Globalizing Leprosy

A Transnational History of Production and

Circulation of Medical Knowledge, 1850s-1930s







Magnus Vollset

























Dissertation for the degree philosophiae doctor (PhD)

at the University of Bergen




2013



Dissertation date: December 13, 2013
 2

© Copyright Magnus Vollset.

The material in this publication is protected by copyright law.























































Year: 2013


Title: Globalizing Leprosy

A Transnational History of Production and Circulation of Medical Knowledge,
1850s-1930s


Author: Magnus Vollset



Print: AIT OSLO AS / University of Bergen

 3



Acknowledgements


This thesis is part of Project History of Science (‘Prosjekt vitenskapshistorie’) and the
research group Health-, welfare and history of science at the Department of
Archeology, History, Cultural Studies and Religion (‘AHKR’) at the University of
Bergen. I would like to thank the University Board and the Faculty of Humanities for
funding this four-year project. I am also grateful for the scholarship from the Meltzer
Foundation, which allowed me research stays at the League of Nations Archives in
Geneva and at the Wellcome Trust Center for the History of Medicine at UCL,
London.
Many people have aided me in this research project, most importantly my
supervisor Astri Andresen. Already when I was a master-student she began to
introduce me to the vibrant scientific community investigating the history of health
and medicine, both locally and internationally. I am grateful for your patience and
guidance, for the many discussions, for allowing me freedom to experiment and
sidetrack, for motivation when I have been overwhelmed and for constructive advice
when I have felt stuck. I might have protested loudly along the way, but in the end
you were usually right.
I would like to offer my gratitude to the members of the project and the
research group, the fierce discussants at the Bjørnson manuscript seminar and the
Nordic Network of Medical History’s PhD-courses. Svein Atle Skålevåg, Morten
Hammerborg, Teemu Ryymin, Tore Grønlie, Sissel Rosland, Ida Blom and Karen
Helle deserve special mention, as well as Iris Borowy for heading my final seminar. I
am grateful to the organizers, opponents and commentators at the various workshops
and conferences where I have presented parts of my research, especially Kathleen
Vongsathorn and Monica Green. I am also grateful for the generous assistance offered
by the staff at the University of Bergen Library, the Wellcome Library in London, the
College of Physicians of Philadelphia’s Historical Medical Library, the State Archives
in Bergen and at the League of Nations Archives in Geneva.
 4

To my colleagues in Bergen, thank you for a good working environment. I
would especially like to mention Gunnar Ellingsen, Runar Jordåen and Dunja
Blazevic. I will always remember the lunches in Øysteinsgate 3 and Dokkeveien 2.
Cecilie Boge, Svein Kåre Sture, Jan Oldervoll, Frode Ulvund, Arne Solli, Anne
Mailin Selland, Sven-Erik Grieg-Smith, Hilde Grønvik, Bjørnar Mortensen Vik, Rune
Hornnes, Per Kristian Sebak, Dag Hundstad, Eirik Hovden, Harald Stokkedal Bokn,
Thomas Slettebø, Evind Urkedal York, Ingrid Birce Muftuoglu, Helen Leslie,
Synnøve Lindtner, Pål Berg Svennungsen and Karine Aasgaard Jansen, thank you.
Thanks also to the members of the editorial board of Historikeren.
I am also grateful for the friends and colleagues I have made around the world,
especially Lauren Cracknell, Bill MacLehose, Tom Quick, Adam Wilkinson, Åsa
Jansson, Chris Millard, Anne Hardy, Sarah Chaney, John Mathew, Jordan Knapp,
Lisa Tassone Knapp, Chantal Marazia, Fabio De Sio, Jenny Adlem and Tony Gould.
Many thanks also to Alison, Francisco, Katrina, Paola, Isabel, Miguel and Anna-
Karin who have made me feel welcome on my trips to Umeå.
Thanks to my friends for patiently enduring my constant anecdotes from the
history of leprosy and having to suffer my unfinished arguments on how the different
elements were connected. Andreas, Henning, Jan, John, Kiel, Idunn, Marie, Eirik, and
Ørjan – you have kept me sane. I am especially thankful to Andreas Berre for
collaborating on a digital tool for mapping the circulation of knowledge.1 Although
this sidetrack did not make the final cut, it helped me clarify my perspectives.Finally,
I would like to thank my family, Dag and Eva for always being available to read my
unfinished manuscripts, and Sara for being my sister and all that that entails.
And, because in Guatemala the most important person is always left for the

very end, I would like to thank Lorena for making a family with me. I love you.





1
Berre, Andreas. lepraMap; Prototyping a Tool for Modeling Historical Sources. MA-thesis. Molde University
College. 2011. Online: http://brage.bibsys.no/hsm/retrieve/1318/master_berre.pdf. My comments on the
collaboration is found in Berre 2011: Appendix 1. The source code for the project is available online:
https://github.com/andreasBerre/lepraMap, and parts of the project was presented in the paper
“Transdisciplinary history of medicine: A ‘Mode 2’-approach” at the conference “The Future of Medical
History” arranged by the Wellcome Centre for the History of Medicine in London in July 2010.
 5


Contents



ACKNOWLEDGEMENTS .............................................................................3


CONTENTS ......................................................................................................5


1. INTRODUCTION ........................................................................................9
THREE DEBATES ...........................................................................................15

OUTLINE AND RESEARCH STRATEGY............................................................27

SOURCES: ‘BACKWARDS’ AND ‘SIDEWAYS’.................................................33

‘THE LEPER’, TERMINOLOGY AND ETHICAL CONSIDERATIONS ....................38

LEPROSY TODAY...........................................................................................40


2. RECOGNIZING ‘THE LEPER’ ..............................................................45
BACKWARDS FROM THE CORPSE ..................................................................47

OF PATHOGENS AND EXPERTISE ...................................................................51

A NOSE FOR THE ULTIMATE PROOF...............................................................57

SHOWCASING THE LIVING BODY ..................................................................66

THE ELUSIVE TEST ........................................................................................70

DIAGNOSTIC PLURALISM AND LOCAL VARIATIONS ......................................74

CONCLUSION ................................................................................................81


3. TREATING LEPROSY: CARE OR CURE?..........................................85
THE TUBERCULIN TRIALS .............................................................................86

SPREADING THE RESULTS .............................................................................91

RUBBING LOTION ON THE SKIN .....................................................................96

SERUM FAILURE AND A NEW BENCHMARK .................................................101

LEPROLIN: TUBERCULIN FOR LEPROSY ......................................................105

NASTIN OVER THE COUNTER ......................................................................111

DID THE TREATMENTS WORK? ...................................................................118
 6

THE BEST CASE SCENARIO .......................................................................... 125

REINVENTING CHAULMOOGRA .................................................................. 129

CONCLUSION .............................................................................................. 142


4. THE QUESTION OF PREVENTION ................................................... 147
QUARANTINE: STOPPING LEPROSY AT THE BORDER .................................. 149

THE RISE OF SEGREGATION: TOWARDS BERLIN 1897 ................................ 158

PUSH, PULL, RESTRICT ................................................................................ 173

A MATTER FOR THE STATE ......................................................................... 183

BURNET’S COMPROMISE ............................................................................ 187

CONCLUSION .............................................................................................. 195


5. APPROPRIATING CONTAGION........................................................ 199
BEFORE LEAVING INDIA ............................................................................. 201

REPORTING HOME; FALLING FROM GRACE ................................................. 204

MEANWHILE, IN NORWAY .......................................................................... 212

CONTAGION AND THE LAW ........................................................................ 224

ENTER THE BACILLUS ................................................................................. 232

PROOF AND HUMAN EXPERIMENTS ............................................................ 245

REMATCH IN THE BRITISH EMPIRE............................................................. 247

CONCLUSION .............................................................................................. 256


6. CONNECTING THE WORLD OF LEPROSY.................................... 259
THE RISE OF INTERNATIONAL CONGRESSES ............................................... 260

THE CONGRESS THAT NEVER WAS.............................................................. 263

ALL TALK AND NO ACTION? ....................................................................... 271

INTERPRETING THE LEPROSY CONFERENCES ............................................. 278

LEPRA BIBLIOTHECA INTERNATIONALIS ................................................... 282

LEPROSY AND CANCER............................................................................... 289

CONCLUSION .............................................................................................. 299
 7

7. INTERWAR GLOBALIZATION ..........................................................301
THE WORLD IS NOT THE SAME ....................................................................303

A CONTESTED LEGACY ...............................................................................310

ORGANIZING AND EDUCATING ...................................................................315

THE LEAGUE GETS INVOLVED ....................................................................321

THE LEAGUE IN LATIN AMERICA ...............................................................328

THE LEAGUE’S LEPROSY COMMISSION ......................................................331

A MATTER FOR TECHNICAL EXPERTS .........................................................335

LEPROSY IN THE FAR EAST ........................................................................340

AN UNPRECEDENTED COMPROMIZE ...........................................................346

THE SYMBOL OF BERGEN ...........................................................................350

CONCLUSION ..............................................................................................354


8. FINAL REMARKS ..................................................................................357
RETHINKING A GENESIS ..............................................................................357

DIAGNOSIS, TREATMENTS AND PREVENTION .............................................360

MAKING KNOWLEDGE MOVE ......................................................................364

WIDER CONTRIBUTIONS .............................................................................367
 8



APPENDIX 1. “THE DISCOVERER OF THE LEPROSY BACILLUS”,
1901................................................................................................................ 371


APPENDIX 2. INTERNATIONAL LEPROSY CONFERENCES,
RESOLUTIONS........................................................................................... 372
A) BERLIN, 1897 ......................................................................................... 372

B) BERGEN, 1909 ........................................................................................ 374

C) STRASBOURG, 1923 ............................................................................... 375


APPENDIX 3. “NORWEGIAN LEPROSY”, 1852 .................................. 377


APPENDIX 4. “THE PRINCIPLES OF THE PROPHYLAXIS OF
LEPROSY”, 1931......................................................................................... 378


LITERATURE ............................................................................................. 381


PRINTED SOURCES.................................................................................. 394


UNPUBLISHED SOURCES ....................................................................... 419


ARCHIVES VISITED ................................................................................. 420


ONLINE RESOURCES .............................................................................. 421
 9



1. Introduction


On August 10th, 1901, a bust of Dr. Gerhard Armauer Hansen was unveiled in the
garden of Bergen Museum, and King Oscar II conferred on Hansen the distinction
Commander of the Cross.2 The initiative came from the Norwegian Medical
Association, and the ceremony was headed by the German professor in dermatology
Oscar Lassar on behalf of the Leprosy Committee established at the First
International Leprosy Conference in Berlin four years earlier. The inscription on the
bust in the town in Western Norway reads “Dr. G. Armauer Hansen, discoverer of the
leprosy bacillus - a gift from physicians of all countries”.3
Today, the bust of Hansen is easily overlooked. But in its time both bust and
distinction were symbols of honor, a celebration of the Norwegian physician’s status
as discoverer of the leprosy bacillus. The event can also be seen as the pinnacle of the
history of leprosy in Norway: National and international recognition of a successful
campaign against the disease. Alarming reports on increasing numbers of leprosy
sufferers in the 1840s had led to the state establishing four new leprosy institutions:
The research hospital Lungegaardshospitalet (Bergen, 1849), Pleiestiftelsen No. 1
(Bergen, 1857), Reknæs Pleiestiftelse (Molde, 1861) and Reitgjerdet (Trondheim,
1861). The institutions were accompanied by a system of continuous local
surveillance of every individual that had the disease, and in 1856 the world’s first
national patient registry was established. In 1877 and 1885 new and increasingly
strict leprosy legislations were put in place. The intervention led the number of cases
to decline from almost three thousand in 1856 to less than six hundred at the turn of
the century. This study, however, goes beyond the Norwegian state borders and will
present a different narrative.







2
Waaler, Erik. “Patolologi og mikrobiologi i Bergen. Det første sentrum for lepraforskning.” Nordisk
Medicinhistorisk Årbok, Supplementum XI. 1985: 43.
3
“Dr. med. G. Armauer Hansen, leprabacillens opdager. Reist af kolleger og venner fra alle lande”. All
translations are by me, unless otherwise stated.
 10

According to Lassars’ speech, “With this initially little appreciated discovery,
he [Hansen] alone put down the foundation for the now ruling view of the disease
that is leprosy.”4 The bacillus is at the core of this thesis, which seeks to answer what
this ‘now ruling view of leprosy’ was in 1901, and how the view changed over time.
Secondly, I investigate how medical knowledge regarding leprosy travelled. How did
the knowledge of the bacillus move from being an entity observed by one person in a
laboratory in Bergen, to being accepted as the defining character of the disease all
over the world?
Medicoscientific knowledge sets the main premises when it comes to leprosy
today; both cure, care and policies. The central role of the bacillus can be illustrated
by the first sentence presenting the disease on the World Health Organization
website: “Leprosy is a chronic infectious disease caused by Mycobacterium leprae, an
acid-fast, rod-shaped bacillus.”5 How was this scientific truth initially created? What
impact did the bacillus have on diagnosis and treatment, and to what extent did the
bacillus set the premises for policies towards those affected by the disease?
This thesis investigates the period between 1847 when leprosy was first
clinically distinguished from other diseases and the first issue of the medical journal
International Journal of Leprosy in 1933. The journal was the outlet of the
International Leprosy Association, established two years earlier. Alongside still
ongoing international leprosy conferences and the active involvement of the League
of Nations (later followed up by the World Health Organization), the organization
and its journal were the last elements in an international framework for the
circulation of knowledge about leprosy that would remain authoritative for more than
seven decades. By 1933 leprosy had become globalized.








4
“Allein er hat mit dieser Anfangs so wenig gewürdigten Wissensthat den Grundstein gelegt für die nunmehr
universal herrschende Auffassung der Aussatz-Krankheit.” Lassar, Oscar. “Gerdhard Arm. Hansen. Foredrag af
O. Lassar”. Medicinsk Revue. 1901: 196.
5
World Health Organization. Leprosy elimination; Leprosy: The disease. http://www.who.int/lep/leprosy/en/.
The presentation also highlights the discoverer: “When M.leprae was discovered by G.A. Hansen in 1873, it
was the first bacterium to be identified as causing disease in man.”
 11

According to the established historiography, the discovery of the bacillus took
place on February 28, 1873.6 The next year, Hansen announced that he had found “in
every leprous tubercle extirpated from a living individual — and I have examined a
great number of them — small staff-like bodies much resembling bacteria, laying
within the cells”.7 His findings were first published in a supplement to a Norwegian
medical journal in 1874 and in a slightly shortened English translation the following
year. The wording was careful: “Though unable to discover any difference between
these bodies and true bacteria, I will not venture to declare them to be actually
identical”.8 It was not until the German physician Albert Neisser published that he
had discovered the bacillus in 1879, and Hansen’s subsequent claims to the discovery
in Norwegian, German, English and French in 1880, that the bacillus received any
real attention. The dispute of precedence was finally settled at the first International
Leprosy Conference in Berlin in 1897, when Hansen was officially recognized and
honored by his peers as the discoverer of the leprosy bacillus, while Neisser was
highlighted as the one who had confirmed the findings. Four years later, the bust was
a material recognition of the achievement.
The event in the garden of Bergen Museum was reported both in national and
international medical journals. According to an editorial in The British Medical
Journal, Hansen’s discovery had led to “that it is now practically admitted by all
those engaged in the study and observation of leprosy, that the disease is
contagious.”9 Although this reflected a majority view, the discussion was far from
over: What was the bacillus actually? What part did it play in the disease and its
causation (etiology)? What consequences should the discovery have in the fight
against leprosy?




6
Irgens, Lorentz. “The Discovery of Mycobacterium Leprae. A medical achievement in the light of evolving
scientific methods.” The American Journal of Dermatopathology. Vol 6, 1984: 337-343.
7
Hansen, G. Armauer. “On the Etiology of Leprosy.” British and Foreign Medico-Chirurgical Review Vol. 55,
1875, as quoted in Irgens 1984: 349. Hansen published the Norwegian original under the title “Indberetning til
det Norske medicinske Selskab i Christiania om en med understøttelse af selskabet foretagen reise for at anstille
undersøgelser angaaende spedalskhedens aarsager, tildels udførte sammen med forstander Hartwig”. Norsk
Magazin for Lægevidenskaben, Vol. 3, ser. 4, no. 9. 1874: 1-88. All quotes are from the English version.
8
Hansen 1875: 489.
 12

In Norway and elsewhere, Hansen has had a prominent role among medical
scientists and is revered with pride.10 ‘Hansen’s disease’ is now the accepted medical
term for the disease. The legacy reflects what the leading German pathologist Rudolf
Virchow stated in a letter read by Lassar in the garden of the museum in 1901:
Hansen’s work “had definitively cleared up a large and difficult field of pathology”,
and his name “is known and celebrated throughout the whole world as a benefactor
of mankind.”11 According to the Norwegian Biographic Encyclopedia, Hansen is “by
far the most famous Norwegian physician of all time.”12 In addition to his own
autobiography, five biographies, two TV documentaries and numerous celebratory
papers have been written about the discoverer.13 However, these have been more
interested in the man behind the discovery than the impact of the ‘discovery’ or how
the knowledge travelled.
Hansen’s discovery is often presented as the second scientific breakthrough in
the medical understanding of leprosy. The first was Daniel Cornelius Danielssen and
Carl Wilhelm Boeck’s publication Om Spedalskhed (On Leprosy, 1847), which






9
Editorial. “The Discoverer of the Leprosy Bacillus”. The British Medical Journal, August 24, 1901: 494. See
Appendix 1.
10
In the final stages of writing this thesis, for instance, the centenary of Hansen’s death in 1912 was celebrated
with a two-day international medical conference. (http: //www.uib.no/matnat/en/seminar/2012/09/armauer-
hansen-100-aars-markering). The University of Bergen has also recently renovated the “Armaer Hansens hus”,
a building named after the discoverer (http: //nyheter.uib.no/?modus=vis_nyhet&id=52515). Outside Norway,
several similar statues of Hansen have been put up to celebrate the discoverer.
11
“Möge Ihr Herz offen bleiben für die Empfindungen der Freunde, dass Ihre Arbeit ein grosses und schweriges
Gebiet definitive geklärt hat, und dass in der ganzen Welt Ihr Name als der eines Wohlthäters der Menschheit
gekannt und gefeiert ist.” Virchow, Rudolf. “Hochgeehrter Freund und College!” Medicinsk Revue. 1901: 198.
Virchow was head of the committee that raised funds for the bust.
12
“Gerhard Armauer Hansen er uten sammenligning den mest berømte norske lege gjennom tidene.” Lærum,
Ole Didrik. “Gerhard Armauer Hansen.” Norsk biografisk leksikon. 2001.
13
The biographies are: Kobro, Isak. Gerhard Henrik Armauer Hansen (1841-1912). 1924; Gade, Fredrik
Georg. G. Armauer Hansen 29 juli 1841-11 februar 1912. 1931; Vogelsang, Th. M. G. H. Armauer Hansen.
1968; Patrix, Johanne-Margrethe. Armauer-Hansen. 1976; Patrix, Johanne-Margrethe. Gerhard Armauer
Hansen: leprabasillens oppdager. 1997. For celebratory papers see: Lie, H. P. “Armauer Hansen,
Leprabasillens oppdager (1841-1912).” Nordisk Medisin. No. 11. 1941; Lærum, Ole Didrik. “Gerhard Henrik
Armauer Hansen (1841-1912).” Det norske Videnskaps-Akademi, Årbok 2001. 2003. The documentaries:
Sandberg, Sverre and Sandberg, Haakon. Armauer Hansen. Svekon Film. 1974; Herland, Ole Geir. “Gerhard
Armauer Hansen – bergenslegen som oppdaget leprabasillen”. Mediakey. 2012. For a studies situating
Hansen’s discovery in a contemporary medico-scientific context, see: Irgens 1984; Irgens, Lorenz. “Hansen,
150 Years After His Birth, the Context of a Medical Discovery”. International Journal of Leprosy. 1992: 466-
469. For a commented overview, see: Vollset, Magnus. Fra Lidelse til Trussel. Spedalskheten i Norge på 1800-
tallet. Masteroppgave, Historisk institutt. University of Bergen 2005: 4-5.
 13


clinically distinguished leprosy from other afflictions of the skin.14 At the unveiling
of the bust in 1901, Lassar highlighted Danielssen and Boeck as the ones who
recognized the anatomical pathology of the disease and thus made leprosy an object
for scientific study.15 The third breakthrough was the first experiments with treating
leprosy using the sulfone drug Promin in Carville, Louisiana (USA), in 1941.16 Since
no other breakthroughs were made, the implicit assumption is that when it came to
medical research, nothing of much interest took place in the intervening seven
decades.
The lack of breakthroughs stands in stark contrast to the medical research that
was actually conducted. Between 1943 and 1948, Índice Bibliográfico de lepra was
published in three volumes by the Library of the Leprosy Prevention Department, São
Paulo, Brazil. The index was 1,935 pages long and contained more than 30,000
entries. The vast majority was research papers on leprosy published in the period
stretching from the 1870s to the Second World War. According to the introduction, it
was written “with the constant purpose of contribution to, and making easier, the
study of leprosy”.17 It was also a way to save time: Prior to this, the library answered
an average of 185,000 consultations by correspondence from all over the world,
annually. The index is a reminder that research into leprosy was conducted in
numerous sites, that medical research is more complex than a handful of




14
Danielssen, D. C. and Boeck, C. W. Om Spedalskhed. 1847; Danielssen, D. C. and Boeck, C. W. Traité de la
Spédalskhed ou Éléphantiasis des Grecs. 1848. In 1856, a translation of Danielssen and Boeck’s monograph
was published in a series of eight articles under the title “On the Nature and Treatment of Leprosy” by Erasmus
Wilson in The Lancet. (Buckingham, Jane. Leprosy in Colonial South India. 2002: 120; Edmond, Rod. Leprosy
and Empire. A Medical and Cultural History. 2006: 46).
15
Lassar 1901: 196. Similar phrases have been repeated by historians such as Sanjiv Kakar, who has stated that
the book “laid the foundation for the scientific study of leprosy.” (Kakar, Sanjiv. “Leprosy in British India,
1860-1940: Colonial Politics and Missionary Medicine.” Medical History. Vol. 40, no. 2. 1996: 217.) Tony
Gould goes further and argyes that the book “brought about a revolution in thinking about leprosy and marks
the beginning of a modern, scientific era in the approach to – and treatment of – this disease.” (Gould, Tony.
Don’t fence me in. From curse to cure: Leprosy in modern times. 2005: 37.)
16
Faget, Q. F. Johansen, J. Dinan, B.Prejan and C. Eccles. “The promin treatment of leprosy”. Public Health
Report. No. 58, 1943: 1729-1741. See also: Lechat, Michel. “La Lèpre après Père Damien”. AMA. No. 65, May-
June 2010. (http: //www.md.ucl.ac.be/ama-ucl/Lepre65.html). Promin is a derivative of dapsone, one of the
three main compounds of the Multidrug therapy (MDT) used today. The others components of the currently
used medication is rifampicin, and clofazimine.
17
Keffer, Luiza (ed.). Índice Bibliográfico de lepra 1500-1943. Biblioteca do Departamento de Profilaxia da
Lepra do Estado de São Paulo – Brasil. Vol. 1. 1944: XIX. According to the introduction: “We have collected
one of the greatest specialized bibliographies in medicine, which at present has more than 100,000 cards.” (IX)
 14

breakthroughs, and that the knowledge was relevant to other geographical locations
than where it was produced. Medico-scientific knowledge went ‘beyond borders’.18
My ambition in this thesis is not to offer a global history of leprosy, but a
history of how the research into leprosy was organized on a global scale. I will argue
that in the beginning of my period, there were a wide range of competing medical
interpretations of ‘leprosy’ and disagreements on what observations medical
knowledge should be based on. By the early 1930s, the chronological end-point of
my discussion, the leprosy bacillus was accepted as the cause of the disease all over
the world. For this to be possible, the circulation of medical knowledge regarding the
disease had to be organized on a global scale. This is indeed what happened.
The thesis offers an alternative to what James Secord and several others have
termed science historians’ “obsession with novelty and the places in which novelty
begins”.19 Instead of focusing narrowly on Hansen’s discovery, I will follow Secord’s
suggestion of seeing science as a form of communication, a collective activity taking
place in various locations – an activity that needed to be organized. For the bacillus to
have an impact, people needed to be convinced that it existed and that its existence
was relevant. As the title of the thesis suggests, the production and circulation of
knowledge will take center stage. The aim is to explain how this extremely successful
medical community established an international infrastructure for the circulation of
knowledge. I will argue that an important consequence of the bacillus was that it
provided a shared point of reference to a range of research efforts taking place in
various sites around the world. In this perspective, how the bacillus was enacted in
debates and its role as an impetus for collaboration becomes more interesting than its
genesis.












18
I have borrowed the term ‘beyond borders’ from Simon, Josep and Néstor Herran (eds). Beyond Borders.
Fresh Perspectives in History of Science. 2008.
19
Secord, James A. “Knowledge in Transit”. Isis. 2004: 654-672, quote on p. 662.
 15

Three debates


This thesis is informed by, and seeks to add to, three distinct research fields and
traditions: The first is debates on whether bacteriology constituted a radical break
with previous understandings of disease; the second is debates within the history of
science regarding transnationalism, localism and the place of scientific practice; the
third is the growing body of research on the history of leprosy.
Gerhard Armauer Hansen’s discovery of the leprosy bacillus has been
presented as an “epoch-making achievement”, marking a break with previous
knowledge of the disease.20 This interpretation balances between history of medical
science as an accumulation of new and increasingly accurate knowledge on the one
hand, and as radical shifts where bacteriology constituted a revolution on the other.
To what extent there really was such a revolution has been a source of debate among
historians. Based on studying medical customs in Britain between 1870 and 1910,
Michael Worboys found that bacteriology did not lead to changes in medical
practices, and he has therefore argued that there was no “bacteriological revolution”.21
Andrew Cunningham, to the contrary, has argued in a study of the plague that
bacteriology meant the introduction of single causes of diseases, that it heralded an
epistemological transformation which lasted until the 1930s, and that the shift was so
radical that we today can hardly imagine a world without diseases having a specific
cause: “The identities of pre-1894 and post-1894 plague have become
incommensurable. We are simply unable to say whether they were the same, since the
criteria of ‘sameness’ have been changed”.22 There have also been studies that bypass
the discussion of bacteriology as a revolution, and instead add nuances through





20
Irgens 1984: 337.
21
Worboys, Michael. “Was there a Bacteriological Revolution in late nineteenth-century medicine?” Studies in
History and Philosophy of Science. Part C: Studies in History and Philosophy of Biological and Biomedical
Sciences. Vol. 38, issue 1. 2007: 20-42. Elsewhere, Worboys has demonstrated that ‘germs’ was a flexible
concept with multiple meanings, and that there was not a single bacteriological model. See: Worboys, Michael.
Spreading Germs. Disease theories and medical practice in Britain, 1865-1900. 2000.
22
Cunningham, Andrew. “Transforming plague. The laboratory and the identity of infectious disease”. In:
Cunningham, Andrew and Perry Williams. The laboratory revolution in medicine. [1992] 2002: 209-244; quote
on p. 242.
 16

detailing the scientific work actually conducted in the bacteriological laboratory, such
as Christoph Gradmann’s Laboratory Disease (2009), which discusses the history of
medical bacteriology though the biography of Robert Koch.23
The question of a bacteriological revolution is part of a larger debate on the
nature of scientific progress and the question of disruption versus continuity. In the
seminal paper “The disappearance of the sick-man from medical cosmology, 1770-
1870” (1976) Nicholas Jewson argued that medicine in the laboratory represents a
transformation which “precipitated a total reconstruction of the epistemological
foundations of medicine as a field of knowledge.”24 The introduction of laboratory
medicine in the 1870s was the third such transformation, preceded by bedside
medicine and hospital medicine. These shifts were not just theoretical. Rather, the
modes of production of medical knowledge led to changes in social relations between
physicians and in their relations to the individuals affected by disease: Instead of
relating to patients directly, only samples made their way into the laboratories. Status
from medical peers became more important than meeting the expectations of the
persons suffering from disease.

Later commentaries have pointed out that Jewson’s analysis was strongly
influenced by Thomas Kuhn’s The Structure of Scientific Revolutions (1962), and his
model of science as ‘puzzle-solving’ working within successive and
25
‘incommensurable’ paradigms. Kuhn in turn drew on Ludwig Fleck’s Genesis and
Development of a Scientific Fact ([1935] 1979), which presents science as a collective
endeavour which not just accumulates new pieces of information, but also overthrows
old ‘thought-styles’.26




23
Gradmann, Christoph. Laboratory Disease. Robert Koch’s Medical Bacteriology. 2009.
24
Jewson, N. D. “The disappearance of the sick-man from medical cosmology, 1770-1870”. Sociology. Vol. 10.
1976: 225-244, quote on p. 237. Jewson defines ‘Medical Cosmology’ as “conceptual structures which
constitute the frame of reference within which all questions are posted and all answers are offered.” (Op. cit.:
225.)
25
Armstrong, David. “Indeterminate sick-men—a commentary on Jewson’s ‘Disappearance of the sick-man
from medical cosmology’.” International Journal of Epidemiology. No. 3. 2009: 642–645. See also: Nicolson,
Malcom. “Nicholas Jewson and the disappearance of the sick man from medical cosmology, 1770–1870”.
International Journal of Epidemiology. No. 3. 2009: 639-642.
26
Fleck, Ludwig. Genesis and Development of a Scientific Fact. [1935] 1979. Kuhn wrote the foreword to the
first English translation of Fleck’s Genesis and Development in 1979, edited by T. K. Trenn and R. K. Merton.
 17

Despite endorsing Kuhn and Fleck’s argument that science must be understood
as a social and collective endeavor, the model of succeeding and incommensurable
paradigms (or thought-styles) seems inadequate when it comes to the history of
medicine. Novelties does not mean that old knowledge is suddenly no longer relevant:
Bacteriology did not mean an end to clinical diagnosis, that the physicians stopped
compiling medical statistics, or that that measuring the vitals of a patient had become
obsolete.
To me, John V. Pickstone’s framework from Ways of Knowing (2001) is more
compelling.27 Pickstone presents five ‘ways of knowing’, the first three of which
correspond relatively well to Jewson’s three step model: Natural history (description
and classification), analysis (uncovering elements), experimentation (controlling
phenomena), technoscience (creating novelties), and world readings
(hermeneutics/interpretation).28 Pickstone agrees with Jewson in that new ways of
knowing were developed at specific points in time and were entangled with new ways
of working. To describe and classify kinds to create ‘natural history’ demands a
different set of activities than to learn about phenomena through experimentation. But
instead of replacing the old, the new ways of knowing add to the repertoire of
possible ways of knowing. They must be understood “like elements in modern
chemistry and not as taxonomic boxes into which instances of STM [Science,
Technology and Medicine] are to be placed, or forced.”29 Different ways of knowing
and working make up ‘compounds’ that are given different emphasis in different
contexts and at different points in time.30






27
Pickstone, John V. “Ways of Knowing: Towards a Historical Sociology of Science, Technology and
Medicine.” The British Journal for the History of Science, Vol. 26, No. 4. 1993: 433-458; Pickstone, John V.
Ways of Knowing. A New History of Science, Technology and Medicine. 2001; Pickstone, John V. “A Brief
introduction to ways of knowing and ways of working”. History of Science. 2011: 235-245.
28
Another important distinction between Pickstone and Jewson is that while the latter’s argument concerns the
history of medicine, the explicit ambition of Pickstone’s ‘ways of knowing’ is to transcend disciplines. The
analytical categories are equally relevant to all fields of knowledge, Pickstone argues. For Pickstone’s
comments on Jewson, see: Pickstone, John V. “From history of medicine to a general history of ‘working
knowledges’”. International Journal of Epidemiology. 2009: 646-649.
29
Pickstone 2011: 235.
30
Lorraine Daston and Peter Galison have presented a similar line of reasoning in their study of the changing
meanings of ‘objectivity’ in scientific atlases from the eighteenth to the twenty-first century: “Epistemic virtues
 18

Pickstone’s repeated emphasis that ways of knowing are intertwined with ways
of working is a reflection of another long-standing criticism of Kuhn’s perspective on
science, namely that by only examining the arguments scientists make, the practical
implications of science are downplayed. Arguments and dominant positions are
important, but they are not the only aspects of science. In the late 1970s the
Edinburgh-school argued that this perspective in effect placed science in a realm
outside society: Only when the historical actors made a mistake ‘outside forces’ were
brought in to explain the mistake. If the argument was correct, given today’s
standards, there was no need for further investigation.31 To the contrary, the sociology

of knowledge has convincingly shown that all knowledge – not just what in hindsight
turned out to be false – is influenced by social and cultural factors.
The solution suggested by the Edinburgh-school’s “Strong Programme” was a
doctrine of causality, impartiality, symmetry and reflexivity.32 The goal was to create
a methodological antidote to teleology (a predefined history where science is nothing
but a linear progression of clearing up mistakes unavoidably leading to what we today
hold to be true) that would avoid relativism (that any statement about the world is
subjective and thus equally valid). In practice, the programme has meant that the
standards for investigating the actors who in hindsight were ‘correct’ and those who
turned out to be were ‘wrong’ must be the same. Second, science cannot be explained
without investigating the social and cultural context in which the production of
knowledge took place. Especially the latter argument has been hugely influential for

later historical investigations.






do not replace one another like a succession of kings. Rather, they accumulate into a repertoire of possible ways
of knowing.” Daston, Lorraine and Peter Galison. Objectivity. 2007: 111-113.
31
“When a thinker does what is rational to do, we need enquire no further into the causes of his action;
whereas, when he does what is in fact irrational – even if he believes it to be rational – we require some further
explanation.” Laudan, Larry. Progress and Its Problems: Towards a Theory of Scientific Growth. 1977: 188-
189. In: Enebakk, Vidar. Vitenskapsstudier. Historie, teori, kritikk. 2008: 99. In my opinion an equally valid
criticism of this perspective is that through dismissing the blind alleys, the science that ‘failed’, the narratives
end up framing the history of science as one of inevitable and streamlined progress, simply because of the a
priori choice of dismissing everything that does not fit this picture. This might lead to unrealistic expectations
to science.
32
Bloor 1991: 7. The study most commonly highlighted as exemplary within this tradition is: Shapin, Steven
and Simon Schaffer. Leviathan and the Air-Pump. 1985.
 19

The vast majority of historical studies into the history of science and medicine
have defined ‘social and cultural context’ geographically, and consequently
investigated science as an intrinsically local activity. According to Peter Galison “The
turn toward local explanation in the historical, sociological, and philosophical
understanding of science may well be the single most important change in the last
thirty years.”33 This has provided unprecedented insights into how the relation
between knowledge and practice is expressed, and compared to Kuhn’s emphasis on
arguments it has definitively helped bring science down to earth. Even so, the
perspective is not unproblematic.
A major drawback of the turn to local explanations is that it creates an
artificial boundary between the geographically defined ‘inside’ to be studied through
archival sources, and the ‘outside’ which either influences or is influenced by events
taking place elsewhere. This leads to looking for explanations primarily in previous
or concurrent events taking place in the same geographically predefined area, and
makes it difficult to explain similarities in how issues were addressed in widely
different contexts at more or less the same time.34 In the entry on ‘Medicine’ in The

Palgrave Dictionary of Transnational History (2009), Sanjoy Bhattacharya pointed
out that the construction of medical knowledge took place in several sites: Ideas were
developed in one region, tested in another and often implemented elsewhere.
“Medical ideas constantly flowed in all directions.”35 I wish to fill this catchphrase
with content. The first step is finding good questions to ask.
The Finnish historian and philosopher Jouni-Matti Kuukkanen has asked: If
science is inherently local, how can we explain that its knowledge is universally
applicable? He phrases the challenge as follows: “The problem of the globality of
science challenges localism to offer an account of the mechanism through which






33
Galison, Peter. “Ten Problems in History and Philosophy of Science”. Isis. Vol. 99, No. 1. 2008: 111-124,
quote on p. 119.
34
For examples of this, see for instance Vollset 2005 or Leung, Angela Ki Che. Leprosy in China, a history.
2009.
35
Bhattacharya, Sanjoy. “Medicine”. In: Iriye, Akira and Pierre-Yves Saunier (eds). The Palgrave Dictionary
of Transnational History: From the mid-19th century to the present day. 2009: 708.
 20

science can move from one locality to another.”36 Likewise, James Secord has argued
that instead of looking for the genesis of new knowledge, more fruitful research
questions are: “How and why does knowledge circulate? How does it cease to be the
exclusive property of a single individual or group and become part of the taken-for-
granted understanding of much wider groups of people?”37 The thesis is an attempt at
addressing these questions.
These are not new concerns. Already in the early 1930s, Ludwig Fleck
challenged the assumption that it is possible to pinpoint scientific breakthroughs to a
place and a discoverer. In his study of the relation between syphilis and the
Wasserman test, Fleck pointed out:

Very often it is impossible to find any originator for an idea generated during discussion and
critique. Its meaning changes repeatedly; it is adapted and becomes common property.
Accordingly, it achieves a superindividual value, and becomes an axiom, a guideline for
thinking.38


Although Fleck underestimated the importance of physicians allocating individual

honors, for instance through putting up busts or giving diseases or methods the name
of their originators (a narrative he explicitly opposed), his description is valid also
when it comes to medical knowledge about leprosy. Fleck’s solution was to highlight
the individual actors and their arguments, both proponents and opponents stepping
forward to address the community of researchers. Over time these negotiations led to





36
Kuukkanen, Jouni-Matti. “I am knowledge. Get me out of here! On localism and the universality of science”.
Studies in History and Philosophy of Science. Vol. 42. 2011: 590-601, quote on p. 594. Kuukkanen argues that
“strong localism is both historiographically and philosophically untenable”, but suggest a more pragmatic
localism with emphasis on extra-local inferences through studies of circulation and practices of delocalization.
See also: Kuukkanen, Jouni-Matti. “Senses of localism”. History of Science. Vol. 50, No. 4. 2012: 477-500;
Livingstone, David N. Putting Science in its place. Geographies of Scientific Knowledge. 2003: 140-141.
37
Secord 2004, 94: 655. Secord has argued this point since he took initiative to the ‘Big Picture’-debate in
1991, which addressed disciplinary fragmentation within history, and resulted in a special issue in The British
Journal for the History of Science, Vol. 26, No. 4, 1993. See also the The British Journal for the History of
Science’s special issue “Transnational History of Science” (Vol. 45, No. 3. 2012: 319-442). One of the
recommendations in the introduction, is to conduct studies that can explain how locally produced knowledge
becomes globally accepted. (Turchetti, Simone, Néstor Herran and Sorya Boudia. “Introduction: have we ever
been ‘transnational’? Towards a history of science across and beyond borders”. The British Journal for the
History of Science. Vol. 45, No. 3. 2012: 331.)
38
Fleck 1979: 121.
 21

the establishment of a common style of thought (‘Denkstil’) shared by a thought
collective (‘Denkkollektiv’), defined as a community of individuals maintaining
interactions and mutually exchanging ideas.
While I will not adapt the terminology of thought collectives and thought
styles, I will in this thesis place the historical actors in the foreground; both those
who ‘stepped forward to address the community’ and those who were involved in
establishing and maintaining arenas for exchanges of ideas. My focus will be on the
circulation of knowledge, understood as the communication aimed primarily at
medical peers in other locations. This communication, I argue, is the backbone of any
international scientific community.
In the first three chapters, my emphasis is on the content of this
communication: What circulated, and what arguments were made? The last three
chapters will focus on how knowledge circulated, and how this was organized.
Although the cast is larger than in the typical local study, I will show that leprosy was
made into a global disease by a relatively small group of individuals.39
Despite increasing interest in the problem that local studies do not necessarily
add up to today’s science as a global enterprise, there are so far surprisingly few
studies which try to tackle this problem in depth. In my opinion, the most promising
attempt at bridging this gap between the local and the global is the framework
presented by geographer David N. Livingstone in Putting Science in its Place (2003).
His starting point is that “Scientific rationality cannot be conceived of independently
of temporal and spatial location.”40 His suggestion is therefore to put the site of
knowledge production in the center: The ‘venues of science’. Second, the context
should be studied: The ‘cultures of science’. The third part of Livingstone’s model is
circulation, the movements of scientific knowledge. This is what connects the sites
into networks with multiple (and sometimes competing) centers.




39
Biographical studies have also been of much help, such as: Power, Helen Joy. Sir Leonard Rogers Frs.
(1868-1962): Tropical Medicine in the Indian Medical Service. PhD Thesis, University College London. 1993;
Gould 2005. The first is a biography of Sir Leonard Rogers, the latter presents the history of leprosy through a
collective biography of lives that in different ways were shaped by the disease. I have also found obituaries
useful, especially for information about the education and places of work of these historical actors.
 22

I see the circulation of knowledge as a practice in its own right, a practice that
needs to be organized. While chapter 5 will examine how circulation does not abolish
local differences, the last two chapters will detail how the frameworks for circulation
of knowledge related to leprosy was established, which traditions these were built on
and what characterized the practice of circulation. My argument is that the circulation
of knowledge is what made the medical knowledge about leprosy authoritative: It
gave each individual actor access to far more knowledge than had the actor worked in
isolation. The international research community is where truths about leprosy are
constructed, and therefore deserves to be studied in its own right. This, I believe, also
applies to other scientific activities.
In order to explain the local impacts of the circulation of knowledge, I rely
heavily on the term ‘appropriation’. This concept was used by the STEP-network
(Science in The European Periphery) in the 1990s to challenge a framework which
saw scientific communication as characterized by active transmission from a
scientific ‘center’ and passive reception in the ‘periphery’. The center/periphery-
model measured the success of the communication by how fully the center was being
reproduced in the periphery. The term ‘appropriation’ instead signifies that
communication is an active process on all parts, that the outcome is new knowledge
(not reproductions), and that all actors involved in the circulation of knowledge must
be given equal epistemological status.41 As I will show in this thesis, this leads to a

de-centered model of science: The perceptions of what constituted ‘centers’ differed,
and appropriation helps explain how local differences were maintained. At the same
time, through investigating the discussions in taking place in the circulation of
knowledge, it is possible to show how the dominant positions were established and
changed over time.
What was known about leprosy at various times and in different places is not

just a matter of theoretical interest. Especially the knowledge regarding etiology gave




40
Livingstone 2003: 184.
 23

rise to tangible practices with immense consequences on how those affected by the
disease could live their lives. With the exception of studies of scientific
breakthroughs, it is the social aspects of the disease that have been the main concern
in studies of the history of leprosy so far. The attention to detail and nuance has
differed. Michel Foucault, for instance, argued in the first chapter of Madness and
Civilization (1961) that society’s reaction to leprosy must be understood as an
expression of confinement and social control. In the 1300s, “Leprosy disappeared, the
leper vanished, or almost, from memory; these structures remained. (…) Poor
vagabonds, criminals, and ‘deranged minds’ would take the part played by the
leper.”42 Along similar lines, anthropologist Mary Douglas has proposed that leprosy

became a symbol of impurity and that the consequent segregation of leprosy was “part
of the successful attempt to create order that resulted in the highly structured society
of the thirteenth century.”43 These studies use leprosy as a stepping stone to give
insights into fundamental power-relations in society. Further studies into the history
of leprosy, however, have shown that taking for granted that leprosy was a cause of
universal and timeless anxiety is problematic.
Since its publication in 1989, the study Leprosy, Racism and Public Health:
Social Policy in Chronic Disease Control by Zachary Gussow has become a shared
reference point for later investigations into the history of the disease. Gussow’s
project was to challenge the notions of a timeless and universal stigma connected to
leprosy dating back to Biblical times. Through comparing the approaches to leprosy
in mainland United States with Hawaii, Norway, Britain, India and China, Gussow
argued that the social construction of leprosy depended on, and changed with,







41
Guillem-Llobat, Ximo. “Science in the Periphery”. In: Simon and Herran (eds) 2008: 291-299. The STEP-
network emphasizes comparative methods, but with the exception of Chapter 5 which compares leprosy policies
in Norway and British India, this has not been part of my appropriation.
42
Foucault, Michel. Madness and Civilization. 2007: 5. (Folie et déraison: Histoire de la folie à l’âge
classique [1961]).
43
Douglas, Mary. “Witchcraft and Leprosy: Two Strategies of Exclusion”. Man, New Series, Vol. 25, No. 4).
1991: 732. The suggestion that “The initial recognition of anomaly leads to anxiety and from there to
suppression or avoidance” was first put forward in: Douglas, Mary. Purity and danger: an analysis of concept
of pollution and taboo. (1966) 2006: 4.
 24

political forces and social concerns.44 The disease, Gussow argued, was ‘retainted’ in
the late 19th century, and its social practices entangled in imperialism and racism.
Leprosy became a symbolic and tangible threat from the colonies, a medieval disease
that if left unchecked would contaminate the ‘civilized world’. He also emphasized
missionaries connecting the disease with Biblical leprosy, sensationalizing the disease
to raise funds and to present their work as heroic and self-sacrificing. Together, this
gave leprosy the character of a metaphor, a phenomena that needed to be kept apart
from the rest of society. Although irrational fear on behalf of society more often than
not took place at the expense of the individuals who had the disease, the responses
changed over time and varied from country to country.45
A drawback of Gussow’s study is that his historical arguments about
conditions outside the United States relied on a relatively narrow source material. His
presentation of Norwegian leprosy policies as humane and scientific under the title
“The Enlightened Kingdom”, for instance, ignores the physicians’ use of coercion,
the context in which the reports he uses as sources were written, and the fact that
domestically the Norwegian policies and institutions were politically contested and
increasingly unpopular.46 In this thesis I will not go into the missionary activities and
their circulation of knowledge and therefore I cannot comment on their role in
spreading prejudices against those affected by the disease. Still, Gussow’s claim that
secular medico-scientific research disenchanted the negative stereotypes connected to
leprosy was not necessarily the case, at least not in the period I am studying. Rather,
as I will show in this thesis, Hansen, whose status as a discoverer made him an




44
For more on social constructivism, see: Jordanova, Ludmilla. “The Social Construction of Medical
Knowledge.” Social History of Medicine. Vol. 8, No. 3. 1995: 361-381; Hacking, Ian. The social construction
of what? 1999.
45
Gussow 1989. Despite acknowledging that the social responses to the disease has changed with temporal and
geographical location, Gussow and most other studies in the history of leprosy take for granted that the disease
today identified by the leprosy bacillus is unchanging throughout history, and judge the merits of previous
studies by how well they fit the criteria today accepted to be true. For a discussion, see: Wilson, A. “On the
history of disease-concepts: The case of pleurisy”. History of Science. Vol. 38.,2000: 271-319. I will return to
this in Chapter 2.
46
Andresen, Astri. “‘Patients for life’: Pleiestiftelsen leprosy hospital 1850-1920s”. Andresen, Astri, Tore
Grønlie and Svein Atle Skålevåg (eds). Hospitals, patients and Medicine 1800-2000. Conference Proceedings.
Bergen. 2004: 93-116; Pandya, Shubhada. “The first international leprosy conference, Berlin, 1897: the politics
 25

international authority, was a vocal advocate for educating the population that lepers
were to be feared and shunned, first in Norway and then on an international level.
Gussow’s project has been seen by scholars as an open invitation for studies
adding content and nuances to the overall narrative of local differences, changes over
time, and that leprosy is more than ‘just’ a medico-scientific object. The result has
been a rich historiography, including country-specific studies, the studies of
institutions and studies of the experiences of those affected by the disease and
society’s response to it. The main finding is that the approaches to leprosy were
indeed not universal, but unique on a local scale.47 Inspired by social history, these

studies offer an explicit or implicit critique of a depiction of the history of medicine
“as ‘conquest’ of disease by great men and great ideas, independent of social and
political contexts.”48
The works of Jane Buckingham and Shubhada Pandya are prime examples of
the local studies that have been important for this thesis. Buckingham has
investigated the dynamics of colonial power in 19th century South India, especially
the relationship between indigenous and colonial medical and legal systems, and their
impacts on those suffering from leprosy. Her book is exemplary when it comes to






of segregation”. História, Ciências, Saúde – Manguinhos. Vol. 10 (supplement 1). 2003: 161-177; Vollset
2005.
47
For prominent examples of studies of leprosy and social control, see: Edmond 2006; Leung 2009; Moran,
Michelle T. Colonizing Leprosy. Imperialism and the Politics of Public Health in the United States. 2007;
Buckingham 2002; Robertson, Jo. In a State of Corruption: Loathsome Disease and the Body Politic. PhD
Thesis, University of Queensland. 1997; Vollset 2005. For studies emphasizing missionaries and colonialism,
see: Kipp, Rita Smith. “The Evangelical Uses of Leprosy”. Social Science & Medicine. 1994; Vaughan, Megan.
“Without the Camp: Institutions and Identities in the Colonial History of Leprosy”. Curing Their Ills: Colonial
Power and African Illness. 1991; Warwick Anderson, “Leprosy and Citizenship”. Positions, Vol. 6, 1998;
Manton, John. “Leprosy in Eastern Nigeria and the social history of colonial skin”. Leprosy Review. Vol. 82.
2011: 124-134; Kakar 1996: 215-230; Worboys, Michael. “The Colonial World as Mission and Mandate:
leprosy and Empire. 1900-1940”. Osiris. 2001: 207-218; Marks, Shula. “What is Colonial about Colonial
Medicine? And What has Happened to Imperialism and Health?” Social History of Medicine. Vol 10, no. 2.
1997. For studies investigating leprosy institutions, see i.e. Andresen 2004; Robertson, Jo. “The Leprosy
Asylum in India: 1886-1947”. Journal of the History of Medicine and Allied Sciences, Vol. 64, No. 4. 2009.
For studies emphasizing the experiences of those who were institutionalized, see: Seng, Loh Kah. Making and
Unmaking the Asylum. Leprosy and Modernity in Singapore and Malaysia. 2009; McMenamin, Dorothy.
“Recording the experiences of leprosy sufferers in Suva, Fiji”. Oral History in New Zealand, Vol. 17, 2005. See
also: ILA’s “The Oral History Project”, which is part of ILA Global Project on the History of Leprosy:
http://www.idealeprosydignity.org/OralHistoryWeb/OralHistory-Main.html
48
Pandya, Shubhada S. Leprosy in the Bombay Presidency, 1840-1897: Perceptions and approaches to its
control. Phd Thesis, Mumbai. 2001: 4.
 26

demonstrating the importance of local negotiations in specific contexts.49 Likewise,
Pandya has in her PhD-thesis highlighted the limits of colonial power in Bombay
Presidency in India. Between 1840 and 1897, also Judeo-Christian and Hindu
interpretations of the disease played part in shaping the medical, sociopolitical and
administrative responses to the ‘leper problem’.50 While my prime interest in this
study is scientific medical knowledge, this was not the only knowledge in existence.
And not only did the local conditions differ from place to place; so did what
constituted relevant knowledge.
My contribution to the existing literature in the history of leprosy is primarily
the investigation of the transnational circulation of knowledge. How did the dominant
extralocal positions change over time, how were frameworks for the circulation of
knowledge established and maintained, and what were the mechanisms involved in
how knowledge from elsewhere was appropriated (or dismissed)? While a local study
would not be able to answer these questions, the circulation of knowledge both
originated and played back into the local. Even the actors who were in the vanguard
of organizing the circulation of knowledge spent most of their efforts in local
settings. In this thesis I rely heavily on previous research to grasp these local
contexts. It would not have been possible for a single historian to investigate all the
different contexts, and without these localized studies, my transnational project
would not have been attainable. This thesis is not a critique of local studies, but an
addition.
Two more works within the history of leprosy deserve special mention for
charting the course for my study of the circulation of knowledge regarding leprosy:
Leprosy and Empire (2006) by Rod Edmond, and the paper “The first international
leprosy conference, Berlin, 1897: the politics of segregation” by Shubhada Pandya.51
Edmond’s study of leprosy in the British Empire relied on scientific and literary


works published in Britain and the British Empire from the 1770s to the early 20th





49
Buckingham 2002.
50
Pandya 2001.
51
Edmond 2006; Pandya 2003.
 27

century. Inspired by Gussow, the goal of Edmond’s study was to give historical
nuances to how leprosy has been represented in colonial contexts, and “understand
better the varying historical conditions in which it [stigma] has been produced.”52 My
interest is not in stigma but Edmond’s chapters on medical research. These
convincingly show how events in one part of the British Empire, such as developing
or testing new treatments, could have consequences elsewhere. Edmond has also
shown how actors in the colonies took independent initiatives, and despite opposition
from the establishment in London, the center/periphery-model is clearly inadequate.
My thesis is an expansion of Edmond’s perspectives. Pandya’s paper on the first
international leprosy conference in Berlin in 1897 details the competing schemes
aimed at bringing individual actors from various backgrounds together to discuss and
establish the first international recommendations on leprosy.53 This paper is the
starting point for my investigation of how the circulation of knowledge about leprosy
was organized internationally (Chapter 6). Furthermore, Pandya’s perspective was
instrumental in my decision to tell the story focusing on the individual actors involved
in setting up the structures for transnational circulation of knowledge, and to not
overlook the attempts that in hindsight can be portrayed as ‘failed’. As Fleck was the
first to point out, and Pandya’s paper demonstrates: Science is the outcome of debate
and opposition, not the labor of individuals working in isolation.





Outline and research strategy


This thesis is divided into two main parts, each with three chapters. The first part
(Chapter 2-4) investigates the content of the knowledge that was circulated, and what
implications the leprosy bacillus had on three traditional themes in the history of
medicine: Diagnosis, treatment and prevention. Each chapter follows the discussion
from the 1850s to the 1930s.





52
Edmond 2006: 7
53
Pandya 2003.
 28

The second part (Chapter 5-7) problematizes the underlying assumption that
science was a coherent and global conversation throughout the period, and
investigates the frameworks that made the circulation of medical knowledge about
leprosy possible. In each chapter I discuss the specific mechanisms involved in the
circulation of knowledge: The practice of appropriation, the role of conferences and
medical journals, and the tradition of travelling and establishing organizations.
Furthermore, these last three chapters each emphasize specific periods of time: 1850-
1895, 1895-1915 and 1920-1933. Focusing on shorter time periods allows me go
more in depth on the personal relationships between the actors involved. While I have
put emphasis on what I believe to be the predominant traits of each period, the
mechanisms are relevant also across the periodization: Appropriation did not come to
an abrupt end in the 1890s, nor did physicians start travelling only in the 1920s.




FIGURE 1: Structure of the thesis.






Diagnosis, the practice of recognizing disease, is the topic for Chapter 2:
Recognizing ‘the leper’. The chapter opens with Gerhard Armauer Hansen at the
first international leprosy conference in Berlin in 1897 insisting that the dominant
clinically based diagnostics (‘if you look like you have leprosy, you are a leper’), was
 29

wrong. If it was impossible to demonstrate the presence of the bacillus, the patient
was not suffering from leprosy, Hansen argued. In the chapter I will discuss the
dominant approaches to diagnosis and training, the ambition of developing
mechanically objective tests that did not rely on specialist training, and what impact
the bacillus had on the debates. Finally, the chapter will show how the leprosy
bacillus came to play different roles in diagnostics in different parts of the world.
Most importantly, at least from the perspective of those who had the disease, the
bacillus made it possible to look like a ‘leper’ and be paroled as ‘arrested’.
Next, what did medicine have to offer those suffering from the disease? In
Chapter 3: To care or to cure I will discusses treatment of leprosy and the various
attempts at developing a cure. The chapter opens with a clinical trial of tuberculin
taking place in Bergen – with disastrous results. After investigating how the news of
the trial circulated and was put in context with similar experiments elsewhere, I
examine the drugs and treatment regimes that dominated the medical debates. What
impact did the leprosy bacillus have on medical research into treatments? To what
extent did the discussions on treatments reflect local practices? Finally, I will show
how the ancient Indian medicine ‘chaulmoogra’ was reinvented from an ailment to a
possible cure. From the 1920s, chaulmoogra became the center of a global
controversy which split the leprologists into two opposing camps. The dominant
position was still that the disease was incurable and should be met with segregation.
The challenger saw leprosy as curable, thanks to chaulmoogra, and argued for
voluntary treatments and that the era of wholesale segregation must come to an end.
Until the first decade of the 20th century, the physicians generally considered
leprosy to be incurable, and with devastating consequences both for the individual and
society at large. Leprosy was a threat, a problem that needed to be eliminated. But
how was this to be achieved? This is the topic for Chapter 4: The question of
prevention. The chapter opens with a widely publicized letter from an American
visitor to Bergen in 1852, warning that Norwegian migrants were invading America
with a ‘Biblical disease’. After a discussion on quarantine, I will identify the three
main strategies for prevention that dominated the medical debates. In the chapter I
 30

will show how the bacillus increasingly was entangled with the already existing
argument that the disease was contagious, and how the debates on prevention were
primed at finding efficient ways to keep the ‘lepers’ away from the healthy. Norway
was not the only country to launch a campaign against the disease, but came to have a
special position as the only country where the intervention had been successful: The
number of ‘lepers’ was declining. Still, the interpretations of the cause of this success
differed. In the 1920s, both those who argued for continued segregation and those
arguing for voluntary treatment pointed to Norway as a case in point.
Norway and colonial India came to represent two extremes when it came to
leprosy policies. The first chapter in the second part investigates the roots of this
divide, namely how the view that leprosy was contagious was introduced to the
debates in the decades leading up to the international leprosy conferences. Chapter 5:
Appropriating contagion opens with a British physician working in India visiting
Bergen in 1873, asking whether the leprosy he saw in Norway was the same disease
as leprosy in India. This was a necessary but not self-evident premise for knowledge
from other places of the world being locally relevant. The account from the visit was
the first time the observation of a bacillus was mentioned in print, but the impact of
the discovery differed greatly. Focusing on the years surrounding the discovery of the
leprosy bacillus, what were the similarities, contacts and differences between the
leprosy debates in Norway and colonial India? I will show that the period between the
1850s and the 1890s was characterized by competing, contradictory and coexisting
medical models of leprosy. Personal experiences outweighed observations made by
others, appropriation was selective, and not everything that went on in a local setting
was reported elsewhere.
The next chapter investigates the conscious attempts at organizing the
circulation of knowledge, particularly the international leprosy conferences and the
specialized medical journal Lepra Bibliotheca Internationalis (1900-1914). Chapter
6: Connecting the world of leprosy opens with an announcement by an American
physician that an international leprosy congress was scheduled to be held in Bergen in
1897. The goal of the conference was to establish a supra-national committee of
 31

experts tasked with dictating a global leprosy campaign. The American’s scheme
never succeeded, but it shows how gathering leprologists from all ‘civilized countries’
was on top of the agenda at the end of the 19th century. A common trait for those
involved in connecting the world of leprosy was that they all accepted the leprosy
bacillus as the cause of the disease, and believed leprosy to be contagious. In the
chapter I will also discuss the role of conferences and medical journals in general,
before finally showing how the practice of circulation in itself could result in the
production of new knowledge.
After the Great War the shared medical journal was discontinued, and several
of the most prominent actors had died. How leprosy ended up as an issue for the
League of Nations, their activities, and the various initiatives that came together to
form the Manila meeting in 1931 when the International Leprosy Association was
founded is the topic of Chapter 7: Interwar globalization. The chapter opens with
the arrival in Bergen of a Brazilian physician who sponsored by the Rockefeller
Foundation went on a global fact-finding mission for two and a half years. The goal
was to reorganize the leprosy campaign in his home country in light of experiences
elsewhere. During the journey he came to the conclusion that leprologists around the
world needed to organize and collaborate, and he founded an international
organization to this end. Although his international leprosy society never had a single
meeting, it laid the foundations for how the International Leprosy Association should
be organized and who should be involved. Focusing on the practices of traveling and
establishing organizations, as well as the activities of the League of Nations Leprosy
Commission, I will show how several initiatives aimed at organizing leprosy on a
global scale came together in the interwar period and led to initiatives aimed at global
standardization of medical research.
The chapter and the thesis ends in 1933 and the first issue of the quarterly
International Journal of Leprosy. For the next 73 years this would be the main global
arena for publishing and discussing knowledge regarding leprosy. The journal was the
last of the four pillars that made up the leprosy world order which would last for more
than seven decades. Until its final issue in 2005, the journal was where the dominant
 32

medical discussions took place and where the latest and most authoritative research
was published. The journal was published by the organization that made up the
second pillar: The International Leprosy Association (ILA). ILA was established at a
meeting in Manila in 1931 and still organizes leprosy researchers globally. The third
component was the League of Nations Leprosy Commission, which had its first
meeting in Paris in 1928. After the Second World War, its activities were continued
by the World Health Organization (WHO).54 Like its successor, the Leprosy

Commission’s role was to monitor the global prevalence of the disease and support
governments in their leprosy campaigns. Its experts were usually handpicked from the
ILA. The fourth and final component was the International Leprosy Conferences,
which still is the main meeting point for the world’s leprologists. The first conference
was arranged in Berlin in 1897, the 18th conference in the series was arranged in
Brussels in Belgium in September 2013.
In this thesis I pursue three main arguments. First, science is not just clever
ways to produce knowledge about the world in specific sites. Science is also a
collective activity that goes beyond the local. The circulation of knowledge is in itself
a scientific practice, and must be studied as such. Those participating in the
circulation of knowledge got access to more experience than had they worked in
isolation, knowledge that in turn could be translated into prestige and status as experts
on a local scale. In this thesis I show how this framework was organized and how the
dominant positions in three of the most central debates changed over time. Second,
the science of leprosy had direct and practical applications. It was never possible to
fully separate the disease from those affected by it, thus to do something with the
disease meant doing something with those affected by it. Since not much could be
done to cure those already affected, the interventions focused on prevention. Third, a
study of the circulation of knowledge builds on and does not replace the need for
geographically delimited studies. These provide insight both in local practices,
perspectives of other actors such as missionaries and the persons affected by the




54
Today, the leprosy work is organized by the WHO office for Control of Neglected Tropical Diseases. See:
 33

disease, and constraints outside the control of the medical investigators such as
economic and political conditions. Only fractions of what went on in one place were
made part of the circulation of knowledge.





Sources: ‘Backwards’ and ‘sideways’


My main strategy for finding relevant source material has been to work ‘backwards’
and ‘sideways’. My starting point was the establishment of the International Leprosy
Association in 1931 and their medical journal, and I then worked backwards from
there. Since the League of Nations Leprosy Commission was heavily involved in
deciding who was to attend the two-week founding meeting in Manila in 1931, this
brought me to the League of Nations archives in Geneva.55 The Leprosy
Commission’s main ambition was to gather the most recent scientific data concerning
leprosy, bring experts together, and coordinate cooperation between leprosy
researchers all over the world. I was allowed to bring a camera and created a digital
archive of all material related to their leprosy activities.56
In addition to the origins and activities of the League’s Leprosy Commission,
which will be detailed in Chapter 7, the material from Geneva showed that the
initiative for involving the League of Nations in leprosy work came from the
organizers of the Third International Leprosy Conference in Strasbourg in 1923.




http://www.who.int/lep/en/
55
The recommendation on the website of ILA’s Global Project on the History of Leprosy (http:
//www.leprosyhistory.org) was also important in this choice. The project operated between 1998 and 2007 as
collaboration between ILA, WHO and the Wellcome Trust Centre for the History of Medicine at Oxford. It was
funded by the Japanese Nippon Foundation. During the work with my MA-thesis I met with research officer Jo
Robertson who visited Bergen twice, and I have later met with Julia Sheppard, chair of the steering group, and
corresponded with Professor Emeritus Michel Lechat, former President of the International Leprosy Association
and member of the steering group. I have also met with John Porter (UN advisor on questions of leprosy),
interviewed Douglas Soutar, the current General Secretary of the umbrella-organization ILEP which works to
coordinate the work of anti-leprosy organizations, interviewed representatives from the organization LEPRA
Health in Action. I have also met with Helen Bynum who in 1991 wrote her PhD on Leonard Rogers who in
1924 founded the British Empire Leprosy Relief Organization (BELRA), and author Tony Gould.
56
I am especially grateful for the help and friendship offered by archivist Neycho Iltchev, who not only helped
me find the sources I was after but also where to find the best coffee and how to order pizza from the
lunchroom. For a travel report, see Vollset, Magnus. “Tilbake til verdens navle”. Historikeren. No. 2, 2010: 36-
40. Available online: http: //hifo.b.uib.no/2010/06/07/tilbake-til-verdens-navle/.
 34

There the attendees pointed at the League as a potential partner for reestablishing the
international medical journal Lepra Bibliotheca Internationalis (1900-1915). This
was the main motivation behind involving the League of Nations in leprosy work, and
an obvious next step in finding relevant sources.
Consequently, I spent three and a half months at the Wellcome Trust Center for
the History of Medicine in London, both because of their renowned research
community and access to the Wellcome Library, which is among the few libraries that
still hold a complete set of this journal. I also spent a wonderful weekend visiting
author Tony Gould in his home near Newton Abbot, and was allowed to help myself
to the rich archives he had collected doing research for his book Don’t Fence me in.
From curse to cure: Leprosy in modern times (2005).57 Inspired by Pandya’s paper on

the first International Leprosy Conference, I also visited the Ashmead Collection at
the Historical Medical Library at The College of Physicians of Philadelphia, USA.
Working with my MA-thesis, a social history of leprosy in Norway in the 19th
century, I familiarized myself with the Leprosy Archives in Bergen, which in 2001
was accepted to the UNESCO Memory of the World programme.58 The archival
material I have used has mainly consisted of correspondence, reports and minutes of
meetings.
Although circulation of knowledge is only possible to document post factum,
when a reference is made to prior research, an obvious drawback of the strategy
working ‘backwards’ is that it is easy to fall into the trap of teleology through basing
the story only on the voices of those who ended up ‘winning’ the arguments. I
therefore supplemented this by working ‘sideways’. This strategy consisted of
examining the concurrent debates the original texts were part of. The most important
sources for this strategy have been medical journals, reports, conference proceedings




57
Gould’s book has been a valuable starting point for finding information about the actors involved in making
leprosy a global disease, and has served as a constant reminder that leprosy and the responses to the disease has
shaped the lives of people in numerous and dramatic ways.
58
Vollset 2005; Memory of the World: The Leprosy Archives of Bergen. The nomination form is available on
UNESCO’s website: http: //www.unesco.org/new/en/communication-and-information/flagship-project-
activities/memory-of-the-world/register/full-list-of-registered-heritage/registered-heritage-page-8/the-leprosy-
 35

and medical textbooks.
The approach of working both ‘backwards’ and ‘sideways’ reflect the original
dual purposes of these publications. On the one hand they were arenas for ongoing
debates; on the other hand they created an archive for later reference. As Bruno
Latour has pointed out, only what was considered relevant for later researchers was
referred to. Further, the act of referring to previous research is not the same as making
identical copies of the original. Rather “with every new retort added to the debate, the
status of the original discovery (…) will be modified.”59 Through the dual strategy of
working backwards and sideways, it is possible to show not only what was considered
vital concurrently, but the breadth and scope of the debates, and how the dominant
positions changed over time.

Thanks to projects such as The Internet Archive, and the digitalized archives of
both medical journals and newspapers, much source material has been available
online.60 This has been invaluable for my research, especially for the period prior to
1900. But the digital revolution also has its pitfalls: There might very well be biases in
the selection of what to digitalize that I am not aware of. This is obviously a problem
with the historical records preserved in archives and libraries as well, but since the
digitalized sources are only a selection of what has been preserved, the challenge is
only greater. I therefore chose to supplement my research by visiting library holdings.
In addition to the Wellcome Trust Library, which holds a large collection of relevant
research literature, I have spent much time at the University of Bergen Library where
much of the material from the library at the Lungegaarden leprosy research hospital is
found. Still, the value of convenience in the digital revolution has, for me at least,
outweighed the cost of traveling to even more libraries and archives. Although it
probably would have been possible to conduct this study without relying on the
scanned originals available online, it would have been more costly and time





archives-of-bergen/. The archives also has an internet exhibition with digitalized sources and links to previous
research: http: //digitalarkivet.uib.no/lepra-eng/
59
Latour, Bruno. Science in Action. 1987: 27. Italics in the original.
60
http: //archive.org. For other internet resources I have found useful, see the list of “Online resources” at the
end of the thesis.
 36

consuming.

After identifying the sources and getting an overview of the content, the next
step was making a narrower selection and composing stories based on this material.
With the exception of the sections that discuss what went on behind the scenes in the
League of Nations Leprosy Commission and in the run-up to the first international
leprosy conference, I have given priority to the sources that were publicly available
and part of concurrent discussions within the medical community. Apart from those
directly involved behind the scenes, this is what actors elsewhere based their
appropriation on. Accordingly, I have given priority to medical journals and
conference proceedings.
I have chosen to tell my story primarily through medical researchers and their
debates. Although the number of dominant actors was limited, both in the number of
persons involved in organizing frameworks for circulation and in the number of
persons frequently referred to, I have tried to balance their position with focusing also
on those who most vocally represented positions that were later abandoned by the
research community. As Fleck pointed out, ideas are generated and accepted during
discussion and critique. Ignoring the ‘blind alleys’ would therefore give a misleading
impression of how science is actually conducted. As Pandya demonstrated in her
paper on the first international leprosy conference, and as I will expand upon in
Chapter 6, the first leprosy conference and its outcomes would not have been the
same had it not been for the competitive scheme with a different vision for how the
fight against leprosy should be organized internationally.
The choice of focusing on the medical debates in this set of sources has
unavoidably led to a geographical bias. The vast majority of those affected by the
disease were encountered in the colonies by physicians from Europe working for the
colonial authorities. In addition to diagnosing individuals and estimating prevalence
in the population, they were involved in testing drugs and formulating policies. Until
the outbreak of war in 1914, most of the meetings and discussions took place in
Europe and North-America, and this was where those involved in organizing the
circulation of medical knowledge lived. In the interwar period physicians from Latin-
 37

America, South Africa, India and the Phillipines also stepped forward. The
geographical bias of the medical community is reflected in my thesis. This is not to
say that the disease did not exist in other parts of the world, or that those affected by it
did not receive attention. But in Africa and China, for instance, leprosy work was to a
large extent left to the missionaries who had their own frameworks for the circulation
of knowledge. Had I chosen to focus on the missionaries, the geographical bias would
have been different.61

There were some exchanges between missionaries and physicians both on a
personal level and through publications. Lepra Bibliotheca Internationalis (1900-
1914), for instance, printed abstracts of six papers from the Mission to Lepers in India
and the East’s quarterly journal Without the Camp (1897-1971). The founding head of
the Mission to Lepers, Wellesley Bailey, was invited to the first leprosy conference,
and did attend both the follow-up in Berlin in 1904 and the Second International
Leprosy Conference in Bergen in 1909. The replies to the League of Nations calls for
information on leprosy in 1925 found in the archives in Geneva indicate that
missionaries were heavily involved in leprosy work also in areas where the Western
physicians had yet to arrive. Roy Porter has argued that “Leprosy provided a prism for
Christian thinking about disease.”62 Pursuing the various missionary societies
involved in leprosy work would undoubtedly have been fruitful, for instance using a
similar transnational strategy as the one I have developed for this thesis. The
circulation of missionary or religious knowledge about leprosy did tangent the
medical circulation of knowledge, but it mainly existed in parallel. This is a story I
have not had the capacity to pursue. My study is limited to the medical community.













61
For studies in this direction, see for instance: Worboys 2000; Joseph, D. George. “"Essentially Christian,
eminently philanthropic": The Mission to Lepers in British India.” História, Ciências, Saúde-Manguinhos.
Suppl. 1. 2003: 247-275.
62
Porter, Roy. The Greatest Benefit to Mankind. A medical history of humanity. 1997: 122.
 38

‘The leper’, terminology and ethical considerations


In the thesis I use quotations extensively. Due to readability I have translated the
Norwegian, German and French sources into English in the main text, but the original
quotes are found in the footnotes. The words used are never neutral or objective
signifiers, but expressions of the perspectives and situation of those who use them.
How the actors presented their arguments changed both with time and setting, and this
I believe is more readily expressed through direct than indirect quotations.
The quotations show how the medical discourse especially in the 20th century

became increasingly specialized, but my choice is not without its drawbacks. I have
consciously tried to explain the specific meanings of the medical terms used, but after
working with this material for several years I have unavoidably adapted and
internalized some of the terminology. Although my advisor and readers have been
helpful in pointing out what needs further elaboration, I am certain some concepts
should have been explained better. All mistakes are mine.
The use of the term ‘leper’ requires special attention. The term has been seen
as derogatory, and several organizations have argued that refraining from using the
word is an important step in getting rid of the stigma connected to the disease. The
first advocate for abolishing the term was Stanley Stein, a patient at the US leprosy
institution in Carville, Louisiana. From 1931 to 1934 he edited the bimonthly journal
The 66 Star, forerunner to The Star (1941- present). In the patient-run journal, Stein
argued that ‘leprosy’ has Biblical connotations to sin and impurity, and advocated that
the disease instead should be called “Hansen’s disease”.63 The argument that labels
like ‘leper’ is a hurtful stereotype that keeps stigma alive, has later been promoted
especially by the organization IDEA, established in 1994 with 20,000 members in five







63
Stein, Stanley. Alone no longer. The story of a man who refused to be one of the living dead. 1963. While the
connotations to ‘leprosy’ in the bible were important for missionaries justifying their activities, it is beyond doubt
that ‘Biblical leprosy’ and ‘leprosy – the disease’ is not the same, but can be traced to when the Bible was
translated from Hebrew to Greek. As M. J. de Mallac has put it in Hansen’s disease: The shared paradigm:
“That ‘Tsara’ath’ or ‘lepra’ is synonymous with Hansen’s disease has a semantic basis only.” (Mallac 1998:
14)
 39


continents.64 This position has many supporters.65

While I agree that using the term ‘leper’ about individuals affected by the
disease today is derogatory, when studying the history of the disease I have reached a
different conclusion. Terminology and categorization is central to the creation of
knowledge, and going down the alley of re-labeling would inevitably lead to
anachronism. In the period I study, the word ‘leper’ was used both as a metaphor, a
sensationalist expression to incite fear, and an unchallenged medical term. This is part
of what made it so powerful. When it comes to leprosy, Sander Gilman’s term about
images of disease, ‘disease anthropomorphized’, was sadly also inherent in the
language.66 I acknowledge that terminology is a sensitive issue, but for reasons of
historical precision I will stick to the terminology used in the sources.67
A different but related ethical consideration is that the stigma itself for some
can be said to be hereditary. Discovering that the family carried a dark secret, namely
that her grandmother was affected by leprosy and spent her life at “The Leper Island”
Spinaloga in Greece is the theme in Victoria Hislop’s novel The Island. The book was
celebrated as ‘Newcomer of the Year’ at the Galaxy British Book Awards in 2007, and
has later topped various bestseller lists. Although individuals’ referred to in my
sources are deceased, having had ancestors who were affected by the disease can for
some be seen as a reopening wounds that need healing. While the sources often give
the full names of the individuals affected by the disease, I have chosen only give the
initials of the family names, or avoid using names altogether. The only exception is
when the individuals themselves actively sought attention in a public arena – then I




64
See: http: //www.idealeprosydignity.org
65
“By refraining from using the word ‘leper’, either historically or in modern times, we will be challenging the
stigma, restoring the humanity of those who lived hundreds of years ago, and promoting the dignity of those
individuals affected by this disease today.” (Law, Anwei Skinsnes. “The last leprosy communities and the
people who call them home.” In: Roberts, Charlotte A., Mary E. Lewis, and K. Manchester (eds.): The Past and
Present of Leprosy. Archeological, historical, palaeopathological and clinical approaches. BAR International
series 1054. 2002: 7). US president Bill Clinton voiced a similar sentiment in his opening speech at the
exhibition ‘Quest for Dignity’ in the United Nations October 30, 1999: “An important step in our efforts to
ensure that all individuals are treated equally is to permanently strike the hurtful word ‘leper’ from our
vocabulary.” (http: //www.idealeprosydignity.org/OralHistoryWeb/Terminology.html)
66
Gilman, Sander L. Disease and Representation. Images of Illness from Madness to AIDS. 1988.
 40

have used the names they have signed with.68





Leprosy today


In May 1991, the World Health Assembly passed a resolution to eliminate leprosy as a
global public health problem by the year 2000. At the time it was estimated that 5.5
million people suffered from leprosy globally.69 Elimination was defined as reducing
the prevalence rate to less than one case per 10.000 inhabitants, first on a global, then
on a national and finally on a regional scale.
That leprosy is the same disease all over the world is a necessary premise for

‘global prevalence’ to be a meaningful concept. But that leprosy prevalence exists as a
global unit still does not make the approaches to the disease identical on a local level.
There are, for instance, obvious differences between being diagnosed with leprosy in
Norway and in East Timor.70
Today medical experts agree that the causes of leprosy are the same all over the
world, namely the bacillus first observed by Hansen in 1873, Mycobacterium leprae,
or the related Mycobacterium lepromatosis, which was first identified in 2008 by a
team headed by the American pathologist Xiang-Yang Han.71 However, although the
bacilli are necessary, they are not alone sufficient to produce the disease. The
individual affected also needs a hereditary predisposition for the bacilli to cause the





67
This choice, I believe, is in line with Stanley Stein’s own editorial advice in The Star: “We dislike the word
‘leprosy’ intensely, but we dislike the practice of censorship even more.” (“Editorial Policy on Terminology.”
The Star, all issues, p. 2.)
68
Stanley Stein, for instance, was a pseudonym he adapted after being sent to Carville in 1931.
69
Nordeen, S.K., Bravo L. Lopwz and T. K. Sundaresan. “Estimated number of leprosy cases in the world.”
Bulletin of the World Health Organization. Leprosy Unit, World Health Organization. 1992: 7-10.
70
The past 20 years, nineteen new cases of the disease has been identified in Norway. The patients have been
absorbed by the local health systems. Rapp, Ole Magnus. “Fortsatt tilfeller av spedalskhet”. Aftenposten. 25.
June 2012. (Online: http: //www.aftenposten.no/nyheter/iriks/Fortsatt-tilfeller-av-spedalskhet-6907004.html). In
poverty-stricken East Timor, with 160 new cases detected every year, the situation for those diagnosed is
radically different. Mason, Margie. “Tiny East Timor Declares War On Leprosy”. Associated Press. 10.
October 2010. (Online: http: //www.huffingtonpost.com/2010/10/10/tiny-east-timor-declares-_n_757544.html).
71
Han, Xiang-Yang, Y. H. Seo, K. C. Sizer, T. Schoberle, G. S. May, J. S. Spencer, W. Li, and R. G. Nair. “A
new Mycobacterium species causing diffuse lepromatous leprosy”. American Journal of Clinical Pathology.
2008: 856-64.
 41

disease, and an estimated 95 percent of the human population is immune. Third, it
seems a prolonged reduction in the immune system is necessary for the disease to
develop. This can be caused by insufficient diet, poor living conditions or other
diseases, and explains why the disease is often linked to poverty. The disease has a
long incubation time, from months to decades. The genomes of the two leprosy bacilli
have been mapped, but many questions of the precise mechanisms involved in the
transmission and the early development of the disease remain unanswered.
From 1995 the WHO has provided free multidrug therapy (MDT) to all
relevant countries through their Ministries of Health. Cooperation between
international bodies and individual countries has been necessary in order to reach the
global elimination target.72 In November 1999, as the global elimination goal was
within reach, the WHO took the initiative to establish Global Alliance for Elimination
of Leprosy (GAEL). They soon adopted a “Final Push” strategy, moving from
focusing at the global prevalence target to reaching this elimination target at a
national level. The rationale was that reaching the targeted prevalence rate would
make it possible to integrate leprosy treatment into the general health services.
Over the past 20 years, more than 14 million patients have been detected and
cured using MDT. At the time of writing, pockets of high prevalence still remains in
areas of Brazil, Indonesia, Philippines, Democratic Republic of Congo, India,
Madagascar, Mozambique, Nepal, and the United Republic of Tanzania.73 Throughout
the past decade, the global leprosy prevalence has been in steady decline (see Table 1
on the following page). According to the WHO, there were 181.941 cases worldwide
at the end of 2011.













72
In October 2010, WHO and the pharmaceutical company Novartis signed an agreement to continue to
provide free MDT free of charge to all countries where the disease is endemic until 2015. See:
http://www.who.int/lep/resources/press_releases/en/index.html
73
WHO. Leprosy Fact Sheet. Available online: http: //www.who.int/mediacentre/factsheets/fs101/en/index.html
 42




Table 1. Detection of new cases of leprosy, 2001-2010 (excluding European Region)
2001 2002 2003 2004 2005 2006 2007 2008 2010
763,262 620,638 514,718 407,791 299,036 265,661 258,133 249,007 228,474

Sources: W HO. Weekly epidemiological record, No. 33, 2009, 84: 33-340; Nr. 32, 2006, 81: 309-

316; http: //www.who.int/lep/situation/



The decline of leprosy prevalence has had consequences for the campaign against the
disease. In 2005, the International Leprosy Association (ILA) decided to close down
the International Journal of Leprosy after 73 years.74 The organization LEPRA –
Health in Action, established as British Empire Leprosy Relief Association (BELRA)
in 1924 with the aim “to eradicate the disease altogether”75, continues to publish the
medical journal Leprosy Review in its 83rd volume. However, the organization itself
is moving away from a single-disease focus into the wider area of health-related
development work.
The fight against leprosy has been highly successful in its goal of reducing
leprosy to “just another straightforward, curable disease”.76 However, the WHO
leprosy elimination program has been, and still is, contested. The “Final Push”-
strategy gave attention and resources to the fight against leprosy, but has also been
met with fears that the disease will be neglected, including persons who have
disabilities resulting from having had the disease. Declaring leprosy eliminated by
reaching the 1:10,000 target, some fear, will lead to lack of competence or active
efforts in detecting new cases, and that the prevalence consequently will rise in the
“post-elimination” era.77





74
Scollard, David. “Elimination of (the International Journal of) Leprosy.” International Journal of Leprosy.
Vol. 73, 2005: 303.
75
Oldrieve, Frank. “The Work of the Association.” Leprosy Notes, No. 1, 1928: 2.
76
World Health Organization (WHO). 2003. The Final Push Strategy to Eliminate Leprosy as a Public Health
Problem. Questions and Answers, Second Edition. World Health Organization, Geneva. Available online: http:
//www.who.int/entity/lep/resources/Final_Push_%20QA.pdf
77
See i.e.: Ji, Baohong. “Comments on WHO/AFRO’s ‘Post-Elimination’ Strategy Paper: A New Bottle with
Old Wine of the ‘Final Push’”. International Journal of Leprosy, vol. 73. 2005: 216-218; Khaitan, Binod K. et.
 43

A transnational approach is never disconnected from the local context. Since I
as a historian have been situated in Bergen, an emphasis on the role of the leprosy
bacillus within these medical networks seems given. Had the thesis been written
elsewhere, the starting point would probably have differed. In July 1998, for instance,
127 former leprosy patients filed a lawsuit in Kumamoto District Court against the
Japanese government seeking compensation for being locked up for decades “under
an unconstitutional quarantine policy”.78 Japan’s Leprosy Prevention Law, enacted in
1907, set a standard for forced segregation policies which were abolished only in


1996.79 On May 11th, 2001, the court ruled in favor of the plaintiffs, who received in
total $15 million in compensations; pointing to international scientific
recommendations which from the 1960 has favored outpatient treatment. The story
was widely reported in media all over the world, and led to increased interest in the
history of leprosy from scholars and general audiences alike. Had I been situated in
Japan, this recent event would undoubtedly have influenced the research, both
questions and strategies.
Likewise, had my starting point been in Belgium, Father Damien’s departure
for Hawaii in 1873 could have been a likely starting point.80 In 1889 the news that
the missionary had caught the disease and died caused headlines all over the world.
And had I been situated in Ireland, Wellesley Bailey and the establishment of the
Mission to Lepers in Dublin in 1874 would have been a likely point of departure.81 By
the 1920s the mission ran the majority of all leprosy institutions in India and had
already expanded elsewhere in Asia. Studying how the missionaries established
frameworks for circulation of knowledge would indeed be interesting, but that would
have been a different project.




al. “Final push of leprosy: It is prudent to pause before declaration!” Indian Journal of Dermatology,
Venereology and Leprology. Vol 72, No. 2. 2006: 151-153. For more on this debate, see Gould 2005: 362-365.
78
“State Blamed for Leprosy Misery.” Mainichi Daily News. May 12, 2001. “Japan’s Lepers Win Long-
Awaited Compensation.” International Herald Tribune. May 12, 2001.
79
Ohtani, Fujio. The walls Crumble. The Emancipation of Persons Affected by Hansen’s Disease in Japan.
1998.
80
Lechat, Michel. “La Lèpre après Père Damien”. AMA. No. 65, May-June 2010. http:
//www.md.ucl.ac.be/ama-ucl/Lepre65.html.
 44

This thesis is written in Bergen. Although I as a researcher have travelled to
archives and met with colleagues at conferences elsewhere, opening with the
unveiling of Hansen’s bust in 1901 seemed more fitting. Alongside the Second
International Leprosy conference in Bergen five years later, this was the pinnacle of
Bergen as a renowned international center for medical research into the disease. As I
will return to in Chapter 7, by the late 1920s, this was no longer the case.























































81
Davey, Cyril J. Caring Comes First: Story of the Leprosy Mission. 1987.
 45


2. Recognizing ‘the leper’


Four years before the bust of Gerhard Armauer Hansen was unveiled in Bergen, in the
spring of 1897, Hansen received a message from a district physician asking him to
investigate a man suspected of being affected by tubercular leprosy. After examining
the man in his home, Hansen was convinced that the diagnosis was correct. But when
he returned to the laboratory and failed to find the bacillus in the tissue samples he
had taken, he was forced to reconsider. “I cut out nodules and examined them, but
could not find any bacillus. Naturally I had to give up my diagnosis.” A month and a
half later he repeated the examination with the same result: “Again I did not find it
[the bacillus], and I was obviously compelled to conclude: This is not leprosy.”82

At the leprosy conference in Berlin later that year, Hansen argued that
demonstrating the leprosy bacillus was compulsory in order to make the diagnosis,
and that the presence of the bacillus should be given precedence over the clinical
symptoms. For Hansen, the bacillus (or lack thereof) made it possible to look like a
‘leper’ and still be considered a non-leper.
Few historians have examined the impact of bacteriology on diagnosis. Still,
comparing for instance Michael Worboys’ investigation of the impact of bacteriology
on disease theories and medical practices in Britain in the 19th century and Andrew
Cunningham’s study of how laboratory medicine transformed the identity of plague
would indicate that a radical shift took place during the first decades of the 20th
century. In Spreading Germs (2000), Worboys argues that: “Given doctor's
confidence in their existing methods of diagnosis, bacteriological methods were





82
“Ich schnitt Knotten heraus, konnte in diesen keine Leprabacillen finden und musste da natürlich meine
Diagnose aufgeben. 1 ½ Monate später sah ich die Patientin wieder, schnitt aufs neue einen Knoten aus, härtete
ihn in Alkohol und machte Schnitte, um erneut auf Bacillen zu suchen. Ich habe sie auch da nicht gefunden,
muss also ganz bestimmt sagen: das ist keine Lepra.” Hansen, Gerhard Armauer. “Inwieweit ist man berechtigt,
den Leprabacillus als die Ursache der Krankheit anzunehmen?” (Discussion). Mittheilungen und Verhandlungen
der internationalen wissenschaftlichen Lepra-Conferenz zu Berlin im October 1897. II. Abtheilung. 1897: 43-
44. (Hereafter: ‘Mittheilungen 1897’) See also: Neisser, Albert. “Inwieweit ist man berechtigt, den
Leprabacillus als die Ursache der Krankheit anzunehmen?”. Mittheilungen 1897. I. Abtheilung.
1897: 1-10; Looft, Carl. “Die anästhetischen Formen der Lepra”. Mittheilungen 1897. II. Abtheilung. 1897: 99-
101.
 46

largely used to confirm clinical judgments or used in doubtful cases.”83 Worboys has
later argued that there was indeed no bacteriological revolution between the 1870 and
1910, at least not in Britain. Instead, the period was characterized by richer
uncertainties and possibilities regarding etiology and pathology, a growing repertoire
of techniques and technologies, and new possibilities for analogical and analytical
reasoning.84 Cunningham, on the other hand, argues that the discovery of bacteria
meant the introduction of single causes of diseases, and that laboratory medicine
transformed the identity of disease. Clinical diagnosis could only suspect. “The only
way a suspicion of plague can be confirmed or established is by bacteriological
methods; in other words, by a laboratory.”85 Cunningham then goes on to argue that
by accepting that a disease has a specific cause, we have all in essence become
bacteriologists. “To oppose the claims of bacteriology is now not a rival view, nor an
alternative view, nor even a dissident view. It is now a lunatic view.”86
Identifying the disease and thereby deciding who was to be considered a
‘leper’, was the first step in dealing with leprosy. As Hansen’s example in the
discussion in Berlin shows, the results from diagnosing clinical signs and diagnosing
in the laboratory were not necessarily overlapping. This chapter will investigate what
diagnosis was based on prior to the bacillus, and to what extent Hansen’s insistence
that demonstrating the bacillus was compulsory for diagnosis was accepted by
colleagues elsewhere. To what extent did the bacillus lead to global standards for
diagnosis of leprosy? What new research on diagnosis did the bacillus inspire? What
practical implications did the bacillus have when it came to recognizing the leper?













83
Worboys 2000: 214.
84
Worboys 2007: 20-42.
85
Cunningham 2002: 209-244; quote on p. 213.
86
Cunningham 2002: 239. For a related discussion on the assumed conflict that arose between the laboratory
and the clinic, see: Sturdy, Steve, Morten Hammerborg, Rosemary Wall and Mirjam Stuij. “Bedside and Bench
Revisited”. Social History of Medicine, Vol. 24, issue 4, 2011: 739-812.
 47

Backwards from the corpse


Establishing how to clinically recognize leprosy and separate it from other illnesses
was the main ambition of Daniel Cornelius Danielssen and Carl Wilhelm Boeck’s
monograph Om Spedalskhed (‘On Leprosy’) published in 1847.87 For the two
Norwegian physicians, leprosy was a unique illness that slowly made its presence
known. As they summarized their presentation of the diagnosis: “We hope that we in
our description of leprosy have portrayed this as a distinctive disease which, fully
developed, cannot be mistaken for any other.”88
Leprosy manifest was the end point; the dead body. By opening the corpse,
observing how the disease had affected the internal organs, the disease was no longer
obscured. Only when observing the internal organs, the pathological changes could be
contrasted with the complaints made while the sufferer was still alive. Death was thus
the starting point for unraveling the mysteries of the disease. In the monograph, the
disease was traced backwards from the corpse, via the symptoms to the early, non-
specific signs. As I will expand upon in Chapter 5, in the majority of the cases the
authors argued that the disease could even be traced further back in the lineage.
In On Leprosy the presentation of the disease was in chronological order,
starting with the prodromes – the stage where the disease was lingering but had not
yet made itself firmly known. Then the progress of the disease was presented both in
general terms and with 70 detailed case stories from St. Jørgen’s Hospital in Bergen
observed by Danielssen, most of which ended in autopsies conducted between five
and forty hours after death. The observations were supplemented by chemical analysis
and microscopy. Emphasizing that the disease was the same in other places, there
were also eleven ‘foreign’ cases, patients observed by Boeck in Varazze (6), Athens
(2), Hamburg (1), Turin (1) and Rognac (1).




87
The monograph was published in Norwegian in 1847 with the title Om Spedalskhed, and the following year in
a French translation with the title Traité de la Spédalskhed ou Éléphantiasis des Grecs. In 1855, the book won
the Prix Monthyon from the Academy of Sciences in Paris, and in 1856 the findings were summarized in
English under the title “On the Nature and Treatment of Leprosy”, a series of eight papers by Erasmus Wilson
in The Lancet. (Edmond 2006: 46.)
88
Danielssen and Boeck 1847: 269.
 48

Learning to recognize the disease as early as possible was a goal in itself. The
logic was that in order to find a cure, treatment must start early. Finding a cure was
the objective for the research hospital which was being built while the book was
finalized (Lungegaardshospitalet). Although the reaction to medication given to the
patients was documented as part of the progress of the disease, treatment as such was
not an ambition of the work.
Danielssen and Boeck separated leprosy into two distinct forms based on their
symptoms, the nodular (‘Den knudede Form’) and the anesthetic (‘Den anæsthetiske
Form’). The prodromes were identical: Fatigue, stiffness, sleepiness, occasional light
chills, passing pain, lack of appetite and nausea sometimes leading to vomiting. More
often than not, the patient would then develop symptoms from both forms, sometimes
to the extent that neither stood out as the dominant. These sufferers would be
classified as ‘mixed’. The descriptions reveal how the act of producing the accounts
demanded close observation over time and the patient explaining the sensations
accompanying the visible changes in their bodies.
For the nodular form, the specific symptoms consisted of slightly elevated
spots in the face and on arms and legs, scarlet to dark brown in color, sizes ranging
from that of a coin to the palm of a hand. The spots were less sensitive to touch than
the rest of the skin; they sometimes itched and were made more visible when exposed
to extreme cold or extreme heat. After a few days, weeks or months the spots would
disappear, only to reoccur at a later point in time. At some point, the spots would
become permanent and swollen, usually first on the back of the hands and in the face,
leading to the eyebrows falling out. Often the eyes were attacked leading to blindness.
Over time, the spots would turn into nodules, accompanied by deep pain. While the
nodules themselves were dry, the rest of the body would sweat, making the skin
appear smeared and greasy. Next, spots would appear on the inside of the mouth and
throat, leading to a distinct hoarse voice, trouble with breathing and sometimes fatal
suffocation. The nodules would continue to grow and gain a brown color. Sometimes
the nodules would burst with liquid floating out. The whole process could take years,
but the disease could also enter more active periods, usually lasting up to two weeks,
 49

producing fevers, a feeling of heaviness, headache, delirium, thirst, and high pulse.
“The disease can now in few weeks produce the destruction that it in the chronic
phase takes years to achieve.”89 While some patients would experience periods of
apparent recovery, these were with but a few rare exceptions all passing stages – the
disease would inevitably return. In the end leprosy would produce diarrhea and
dramatic loss of body weight (marasmus). Finally, sometimes after decades of
suffering, death would come as a relief.
The anesthetic form had a more chronic and covert development. Often the one
affected would experience chills, making the whole body stiffen and cause “an
unexplainable indisposition, sometimes forcing him to solitude”.90 This stage could
last for months or years. Then, with no prior warning, blisters the size of walnuts or
hens eggs would form on the arms and legs, filled with a yellow-green, sometimes
milky, viscous (thick and sticky) fluid. After bursting and then healing like a normal
wound, the affected areas would more often than not be less sensitive to touch than
the rest of the skin. The phase of producing blisters could last up to five years. The
next step would be intense and lasting pain, often located in deeper and previously
unaffected parts of the body, producing hypersensitivity where even the slightest
touch or movement would cause stabbing anguish. Then spots of anesthesia set in.
The skin would go pale, dry and with no production of sweat, often leaving the skin
tough and with no elasticity. Over time the anesthetic spots would spread to larger
parts of the body, the face would take on a pale yellow color with hints of purple.
Like the nodular form, the disease would attack the eyes causing blindness, and
produce lesions inside the mouth and in the gums. As the disease progressed, the
tissues and bones would begin a ‘necrotic’ phase, causing the attacked areas to be
insensible to the extent that they could be cut without causing pain. Muscles in the
face would stop holding the facial expressions up, leading the sick to drool; palms and
feet would contract. The loss of sensibility would usually be combined with a deep




89
“Sygdommen kan nu I faae Uger frembringe alle de Ödelæggelser, hvortil behöves Aar under den chroniske
Gang.” Danielssen and Boeck 1847: 152.
 50

pain that felt like originating in the bones. This was in turn followed by strong fever,
violent shakes, headache, and delirium, burning thirst, pressure in the stomach,
frequent vomiting and an ‘annihilating powerlessness’.


Under too frequent and harsh suffering, years go by while the disease slowly and surely
progresses. Anesthesia takes over the whole body, the breath finally fades, and one can with
good reason claim that the body is dead long before the sick end their days. It is like all parts
diminish, and life goes out unnoticed.91

The last part of the monograph was a colored atlas with 24 plates made by the
Norwegian lithographer Johan Ludvig Losting, Atlas Colorié de Spedalskhed
(Elephantiasis des Grecs). The plates depicted faces, eyes, body parts, magnified skin
lesions and internal organs, set against a neutral white background. The images were
realistic but slightly exaggerated, representing the archetypes of the disease as it
appeared in different parts of the body. Frequent references in the text make it clear
that the atlas was to serve as a visual guide to the disease, exemplifying what to look
for when making a diagnosis. In Lorraine Daston and Peter Galison’s vocabulary, the
atlas can undoubtedly be classified as ‘truth-to-nature’; idealized, selecting the
essential and leaving out the accidental.92 Again, the atlas played into making the
monograph decidedly useful in making the diagnosis. It equipped the physician facing
a patient in different stages of the disease not only the tools to decide if it really was
leprosy or not, it also gave insights into the probable case history, how the patient was
likely to describe his or her symptoms, and predictions on what would happen next.
The usefulness of On Leprosy would ensure its status as a standard reference
work on diagnosis for more than half a century. Apart from less emphasis on
communicating with the sufferer, not much would change in clinical diagnosis until




90
“(…) sætte den Syge I et for ham uforklarligt Ildebefindende, der undertiden tvinger ham til at söge
Eensomhed.” Danielssen and Boeck 1847: 204.
91
“Under alt for hyppige og haarde Lidelser hengaae mangfoldige Aar, hvori Sygdommen gaaer sin sikkre Gang
fremad. Anæsthesien indtager hele Legemet, Aanden slöves omsider, og man kan med god Grund sige, at
Legemet er dödt længe förend den Syge ender sine Dage. Det er ligesom om alle Dele svinde hen og Livet
udslukkes fast umærkeligt.” Danielssen and Boeck 1847: 213.
92
Daston and Galison 2007: Chapter 2.
 51


the advent of the leprosy bacillus.93 In short, leprosy was a horrible disease identified
through clinical diagnosis. It was the appearances and progression associated with
leprosy that decided if you had the disease or not.94





Of pathogens and expertise


When Gerhard Armauer Hansen and Carl Looft wrote the next major textbook on
leprosy in Bergen almost half a century later, leprosy was no longer described as a
disease slowly overtaking the healthy body causing suffering and pain, but as the
effect of the leprosy bacillus acting on the body. In Die Lepra vom klinischen und
pathologish-anatomischen Standpunkte (1894), the two Norwegian physicians
described the disease not as a mystery to be unraveled in collaboration with the
sufferer, but as an object to be discussed among experts.95
Hansen and Looft also separated the disease into two main forms, but used a
different nomenclature than Danielssen and Boeck. The form producing nodules they
named Lepra tuberose (Lepra tuberculosa), while skin reactions and nerve affections
were the distinguishing features of Lepra maculo-anæsthetica. What bound the two
forms together was not that they could appear as ‘mixed’ forms in the same patient,
but that both forms were caused by the presence of the leprosy bacillus: “We must




93
The feeling and localization of pain was not something that could be observed, but relied on what the patient
could tell about his or her experience. For Danielssen, the patient was not (only) an object containing disease,
but a partner in unraveling its mysteries. This emphasis on the patients’ experiences was also reflected in
Danielssen’s tuberculin trials, which I will investigate in Chapter 3.
94
Danielssen and Boeck’s monograph was but one of several descriptions of the disease. Most accounts divided
the disease into several categories based on its clinical signs. In 1852 Dr. W. S. Oke at the Royal South Hants
Hospital in Southhampton, for instance, reported in The British Medical Journal that the disease had “three
principal species – the albida, nigricans and candida.” Albida was “characterized by elevated patches of
squamous matter and of a dull white colour”, candida by its “bright whiteness […] the denomination has a
complete agreement with that emphatically given to it in several parts of the Old Testament, such as ‘leprous as
snow’.” The last form was not found in Britain and was therefore not described. According to Oke, the disease
caused “considerable local irritation; but although it continues for a long time, [leprosy] does not produce any
great amount of constitutional disturbance.” (Oke, W. S. “Notes on the Treatment of Curable Diseases”. The
British Medical Journal. 1852: 138.)
95
The book was translated to English by Norman Walker from Edinburgh in 1895 and given the title Leprosy:
In its Clinical & Pathological Aspects. Two years later Hansen and Looft authors published a Norwegian
 52

regard them as the same disease, only with varied intensity in the action of the
bacilli.”96 Again, the descriptions reveal what activities went into producing the
accounts: Observation over time was still indispensable, but the experiences of the
patients were supplanted by what could only be observed either by the naked eye or
through a microscope. Leprosy was becoming an object, not a subject.
Lepra tuberose was characterized by massive amounts of bacilli producing
oblong nodules, from one to two millimeters in diameter; first of red color, later
yellow. The nodules initially appeared on the backs of hands, on top of the wrists and
in the face. Eyebrows, eyelids, eyes and the soft parts of the nose were especially
prone to attack. This, they speculated, was probably due to being exposed to climate,
and possibly connected with peculiarities in the structures of the tissues making them
more fertile to the bacilli.97 Next, nodules would appear near the joints of the limbs

before spreading to other parts of the body. In addition, the lymphatic glands were
always swollen.
This nodular form always advanced through outbreaks or eruptions
accompanied by fever, repeating at longer or shorter intervals. For some the eruptions
lasted only a few days with almost unnoticeable rise in body temperatures and almost
no growth of the nodules. For others the fever could reach 40° C, last for weeks or
months and lead to dramatic development of new nodules. Stronger and more
frequent eruptions meant a quicker course and a worse outlook. Whether the
individual differences were caused by the virulence of the bacilli or the structural
conditions of the individual was impossible to say, but either way the consequence
was that the fate of each patient could differ greatly. Intermittently all affections could
spontaneously disappear and the patient would heal, but in general the life of the
patient would end after eight or nine years. Death was not a direct effect of the




edition: Lepra (spedalskhed): klinisk og pathologisk-anatomisk fremstillet (1897). All quotes are all from the
English translation.
96
Hansen and Looft 1895: 52. Here, the discovery of the bacillus was dated to 1871 and all observations made
before this point were labeled ‘pre-bacillary era’.
97
Climate was also put forward as a possible explanation for which form of the disease a patient developed.
Geographically the nodular form dominated along the moist coast of western Norway, while maculo-anæsthetic
 53

bacillus proper, but a consequence of the internal organs degenerating under fatigue
caused by ulceration (the inflammatory response). Most patients suffering from Lepra
tuberose died before the disease had run its full course.
The maculo-anæsthetic form of leprosy was more chronic and could last ten,
twenty or even forty years or more. Its distinguishing feature was that the bacilli were
fewer in number and attacked mainly the nerves and skin causing anesthesia and
spots. The marks were observed first in the face, on the back and on the extremities;
shapes and sizes varied, the colors ranged from bluish red to yellowish or brown and
were made more visible with changes of temperature or by friction. Some spots were
gone in days, others could last for years. If the macula (the discolored spots)
remained, the affected skin would become thin, shiny, slightly scaly, and hinder the
secretion of sweat. Usually the spots only affected the surface of the skin, but it could
sometimes affect the tissue as deep as the bone. Initially the spots would be
hypersensitive, but over time anesthesia (the loss of sensation) set in. The anesthesia
would often lead the patients to accidentally injure themselves, and the resulting
wound was prone to infection. Accompanying the spots were painful, tender and stiff
joints that often appeared swollen. Often the face was attacked by anesthesia, causing
blindness as the eyelids could not be closed due to paralysis. In most cases, however,
the disease would at some point cease to progress.


Thus the specific leprous affections gradually disappear, and only their results remain – in
other words, the leprosy is healed. Most maculo-anæsthetic patients become in time purely
anæsthetic; they no longer suffer from leprosy, but only from its results.98



This was the greatest implication of Hansen and Looft’s bacteriological disease
model: Leprosy was now a disease you could get well from. While clinical diagnosis
meant that if you looked like a leper you had the disease, bacteriological diagnosis






cases were more frequent in the dry climate in the east of the country and in the more sheltered villages along
the western fjords.
98
Hansen and Looft 1895: 67. Italics in the original.
 54

meant that you could have had leprosy some point in the past and now suffered from
the results of the disease – not the disease proper.
On the other hand, Hansen and Looft were quick to point out that the disease
could reappear at a later point in time, indicating that the bacilli could remain hidden
inside the body. And even if the disease never returned the results of having had the
disease were devastating, possibly a fate worse than death:


We have occasionally a complete subject with vigour and good health, but usually only a
miserable rudiment of a human being, with more or less paralysed and deformed hands and
feet, with unclosable eyes, of which the lower part of the cornea is opaque, and from which
the tears run down over the cheeks, and with paralysed facial muscles unable to close the
mouth, so that the saliva constantly dribbles from it. Such cases may, however, live long and
reach great ages, if under such circumstances this can be looked upon as any advantage.
They die usually from some intercurrent disease.99

Determining the exact genesis of the disease, Hansen and Looft considered
impossible. This would rely on the patients’ own observations. Unlike Danielssen and
Boeck, Hansen and Looft found the patients not to be trusted, since “the patients
either observe themselves insufficiently, as may frequently be noted, or they conceal
many facts”.100 When Danielssen and Boeck saw leprosy as a disease that slowly took
over the whole body, the experiences of the person suffering from the disease were
relevant in uncovering its mysteries. In comparison, Hansen and Looft perceived the
observations made by the sufferers to be of little interest. Consequently, Leprosy in its
Clinical & Pathological Aspects contained no detailed patient stories. The purpose of





99
Hansen and Looft 1895: 85.
100
“If at the commencement only the extremities are affected the patients may conceal their condition for years,
and through this concealment become so accustomed to lie, that later it is impossible to receive from them
correct information.” (Hansen and Looft 1895: 17). That lepers were considered untrustworthy was also reflected
in their discussion on surgical removal of necrotic (dead) tissue as part of the treatment. “In such operations it is
a frequent experience that the bone is reached before the patient feels anything, but he immediately feels pain
when the periosteum [the membrane covering the bone] is scraped or the bone attacked with forceps or saw. We
believe, however, that it is only nervous individuals who complain of pain; though it is certain that when the
bone is meddled with, something is felt. Probably in this connection may be explained by the statement of the
patients, that when walking they feel the ground.” (Hansen and Looft 1895: 64, italics in the original.)
 55

the book was to uncover the underlying mechanisms governing the development of
the disease. With the disease being juxtaposed with the bacillus, the experience of
having the disease was simply not relevant. The cause of the disease, the bacillus, was
an object found within the sick body. Exposing the true nature of the disease required
special expertise, not merely the experience of being host to the bacillus.
Expertise meant accuracy and impartial observation. In the text, with but one
exception, analogies to other objects were replaced by metric measurements.101 The
use of illustrations further underline the authors’ emphasis on the pathogen rather than
clinical signs: In addition to five photographs in the English edition, selected not to
highlight the typical but to produce unedited and accurate accounts of the disease,
were eight plates containing forty chromo-lithographs (colored prints) based on
microscopy, the position of the bacilli in the tissue and the cells. Instead of Danielssen
and Boeck’s idealized highlighting of the typical, this was ‘nature speaking for itself’
in all its complexity. In the terminology of Daston and Galison, the scientific ethos
was governed not by ‘truth-to-nature’ but by ‘mechanical objectivity’.102 The major
discussions revolved around where in the body the bacillus was to be found,
commenting observations made by other experts. Did the bacilli reside inside or
between the cells? What was the nature and role of the characteristic ‘globi’, the
brown collections of what appeared to be dead bacilli broken down into granules
(small compact particles)? These were questions for experts familiar with ongoing
debates, not an introduction to the disease for laymen – and definitively not a
reflection of the experiences of those being hosts to the bacillus.
Compared to Danielssen and Boeck, Hansen and Looft presented a new and

different way of knowing leprosy. The patients were still ‘lepers’, suffering from the





101
The only exception not using actual measurements was a reference to the French dermatologist Henri
Leloir’s description of the ulcerating blisters that maculo-anæsthetic cases sometimes developed: “They vary in
size – they may be small, from the size of a pea to that of a bean, or as large as the palm of the hand.” Hansen
and Looft 1895: 59. Leloir’s study, Traité pratique et théoretique de la lèpre (1886), was based on direct study
of 900 cases, many of them observed during a prolonged stay in Norway in 1884. See: Beeson, B. Barker.
“Henri Leloir, M. D.” Archives of Dermatology and Syphilology. Vol, 23, No. 3. 1931: 532-533; Sandmo,
Sigurd. “Portretter av en sykdom. Fotohistoriske perspektiver på det norske lepraarbeidet”. In: Irgens, Lorentz
M, Yngve Nedrebø, Sigurd Sandmo and Arne Skivenes. Lepra. 2006: 51-64.
102
Daston and Galison 2007: Chapter 3.
 56

same disease, but how they were to be studied, and what made the observations
interesting, differed. When what the experts see as relevant observations to produce
knowledge change, so do the activities necessary to produce the observations. As
John V. Pickstone has argued, each way of knowing is associated with a way of
working.103 For Hansen and Looft recognizing leprosy was no longer primarily a
question of looking for clinical signs, asking the patients about their experiences and
family background, or uncovering patterns in how the disease progressed over time,
but a matter of gathering tissue samples, mixing them with chemicals and observe
them through a microscope. For leprosy, as the opening example from Hansen
illustrates, the two approaches could ultimately lead to different conclusions in
deciding if a person was in fact a ‘leper’.
New ways of knowing are not like Kuhninan paradigms, replacing the old.
Instead they add to the repertoire of possible ways of knowing.104 This was also the
case for leprosy. Hansen and Looft’s study did not replace clinical diagnosis, it was
an addition. Despite the emphasis on the pathogen, the first act in making a diagnosis
was based on recognizing the characteristic clinical signs, especially nodules, local
anesthesia and swollen lymph glands. Despite presenting the bacillus as the ultimate
cause of the disease, actually detecting it was a backup. If in doubt, “a piece of skin
may be removed and examined for the presence of bacilli, which, at least in the
nodular form of the disease, are never absent.”105 Compared to On Leprosy (1847),
which aimed at teaching others to recognize the disease,106 Hansen and Looft’s book
was not as practically useful in making a diagnosis. Hence, Danielssen and Boeck’s
monograph would remain the celebrated go-to reference for clinical diagnosis also
after the publication of Hansen and Looft’s textbook.








103
Pickstone 2011: 235-245.
104
Op. cit.; Pickstone 2001; Pickstone 1993: 433-458.
105
Hansen and Looft 1895: 13-14.
106
The same can be said about Leloir’s richly illustrated monograph from 1886, which contained 12
photographs of patients and 10 colored prints of dermatological details. For an analysis of the use of
photography in leprosy research, see: Sandmo 2006.
 57

A nose for the ultimate proof


At the international leprosy conference in Berlin in 1897, the bacillus was one of the
highlights. In the widely published report of the conference the bacillus was the first
topic that was addressed: “As might be expected, a considerable portion of the
discussion has related to the bacillus Leprae, which the Conference accepts as the
Virus of Leprosy, and which for upwards of 25 years has been known to the scientific
world through the important discovery of Hansen and the able investigations of
Neisser.”107 What did the bacillus entail when it came to diagnosis?
The claim that the leprosy bacterium should impact diagnosis was first made
by the German physician Albert Neisser in 1884 in his chapter on chronic infectious
skin-diseases in the 16th volume of Hugo Wilhelm von Ziemssen’s edited series
Handbuch der speciellen Pathologie und Therapie.108 Drawing on Danielssen and
Boeck’s distinction between tubercular and anesthetic forms, Neisser stressed that
diagnosis primarily meant looking for clinical signs. The role of the bacillus was to
confirm the clinical diagnosis: Instead of having to wait (sometimes for years) to see
if the disease continued the path towards overtaking the body, a simple detection of
the bacillus was enough to remove all doubt. The bacillus was thus not only the cause
of the disease, but the ultimate proof that the disease was present.
In tubercular cases, finding the bacillus in samples from the affected areas was
relatively straightforward, Neisser withheld. “The diagnosis presents no difficulty in
the tubercular form. But it is the demonstration of bacilli which facilitates the
diagnosis of tubercular leprosy in the same way as it places each individual case
beyond doubt.”109 Diagnosing the anesthetic variety was more complicated: The
bacilli were fewer, and only found in the nerves and not in the surface on the skin.
Therefore, diagnosis had to be made based on clinical signs alone:






107
“Report of the general conclusions”. Mittheilungen 1897. II. Abtheilung. 1897: 190-192. The full text of the
reports and resolutions from the international leprosy conferences are found in Appendix 2.
108
The volume on Hautkrankheiten was translated to English by William Wood & Co in 1885, and published in
the United States as Handbook of Diseases of the Skin. All quotes are from the English translation.
 58

An accurate knowledge of the symptomatology is all the more requisite for these cases
because the criterion valid for the tubercular form, the presence of the bacilli, cannot be
utilized during life, of course, owing to the localization of the leprous process in the
peripheral nerves.110


At the conference in Berlin thirteen years later most physicians limited the importance
of the bacillus to confirming the symptom-based diagnosis in early or doubtful cases.
As for instance the Hungarian dermatologist Moritz Kaposi, professor at the
dermatological clinic at the University in Vienna, argued: Revealing the presence of
the bacillus was an ideal, but in practice not always possible. While Hansen argued
that without the bacillus there was no leprosy, Kaposi argued that if it was not
possible to detect the bacillus, clinical symptoms, especially local anesthesia, should
take priority.111 Judged by the discussions published in the proceedings of the
conference, published less than three months later, this was the majority view.
The main problem with basing diagnosis on clinical symptoms was that it
relied on judgment, and the judgement could differ. When American physician J. G.
McDougal presented two sisters at the Ohio State Medical Society in 1895 and asked
for help in making the diagnosis, for instance, the colleagues only hesitantly agreed
the sisters were suffering from leprosy.112 Some saw the clinical symptoms and
progress of the disease as a textbook example of leprosy, others pointed at the lack of
nodules and that the progress, color and location of the symptoms were strange. The
legs and hands were most severly affected, and several of the digits had been utterly
destroyed. The anesthetic patches were black. Although the disease appeared to
progress in stages, the fevers were not as disabling as usually the case with leprosy.

According to McDougal “Even though they have not true leprosy, they suffer from






109
Neisser 1885: 327.
110
Neisser 1885: 327.
111
Kaposi, M. “Allgemeine Bemerkungen”. Mittheilungen 1897. I. Abtheilung. 1897: 182-183.
112
McDougal, J. G. “Is this leprosy?” Transactions of the Semi-centennial meeting of the Ohio State Medical
Society held at Columbus, May 15, 16 and 17, 1895. 1895: 232-259. The conclusion of the debate is found on
page 25. The presentation and discussion, including a photograph, was reprinted in Journal of the American
Medical Association on November 2, 1895: 762-765.
 59

some disease so nearly like it in all its apparel of symptom as to afford me ample
apology for choosing the inquiry I did as the subject of my paper.”113
Further complicating the matter, the bacterial diagnosis pointed in a different
direction. Some months before the presentation, the left hand of the elder sister was
amputated and sent to the Military Health Service in Washington for bacteriological
examination. Surgeon M. J. Rosenau who conducted the bacteriological work could
not find a single bacillus and therefore concluded that the two were suffering from
syphilis.114 This, in turn, was countered by the argument that since the two sisters
probably suffered from anesthetic leprosy, detecting the bacillus was not always
possible and the lack of bacteriological evidence was irrelevant.115
After the proceedings were published, the discussion continued in the columns
of the Journal of the American Medical Association. New York-based physician
Albert S. Ashmead insisted that the sisters were probably syphilitic, pointing at the
unusual clinical signs, the missing leprosy bacillus and the fact that although the
father had experienced similar symptoms the mother was not affected.116 Physician D.
C. Newman, however, argued that no two cases of leprosy were exactly alike, but that
the two sisters were ‘close enough’ to the textbook examples for a definitive clinical
diagnosis. “I am sure that if Dr. McDougal’s two patients were to go before any








113
McDougal 1895: 239.
114
“All the sections were stained for lepra bacilli, with negative results. Those sections containing giant cells
were also stained for tubercle bacilli. None were found. The disease, therefore, in my opinion is neither leprosy
nor tuberculosis, which, by exclusion, throws some weight upon the suspicion of syphilis.” Letter from Assistant
Surgeon M. J. Rosenau, dated Washington, D. C, March 28, 1895. (Op. cit: 241.)
115
As physician J. B. Keber, who attended the meeting, put it: “I should be inclined to doubt the accuracy of the
diagnosis of tubercular leprosy if the diagnosis could not be confirmed by the discovery of the bacillus, but I
personally would not feel it necessary to modify my diagnosis of anesthetic leprosy one iota if a bacteriological
investigation failed to demonstrate the characteristic bacteria. That is the rule and not the exception. The
clinical symptoms are amply sufficient for accurate diagnosis.” (Op. cit: 258-259.) When J. G. McDougal again
presented the cases at the Section of Cutaneous Medicine and Surgery of the Fiftieth Annual Meeting of the
American Medical Association in Ohio in 1899, he had reached the same conclusion: “The fact that on
examination no lepra bacilla were found in the amputated hand can not mitigate as has been said, against the
diagnosis of anesthetic leprosy, because in this form of the disease their presence can but exceptionally be
demonstrated.” (McDougal, J. G. “Some Questions Relative to the Diagnosis of Anesthetic Leprosy”. The
Journal of the American Medical Association, January 27, 1900: 211.)
116
Ashmead, Albert S. “The Ohio Cases not Leprosy”. The Journal of the American Medical Association,
November 16, 1895: 872.
 60

medical examining board at Honolulu, they would be sent to Molokai without a
dissenting voice.”117
In the columns of the medical journal Lepra Bibliotheca Internationalis, papers
on diagnosis made up about a sixth of the 833 items published throughout the lifetime
of the journal (1900-1915). In general, clinical judgment took precedence over
laboratory findings.118 The case-studies typically began with describing the clinical
symptoms in the patient, often combined with the history of the patient’s travels and
speculations on where he or she could have caught the disease. The bacillus was often
highlighted as the decisive argument for settling the diagnosis, but usually mentioned
only after the clinical symptoms were exposed.119 In cases where the bacillus was not
found, this was emphasized as an abnormality but I have found no cases where this
had any impact on the diagnostic verdict.120
In principle, demonstrating the bacillus was an increasingly easy task. New
staining techniques were continuously being developed, making the bacteriological
examination both faster and more precise. In addition to being demonstrated at
conferences, the methods were frequently referred to in both textbooks and medical








117
Newman, D. C. “Was It Leprosy?” The Journal of the American medical Association. November 30, 1895:
965. From the late 1860s Molokai was used as Hawaii’s main leper colony. More on this in Chapter 4. See also:
Tayman, John. The Colony: The Harrowing True Story of the Exiles of Molokai. 2006.
118
The journal referred to 64 studies on diagnosis, in addition to 69 case studies which put more emphasis on
the patient’s prehistory in an attempt to find out where and when they caught the contagion but also described the
symptoms of the disease. There were also abstracts of sixteen studies which described smaller groups of patients,
ranging from two to forty cases. For more on Lepra Bibliotheca Internationalis and the role of medical journals,
see Chapter 6.
119 119
See i.e: Fabio, G. “Un caso di lepra tubercolare: herpes zoster in un lebroso”. Lepra Bibliotheca
Internationalis. 1903: Fasc. 3, originally published in: Gazzetta Medica Italiana 1902, No. 16; Dekeyser, L.
“Cas de lèpre anesthésique mutilante”, and Asselberg “Cas de lèpre maculeuse anesthésique”.Lepra Bibliotheca
Internationalis. 1903: Fasc. 3, reprinted from Bulletin de la Société Belge de Dermatologie et de
Syphiligraphie. March 1903, and Journal des Maladies Cutanées et Syphilitiques, October 1903: 743;
Matagne. “La lèpre à Bruxelles” Lepra Bibliotheca Internationalis. 1904: Fasc. 4, originally published
in Annales de la Sociéte Scientifique de Bruxelles. 1904; Grön, Kristian. “Leprafälle in Christiania in 1903”.
Lepra Bibliotheca Internationalis. 1905: Fasc 1, originally presented as a lecture in Christiania Medical
Association, 18. Mai 1904; Beurmann and Gougerot “Troubles sensitifs des lépromes”. Lepra Bibliotheca
Internationalis, 1907: Fasc. 4, originally presented as a lecture in Société francaise de dermatologie, 7.
December 1907.
120
See for instance Poirier’s presentation of two leprosy cases diagnosed in Antwerp in 1908. Poirier. “Deux
cas de la lèpre”. Lepra Bibliotheca Internationalis, 1908: Fasc. 4, originally published in: Societé Belge de
dermatologie et de syphiligraphie. 1908, No. 3.
 61


journals.121 But staining was not the only laboratory technique necessary in order to
find the bacillus. At the First International Leprosy Conference in Berlin in 1897, the
American bacteriologist Luis F. Alvarez, in charge of leprosy research in Hawaii,
argued that especially in the early stages of the disease, the elusive bacillus could hide
inside the tissue samples. Failure to detect the bacillus thus only proved that the
physicians sometimes were unlucky when selecting what piece of the body to look at
under the microscope. The solution, Alvarez argued, was a new technique for
preparing the sample prior to staining. This consisted of washing the tissue in saline
solution (and if necessary boiling it), and then grinding it in a mortar before staining.
This would ensure that no bacilli avoided detection by hiding inside the sample. This
was not the only solution to the problem, but unlike its alternatives, it was fast and
required no special equipment, like a centrifugal machine.122 In the following

decades, varieties of Alvarez’ method were adapted in several places, for instance


Calcutta.123
Grinding, boiling and staining did not assist in bacteriological diagnosis if the
physician chose a sample which contained no bacilli in the first place. Another hot
topic at the conference in Berlin was where in the body the bacillus was to be found.
In addition to skin snippets of leprous lesions, especially in the tubercular cases, the
nasal mucus, sputum and nasal excretion were long considered the most promising
sites for early detection. In Die Lepra Auf Madeira (1891) the German physician and
medical superintendent at the Lazaretto Hospital in Funchal, Julius Goldschmidt,
argued that he had found the bacillus in the nasal cavities in several of his patients,
and suggested that this might be the primary lesion of the disease. Leading up to the
conference in Berlin, several studies confirmed that the bacillus was detected in the





121
See i.e. Fick, James. “Zur Färbung der Leprabazillen in dünnen Gewebsschnitten”. Lepra Bibliotheca
Internationalis, 1907: Fasc. 4, originally published in: St.Petersburger Medicinische Wochenschrift. 1907, Nr.
27; Unna, Paul Gerson. “Über eine neue Doppel-färbung normaler und abgestorbener Bacillen im
Lepragewebe”. Lepra Bibliotheca Internationalis, 1907: Fasc. 4, originally published in: Monatsschrift für
Praktische Dermatologie. 15. February 1907.
122
Alvarez, Luis F. “A New Method of Bacteriological Diagnosis of Leprosy”. Mittheilungen 1897. II.
Abtheilung. 1897: 123-124.
123
For a slightly updated modification of the procedure, see: Rogers, Sir Leonard and Ernest Muir. Leprosy.
[1925] 1940: 210-213.
 62

patients’ nasal secretion.124 At the conference proper, the French physician Edouard
Jeanselme argued that the nasal membranes were the best spot to examine in order to
make early diagnosis, and in addition to being the initial lesion of the disease this
might be a pathway for contagion.125 In the concluding report from the conference,
examination of the tissue and excreta originating inside the nose was highlighted as a
promising avenue for further research.126 In Norway, it inspired Hansen to organize a
collection of nasal excretions from family members of home-living patients, not
necessarily to develop an ‘early warning system’, but with the hope that this could
bring light on the initial lesion of the disease.127 In several leprosy institutions, the
physicians began systematic testing of the noses of the patients. The results from the
nasal test did, however, differ greatly. While Georg Sticker found the bacillus in 127
of 153 cases in Germany (83%),128 Wilhelm Kolle detected the bacillus in 88 of 137
cases in South Africa (64%).129 At the Pleiestiftelsen leprosy asylum in Bergen,
Norway, H. P. Lie discovered the bacillus in only 35% of the patients’ nasal mucus.130
In the medical textbooks published after the Berlin conference in 1897, the


leprosy bacillus was elevated as the decisive cause of the disease.131 There were also




124
For details, and also an overview of studies aimed at detecting the bacillus in saliva, urine, faeces, sweat and
lachrymal (eye) secretions, see: Hollmann, Harry T. “The presence of acid-fast bacilli in secretions and
excretions of lepers.” Public Health Bulletin. No. 61. 1913: 15-17. For a list of 30 studies examining the
presence of the leprosy bacillus in the nose, see: Hollmann, Harry T. “A statistical study of the nasal lesions in
leprosy”. Public Health Bulletin No. 50. 1911: 21-23
125
Jeanselme, E. and Laurens. “Des localisations de la lèpre sur le nez, la gorge et le larynx.” Mittheilungen
1897. II. Abtheilung. 1897: 18-48. The argument was backed by 31 cases.
126
‘Report of the general conclusions’. Mittheilungen 1897. II. Abtheilung. 1897: 190-192. See: Appendix 2.
127
Hansen, G. Armauer. “Nogle leprasprgsmaal”. Medicinsk Revue, 1897: 324-325. A year later, having
received only two replies, he repeated the request. Hansen, G. Armauer. “Spedalskhedens overførelse”.
Medicinsk Revue. 1898: 297. The project was later abandoned.
128
Sticker, G. “Untersuchen über die Lepra.” Arbeiten aus dem Kaiserliche Gesundheits-Amte, Band 16, 1899:
38.
129
Kolle, W. “Mittheilungen über Lepra nach Beobachtungen in Südafrica.” Deutsche Medizinische
Wochenschrift, 1899: 647.
130
Lie, H. P. Beretning fra Plejestiftelsen for spedalske No. 1 i Bergen for årene 1895 til 1898. 1899. Referred
to in Norsk Magazin for Lægevidenskaben. 1899: 1217 and Lepra Bibliotheca Internationalis. 1900. For more
results from nasal tests, see: Rogers and Muir [1925] 1940: 153-155.
131
The opening statement on the entry on leprosy in An Introduction to Dermatology (1899) by Norman Walker
(who translated Hansen and Looft into English four years earlier) was that: “Leprosy is a chronic disease caused
by the presence of the lepra bacillus.” (Walker, Norman. An Introduction to Dermatology. [1899] 1902: 257.)
With some differences in emphasis, identifying the disease with the bacillus soon became a standard formula,
both in general textbooks and books on dermatology and tropical diseases. Some examples: “A chronic
infective granulomatous disease produced by a specific bacterium, and characterized by lesions of the skin,
nerves and viacera eventuating in local anæsthesia, ulceration, and a great variety of trophic lesions. After a
 63

frequent references to the nasal test. For Richard L. Sutton “the quickest and most
certain method of diagnosing the disease is by the recognition of the bacilli in the
affected tissues, in serum or blood obtained from the lepromatous nodules, or in the
nasal discharges.”132 Ludwig Török argued that changes in pigmentation and
anesthetic lesions were the first signs to look for; the bacillus in the lesions and nasal
discharges was the second.133 For W. Hamilton Jefferys and James L. Maxwell early
diagnosis should focus on whether the patient experienced loss of temperature
reaction and absence of sweating from the affected areas. Detecting bacilli in the
nasal secretion was not strictly necessary, but offered “considerable assistance” in the
diagnosis.134 Sir Leonard Rogers and Ernest Muir argued in Leprosy (1925) that: “The
examination of the nasal mucous membrane is almost as important as that of the skin.
It occasionally gives positive bacteriological findings when the skin is negative.”135
The nasal test was also made part of the medical education. In two lectures to students
at the St. Thomas Hospital in London in 1907 referred to in Lepra Bibliotheca
Internationalis, for instance, British epidemiologist Fleming Sandwith stressed that
the nose should always be tested.136








long course it is almost invariably fatal.” (Manson, Patrick. Tropical Diseases. A Manual of the Diseases of
Warm Climates. [1898] 1903: 478); “Leprosy is a chronic, infectious malady, due to the bacillus leprae of
Hansen, characterized by alteration and destructive changes in the cutaneous, nervous or bony structures of the
body.” (Sutton, Richard L. Diseases of the skin. 1919: 803); “Leprosy is a general disease with a chronic and
paroxysmal course, due to the Bacillus leprae of Hansen, and characterised by lesions in the skin, macous
membranes, nerves and viscera. It is transmissible from man to man, but the method of infection is unknown.”
(Macleod, J. M. K. Diseases of the Skin. A Text-Book for Students and Practitioners. 1920: 496.)
132
Sutton 1919: 814.
133
Török, Ludwig. Spezielle Diagnostik der Hautkrankheiten für Praktische Ärtze und Studierende. 1906: 319-
325.
134
Jefferys, W. Hamilton and James L. Maxwell. The Diseases of China. Including Formosa and Korea. 1911:
100. Interestingly, Jefferys and Maxwell also included a third form of leprosy in addition to the nodular and
nerve (their term for anaesthetic) leprosy, namely the ‘macular’ variety. The aacular form produced small,
lightly raised patches less sensitive to pain and recognizing hot and cold, but it never produced mutilations.
Their argument for this being a variety of leprosy was that it was only found in areas where the disease was
endemic; that the loss of temperature sensation was rare in other diseases; that it often mixed with the other
forms; and finally “Because occasionally lepra bacilli are to be found in the nasal secretion of these patients.”
(Op. cit.: 97.) Unlike the other textbooks, Jefferys and Maxwell underlined that “the discovery of the bacillus
has hardly increased our knowledge of the pathology and treatment of the disease.” (Op. cit.: 92.)
135
Rogers and Muir [1925] 1940: 211.
136
Sandwith, F. M. “Two Lectures on Leprosy”. Lepra Bibliotheca Internationalis. 1907: Fasc. 4, originally
published in Clinical Journal, 1907: 782-3.
 64

But did the nose test settle diagnosis? Several physicians were critical. In
Lisbon in 1906, at the fifteenth International Medical Congress, the Portuguese
dermatologist Zeferino Falcão pointed out that occasionally family members of lepers
also tested positively on the nose-smear test, without ever producing clinical
symptoms of the disease.137 In his view, the test was unreliable because it detected too
many cases. Jonathan T. MacDonald at the leprosy investigation station in Hawaii
argued, to the contrary, that the nasal examinations were worthless because they did
not detect enough cases. After studying 150 cases in 1903, he concluded: “After many
faithful trials in every stage of the disease I have found them so seldom that I now
attach but little importance to it as a means of diagnosis.”138 Seven years later,
leprologists Walter Ramson Brinkerhoff and William J. Moore, also working on
Hawaii, agreed that the nasal test alone was secondary to clinical diagnosis but that it
could detect ‘the most dangerous’ cases:

When it is not practicable, to make a complete physical examination of all individuals of a
class suspected of leprosy, the examination of the nasal septum and the bacteriological
examination of the nasal secretions will prove of value by permitting the recognition of the
most dangerous type of the disease, and is therefore worthwhile, even if it does not reveal all
cases of the disease in those who come under observation.139

By the 1930s, however, the premise for the nasal test had changed. Subsequent
studies of 250 leprous children in the Philippines showed that the bacillus was
detected in the skin before it reached the nose, and that instead of being a primary











137
Zeferino Falcao. “La rhinite lépreuse. Communication au Congrès internat. De Lisbonne 1906.” Lepra
Bibliotheca Internationalis. 1907: Fasc. 1, originally published in: Presse de médecine 1906.
138
MacDonald, J. T. “A Diagnostic Examination of One Hundred and Fifty Cases of Leprosy.” The Journal of
the American Medical Association. 1903: 1567.
139
Brinckerhoff, W. R. and W. L. Moore. “The Utility of the Examination of the Nose and the Nasal Secretions
for the Detection of Incipient Cases of Leprosy”. Lepra Bibliotheca Internationalis, 1910: 174, also referred to
in Pinkerton, F. J. “Leprosy of the Ear, Nose and Throat. Observations on more than two hundred cases in
Hawaii.” Archives of Otolaryngology, No. 4. October 1932: 469-487.
 65

lesion, the nasal mucous membrane was one of the last places the bacillus persisted in
those who reacted positively to treatment.140
Despite questions of its reliability, the nasal examination would be used not
only to detect new (or dangerous) cases; it was also employed in leprosy institutions
to decide if a patient could be released. In South Africa, where the passing of the
Leprosy Repression Act in 1892 made segregation compulsory, the leper asylums was
a final destination. Once admitted, the patients were imprisoned for life. This changed
in 1908, when a national Leprosy Commission began periodic visits to the institutions
to look for misdiagnosis and ‘arrested’ (bacteria-free) cases. On Robben Island
leprosy colony, which had hosted leprosy sufferers since 1846 and was massively
expanded after 1892, the Commission’s first visit in March 1908 led to four patients
being discharged. In September, one more patient was released and ten more subject
to further testing at their next visit. At the nearby Emjanyana Leper Asylum, which
opened in 1897, six patients were discharged at the Commission’s first visit.141
From around 1915 similar procedures were introduced on Hawaii. An absence
of the leprosy bacillus in three successive microscopic examinations at intervals of
three months was grounds for ‘parole’. After four years of out-patient treatment, a
final examination could result in a release.142 Between 1915 and 1925, 104 patients
from the Kalihi Hospital received the ‘final release’, while in 102 cases the disease
relapsed during parole.143 The nasal test was thus redefined from initial diagnosis to a
test employed in deciding if someone could be released. As physician Forrest Joy
Pinkerton put it in 1932:




140
Solis and Wade’s study of Philippine children was published in Journal of the Philippine Island Medical
Association, Vol. 5, December 1925, the follow-up in the same journal in 1927 (No. 1). Referred to in: Burnet,
Et. “Provisional report presented at the Leprosy Commission at its meeting at Tokyo in April 1930:
Consideration of urgent matters to which the commission drew attention at its May session, 1928”. League of
Nations, C. H./Leprosy/7a, Geneva, January 1930: 5
141
Gregory, John A. “Report of the Medical Officer of Health for the Colony of Cape of Good Hope (1908).
Lepra Bibliotheca Internationalis. 1909: Fasc. 3.
142
A similar system was set up at the leprosarium in Carville, Louisianna, after it came under Federal control in
1921. Patients who tested negatively on a bacteriological test were moved to a ‘non-contagious section’ and held
there for two years before being submitted to a final examination. After release, they were subject to
examinations every six months for three years before receiving a definite discharge as ‘arrested’ and no longer a
danger to public health. De Souza-Araújo, Heráclides César. Leprosy Survey made in Fourty Countries (1924-
1927). Instituto Oswaldo Cruz, Rio de Janeiro. 1929: 32.
 66



In Hawaii, so much do we depend on the nasal examination that no patient is recommended
for release as having a quiescent case until his nasal ‘snippings’ have been bacteriologically
negative for a period of three months, or even longer, even though the disease is otherwise
clinically inactive before the nasal investigation is begun.144


On the Philippines, a similar system was introduced in March 1922. By September

1925, 545 ‘lepers’ at the leprosarium on Culion were reported as ‘bacteriologically
negative’; 238 had been discharged.145 The introduction of the bacillus as the cause of
the disease thus made it possible to develop the terms ‘quiescent’, ‘arrested’ or
‘bacteriologically negative’. These terms were introduced by the end of the first
decade of the 20th century (followed by the term ‘burnt-out case’), and ultimately
made it possible to look like a ‘leper’ and still be released from confinement.146 For
the individuals concerned, this could have dramatic consequences. The bacillus, or
more precisely the lack of the bacillus, was what set them free.
At the same time, bacteriologically negative did not mean that
mutilations healed. In the Philippines, for instance, several of those discharged from
Culion returned to live in the colony. As physician Heráclides César de Souza-Araùjo
from Brazil reported after a visit in the mid-1920s: “…either they were not welcomed
by their families or by the society, having been considered lepers on account of their
scars or mutilations. Here is a new economic-social problem to be solved.”147




Showcasing the living body


Identifying the bacillus was an addition to, not a replacement for, clinical diagnosis.
Besides opening for possible disagreements, a problem with symptom-based




143
De Souza-Araújo 1929: 75-78.
144
Pinkerton, F. J. “Leprosy of the Ear, Nose and Throat. Observations on more than two hundred cases in
Hawaii.” Archives of Otolaryngology, No. 4. October 1932: 475.
145
De Souza-Araújo 1929: 152; 205-206.
146
The term ‘burnt-out’ seems to be in use from the late 1920s, and was made famous by Graham Greene’s
novel with the same title published in 1960, set in a leprosy colony in Congo.
 67


diagnosis was that it required experience and specialist training.148 Reading

descriptions or looking at images and photographs was helpful, but not sufficient
when learning how to recognize the disease. The solution was learning from living
patients.
From the published proceedings of the medical meetings, often printed in
abstracts in the medical journals, it seems the practice of showcasing living patients
was widespread. There were mainly two motivations behind bringing patients to
medical meetings: To teach others what clinical signs to look for, and to determine
diagnosis in uncertain cases – sometimes with lifelong consequences for the
individual put under scrutiny.
The most prominent exhibition was arranged by the British physician Jonathan
Hutchinson at the Seventh International Medical Congress in London in 1881.
Beneath the chandeliers of the boardroom of the Geological Society at the Burlington
House, seven patients with leprosy, six diagnosed with myxedema and several cases
of lupus were exhibited in a makeshift medical ward.149 The exhibition was, however,
a victim of its own success: As Hutchinson noted: “confusion and crowding (…). Our
exhibition was more popular than we had expected: every morning at the hour
announced, the room filled. The weather chanced to be very hot, and as the room
looked into Piccadilly, it was exceedingly noisy.”150 Still, already the next










147
De Souza-Araújo 1929: 152. More on de Souza-Araújo’s travels in Chapter 7.
148
The same could be argued for bacteriological diagnosis. In 1909, in the case of John Early, a former soldier
and suspected ‘leper’, samples of skin tissues was sent to Armauer Hansen in Norway for a final verdict.
Johnson, Felix S. S., American Consul to Norway. Letter to The Honorable Assistant Secretary of State, dated
Bergen August 20, 1909. The National Archives, Washington, USA. Five years later, John Early caused a
public outcry when traveling to Washington to meet with politicians demanding that the government provided
better care for people in his situation. See: Moran 2007: Chapter 1.
149
Schupbach, William. “The Exhibition of Living Patients, 1881” Wellcome Library Blog. 2009. (http:
//libraryblog.wellcome.ac.uk/libraryblog/2009/10/the-exhibition-of-living-patients-1881/). In the adjoining
exhibition, among more than 700 items, there were also twelve pictures of leprosy patients and two
microscopical demonstrations. See: International Medical Congress. Catalogue of Temporary Museum held at
the Geological Society, Burlington House. 1881.
150
Transactions of the International Medical Congress, 7th session, London 1881, vol. 1, pp. 109-132, referred
to in Schupbach 2009.
 68

International Medical Congress in Copenhagen in 1884 saw a similar exhibition,
though with fewer patients and more wax-models and images.151
Showcasing patients neither started, nor ended, at the International Medical
Congresses.152 But instead of arranging exhibitions, displaying local cases in smaller
sessions seems to have been more common. After J. G. McDougal again had
presented the two Ohio-sisters suspected of having leprosy at the Fiftieth Annual
Meeting of the American Medical Association in 1899, Dr. Bishop of New York City
argued that showcasing living patients was necessary in order to teach physicians how
to recognize the disease. The rationale was not primarily that the individuals could be
treated, but because it would promote early segregation and thus prevent new cases:


The general practitioner is very much interested in leprosy, always, and when he gets hold
of a case he generally shows it around. Last winter, I borrowed some cases from Dr. Fox
and showed them at the session of the General Academy, and they excited much interest.
General practitioners, myself included, do not know these conditions until they are brought
before them. I think many of these cases abound and many might be saved from infection if
these patients were more generally recognized.153

In addition to showcasing patients at meetings, leprosy institutions opened their doors
to visiting physicians. As Ashburton Thompson, head of the leprosy services in New
South Wales (Australia), stressed: “Every opportunity has been given to members of




151
“Of the many diseases under consideration, leprosy claimed a large share of notice. Four living examples
were shown – two adults by Mr. Hutchinson, and two boys aged respectively eight and nine years by Dr.
Radcliffe Crocker. All these had contracted the disease abroad, and the chief points of interest were the gradual
dying out of the disease in an elderly woman (…) Many wax models, photographs and portraits of leprosy were
on view in the museum from the collection of Dr. E. de Wahl of Dorpat, and Guy’s Hospital, &c.” Editorial.
“Disease of the Skin at the Congress in Copenhagen.” The Lancet. 13. August, 1881: 307.
152
Although no living patients were showcased at the international leprosy conference in Berlin, several
pictures and microscopic preparations were exhibited. A. Grünfeld from Rostow brought one hundred
photographs, while Phineas S. Abraham from London brought 18 lantern slides. Abraham also brought an
installation showing the leprosy bacillus stained with different techniques and at different levels of
magnification, prepared by Dr. Lawrence Herman, also from London.
153
McDougal, J. G. “Some questions relative to the diagnosis of anæsthetic leprosy.” Lepra Bibliotheca
Internationalis. 1900: 246, originally published in: The Journal of the American medical Association, Jan. 17,
1900: 210. The discussion led to no firm conclusion on whether the disease the sisters suffered from actually
was leprosy. As McDougal concluded: “I hope that the character of these cases may yet be positively
ascertained, and if it is, I hope it may be found to be some other disease than leprosy, for it would seem a
 69

the medical profession to visit the lazaret for the purpose of seeing such patients as
were formerly under their care, and for study of the disease.”154 As I will return to in
Chapter 7, the practice of traveling to visit leprosy institutions was a common
practice. Visiting institutions also included investigating patients.
The patients in the institutions had already been diagnosed. The verdict leading
to institutionalization was often organized in health boards, which too involved
inspecting living patients. The procedures were often detailed in books and medical
journals, and indicate that in practice clinical and laboratory techniques were
complimentary, not mutually excluding. In the Philippines, for instance, former
Director of Health Victor G. Heiser described:


For the clinical examination of the anesthetic form the suspect was blindfolded. Then his
skin was touched with a cotton swab, a feather, a camel’s hair brush or a paper spill, and he
was asked to indicate where he had been touch. The head and the point of a pin were
pressed alternately against suspected spots, and the patient was asked which caused the
more pain. Test tubes, one filled with hot water and the other with cold, were held against
his skin, and he was asked to tell which was warm and which was cold. Finally, a scraping
was taken from the septum of the nose with a blunt, narrow-bladed scalpel, and put under
the microscope.155


In Calcutta, Sir Leonard Rogers and Ernest Muir described a similar procedure:


The patient is stripped as far as possible and blindfolded. Sensation is tested by touching
different points on the skin surface with a light object such as a feather or camel-hair brush,
the patient being instructed to place his index finger exactly on the points touched. (…) The
most conclusive proof of leprosy is finding Hansen’s bacillus in the tissues. But, as we have
shown, it may be difficult or impossible to find bacilli in lesions of the neural type, and in
these we must rely chiefly on clinical signs.156





menacing disclosure to learn that the bacillus of leprosy can be carried from a distant place to a fertile soil in the
interior of the United States.” (Op. cit: 248-249.)
154
Thompson, Ashburton. “On leprosy in New South Wales, for the year 1904”. Lepra Bibliotheca
Internationalis 1906: 125.
155
Heiser, Victor. An American Doctor’s Odyssey: Adventures in Fourty-Five Countries. 1936: 232.
156
Rogers and Muir [1925] 1940: 207-208.
 70

In the columns of Lepra Bibliotheca Internationalis, there were those that argued that
the leprosy bacillus had stolen the limelight from much needed clinical research. In
1914 American physician James Albert Honeij published a study based on examining
fifteen patients at the Massachusetts leprosy colony on the island of Penikese.157 His
main finding was that the patients all had a very high pulse, and that recognizing this
sign should be part of the diagnostic toolbox. Had the physicians spent more time at
the bedside, and less time in the laboratory, he argued, this would have been noticed
much earlier.158 In general, however, there does not seem to have been much conflict
between the clinic and the laboratory. Identifying the leprosy bacillus in the laboratory
was by most considered an addition to clinical judgment and not a replacement.





The elusive test


Diagnosis could sometimes lead to disagreements among the experts, and much
research was driven by an aspiration of finding a test which quickly and decisively
could determine whether a person was affected by leprosy or not. The tests built on
different strategies, but all had one thing in common: They failed to achieve the
objective. Some of the tests initially designed to decide whether a person was affected
by leprosy would instead be reinterpreted and used in classification of cases, or used
in the hope that they could help predict the progression and outcome of treatments.
The first test which ended up as part of the diagnostic toolkit was uncovered by
mistake when Danielssen, probably in the 1860s, tried using potassium iodide to treat
patients. Administering the chemical compound orally did not lead to improvement,
rather the opposite: The patients consistently reacted with a strong fever. Instead of




157
The Massachusetts leprosy colony was established in 1905, and closed down in 1921. The thirteen remaining
patients were then transferred to the U.S. National Leprosarium in Carville, Louisiana.
158
Honeij, J. A. “Leprosy. Some Notes on Symptoms” and “Leprosy. The Pulse as a possible Indicator of the
Progress of the Disease”. Lepra Bibliotheca Internationalis 1914, Fasc. 2, originally published in Boston
Medical and Surgical Journal, 15. January and 22. February 1914, and also printed in Tropical Disease
Bulletin, May 1914. The paper also shows how the same observations could be presented as new discoveries
several times. In 1908, Japanese dermatologist Takekichi Sugai had discussed the exact same symptoms. Sugai,
T. “Über die Erweichung und Vereiterung der Lepraknoten”. Lepra Bibliotheca Internationalis. 1908: Fasc. 3.
 71

putting the drug on the shelf, this became Danielssen’s final test in deciding if a
patient could be released as ‘cured’ from the Lungegaarden research hospital in
Bergen: If the compound did not produce a fever, the patient was cured.159 At the
Berlin conference in 1897, where Jeanselme advocated the nose as a place to look for
the leprosy bacillus, administering potassium iodide was suggested as a way to incite
the bacillus so that it did not avoid detection. When Etienne Burnet, secretary of the
League of Nations Leprosy Commission, in the late 1920s took stock of the numerous
diagnostics methods in use, he referred to potassium iodide as the best known method
for making a ‘biological diagnose’.160
While potassium iodide was quietly adopted in numerous locations, the Bordet-

Wassermann-test led to far greater attention. This method was developed in Berlin in

1906 by August Wassermann, Carl Bruck and Albert Neisser to detect syphilis, and
drew on Jules Bordet and Octave Gengou’s research on complement-fixation that had
begun five years prior.161 The test consisted of collecting blood serum from a
suspected case and mixing it with an antigen consisting of alcohol-treated muscle
extract from a bulls’ heart in a glass cylinder. The intensity of the reaction correlated
with the intensity of the infection. Ludwig Fleck has argued that the test in fact
redefined syphilis from a display of symptoms to testing positively on the
Wassermann-test.162
For leprosy patients, like the nasal test (and unlike potassium iodide), the
results of the Wassermann-test were highly inconsistent. When the three Swedish
physicians J. Jundell, Johan Almkvist and F. Sandmann in 1908 tested 26 ‘lepers’ in




159
Opposed to Hansen and Looft’s bacteriological diagnosis, it seems Danielssen’s demanded the patients to be
symptom-free before using the label ‘cured’. When discharging patients at their request, he often used the term
‘improving’. For a review of potassium and other compounds producing fevers, subcutaneous haemorrhage and
other side effects, see Siebert, C and V. F. K. Klingmüller. “Beiträge zue Kenntnis der Jodreaktion der
Leprösen.” Lepra Bibliotheca Internationalis. 1904: Fasc 4; Pautrier, L.-M. “Le Diagnostic de la Lèpre par les
Méthodes de Laboratoire.” Lepra Bibliotheca Internationalis. 1915: Fasc 1, originally published in: La Presse
Medicale, 14. March, 1914.
160
Burnet, Et. “Provisional report presented at the Leprosy Commission at its meeting at Tokyo in April 1930:
Consideration of urgent matters to which the commission drew attention at its May session, 1928”. League of
Nations, C. H./Leprosy/7a, Geneva, January 1930: 5.
161
Wassermann, A. P., A. Neisser and C. Bruck. “Eine seriodiagnotische Reaktion bei Syphilis. ” Deutsche
medizinische Wochenschrift. No. 19, 1906: 475-476.
162
Fleck [1935] 1979.
 72

Sweden’s only specialized leprosy institution in Järvsö, they found 4 positive
reactions, 4 partial reactions and 16 negative reactions. The positive reaction, they
speculated might indicate that some of the lepers had in fact syphilis.163 Divergences
were noticed also in other studies, and led to different strategies for classifying the
cases in order to explain the results. Two years after the Swedish study, German
physicians Carl Bruck and E. Gessner found that five out of seven of their tubercular
patients reacted positively to the test, but none of the anaesthetic cases.164 That the
reaction was more common in tubercular cases was also argued by the Berlin-based
bacteriologist (and later Robert Koch-biographer) Bernhard Möllers. Not having
access to any patients of his own, he received 32 serum samples from Memel,
Southern Karpaten in Romania, Egypt, Bosnia and Tokyo and found that all but seven
reacted positively. The reaction was stronger in the more tubercular cases.165 In 1923
the Calcutta based researchers R. B. Lloyd, Ernest Muir and G. C. Mitra found that of
286 cases of ‘undoubted leprosy’, 41,7% of all cases tested positive, with a higher
proportion in nodular cases and “very much higher figures” in children than in
adults.166
The Wasserman test was also used in differential diagnosis. In 1913, American
bacteriologist Moses Tran Clegg found that 11 of 24 cases at the United States
Leprosy Investigation Station in Hawaii tested positively to the test, and suggested
using lutein as a tool to decide whether the positive results were caused by syphilis or
leprosy. Lutein was an inactive solution of the syphilis spirochete which Clegg argued
reacted with syphilis but not with leprosy.167






163
Jundell, J., Johan Almkvist and F. Sandmann. “Wassermanns Syphilisreaktion bei Lepra”. Lepra Bibliotheca
Internationalis. 1909: Fasc. 4, originally published in: Centralblatt für Innerren Medicin, 28. November 1908.
Järvsö hospital in Hälsingland was the only state leprosy institution in Sweden. It was established in 1867, and
closed in 1943.
164
Bruck, Carl and E. Gessner. “Über Serumuntersuchungen bei Lepra.” Lepra Bibliotheca Internationalis.
1910: Fasc. 1, originally published in: Berliner Klininische Wochenschrift, 29. March 1909.
165
Möllers, Bernhard. “Serologische Untersuchingen bei Leprösen.” Lepra Bibliotheca Internationalis. 1913:
Fasc. 3, originally published in: Deutsche Medizinische Wochenschrift. 1913, no. 13.
166
Lloyd, R. B; Muir, E; Mitra, G. C. “The Wasserman Reaction in Leprosy”. Indian Journal of Medical
Research. Vol. 11, No. 1, July 1923: 229-233.
167
M. T. Clegg. “Absence of luetin reactions on lepers showing a positive Wassermann reaction.” Lepra
Bibliotheca Internationalis. 1915: Fasc. 1, originally published in: Public Health Bulletin no. 61, July 1913.
 73

There were also attempts at changing the doses, administering the test using
different temperatures, as well as using other sources than bovine heart or muscle-
extracts to produce the antigens used in the test.168 After analyzing 75 papers on the
Wasserman test in the mid-1920s, H. C. de Souza-Araùjo found that the proportion of
cases reacting positively varied between 30 and 90 percent, and that “in cold and
temperate climates the percentage of positive reactions nearly doubles.”169 This was
not the only interpretation. Did the results prove that leprosy was closely related to
syphilis, or was it an indication that many had both diseases? Did the stronger
reaction in children prove that disease caused the patient’s antibodies to change over
time? Could the reaction (or lack thereof) be used to predict the progress of the
disease? At the end of the 1920s, Dr. Etienne Burnet concluded on behalf of the
League of Nations Leprosy Commission that “the value of this test for the diagnosis
of leprosy would seem to be very small”, and recommended that the researchers
instead focused their efforts elsewhere.170
One of the attempts at finding an alternative to the Wassermann-test did have

lasting consequences. Inspired by Clemens von Pirquet and Charles Mantoux’ skin-
test which assessed the immune response to tuberculosis, developed in 1906, Japanese
leprologist Kensuke Mitsuda published a paper on Lepromin in 1919 which argued
that the substance could be used in a similar way to decide if someone had leprosy.171
The research was presented at the International Leprosy Conference in Strasbourg in
1923 but received little attention outside Japan. Ten years later it was reworked by
Fumio Hayashi and featured as one of the major pieces in the first issue of the
International Journal of Leprosy.172 By then it was clear that the Mitsuda’s test had
failed to achieve the objective of making a decisive diagnosis, but it remained in use





168
See i.e. Bruck and Gessner 1909.
169
De Souza-Araújo 1929: 29.
170
Burnet 1930: 9.
171
Mitsuda, K. “On the value of skin reaction with emulsion of leproma”. Japanese Journal of Dermatology
and Urology. No. 19. 1919: 697-708. In 1931, Mitsuda was appointed to be the first Vice-Chairman of the
Eastern Section of the International Leprosy Association. (“Association News.” International Journal of
Leprosy. No. 1, 1933: 95-96.)
172
Hayashi, F. “Mitsuda’s skin reaction in leprosy”. International Journal of Leprosy. No. 1, 1933: 31-38.
Thanks to Bjørnar Mortensen Vik for scanning this for me.
 74

for decades to distinguish between different types of the disease, and to monitor the
impacts of treatment.





Diagnostic pluralism and local variations


While the presence of the leprosy bacillus from around 1900 had dominated as a
decisive proof when making a diagnosis, the 1920s saw a new dawn for disease
models arguing that the bacillus alone was not sufficient to produce the disease. Some
predisposing cause was also necessary. Originating at the medical community at the
School of Tropical Medicine and Hygiene in Calcutta, the main argument was that if
the bacillus alone had been enough to produce leprosy, more people would have
caught the disease. As Sir Leonard Rogers and Ernest Muir put it; “We consider that
it is highly probable that in an endemic area less than half of those who are inoculated
with the germs of leprosy develop the disease.”173 The same objection, that
developing the disease took more than just the bacillus, had also been raised in the
decades surrounding the turn of the century but was not pursued as a line of
research.174
Emphasis on predisposition was closely linked to early diagnosis and the
argument that treatment should begin as early as possible, ideally before the clinical
signs became severe.175 In the 30-page booklet Leprosy: Diagnosis, Treatment and
Prevention (1924), head researcher in Calcutta, Ernest Muir, argued that “a relative
cure can in the large majority of cases be obtained if the disease is taken in hand in





173
Rogers and Muir [1925] 1940: 220.
174
One of the strongest opponents of predisposition was Gerhard Armauer Hansen. In his review of Leopold
Glück’s Die Lepra in knapper Darstellung (1900), for instance, he argued: “We are too ignorant to know what
confers the predisposition. (…) To say that poor people are more predisposed to these diseases than the well to
do is in my opinion only to clothe our ignorance in high sounding words which tell us nothing. While it seems
to me tolerably certain that the greater the overcrowding and intercourse among the poorer classes the greater
the chances of infection; and in consequence I prefer this interpretation, for as far as I know leprosy everywhere
prevails where the chances of infection are increased. Well to do people often get the disease when they expose
themselves to such conditions.” (Hansen, G. A. “Die Lepra in knapper Darstellung”. Lepra Bibliotheca
Internationalis. 1900: 217.)
175
I will discuss in more details the Calcutta school’s line of reason in Chapter 7.
 75

the first stage; but this becomes increasingly difficult and requires an increasingly
long course of treatment as the disease advances.”176 The publication was distributed
by The British Empire Leprosy Relief Association (BELRA), both within the British
Empire and Mission to Lepers.177
The two cardinal points in diagnosis, according to Muir, was “finding of lepra
bacilli and the presence of anæsthesia, the former in the skin type and the latter in the
nerve type.”178 In absence of the bacillus or anesthesia, a combination of two of more
of the following signs would arouse a strong suspicion of leprosy: Deep analgesia
(insensitivity to the prick of a pin or the cut of a knife), loss of the sense of heat and
cold in the areas around a patch of anesthesia, hyperanesthesia (an abnormal increase
in sensitivity to stimuli), depigmentation, erythematous patches (redness of the skin),
thickening of superficial nerve trunks, parakeratosis (scaly, dry, thickened and glossy
skin), anhydrosis (the inability to sweat), interfollicular swelling (enlargement of the
lymph nodes), dry rhitintis with ulceration (infection in the nostrils), irregular pyrexia
(fluctuating body temperature), tropic blisters and later tropic ulcers in the midst of
anesthetic areas.


The presence of one or more of these subsidiary signs should be considered a sufficient
reason for keeping a patient under observation. As a rule, if the case is one of leprosy, one
of the two important signs will soon establish itself and clear up the diagnosis.179



Two points separated the Calcutta-school from the bacteriological school of thought
that had dominated before the Great War: A firm belief that leprosy in most cases
could be cured, and an emphasis on predisposing causes.180 Or, as Muir put it: “Some
predisposing cause or loss of natural resistance must also be present to change the






176
Muir, Ernest. Leprosy: Diagnosis, Treatment and Prevention. Illustrated. Cuttack: Orissa Mission Press.
1924: 2. The arguments were repeated in Rogers and Muir 1925.
177
Correspondence between the League of Nations and BELRA, 1925. (LNHO: 12B-R898/2942/42641).
Muir’s work was also reprinted in Chinese medical journals.
178
Muir 1924: 2.
179
Muir 1924: 8.
180
The specific treatments will be addressed in Chapter 3.
 76

tissues of the human body into a medium fit for the growth of the lepra bacillus.”181 In
the monograph Leprosy published in 1925, he expanded: “When a case has been
established beyond all doubt as one of leprosy, only half the diagnosis has been made;
it is no less necessary to find out what is the predisposing cause.”182 The predisposing
cause was what lowered the resistance of the body and made the attack of the lepra
bacillus successful. The main predisposing causes were temporary diseases such as
influenza, chronic ailments such as bowel diseases, syphilis, malaria or hookworm;
climatic conditions, unhealthy and insanitary surroundings; lack of sufficient exercise
or unsuitable diet. Early treatment did not primarily address the bacillus but the
predisposing causes: “Failure in treatment is frequently due to failure to diagnose and
eliminate the predisposing cause.”183
Although this led Muir to suggest a classification based on the numbers of

bacilli found under the skin of the patients, it is possible to argue that Muir’s
emphasis on predisposing causes led to a more holistic disease model. While Hansen
emphasized that the leper was to blame for catching the disease, the Calcutta school
saw the disease as the result of unfortunate circumstances for which the ‘leper’
himself could not be blamed, such as poverty or poor sanitary conditions. While
BELRA did work on a specific cure for leprosy, they also emphasized elevating the
sufferer’s circumstances through education and sanitary improvements.
This was not the only interpretation of predisposition. The researchers in
Calcutta cooperated closely with Philippine researchers at the Culion leprosy colony
and in Manila, and were a clear inspiration when the Philippines in the 1920s
abandoned their segregationist line which had relied solely on compulsory
segregation. The replacement, the “Dual Plan”, added two more layers to the leprosy
approach: Voluntary outpatient treatment for those in the early stages of the disease,
and hospitalization for those in need of extensive treatment. Segregation at Culion
should, at least in theory, be reserved for those who did not respond to the





181
Muir 1924: 9.
182
Rogers and Muir [1925] 1940: 220.
183
Muir 1924: 9.
 77


treatment.184 The policies were made possible by a disease model which did not
require the presence of the leprosy bacillus in order to establish the diagnosis. As the
American pathologist Herbert Windsor Wade and colleague Jose N. Rodriguez put it:


While the finding of acid-fast organisms that are sufficiently characteristic to permit their
recognition as M. leprae settles the diagnosis, it must be realized that negative
bacteriological findings do not necessarily rule out leprosy.185


The Manila researchers agreed with the Calcutta school that local anesthesia was a
‘cardinal sign’, but their classification saw cutaneous (skin) lesions as second
necessary determinant for confirming diagnosis and not the bacillus. From this
premise they reached a classification with wide-reaching consequences for the
individual sufferer. Those who had at least one of these signs (anesthesia or skin
lesions) were diagnosed ‘clinically positive’, and were to be offered regular treatment
locally, without segregation. If the leprosy bacterium was detected, the patient was
labeled ‘bacteriologically positive’ and was to be treated in regional stations open to
visits from friends and family. “Third, cases that prove not satisfactorily to treatment
will be removed to the Culion Leper Colony. It is important that such patients do not
accumulate in the stations, for they tend to discourage others.”186
Instead of seeing predisposition as something found in society that could be
combated by raising the general health of the population, the Manila school focused
on ‘individual resistance’. This was not linked to poverty or unfortunate
circumstances, but improper feeding or weakening disease, sexual over-activity, age
(those between ages 10 and 20 were particularly susceptible), and race. Individual
resistance was one of five conditions involved in contagion, the others revolved




184
Despite being the world’s largest leprosy camp, with 5,257 lepers registered at the end of 1925, Culion did
not have enough capacity to segregate all of the estimated 20,000 suffering from the disease in the Philippines.
The change was also influenced by political turmoil and increasing public criticisms of the vast expenses
connected with the leprosy program (see Chapter 7). The meager impact the segregationist policies had on
reducing the number of new cases was repeatedly put forward as case in point by the Calcutta-school, arguing
that the main effect of segregation was that the lepers went into hiding to avoid detention.
185
Wade, H. W. and J. N. Rodriguez. A description of leprosy: Its etiology, pathology, diagnosis and
treatment. Manila. 1928: 52, emphasis in the original.
 78

around the bacillus: The release of bacilli in contact with other lepers, type of contact,
the number of bacilli involved in the contact and its portal of entry.
While the diagnosis in Calcutta and on Manila in most cases overlapped, the
systems were not identical. In borderline cases, diagnosis could differ depending on
where the suspected case was diagnosed.
When Etienne Burnet, the secretary of the League of Nations Leprosy
Commission, in the late 1920s was asked to prepare a memorandum on diagnosis, he
was painfully aware that diagnosis varied from place to place. Instead of focusing on
one method, he cautiously outlined five concurrent strategies in use or being
researched in different configurations in different locations: Clinical diagnosis,
bacteriological diagnosis, biological diagnosis, serological diagnosis, and chemical-
and physiochemical diagnosis – all with different strengths and weaknesses.187
Clinical diagnosis meant looking for symptoms. The problem was that it
required training by specialists to know what discolored spots (‘maculae’) to look for.
There was, according to Burnet, a desperate need for “a collection of colored
photographs which could be printed off in a suitable number of copies. (...) Nothing is
more instructive than to see the real thing side by side with the picture. We remember
with reverence the plates published by Danielssen, the pioneer of the modern study of
leprosy.”188 Burnet did not accept ‘predisposition’ as part of the disease model, but
was closer to Danielssen and Boeck’s ‘prodromes’ when he argued that physicians,
especially in areas where leprosy was endemic, should pay more attention to general
symptoms: Fever, lack of appetite, sensation of chill, skin irritation, fatigue, headache,
pains of rheumatic type, vasomotor troubles (changes in the blood vessels) and
anemia should all rise suspicion of leprosy.
Bacteriological diagnosis consisted of detecting the presence of the leprosy
bacillus in samples taken from the skin, the nasal mucous membrane, the lymph





186
Wade and Rodriguez 1928: 7.
187
Burnet, Et. “Provisional report presented at the Leprosy Commission at its meeting at Tokyo in April 1930:
Consideration of urgent matters to which the commission drew attention at its May session, 1928”. League of
Nations, C. H./Leprosy/7a, Geneva, January 1930: 1-20.
188
Burnet 1930: 2.
 79

glands and other organs, such as the testicles. Burnet was, however, critical of using
the bacillus as an ultimate proof: Referring to four independent studies from Brazil
and the Philippines, he repeated the argument made by Zeferino Falcão in 1906, that:
“Persons in whom it (the bacillus) was found did not always develop leprosy”.189 In
other words: Leprosy was not merely the presence of the bacillus, but the symptoms
caused by this presence.
Biological diagnosis consisted of influencing the organism by compounds that
produced a reaction, with Danielssen’s potassium iodide producing fever as the best
known and most widely used. In addition, injections of Koch’s Tuberculin, Babes’
Leprin, Rost’s Leprolin, Mitsuda’s Leproma and Deycke’s Nastin were all used or
tested to determine specific reactions in lepers.190 Reacting to leprosy-specific stimuli
indicated the presence of the disease.
Serological diagnosis meant producing serum from blood samples and testing
them with fixation techniques in test-tubes. While the Wasserman-test had received
most attention, Burnet concluded that this research had been of limited value.191 This
did not mean that the numerous attempts at modifying the test to give it a higher
degree of specificity to leprosy should be abandoned. Using de-fatted streptothrix
leproides as antigen, a procedure that was extensively tested in São Paulo, was
highlighted as a promising alternative. Some potential was also found in precipitation
tests consisting of mixing serum and distilled water or alcohol to produce a deposit in
the bottom of the small test tubes, a technique researched in the Philippines and in the
Netherlands respectively. A related line of research focused on measuring not the
intensity of the reaction, but the speed of sedimentation of the red blood corpuscles,
the hypothesis being that the blood of lepers would sediment faster than ‘healthy’
blood.


Finally, chemical and physiochemical diagnosis consisted of analyzing the


proportions of different substances in the blood, such as calcium, the reserve of alkali





189
Burnet 1930: 5.
190
I will discuss these drugs in detail in the following chapter.
191
Burnet 1930: 9.
 80

and cholesterol. There were also more specialized tests, such as the proportion of
albumin in the nasal mucus. Increasingly, these tests were seen as useful not in
deciding if someone was a leper, but in classification of cases and a way to monitor
and ideally predict the effects of treatment.
Despite local variations, by the 1920s the discussion on diagnosis had moved
from setting standards for deciding if someone was a leper or not, to finding a
common classification of the different varieties of the disease. Since local diagnostic
practices differed, classification had consequences for how reports from afar could be
interpreted and to what extent it was possible to compile and compare the results. At
the 1931 Leonard Wood Memorial Conference on Leprosy in Manila, which I will
discuss in more detail in Chapter 7, establishing a global standard for classification
was high on the agenda. The outcome was the “Memorial Conference classification”,
soon renamed “the Manila classification”. This divided leprosy into two main types
based on clinical features: the Neural and the Cutaneous. The Neural resembled
Danielssen and Boeck’s “Anesthetic” form, and was defined by alteration in the
nerves causing anesthesia, contractures (hardening of tissue) and ulcerations but no
skin lesions. The Cutaneous form referred to “All cases showing leprotic lesions in
the skin.”192 These were in turn divided into three subtypes each based on the degree

of severity of these clinical signs.

Within months after being published, the Manila classification was criticized.
In the columns of the quarterly journal Leprosy in India (started by Ernest Muir in
1929), Indian physician S. N. Chatterji working at Muir’s clinic in Calcutta argued
that all cases in reality had mixed clinical signs, and that “any classification on
anatomical or pathological grounds (...) is but arbitrary”.193 Instead of symptoms,
Chatterji argued, classification should rest on bacteriological findings. Hansen’s
bacillus was, after all, the cause of the disease.




192
Wade, H. W. “A proposed revision of the Memorial conference classification of leprosy”. The American
Journal of Tropical Medicine, Vol. 17, No. 6. 1937: 773-801, quote on p. 775. The term ‘leprotic’ was in turn
defined as: “those changes which present clinical or microscopic evidence of inflammatory processes, typically
of granulomatous nature, which are apparently caused by Mycobacteria leprae in them.” (Op. cit.: 776.)
 81

The debate continued in the columns of the International Journal of Leprosy
and other medical journals. When the founding editor of the journal, the American
pathologist Herbert Windsor Wade working on Culion in the Philippines, in 1937
suggested a compromise at least seven different alternatives had been laid on the
table.194 At the Fourth International Leprosy conference held in Cairo the following
year, classification, and thus indirectly diagnosis, would be one of the main
discussions.195





Conclusion


Danielssen and Boeck’s clinical diagnosis from the middle of the 19th century meant
that if you look like a leper, you have leprosy. Diagnosis was made in the meeting
between the individual suspected of having the disease and an expert who knew what
signs to look for. Hansen and Looft’s bacteriological diagnosis from the 1890s
focused on detecting the bacillus in tissue samples, removed from the person
suffering from the disease. What defined the disease was the bacillus, and what the
physicians could observe in the clinic was merely a consequence of its effect on the
human body.
In theory, establishing the bacillus as the cause of the disease made the clinical
symptoms secondary. From the 1890s, several bacteriologists argued that the bacillus
reduced the clinical signs from a decisive argument to a suspicion that needed








193
Chatterji, S. N. “Critical review of the Leonard Wood Memorial Conference report.” Leprosy in India, No.
3. 1931: 142-146, as referred to in Wade 1937: 777.
194
Wade 1937: 778-782.
195
The discussion in Cairo concluded with a new classification, but already the next international leprosy
conference in Habana, Cuba, in April 1948, this was overturned by a new standard. See i.e. Canizares, Orlando.
“New Official Classification of Leprosy”. Archives of Dermatology. No. 5. 1949: 584-586. Discussions on
classification continue to this day, for instance on Dr. Salvatore Noto’s “Leprosy Mailing List” (LML). [http:
//www.aifo.it/english/resources/online/lml-archives/index.htm]. Medical anthropologist Annemarie Mol’s astute
observation based on studying atherosclerosis in a Dutch hospital, that parallel (and sometimes competing)
ontologies are at work and that diagnosis and interventions are decided on a case to case basis, seems to be the
case also for leprosy. (Mol, Annemarie. The body multiple: ontology in medical practice. 2002.)
 82

confirmation in the laboratory.196 From around 1910, several leprosy institutions
introduced bacteriological tests in deciding whether a person could be released from
segregation. This was the most dramatic consequence of the bacillus: It made the
disease something you could get well from.
When establishing whether or not a suspect was indeed ‘a leper’, however,
most saw the bacillus as a welcome confirmation of uncertain cases, but not as a
necessity. Hansen’s attempt at redefining leprosy as based not on its clinical signs but
on the presence of the bacillus alone failed. Bacteriogical diagnosis was was a
supplement to clinical diagnosis but never a replacement.
The introduction of the laboratory in diagnosis was not limited to detecting the
bacillus. There were numerous attempts at finding a decisive test to decide if a patient
was suffering from leprosy or not and thus leave the question of clinical judgement
out of the picture. After failing to meet the objective of conclusively separating
‘lepers’ from ‘non-lepers’, some of the tests were reinterpreted and used to create new
subcategories of the disease and to monitor the effects of treatments. But instead of
giving birth to unifying diagnostic practices globally, these techniques played
different roles in different locations. In borderline cases, the final verdict depended on
where the suspected ‘leper’ was diagnosed.
This diagnostic pluralism was challenged in the early 1930s as part of
initiatives to organize leprologists around the world. This is hardly coincidental. As I
will expand upon in the following chapter, in order to compare the efficacy of
treatments, a common set of definitions was perceived to be a necessity. Instead of
addressing diagnosis directly, the approach was to establish global standards for
classifying the forms and varieties of leprosy so that the results of local studies could
be disentangled from their site-specific origins and thus be more useful for
researchers elsewhere.
So did bacteriology lead to a revolution when it came to diagnosis? Worboys is

probably right that the changes read into the 1880s took longer time, and the 1880s




196
The same argument has been made by Andrew Cunningham regarding the plague. See: Cunningham [1992]
 83

was certainly not a decade of a rapid and universal reductionist trajectory in medicine.
Rather, the immediate consequence of bacteriology was that it opened for a plethora
of new ways of conceptualizing disease. Likewise, Cunningham is correct in pointing
out that by the 1930s medical understanding of disease was transformed. Diseases
now had a clear cause.
The introduction and interpretations of bacteriology changed over time and
differed from place to place and from actor to actor. Not only did it take time before
the new ways of knowing were made available, simply reading about new theories
was not enough for everyone to be convinced. As I will expand upon later, it does
seem that the medical elite in Britain were slower and more reluctant in accepting the
bacteriology than similar elites in continental Europe and in the colonies, at least
when it came to leprosy. At the same time, even those who accepted the bacillus as
relevant only later dated its genesis not to when it was introduced locally, but to the
first time it was observed. Agreeing on a common genesis seems to have been a
shared trait in the medical community.
To the physicians in the 1920s, the late 1870s and early 1880s were indeed
seen as a time of medical revolution. The explanation lays not only in the numerous
new medical techniques or the rise of new specialties, but in the practice of
backdating. When Hansen and Looft in 1895 dated the discovery of the leprosy
bacillus to 1871, they labeled all medical observations made earlier as belonging to
the ‘pre-bacillary era’. Likewise, as the presence of the leprosy bacillus from turn of
the 1890s was increasingly accepted as a more definite proof of disease than
diagnosis based on clinical judgment alone, the genesis of this new way of
understanding disease was backdated it to its origins in the 1870s and 1880s.
The ‘revolution’ happened over decades. Despite the development of new
staining techniques continuing into the 1900s, this too was seen as part of the changes
in the late 1870s. In hindsight ‘bacteriology’ and the ‘bacteriological revolution’
became the catch-all concept to give meaning to the change that had taken place.





2002: 209-244.
 84

Already from the first decade of the 20th century, the understanding that there had
been a bacteriological revolution, starting in the 1880s, had commenced.
 85



3. Treating leprosy: Care or cure?


A quarter past nine in the morning on Tuesday January 16, 1891, 26 year old Johan P.
S., affected with ‘tuberculo-anesthetic’ (mixed) leprosy, received an injection of one
milligram tuberculin at Lungegaardshospitalet in Bergen.197 This was the beginning
of what became the world’s largest tuberculin-trial on leprosy patients in 1891. Over
the next three months fourteen patients received injections. The results were
disastrous.
This chapter will investigate the medical discussions regarding the treatment of
leprosy. What did medicine have to offer those who suffered from the disease? What
efforts were made to find new medications, and what impact did the leprosy bacillus
have on treatment?
In hindsight the short answer to what medicine had to offer is ‘not much’. Most
leprosy histories discussing treatment take the successful trial of Promine at Culion in
1941 as their starting point.198 This was the first time dapsone drugs were used against
leprosy, and dapsone is part of the Multidrug therapy that the World Health
Organization (WHO) has offered free of charge to all countries where leprosy is
endemic since 1995.199 Since the drugs used earlier followed radically different
rationales and thus were not steps on the way to a cure, prior treatments are explicitly
or implicitly seen as ‘mistakes’ or ‘failed science’.200 I will argue for the contrary:
This period was one of the most active when it came to developing and testing new






197
Danielssen, D. C. “Tuberkulinen (Kochs lymfe) anvendt paa spedalske i Lungegaardshospitalet”. Medicinsk
Revue. 1891: 185.
198
Faget, Q. Johansen, F. Dinan, J. Prejan, B. and C. Eccles. “The promin treatment of leprosy”. Public Health
Report. No. 58, 1943: 1729-1741.
199
World Health Organization. “Leprosy elimination”. [Online: http: //www.who.int/lep/mdt/en/index.html]
200
Ironically, the sulfones that Promin was based on were first synthesized in 1908 and published in a chemical
journal. (Fromm, E. and J. Wittmann. “Derivate des p-nitrophenols.” Berichte der Deutschen Chemischen
Gesellschaft. Vol. 41. 1908: 2264-2273.) Sulphones were not picked up by medicine until the 1930s. (Gottfried,
Wozel. “The Story of Sulphones in Tropical Medicine and Dermatology.” International Journal of Dermatology.
1989: 17-21; Zhu, Y. Isabel and Matthew J. Stiller. “Dapsone and sulfones in dermatology: Overview and
update.” The Journal of the American Academy of Dermatology. Vol. 45, No. 3. 2001: 420-434.) Since the
dapsone drugs were not discussed among leprologists in the period I am interested in, it will not be
not part of the story I will tell in this thesis.
 86

remedies. Concurrently, medicine had much to offer – but whether or not the
treatments actually worked was contested.
In this chapter I will first unpack the tuberculin trial in Bergen and investigate
what happened as the findings were circulated in medical journals. I will then outline
the most discussed remedies developed specifically for leprosy both prior and after
the bacillus became a target for new medications, and ask how the rationale behind
the treatments changed over time. Next, did the treatments work, and to what extent
were the medical trials representative of local treatment practices?
Finally, I will investigate how chaulmoogra, an ancient wood-oil from India,
around the turn of the 20th century was reinterpreted as a cure instead of a temporary
relief. The efficacy of chaulmoogra was at the core of the controversy where
leprologists at the end of the 1920s could be separated in two opposing camps: One
saw leprosy as curable and argued for voluntary treatment, the other saw the disease
as incurable and argued for segregation and prosecution.
I will also show how the ‘lepers’ were not passive recipients, but active
partners in the search for a way to get rid of the disease. Some traveled far in search
for treatments that promised a cure, others convinced their physicians to conduct
experiments or threatened with violence if treatment was not offered. Yet others ran
away when it turned out that the treatments were both painful and failed to make them
better.





The tuberculin trials


In 1891 tuberculin was tested on leprosy patients in at least twelve different locations
around the globe. The trials were promptly compiled and compared, and neither the
rationale nor the outcomes of the trials can be explained based on studying only the
sites in which each individual trial took place. The trials will therefore be investigated
not primarily as a series of local events, but as expressions of debates which went on
in conferences and medical journals. How was the news of the alleged ‘miracle cure’
spread? How were the experimental observations disseminated, and how did the trial
 87

in Bergen relate to tuberculin trials elsewhere? What happened with how the studies
were represented as they were circulated?
The genesis of the tuberculin trials was not the injections in Bergen in 1891,
but a presentation at the Tenth International Medical Congress in Berlin five months
prior. Arranged the first week of August, the congress was the largest event for
medical science in 1890. In total, 5,737 people attended the six day conference; there
were eighteen parallel sessions, daily excursions to Berlin hospitals, and daily
journals publishing highlights and changes to the program in German, French and
English.201 Afterwards, the proceedings were published in five comprehensive


volumes.202
The highlight of the conference was the presentation by bacteriologist Robert
Koch. Nine years earlier, at the Seventh International Congress in London, he had
made his fame by demonstrating a method for cultivating microbes on solid medium.
His paper at the first plenary session of the Berlin conference lived up to the
expectations. After first presenting the history of bacteriology as fifteen years of
progress, he concluded with the ultimate breakthrough: Tuberculin. This was a new
substance that had brought the disease process in tuberculosis to a complete standstill
both in the Petri dish and in guinea pigs. This was a proof, Koch argued, that it was
possible to render disease-producing (pathogenic) bacteria harmless in living
organisms without harming the host.203
Although Koch refused to disclose how the drug was manufactured, the lecture
was an immediate success. This is perhaps not surprising given that tuberculosis was
estimated to be the cause of one in seven deaths globally.204 “Koch’s miracle cure”










201
Hanssen, Klaus. “X. internationale medicinske kongres i Berlin”. Medicinsk Revue. Vol. 7, No. 9. 1890: 273.
202
Verhandlungen des X. Internationalen medicinischen congresses, Berlin, 4.-9. august 1890.
203
Koch, Robert. “Ueber bakteriologische Forschung.” Verhandlungen des X. Internationalen medicinischen
congresses, Berlin, 4.-9. august 1890. Bd. 1. 1891: 35-47.
204
This estimate was made by Koch some eight years earlier, and was widely accepted. Koch, Robert. “Die
Ätiologie der Tuberkulose.” Berliner klinische Wochenschrift. No. 15, 1882: 221-230.
 88

was widely reported in both medical journals and the popular press.205 Tuberculin
showed that bacteriology held the promise of a cure.
Known among physicians as “Koch’s lymph” or “tuberculin”, the drug was put
up for sale on November 13, 1890.206 Danielssen was among those who sent an order,
leading to the clinical trials which started in January 1891. According to Danielssen,
the initiative for testing tuberculin at the Lungegaardshospitalet research hospital in
Bergen came from the patients themselves who had read about it in the local
newspaper.207
The stories of Koch’s lecture were not the only thing that needed to travel for
the trial to take place, so did the drug itself. Just like the news moved through several
channels, so did access to tuberculin. Although Koch was the only producer, it was
also possible to get hold of his drug via proxy. On December 20, 1890, the Medical
Secretary of the National Leprosy Fund in Britain and editor of the Journal of the
Leprosy Investigation Committee (1890-1891), Phineas S. Abraham, published a
small note in the British Medical Journal informing that he had received a supply of
tuberculin from Robert Koch and was inviting physicians to try it.


I shall be glad to hear from any medical man who has a case of the kind at present in
England, and willing to be treated. A definite effect has, I believe, already been obtained in
Vienna by Professor Kaposi in a leper, and I understand that the remedy is now being tried
by Dr. Koch’s advice, for leprosy in Germany.208

Danielssen made two basic assumptions to justify acquiring tuberculin and testing it
on his patients, reflecting how clinical and bacteriological arguments were in practice




205
Various medical journals printed full translations, abstracts and reprints within weeks, such as The British
Medical Journal (1890: 380-383), Deutsche medizinische Wochenschrift 1890: 756-757, Medicinsk Revue
(1890: 280-284). For an extensive review of the reception and the following tuberculin-trials on patients
suffering from tuberculosis, see Gradman 2009: Chapters III and IV.
206
Gradman 2009: 126.
207
Already on August 13, 1890, nine days after the lecture in Berlin, the local newspaper Bergens Tidende
published a short note about the lecture (1890: 2). Danielssen himself did not attend the meeting in Berlin, but
several of his colleagues from Bergen were among the 57 Norwegian physicians who participated and it is not
unlikely that they told Danielssen about Koch’s lecture. (Hanssen 1890: 273-276.)
208
Abraham, Phineas S. “Leprosy and Professor Koch’s Treatment”. The British Medical Journal. December
20, 1890: 1438.
 89

entangled. First, tuberculosis and leprosy had “remarkably similar clinical
expressions”. Second, the tubercle bacillus and the leprosy bacillus seemed identical
in the microscope, “a similarity so great, that even Dr. G. Armauer Hansen, the
discoverer of the leprosy bacillus who for many years has concerned himself with
bacteriological research, no longer is able to separate them”.209 The first argument
relied on experience tending to patients suffering from the disease, the second on
what had been observed through the microscope. Both the clinic and the laboratory
suggested that the mysterious drug developed for tuberculosis would work equally
well on leprosy patients. To my knowledge, this was the first time the leprosy bacillus
itself was presented as a rationale for a clinical trial, and the first time Danielssen
publicly endorsed Hansen as its discoverer.
When the trial started, 75 year old Danielssen was “the grand old man” of
leprosy research. For five decades he had tried – and failed – to find a cure for the
disease.210 Danielssen and Boeck’s monograph On Leprosy from 1847 was still seen
as a leading reference work, and was regularly referred to all over the world.211





209
“(…) en lighed, der er saa stor, at selv dr. G. Armauer Hansen, som er leprabacillens opdager, og som i
mange aar har beskjæftiget sig med bakteriologiske undersøgelser ikke nu længer i stand til at kunne adskille
dem.” Danielssen 1891: 177.
210
Already in Om Spedalskhed (1844) Daniellsen proclaimed that “From now on one of the author’s principal
activities shall be devoted to leprosy therapy; this is his goal in life, which he with the healthiest of hopes will
respond to.” (Danielssen and Boeck 1847: 288.) In 1891 Danielssen’s colleagues in Norway published a
Festschrift, a memorial volume celebrating his 50 year anniversary as a civil servant: Festskrift i Anlædning af
Overlæge Dr. Med. D. C. Danielssen’s 50aarige Embetdsjubilæum. Udgivet af Medicinsk Revue. 1891.
Available online: http: //www.nb.no/utlevering/nb/4ce01326e33d24956f3ef1cf91b11ff6. For a list of the honors
bestowed upon Danielssen, see: Brunchorst, J. Bergen Museums Aarbog 1893. D. C. Danielssen. A
biographical sketch. 1894. Karen Helle is currently working on a biography of Danielssen.
211
While a common reference, the interpretations of its importance differed. In Treatise on Diseases of the Skin
for the use of Advanced Students and Practitioners by Philadelphia dermatologist Henry Weightman
Stelwagon, for instance, Danielssen and Boeck was presented the primary reference work on diagnosis of
leprosy i until at least its 7th edition. (1914: 914). In A Handbook on Leprosy (1896: 19), medical
superintendent Samuel Patton Impey at Robben Island Leper and Lunatic Asylum referred to Danielssen and
Boeck as the authority when it came to deciding the relative frequency of anæsthetic, tubercular and mixed
cases. This distinction was introduced by the two Norwegian physicians in 1847, and was and in general use
until the 1920s. Despite the fact that Danielssen at this point had acknowledged the leprosy bacillus as the cause
of the disease, The British Leprosy Commission in India (1893: 204ff), put Danielssen and Boeck forward as
the main proponents of the theory of heredity. Later Danielssen and Boeck’s theory of heredity was highlighted
and ridiculed by Leonard Rogers and Ernest Muir as “strongly supported on very inconclusive evidence by the
Norwegian authorities Danielssen and Boeck in their work of 1848”. (Rogers and Muir 1940: 64.) After the entry
on leprosy was rewritten for the eleventh edition of The Encyclopedia Britannica, Danielssen and Boeck’s
monograph was highlighted as one of the “primary treatises on modern leprosy in particular locations.”
(Encyclopedia Britannica. Volume XVI, 1911: 481.)
 90

The trial at the Lungegaarden research hospital consisted of injections every
morning, starting at 1 milligram per dose and increasing over time to a maximum of
320 milligrams. Temperature and pulse were measured three times daily for as long as
the trial ran. These observations and the patients’ own experiences made up the main
bulk of Danielssen’s study.
Johan P. S., who had been admitted to the hospital only three months prior and
was among those advocating that tuberculin should be tested, received his second
injection on January 17. The dose was doubled to two milligrams, and the drug caused
a reaction: A strong headache and pain in the neck was accompanied by a fever rising
to 39.5° Celsius (103.1° Fahrenheit) mid-day. The following day, the temperature rose
to 40.4° C (104.7° F). The nodules in the face turned red with inflammation, some of
them burst with seropurulent liquid oozing out.212 When his part in the trial was

terminated at his request five weeks later, Johan could no longer walk; the leprosy
nodules on the face, arms and legs had increased both in number and size.213
One by one, the trials were aborted, either by Danielssen or the patients
themselves, in several cases to avoid the loss of lives. In the case of a 20 year old
woman, Ingeborg A. T., the trial was terminated by Danielssen in March. “Continuing
the treatment was out of the question; I am convinced that continued treatment would
have led to a fatal result.”214 For 31 year old Inga A. H., who had interrupted her other
medication to be part of the tuberculin-trials, the first reaction came after five weeks
when the doses had reached 15mg: Heat spells followed by chills, nausea and red-
brown patches spreading over the face and arms. Over time, the symptoms grew only
worse. “The hope I once had regarding her cure is extinguished. Worse, this is thanks
to tuberculin”, Danielssen concluded.215
The last trial was stopped April 15, 1891. By then it was clear that the effects

of the drug were immediate, generalizable and relatively consistent: Between four and




212
Danielssen 1891: 180. Seropurulent: Liquid consisting of both serum and pus.
213
Danielssen 1891: 185.
214
“Der kunde ikke være tale om at fortsætte med behandlingen; thii det er min overbevisning, at en fortsættelse
vilde have ført til en dødelig udgang.” (Danielssen 1891: 196).
 91

six hours after the injection (occasionally delayed up to three days), patients would
develop a strong fever, new eruptions of leprosy would appear, and over time the
health of the patient would dramatically deteriorate. In some cases, the patient would
develop a resistance to the drug, but this seemed to have no impact on the progress of
the disease.
Danielssen’s conclusion did not question the premise that leprosy was caused
by a bacillus, nor that ‘Koch’s lymph’ reacted with this bacillus. Rather, he strongly
warned against using tuberculin because of this connection.


The tuberculin does not kill the leprosy bacillus, but it seems to provide good nutrition to
the bacillus, so that it with increased vigor enters the bloodstream, travels around in the
body and with larger productivity spreads its destruction faster and with greater intensity
than had the disease been left to itself. (…) After a time, a sort of immunity to tuberculin
can be developed, but this does in no regards bring a stop to the disease. No, the leprosy
bacillus is very well under this apparent immunity. It quietly produces its destructive poison,
and the effects are visible in the increase of disease phenomena.216


By accepting the bacillus as the cause of the disease, it was also the correlating
explanation for the clinical outcomes of the use of Koch’s drug.





Spreading the results


Danielssen’s study was initially published as a 63-page report in the Norwegian

journal Medicinsk Revue, and then in a two-part series the German Monatshefte für




215
“Det haab, jeg engang kunde have om hendes helbredelse, er ganske udslukt. Tuberkulinen har desto verre
sørget derfor.”(Danielssen 1891: 222).
216
“Af de ovenanførte i Lungegaardshospitalet anstillede forsøg af prof. Kochs lymfe fremgaar: (...)
At tuberkulinen ikke dræber leprabacillen, men at den synes at være et godt fodringsmiddel (eller om man vil
et godt livsmedium) for bacillen, saa at denne med vigør og større produktivitet vandrer ved blodinokulationen
omkring i legemet og anretter sine ødelæggelser hurtigere og med større intensitet, end om sygdommen
overlades til sig selv.
At der, efter at tuberkulinen har været benyttet en tid, kan oppstaa en slags immunitet, men at denne
ingenlunde bringer stans i sygdommen, eller er en følge af, at leprabacillen er tilitetgjort. Nei, leprabacillen
 92

praktische Dermatologie.217 Both publications focused on Danielssen’s bedside
experiences during the trial, detailing observations of each individual patient; body
temperature, pulse and clinical signs, as well as how the patient’s outlooks for cure
changed over time. The conclusion was phrased as a warning to other physicians
stating that the drug was dangerous and should not be used.
Danielssen’s choice of publishing the results of the trial in both the Norwegian
and the German journal was not arbitrary. The Norwegian journal was founded by the
research community in Bergen that Danielssen himself had been a key figure in
establishing, and its main asset was the 148 different medical journals that the library
at the research hospital subscribed to.218 Not everybody read Norwegian. While
French was the ‘international’ language of choice in around 1850, German had by the
1890s taken over, at least for the physicians in Bergen. 86 out of the journals in the
library catalogue were in this language.219 The Monatsheft (established in 1882) was
not the only journal publishing clinical and laboratory experiments on skin diseases,
but it followed tuberculin especially close. In spring 1891 the German journal
published 35 studies on the effects of the drug in various diseases. In addition,
Danielssen knew some of the editors personally.220
Outside the medical conferences, medical journals were the fastest way to
reach colleagues domestically as well as abroad. First, they reached the immediate
subscribers. Second, the studies were referred to in other journals. Most of the 35
reports on tuberculin in the Monatsheft were abstracts of papers published in other






befinder sig meget vel under denne tilsyneladende immunitet, og producerer i al stilhed sin ødelæggende gift,
hvis virkninger viser sig i den stadige tiltagen af sygdomsfænomenerne.” (Danielssen 1891: 240).
217
Danielssen, D. C. “Tuberculin im Lungegaardshospital gegen Lepra angewendet.” Monatshefte für
praktische Dermatologie. Vol. XIII, No. 3 and 4. 1891.
218
Dethloff, H. G. Katalog over Lungegaardshospitalets bibliothek ved udgangen af aaret 1904. Bergen. 1905.
More on Medicinsk Revue and circulation of knowledge through medical journals in Chapter 6.
219
The second largest category was “French, Italian and other” journals (23 titles), followed by “Scandinavian,
Danish and Finish” (22), and “English and American” (17).
220
The main editor, Paul Gerson Unna, visited Danielssen in Bergen in 1884. (Romiti, Ney. Anais Brasilieros
de Dermatologia. Vol. 80, No. 1. 2005: 89.) While it is unclear if co-editor Hans von Hebra ever visited
Bergen, his father Ferdinan Ritter traveled there in 1852, when Hans von Hebra was five years old (http:
//www.whonamedit.com/doctor.cfm/708.html). The third editor, Oscar Lassar, was the one unveiling the
memorial for Danielssen after his death in 1894. (Lassar, Oscar. “Zur Erinnerung an Daniel Danielssen”.
Dermatologische Zeitschrift. Vol 2, No. 5. 1894: 534-544.)
 93

journals. Also for Danielssen’s report, this was how the results were disseminated –

through abstracts in other journals.

The first English-language reference to the tuberculin trials in Bergen was
published as a 200-word note in Weekly Epitome of Current Medical Literature, a
supplement to The British Medical Journal, in the end of August 1891.221 In
December, a 6-point conclusion was published by Dr. P. Ferrari in the short-lived
London-based Journal of the Leprosy Investigation Committee.222 The following
spring the result of the tuberculin trial in Bergen was referred to in The Lancet and
put in context with other trials, book reviews, official reports, and abstracts from
discussions on the use of tuberculin against leprosy in various medical meetings.223
Danielssen’s trial was also highlighted in Paul von Baumgarten’s Jahresberichte über
die Fortschritte in der Lehre von den pathogenen Organismen for 1891, published
two years later.224 As the distance in time increased, the abstracts were increasingly
void of all traces of local context. The names or daily experiences of the individuals
taking part in the trials never travelled past the original publication. The clinical gaze,
local particularities, or the voices of the sufferers were not mentioned; only the
generalized findings remained: 14 ‘lepers’; 0,001-0,320 gram doses; reactions after
12, 48 and 72 hours; bacillus detected in the blood.225
While Danielssen’s trial was the largest, he was by far the only one testing
tuberculin on leprosy patients. In 1891 alone, tuberculin-trials on leprosy patients
were performed in at least twelve different locations on three continents: Bergen,






221
Editorial. “Tuberculin in Leprosy”. Supplement to the British Medical Journal. August 29, 1891: 69-70. A
120-word abstract of the second part of Danielssen’s German paper was referred to in the same supplement on
November 28, 1891: 174.
222
Ferrari, P. “Koch’s Tuberculin in Leprosy”. Journal of the Leprosy Investigation Committee. No. 4,
December 1891: 46-47.
223
Editorial. “The tuberculin treatment of leprosy”. The Lancet. April 16, 1892: 877-879.
224
Baumgarten, Paul von. Jahresbericht über die Fortschritte in der Lehre von den pathogenen
Mikroorganismen umfassend Bakterien, Pilze und Protozoën. Vol. 7. 1893: 284-285.
225
Currie, Donald H., Moses T. Clegg and Harry T. Hollmann. “XV. Attempts at specific therapy in leprosy.”
Public Health Bulletin No. 47: Studies upon Leprosy. 1911: 25. Removing traces of local contexts in concurrent
summaries was characteristic for abstracts as a genre, see: Chapter 5. That the tuberculin trials were revisited by
researchers on Hawaii twenty years later shows how published research did not merely have concurrent interest,
but also created an archive for later reference. On the other hand, only what was considered relevant to the
research question at hand was referred to – in this case attempts at developing a specific immunity to leprosy.
 94

Bucharest, Hamburg, Hong Kong, London, Madeira, Madras, Mauritius, New York,
Tallinn, Tokyo, and Tunisia. Initially the results differed greatly.
Reporting in Deutsche medizinische Wochenschrift, Dr. Truhart in Tallinn
noted that he had tested tuberculin on six cases, and found that leprous ulcers healed
promptly using tuberculin, more so in tubercular cases than in mixed or nerve
cases.226 In an attempt to use tuberculin reaction as a tool for differential diagnosis,
Eduard Arning tested the drug on two cases of anaesthetic leprosy and one case of
lepra tuberosa in Hamburg. The anaesthetic cases had no reaction to the drug, while
the man suffering from lepra tuberosa developed a strong fever.227 Publishing in the
same journal, physicians Babes and Kalindro in Bucharest tested in total eleven cases
with mixed results. In two cases the reaction was so severe that it threatened the life
of the patients.228 For the nine others, local reactions about nodules were interpreted
as signs of improvement, but none of the patients progressed to a complete cure.
At the Lazzaretto Hospital in Madeira, Medical Superintendent Julius
Goldschmidt first tested five cases in May 1891, and was hopeful that it would result
in a cure. After a second trial on eleven more cases, he concluded in the columns of
Berliner klinische Wochenschrift that the best possible outcome was that the disease
remained stationary. In most cases the treatment made the health of the patient
deteriorate.229 In Hong Kong, James Cantlie found bacilli in the blood of the patients









226
Truhart. “Ein Beitrag zur Leprabehandlung mittels Tuberkulin.” Deutsche medizinische Wochenschrift.
1891, No. 36-38.
227
Arning, Eduard. “Über die wirkung des Kochschen Heilmittel bei Lepra und Lupus erythatiodes”. Deutsche
medizinische Wochenschrift, 1890, no. 50; Arning, Ed. “Mittheilungen über Versuche mit der Koch’schen
Injectionsflüssiggkeit bei Lepra und Lupus erythematodes.” Robert Koch’s Heilmittel gegen die Tuberculose. 2.
Heft, 1890:63-70. The conclusions were summarized in in: Monatshefte für praktische Dermatologie 1891:
101-102.
228
Babes and Kalindro. “Resultate, erhalten durch Injectionen mit Koch’scher Lymphe bei den verschiedenen
Formen der Lepra.” Revue de Médecine, October 1891; Babes and Kalindro. “Ueber die Wirkung des
Koch’schen Heilmittels bei Lepra.” Deutsche medisinsche Wochenschrift. 1891, No. 3; Babes and Kalindro.
“Zwei Fälle von mehrere Wochen lang anauernder Allgemeinureaction bei Leprösen nach einmaliger
Einspritzung von 0,8 mg Tuberkulin.” Deutsche medisinsche Wochenschrift. 1891, No. 14. See also:
Monatshefte für praktische Dermatologie 1891: 243-244, 499.
229
Goldschmidt, J. “Wirkung des Tuberkulins auf Lepra”. Berliner klinische Wochenschrift. 1891, No. 15;
Editorial. “The tuberculin treatment of leprosy”. The Lancet. April 16, 1892: 878.
 95

after administering injections to seven patients, and dryly noted that this was not a
promising sign.230
Tuberculin was also tested at several sites in India. The largest trial was
conducted by Surgeon-Major H. D. Cook at the Government Leper Hospital in
Madras at the request of the Leprosy Commission to India. He treated twelve patients
beginning June 27, 1891, and concluding after a month that “‘Tuberculin’ for leprosy
is a decided failure.”231 At the same time, reports referred to in The Madras Times and
Calcutta Daily News in the end of October 1891 stated that trials elsewhere in India
had produced no negative effects, and a slight improvement in health.232 The reports
were picked up by physicians in London, where tuberculin was tested on one patient
at King’s college Hospital and one patient at University College Hospital.233
In Barkly Asylum Public Hospital on Mauritius, Charles Poupinel de Valencé
reported to the British Colonial Office that he had tested tuberculin on five lepers, and
that three of them had experienced nodules shrinking, improved sense of well-being,
increased weight and general improvements in health.234 This, he argued, was partly
due to the treatment being carried out in alteration with large doses of chaulmoogra
oil. The report was sent by Lord Knutsfor (Henry Thurstan Holland) to The Lancet,
where the editor promptly put it in context with other tuberculin trials, including one
case at His Imperial Majesty’s Army Hospital in Tokyo and two cases treated
separately in New York, both previously referred to in The British Medical Journal.
The editorial in The Lancet stressed that these cases “do not exhaust the list of
experiments”. Still, it shows how it was only when the results of a wide range of
experiments were compiled and compared that larger conclusions could be drawn.




230
Seven years later Chantlie was the co-founder, and for the following 23 years main editor, of the Journal of
Tropical Medicine and Hygiene which was to become the most-referred to journal in Lepra Bibliotheca
Internationalis. His trial with tuberculin was referred to in: Editorial. “The tuberculin treatment of leprosy”. The
Lancet. April 16, 1892: 879.
231
“Surgeon-Major H. D. Cook’s Report on Tuberculin”. Leprosy in India. Report of the Leprosy Commission
in India 1890-91. Appendix II to Chapter VII. 1893: 371.
232
According to the editorial in The Lancet on April 16, 1892, these improvements were soon reinterpreted as
the result of improved hygiene for the patients taking part in the trial.
233
Referred to in: Editorial. “The tuberculin treatment of leprosy”. The Lancet. April 16, 1892: 878.
234
The two other cases had refused to carry on after the first injection. The report from Mauritius was what
sparked the editorial in The Lancet in 1892.
 96

And this was exactly what the Lancet did. In an editorial published in April 1892,
they argued that the results “are sufficient to show that tuberculin is very uncertain in
its immediate effects on leprosy”. Relying heavily on Danielssen, their conclusion
was to recommend the trials be stopped: “the fact of its action being to set free bacilli
rather than to destroy them should make us seek in another direction for remedial
agents for the relief of victims of this much-dreaded disease.”235
While each of these tuberculin-experiments took place in specific locations,

neither the rationale nor the outcomes of the trials can be reduced to the local. For the
physicians, the medical trials were understood and discussed in context of similar
experiments conducted in other locations. The premises for the trials came from a
presentation by Robert Koch in Berlin in 1890, and the news were spread through
both medical journals and the popular press. The drugs necessary to conduct the trials
were dispatched from a single German supplier but could also be acquired indirectly,
for instance through Abraham in London. In turn, the outcomes of the experiments
were published and referred to in medical journals around the world. Finally, the
results were compiled and compared.





Rubbing lotion on the skin


Tuberculin was neither the first nor the last attempt at finding a remedy for leprosy,
but most attempts remained local. It was the claim that a cure that was found that got
attention. The first claim to receive global attention was a treatment regime developed
in in the late 1860s in Cumana, Venezuela, by the French physician Louis Daniel
Beuperthy. The three main features of Beuperthy’s cure were good hygiene (fresh air,
nourishing food including fresh meat and vegetables and abstaining from salted meat
or fish), external application of oils (coconut oil, olive oil and cashew nut oil
massaged into the skin twice a day followed by baths) and internal medicine (either






235
Editorial. “The tuberculin treatment of leprosy”. The Lancet. 1892: 879.
 97


perchloride of mercury or sodium carbonate, both fairly well-known antiseptics).236


The British physician Dr. Bakewell reported favorable on the cure to both houses of
the British parliament in 1871, and Gavin Milroy from the Royal College of
Physicians was sent to investigate.237 When Bakewell in a letter a month later offered
Daniel Danielssen to visit Bergen and teach him techniques involved “against a
negligible compensation”, Danielssen welcomed the visit but refused to offer any
payment.238 From what he had read about Beuperthy’s cure, the only real novelty not
yet tested in Bergen was the cashew nut-oil, and since Danielssen at this point still
believed the disease was caused by an imbalance in the blood (a dyscrasia), rubbing
lotion on the skin was at best palliative.


…none of the numerous irritant agents I have used against leprosy over the years have been
able to elicit any changes in the dyscratic conditions which underlie it, and I do not believe
– based on my understanding of the disease – that any external remedy will ever be found.
The case must differ for Dr. Beauperthy, who believes leprosy to be a local disease caused
by parasites, and with this understanding pursuing a treatment partly with corrosive and
irritant agents, is quite natural.239

Beauperthy died shortly after Milroy arrived in Venezuela, and although his alleged
cure was tested in various locations and was reported to ameliorate some of the







236
Report of the Leprosy Commission in India, 1890-1891. 1893: 333-334.
237
Milroy’s work on the Royal College of Physicians’ report on leprosy in 1867 had made him an authority on
the disease, at least among the British medical and political elites. I will return to this in more detail in Chapter
5.
238
“Skulde den norske Regjering ønske at se Dr. Beauperthy’s Behandling forsøgt, vilde jeg være fuldkommen
rede til at komme over mod en meget ubetydelig Godtgjørelse for at vise Dem Metoden.” Letter from Bakewell
to Danielssen, dated Leicester, England, June 17, 1871. In: Danielssen, D. “Lungegaardshospitalets
Virksomhed i Treaaret 1871-73”. Norsk Magazin for Lægevidenskaben. 1874: 320-321. The correspondence
also included a letter of introduction from the British physician Jonathan Hutchinson.
239
“Men hverken det ene eller andet irriterende Middel af de mangfoldige, jeg i Tidernes Løb har anvendt mod
Spedalskheden, har været istand til at fremlokke væsentlige Forandringer I de dyskrastiske Forholde, som
underholder den, og heller ikke vil, efter den Opfatning af Sygdommen jeg har, et saadant udvortes Middel
nogenside findes. Anderledes maa Sagen stille sig for Dr. Beauperthy, der antager den spedalske Sygdom for
local og foraarsaget ved Parasiter, og at han derfor forfølger den dels med Caustica, dels med lettere
Irritamenter, er jo ganske naturligt.” Danielssen 1874: 332. Despite the skepticism, based on Bakewell’s
descriptions from Trinidad and cashew nut oil from an apothecary in Kristiania, Danielssen did indeed test the
cure on five patients in Bergen. Beyond causing irritation, he found it to have no apparent effects.
 98

symptoms, the consensus was soon that it fell far short of a complete cure.240 Still, the
premise was made: News of alleged cures travelled fast, and many were eager to try.
Beuperthy’s cure was to be the first of many.
In 1873, Surgeon-major J. Dougall at Port Blair on the Andaman Islands in the
Indian Ocean began experimenting with gurjun-oil made from a local tree, mixed with
lime water. Inspired by Beauperthy, the treatment regime consisted of massage and oil
applied both internally and externally. Every morning at the break of dawn, 24
patients would be supplied with dry earth for use as soap and sent to a stream to wash.
They would then be placed in a row and served a drink consisting of gurjun-oil and
lime water in equal proportions.


Having seen this swallowed by all of them, the apothecary sees that each man has some
small vessel (usually half of a coconut shell) into which the compounder puts a quantity of
the gurjun ointment, and with this they proceed to rub themselves all over, not merely by
smearing it on, but thorough and continuous friction is kept up for two hours, and the
compounder all the while is walking up and down the line armed with a tin of the ointment
and a spatula for distributing more of it as it is required amongst the patients, and no limit is
placed upon the amount given further than whatever is given must be well rubbed in.241


The same prolonged rubbing was repeated for two hours every afternoon. Although
Dougall explicitly considered the patients malnourished, he made no changes to the
diet “in order to avoid complications and to test the gurjon oil in its merits”. After
testing the treatment for six months, he concluded that the treatment should be
recommended to others:

The time has been long enough to show that leprosy, both tubercular and anæsthetic, can not
only be arrested, but the condition of the lepers can be greatly ameliorated; and men here









240
Buckingham 2002: 135-140; Edmond 2006: 61-62.
241
“Dr Dougall’s Treatment with Gurjun Oil.” In: Leprosy in Foreign Countries. 1886: 75. The report was first
published in Calcutta in 1875. See also Report of the Leprosy Commission in India, 1890-1891, 1893: 335-338.
 99

who have not for years been able to do more than drag out a miserable helpless existence are
now able and willing to work, and every sore is quite healed.242



Being both inexpensive, readily available and apparently of great use, gurjun oil was
soon tested in Madras and other parts of India, as well as in other parts of the
world.243 Surgeon C. T. Peters at Belgaum near Goa in Western India, for instance,
tested first Beauperthy’s cashewnut oil and then Dougall’s gurjun on 29 cases. He
concluded that while consuming gurjun produced indigestion in some, diarrhea in
others, it had value when applied to the skin externally. His assessment of the
treatment indicates how its effect on the disease was measured under clinical
diagnosis, namely by the ability to produce visible changes in the skin: Chronic
leprous ulcers rapidly healed, and although the gurjun did not stop fresh ulcers from
appearing elsewhere on the body, these too could be contained and forced to retract
using the oil. Finally, the treatment regime introduced much-desired order and
cleanliness.



This emulsion also keeps the skin in a soft condition, and so prevents cracking, which is
often the commencement of an inveterate ulcer. It has, moreover, the advantage of keeping
away flies which infest leprous patients, and in the absence of cleanliness, give rise to
maggots, which increase the extent of the ulcer, but under its use the lepers, as well as their
rooms, presented a very clean appearance.244


It did not take many years before the immediate optimism waned. While many
reported that more or less relief had been obtained by the use of gurjun, none were
cured. When The Leprosy Commission to India summarized the trials in the early
1890s, they concluded that gurjon oil could produce some temporary relief, but found







242
“Dr. Dougall’s Treatment with Gurjun Oil.” In: Leprosy in Foreign Countries. 1886: 76.
243
For instance, two 500-pound barrels of gurjon were shipped to Bergen in 1875, in the hope that the
Norwegians would give the oil a trial. (Buckingham 2002: 141.) For more on Dougall’s treatment, see
Buckingham 2002: 88-91.
244
Peters, C. T. “Extracts from report on cases of leprosy treated”. In: Leprosy in Foreign Countries. 1886: 69-
70.
 100

it doubtful that this was more than could be obtained by skin-massage and cleanliness
alone.


Dr Dougall’s success at Port Blair was probably due to the fact that he was dealing with a
colony of convict lepers under prison discipline, and was, therefore, able to carry out his
plan of treatment far more rigorously than in an asylum where, as a rule, patients are adverse
to any therapeutic measures which involve the least exertion. It is quite possible that the
prolonged frictions with dry earth, and the regular sea-bathing, were quite as potent in
affording relief as the use of the gurjun oil.245

This was also the verdict for cashew nut, gurjun, kowti, chaulmoogra and other plant
oils that were tested, as well as German dermatologist Paul Gerson Unna’s treatment
introduced in 1886, consisting of ichtyol and resorcin. Medical treatment gave some
relief, but “the incurability of leprosy by any means yet known is unfortunately
certain.”246 The same could be said about the treatment introduced in 1890 by
physician Adolpho Lutz at Hawaii, which consisted of oral administration of a mix of
the antipyretic (feber-reducing) salicylate and the newly developed chemical
compound salol, and rubbing the organic powders chrysarobin and pyrogallic acid on
the skin. The treatments reportedly did some good in ameliorating the disease for
some, but did not produce cures.

Still, the Leprosy Commission to India firmly concluded that oils, hygiene,
ventilation, sanitation, as well as improved diet made the disease run a milder course,
compared to no intervention at all. Since all these measures would be easier to
administer in asylums, this was used as an argument for establishing voluntary
asylums throughout India where treatment could be administered under careful
supervision. Although no cure was (yet) available, and the prospect of segregating
100,000 individuals was simply not realistic, voluntary institutions could provide the

necessary discipline and patient motivation to test new drugs and treatments.






245
Report of the Leprosy Commission in India, 1890-1891, 1893: 337.
246
Op. cit: 331.
 101

Serum failure and a new benchmark


The serum therapy developed by physician Juan de Dios Carrasquilla in Bogotá,
Columbia, would follow the same pattern as the other proposed cures. First, the drug
was developed and tested locally. Then, it was published in a medical journal and
picked up by physicians elsewhere. Next, the drug was distributed either directly to
other locations, or manufactured based on the initial descriptions. The drug was then
tested, the experiences compared and discussed – and finally, it turned out that the
drug did not live up to the expectations. Still, the failure was important in that it
would introduce a new benchmark for future treatments.
While lotions and orally administered drugs combined work in the clinic and
chemical laboratories, serum therapy was an outcome of bacteriology. Introduced in
the early 1890s, the ruling principle of serum-therapy was that bacteria produced
poisons and these in turn produced disease. By injecting processed serum under the
skin or directly into the bloodstream, the bacilli’s ability to produce the poison could
be stopped. German physiologist Emil Adolf von Behring’s discovery of diphtheria-
and tetanus antitoxins in 1890, which quickly led to the development of a serum-
therapy that cured the diseases, led to widespread optimism that similar strategies
could be applied to other illnesses.247

Carrasquilla’s serum was tested by himself and five medical students at the
newly opened government-sponsored Serotherapeutic Institute in Bogotá in 1896.248
The first results presented in the Columbian medical journal Revisita Médica in 1896,
including information both on how the drug was manufactured, how it was
administered and the results of treating first fifteen, and then one hundred cases. The
drug was based on serum from blood from leprosy patients, ideally tapped during a
fever attack. The serum was then injected under the skin (subcutaneously) of horses,





247
In 1901 von Behring would be the first recipient of the Nobel Prize in Medicine for his this research.
248
Obregón, Diana. “Building National Medicine: Leprosy and Power in Colombia, 1870-1910”. Social History
of Medicine. Vol. 15, No. 1. 2002: 102. See also: Obregón, Diana. “Lepra e investigación bacteriológica en
Colombia: los casos de Carrasquilla y de Lleras.” Biomedica : Revista del Instituto Nacional de Salud. 2000:
181-189.
 102

mules or asses, causing a fever that would last for up to five days. After repeating the
injections at least three times in ten-day intervals, the animals were bled and serum
again separated from the blood. This serum was then injected subcutaneously into the
persons suffering from leprosy. Two to six hours after each injection, the patient
would develop a fever with chills, anxiety, headache, thirst and ‘general malaise’.
After two hours the fever would enter a ‘hot stage’ with hot and cold flushes, stronger
fever, increased pulse and breath, anorexia (loss of appetite), fatigue and occasional
delirium. This would in turn be followed by a phase of sweat, and the patient would
usually recover within a day. The injections were to be injected every three to five
days, with doses increasing from 1 ccm to 5 ccm or more.
The results of the first hundred cases under treatment, Carrasquilla reported,
were wonderful. Tubercles would soften, flatten and finally be absorbed and heal like
normal wounds. Leprous patches would be replaced by normal skin, skin color would
return, eyebrows and other hair would grow back. Anaesthesia would vanish, nerves
return to normal, sight restored to those previously blind, the sense of taste and smell
would be regained. Appetite, digestion, sleep, health – all would improve. And once
the treatment had begun, no new manifestations of the disease would ever occur. In
August 1896, Revisita Médica reported that the announcement had led to “Lepers
flocking to Bogota” in order to receive the treatment.249
In addition to the reports of astounding success, and serum-therapy being in
vogue thanks to the promising results in diphtheria and tetanus, it was active
promotion by the New York-based physician Albert S. Ashmead that helped spread
the news of the new therapy.250 In January 1897 Ashmead received a shipment of
seventy-two bottles of the serum from Bogotá, and quickly forwarded portions to
Hansen in Bergen, Oscar Petersen in St. Petersburg, and the President of the Board of





249
As reported in: “Lepers Flocking to Bogota”. The Journal of the American Medical Association. December
26, 1896: 1356.
250
Ashmead was told about the experiments already in 1895 by the U.S. Minister Luther F. McKinney when
investigating the prehistory of leprosy in the Americas. McKinney, in turn, had been informed of the
experiments by a private physician who had contacted Carrasquilla after reading about it in a local newspaper in
Bogota. See: Ashmead, Albert S. “Serum-Therapy in Leprosy” The Journal of the American Medical
Association. December 7, 1895: 1008.
 103

Health on Hawaii for them to experiment with and report at the upcoming leprosy
congress.251 Carrasquilla also shipped the drug to Walter Herschel Atherstone and
Robert Sinclair Black at Robben Island; A. C. Smith in New Brunswick; Ludwig
Brieger and Fausto Buzzi in Berlin; Phineas Abraham and Lawrence Herman in
London and Eduard Arning in Hamburg, who all tested it on up to ten cases each. In
Paris, a committee consisting of Jean Alfred Fournier, Ernest Henri Besnier, Pierre
Paul Émile Roux and François Henri Hallopeau was set down to treat nine cases and
evaluate the results. In Dorpat, Karl Gottfried Konstantin Dehio manufactured the
serum using a horse and tested it on eighteen cases. Also using a horse and the
directions Carrasquilla had published, Frank Tidswell in New South Wales, Australia,
tested the serum on two cases. In Algiers, Louis Barillion used an ass to create serum
and tested it on two men suffering from leprosy.252
At the first international leprosy conference in Berlin in 1897, the treatment
was generally considered a failure.253 In South Africa, there were no results, nor in
Algiers, Berlin, Dorpat or New South Wales. In the Paris-trial four of the nine
patients saw some improvements but this was considered nothing more than the usual
fluctuation of the disease. This was also the case in Hawaii, where Louis F. Alvarez
saw some improvements in two out of fourteen cases. In a special correspondence
from “The Berlin Leprosy Conference” in New Orleans Medical and Surgical Journal
for December 1897, Isadore Dyer summarized:

Excepting his own countrymen, no results were reported from the use of his discovery, and
the Germans, the English and others came down in full force to deny not the usefulness but








251
Ashmead, Albert S. “Antileprous serum”. The Journal of the American Medical Association. January 27,
1897: 181. See Chapter 6 for more on Ashmead’s role in preparing the 1897 leprosy congress.
252
Carrasquilla, Juan de Dios. “Memoria sobre la Lepra Griega en Colombia.” Mitteilungen 1897. Bd. 1, Abt.
IV. 1897: 81-124; Discussion. “Die Therapie, insbesondere Serotherapie”. Ibid. 1897: 145-160; Thumpson,
Ashburn. “Serum treatment in Leprosy”. Lepra Bibliotheca Internationalis. 1900: 141-148. Smith, A. C.
“Report on the Lazaretto Tracadie, New Brunswick.” Lepra Bibliotheca Internationalis. 1900: 232.
253
The final resolution from the Berlin Conference simply stated: “The treatment of Leprosy has only had
palliative results up to the present time. Serum therapy has so far been unsuccessful.” Mitteilungen 1897. Bd. 2.
1897: 191-192.
 104

to argue dangers from its employment (…) Poor Carrasquilla, to have travelled so far and
yet found so little at the end of his journey.254


The main objection to Carrasquilla’s serum would however mark a new standard for
justifying the treatments: The problem with the serum was not just that it failed to
produce the promised cure, but that there was no reason why it should work at all.
This was first argued by Ludwig Brieger who tested the serum on two cases in Berlin
and found that the injections had no impact what so ever. Taking serum from a human
and incubating it in a horse for a month, Brieger argued, did not make any
immunological sense: All experience pointed at antitoxins injected in animals quickly
diminished. And since it had been impossible for anyone to detect toxins produced by
the leprosy bacillus, how could one assume that the serum that was injected in the
animals had contained any antitoxins in the first place?255 Thus, in line with other
bacteriological knowledge, the ability to act directly on the leprosy bacillus was
introduced as a new benchmark for future treatments.
Summarizing the experiments in the columns of Lepra Bibliotheca
Internationalis in 1900, John Ashburton Thompson, president of the Board of Health
in New South Wales, had two explanations for why Carrasquilla’s serum quickly lost
interest. First, Carrasquilla appeared to have had no knowledge about proper serum-
production and consequently had taken no precautions against possible contamination
when producing the serum. Second, even if the leprosy bacillus did produce a poison
which so far had eluded detection, nothing indicated that it could interact with bodies
of other animals. In short, failure was to be expected: If the treatment actually
worked, it would be a breakthrough in a range of fields at once.256
It was the lack of specialist skills and an explanation for how the drug
theoretically interacted with the leprosy bacillus that made the physicians declare the




254
As quoted by Ashmead, Albert S. “Poor Carrasquilla.” The Journal of the American Medical Association.
February 5, 1898: 330. Ashmead, the one who had introduced Carrasquilla to many of the physicians who tested
the drug, appears to have been alone in publicly defend the Columbian from the mocking reception of his
alleged cure.
255
Brieger, Ludwig. “Die Therapie, insbesondere Serotherapie”, Mitteilungen 1897. Bd. 2. 1897: 155-156.
 105

serum therapy a definite failure. As one would expect, the justification for the next set
of anti-leprosy drugs was that they interacted directly with the leprosy bacillus.





Leprolin: Tuberculin for leprosy


The first drug aimed specifically at the leprosy bacillus was ‘Leprolin’, developed by
Captain E. R. Rost working in Rangoon, the capital of British Burma, in 1904. The
drug was inspired by Robert Koch’s tuberculin, and a direct outcome of experiments
with cultivating the leprosy bacillus.
Experiments aimed at growing the leprosy bacillus outside the human body had
begun in the 1880s. Bacilli were taken from leprosy sufferers, both fresh and old
cases. The bacilli were then put in a dish containing nutrient media, ranging from agar
to blood serum, from boiled flesh to potatoes, and then stored under different
temperatures for varying amounts of time.257 Despite occasional claims that the
experiments were successful, these proved hard to reproduce. Koch’s four postulates
for proving that a bacillus was causing a disease were never explicitly discussed.
Instead, the case for the bacillus being the cause of the disease (and not an outcome)
was in the 1880s and 1890s made by frequent analogies to the tuberculosis bacillus,
which shared many of the same properties and was made visible through the same
techniques for staining.
During its existence, the medical journal Lepra Bibliotheca Internationalis
published 29 papers on cultivation, about 3.5 percent of the total number of papers.
Again the occasional reports of successful cultivations proved difficult – if not
impossible – to reproduce. Likewise, the results of attempts at inoculating animals
with the cultivations were inconsistent.





256
Thompson, Ashburton. “Serum Treatment of Leprosy”. Lepra Bibliotheca Internationalis. 1900, Fasc. 3:
141-147.
257
For an extensive overview of the early cultivation attempts, the cultivation medias used, as well as the
rationales and outcomes of the experiments, see: Scholtz, W. and Viktor Klingmüller. “Über Züchtungs-
Versuche des Leprabacillus und über sogenanntes ‘Leprin’.” Lepra Bibliotheca Internationalis. 1900: 93ff.
 106

In 1902, lecturer at the pathological department of the University of Moscow
W. J. Kedrowsky introduced the argument that the leprosy bacillus had morphology of
its own.258 The acid-fast bacilli made visible in the microscope through stained
samples from leprosy sufferers were but a certain stage in the development of the
bacillus, Kedrowsky withheld. This explained the inconsistencies in the attempts at
cultivating the bacillus outside the human body: Even if the samples selected for
cultivation contained the end-stage of the bacilli, it was not given that they contained
the bacilli in its fertile stages. As physician H. Bayon later summarized: “Once it is
admitted that Hansen’s ‘bacillus’ is but the end phase in the tissues of a filamentary
and branching organism, a quantity of bacteriological and also clinical observations
finds an easy and satisfactory explanation.”259 This debate continued into the 1920s.
Rost had a different explanation: The reason why most cultivation attempts
failed was that the most common growth mediums contained chloride salts. This
inhibited the growth of the bacillus, Rost claimed. By instead using a medium made
by distilled and superheated beef extract, the leprosy bacillus would grow in three to
five days “as a white, and later as a yellow or brick red, curly, thick growth on the
surface of the agar, very much like the bacillus tuberculosus [sic] grows on the
surface of glycerinized nutrient agar.”260 After six weeks, an extract was suspended in
glycerin in the same fashion as when producing tuberculin from cultures of the
tuberculosis bacillus. Rost named the outcome Leprolin.




258
Kedrowsky’s first paper was published in Robert Koch and Carl Flügge’s Zeitschrift für Hygiene und
Infectionskrankheiten, No. 1, 1901, and was reprinted under the title “Über die Kultur des Leprabacillus” in
Lepra Bibliotheca Internationalis. 1901: Fasc. 4.
259
Bayon, H. “The Present Position of Leprosy Research (Paper read before the Meeting of the British Medical
Association at Cape Town October 24, 1912)”. Lepra Bibliotheca Internationalis. 1913: 54. For a summary of
the cultivation attempts in the first decade of the 20th century, see: Bayon, H. “The Micro-Organism of Leprosy,
has it been cultivated?” Lepra Bibliotheca Internationalis. 1913: Fasc 4.
260
Rost, E. R. “On the Pathology and Treatment of Leprosy”. The British Medical Journal. February 11, 1905:
295; Rost, E. R. “The Cultivation of the Bacullis lepræ”. Lepra Bibliotheca Internationalis. 1905: Fasc 1. The
paper was first read before the Burmah Branch of the British Medical Association and reported in the Indian
Medical Gazette in May and June 1904, before being reprinted in Journal of Tropical Medicine, June 15, 1904.
The first results of the treatment were printed in: E. R. Rost. “Further notes on the treatment of leprosy by
injections of leprolin”. Indian Medical Gazette, December, 1904, and reprinted in Lepra Bibliotheca
Internationalis. 1905: Fasc 2. For details on the production of Leprolin, see also: Rost, E. R. “The Cultivation of
the Bacillus of Leprosy and the Treatment of Cases by means of a Vaccine prepared from the Cultivations”.
Lepra Bibliotheca Internationalis. 1911: 125-130, originally published in: Scientific Memoirs by Officers of the
Medical and Sanitary Departments of the Government of India. No. 42. 1911.
 107

The drug was injected either in the arms or the buttocks of leprosy sufferers,
and like Carrasquilla’s serum it caused a strong fever and high pulse. This, Rost
withheld, proved that the drug was working as intended.


A case of leprosy, after the first injection of Leprolin, will get a severe reaction, which may
come on very soon after the injection, the temperature running up to 104° F. [40° C] or
higher, the anaesthetic areas becoming red, hot, and swollen, and the pulse and respiration
rate going up very soon after injection. (…) As a general rule, the severity of the reaction
may be taken as an index of the benefit that is likely to occur, and this in itself is a good sign
of the beneficial action of this material in the disease.261


After three or four days, the fever would subside and previously anesthetic areas
would regain sensation. Over time ulcers would heal, cramps in hands or feet would
loosen up, the patients would become more energized; the pain and heavy sensation
associated with the disease would disappear.262 Like most concurrent bacteriological
research, exactly how the drug worked in the body was open for speculation. Rost had
two competing theories: Either the Leprolin made the body produce antitoxins which
in turn acted as an antidote (the ‘antautoxic’ view), or the Leprolin poisoned the
bacteria directly by exposing it to their own excreta (the ‘autotoxic’ view).
In addition to testing it on 120 patients in Rangoon, where a majority showed
signs of improvement and four patients were cured within months, the drug was
distributed to thirty different sites in India. But the results were not promising. T. C.
Rutherford concluded after treating 32 patients in Bilaspur District in eastern central
India with Rost’s Leprolin that all but two cases had gotten worse, and that “in at least










261
Rost 1905: 295-296.
262
“The most remarkable effect of leprolin on lepers is the suddenness with which the sensation returns in the
anaesthetic patches. I know that it is hard sometimes to say that some low-class Indians have anaesthesia or not,
but the majority of my patients have been intelligent Burmans, and some Eurasians, and only the minority
jungle folk. I have made absolutely certain before injection that the patient could not feel the prick of a pin in
certain areas, and I am glad to say that in almost every case injected with this material there has at least been
some obvious return of sensation in some anaesthetic area.” (Rost 1905: 295-296.)
 108

one of the cases the downward progress was so very marked that it is difficult not to
hold the treatment as at least partially responsible.”263
At the time Leprolin was introduced, several physicians had again resumed
experimenting with tuberculin. In 1902, for instance, physician M. Sée in Paris
deviced an experiment which would decide if the tuberculin reaction was brought
about simply because the leprosy patients had also been infected with tuberculosis.264
Even in Bergen, the failure of other remedies and occasional positive reports on

tuberculin over time leading to improvements in patients suffering both from leprosy
and other diseases, led to renewed interest for new tuberculin trials. Three years after
the death of Daniel Danielssen in 1894, the Lungegaardshospitalet was closed and
both patients and research activities were transferred to the neighboring Pleiestiftelsen
leprosy asylum. From the turn of the century, director and physician H. P. Lie at
Pleiestiftelsen would repeatedly argue that increased knowledge about doses and
possible positive long term effects justified new trials:

It may perhaps seem useless to make a fresh trial of tuberculin, when both Dr. Danielssen
and so many other observers have tried it with such bad results. There are a few, however,
whose verdict is not altogether unfavorable; and the experience that has of later years been
gained with regard to the employment of tuberculin in tuberculosis, might prove useful in the
application of the remedy to lepra.265

But, as Lie argued in the annual report for Pleiestiftelsen which in turn was printed in
Lepra Bibliotheca Internationalis, the trials would have to take place elsewhere: “The
tuberculin injections were still too fresh in the recollection of the patients who had





263
Rutherfoord, T. C. “Report of Cases of Leprosy treated with Leproline during 1911-12 in Bilaspur District
(Mirror)”. Lepra Bibliotheca Internationalis. 1913: 180, originally published in: Indian Medical Gazette.
February, 1913, and then Tropical Diseases Bulletin. 1913: 564.
264
Sée, M. “Les traitements de la lèpre”. Gazette des hòpitaux. Vol. 25. No. 60. 1903: 559-606, as referred to
in Baumgartens Jahresbericht. Vol. 18, 1905: 373. The claim was contested, see: Satinéano, A and D.
Daniélopolu. “Sur les reactions des lépreux à la tuberculine.” Comptes redus de la Société de Biologique. Vol.
66, No. 25. 1909, as referred to in Centralblatt für Bakteriologie. Vol. 45. 1909: 467 ; Babes, H. “Au sujet de la
reaction des lépreux à la tuberculine.” Comptes redus de la Société de Biologique. Vol. 67. 1909 : 411, as
referred to in Centralblatt für Bakteriologie. Vol. 45. 1909: 555.
265
Lie, H. P. “Report of the Leper Hospital (Pleiestiftelsen no. 1) in Bergen for the 3 years 1899-1901”. Lepra
Bibliotheca Internationalis. 1903: 19.
 109


come from the Lungegaard Hospital to allow me venturing upon them again.”266 In
other words, the same patient body which in the early 1890s had insisted that
tuberculin should be tried now, in light of experience, refused further experiments.
Lie, who had been appointed doctor at the hospitals in Bergen three years after the
trial, tried to convince the patients but was unsuccessful. This is but one of many
examples of how the lepers themselves could influence what medical trials to be
conducted: By refusal to participate.267
The renewed interest for tuberculin helped promote Rost’s Leprolin. But
despite receiving much attention for the potential cure developed specifically for
leprosy, with no other official manufacturer than Rost himself, the availability of the
drug was severely limited.268 The claim that Rost had succeeded in cultivating the
bacillus was also controversial.269 In early 1905, for instance, Rost was invited by
director David Semple to the newly opened Pasteur institute in Kasauli in northern
India to oversee an attempt at producing Leprolin. Despite letting Rost choose the
material and supervise the process, the attempt failed. As Semple concluded:


…we have ended in proving a negative (…). It is unpleasant, no doubt, to produce a piece of
work and find it to be wrong, but that the publication is useless is by no means true.
Mistakes may benefit the man who makes them, and profit to many other men who take up





266
Op. Cit: 20. Lie himself had no direct experience with the drug, since he was employed only in May 1893,
after Danielssen’s trial had been stopped. In 1904 Lie repeated the call for recommenced experiments with
tuberculin as a remedy in Deutsche medizinische Wochenschrift. (Lie, H. P. “Die Therapie der Lepra”.
Deutsche medizinische Wochenschrift, vol. 34. 1904 : 1381.)
267
In 1930, the secretary of the League of Nations Leprosy Commission, Etienne Burnet, summarized: “The
majority of the lepers want to be treated and simply ask that the treatment shall not be too painful; they read the
papers, never miss any item dealing with leprosy and are on the look-out for the newest remedies. If revolts
occur when the lepers are dissatisfied at their compulsory segregation, again cases could be quoted of lepers
who have objected because they were not given sufficient energetic treatment (even threatening to kill doctors
who were opposed to treatment.)” Burnet, E. League of Nations Health Organisation. Report on the Study Tour
of the Secretary of the Leprosy Commission in Europe, South America and the Far East. January 1929 - June
1930. (C. H. 887). Geneva, 1930: 43.
268
In 1910, for instance, the Spanish physicians Juan de Azua and Jose S. Corvisa explained that the reason why
they had not tried Leprolin in treating the two hundred known leprosy sufferers around Madrid was that they had
not reached the point where they could cultivate the bacillus and thereby produce the drug themselves. (Azua,
Juan de and Jose S. Corvisa. “Traitement de la lèpre.” Lepra Bibliotheca Internationalis. 1910: 148-9.)
269
Already in 1905, Frank Tidswell from Sydney concluded that they were unable to verify Rost’s reported
cultivation of leprosy bacilli, and that the premise for producing Leprolin was therefore dubious. Tidswell,
Frank. “Note on Rost’s ‘Achloretic’ Culture Medium (Report of the Board of Health on Leprosy in N. S. Wales
1905)”. Lepra Bibliotheca Internationalis. 1906: 197.
 110

the same line of enquiry. By the mistakes of ourselves and others we learn correct methods
and arrive at accurate conclusions, be they positive or negative, and, from a scientific if not
from a remedial point of view, the one is almost as important as the other.270

At the second international leprosy conference in Bergen in 1909, physicians
Beurmann and Gougerot working in Hôpital Saint-Louis in Paris reported that their
initial tests were promising.271 And should the treatments eventually fail, it was still
useful: Since Leprolin was specifically tailored to leprosy, only those actually
suffering from the disease would react. Hence, it could be used in diagnosis.272
Rost was not the only one trying to produce a tuberculin from cultivated
leprosy bacilli. In the fall of 1907, the director at the Pasteur Institute in Tunis,
Charles Nicolle, reported in a lecture at the Medical Academy in Paris that their
experiments had failed: “our ignorance for what conditions the leprosy bacillus needs
to thrive is almost complete.”273 Some years later, three physicians at the Leprosy
Investigation Station at Molokai, Hawaii, referred to previous tuberculin trials to
justify further experiments into a “vaccine and tuberculin-like extract therapy”.274
Eventually, this attempt failed too.


















270
Semple, D. “Rost’s Leprolin.” Lepra Bibliotheca Internationalis. 1906: 257, originally published in Journal
of Tropical Medicine. September 1. 1905.
271
Beurman, M. de and Gougerot. “Traitement de la lèpre par la lèproline de Rost”. Mittheilungen und
Verhandlungen der Internationalen wissenschartliche Lepra-Konferenz zu Bergen, 1909 (Hereafter
‘Mittheilungen 1909’) and Lepra Bibliotheca Internationalis. 1910: 301.
272
Beurman and Gougerot. “Le lèproline diagnostic”. Mittheilungen 1909 and Lepra Bibliotheca
Internationalis. 1910: 191.
273
Nicolle, Charles. “Réaction à la tuberculine dans la lèpre (inoculations sous-cutanée, dermique et
conjonctivale”. Lepra Bibliotheca Internationalis. 1908: Fasc. 3, first presented at Acadademie de Médecine,
August 12, 1907. Failing to produce a leprosy-tuberculin, Nicolle resorted to the tuberculosis-based tuberculin
administered through subcutaneous inoculation, skin-smears and smears on the skin under the eyelids – and
found that varying the delivery had no impact on the effects.
274
Currie, Clegg and Hollman 1911: 23-62.
 111

Nastin over the counter


Collaboration with a professional manufacturer was the secret to success for the
German researcher Georg Deycke and his drug ‘Nastin’,275 which was produced by
the company Kalle & Co in Biebrich on the Rhine from 1907.276 Deycke’s Nastin was
developed in parallel to Rost’s Leprolin, and was also sparked by attempts at
cultivating the leprosy bacillus. Unlike Rost, Deycke concluded that the organism he
managed to cultivate was not the leprosy bacillus proper but a characteristic
microorganism found in leprous ulcers that he named Streptothrix leproides. This
microorganism could be cultured in a normal salt solution.277
Determining that the organism could be developed into a drug was
serendipitous. In an attempt to ascertain the relationship between the culture and the
leprosy bacillus, he injected it into a patient suffering from leprosy to see what
happened.


Irrespective of a slight induration [hardening] at the place of injection no result was

observed; the patient, however, obstinately maintained that the injection had had a
beneficial effect on him, and he was not satisfied until I repeated the injections at weekly
intervals. Under this extraordinary treatment the patient, whose disease was severe and
accompanied by high fever became completely free from fever, and his extensive leprous
symptoms retrogressed so rapidly and in so remarkable a manner that after two months he





275
Franz Burghardt Georg Deycke from Hamburg developed the drug at the imperial ottoman hospital Gülhane
in Constantinople where he worked from 1898 to 1907, from 1903 as its director. Deycke returned to Hamburg
in 1907. At the end of 1908 Deycke visited the Public Leper Asylum at Mahaica in British Guiana for six months
in order to direct a trial of Nastin on 135 cases, before returning to continue his research in Hamburg. (Editorial.
“The Nastin Treatment of Leprosy”. The Lancet. July 22, 1911: 237-238). The initial research was made in
collaboration with Reschad Beyer and published in Deutsche Medizinische Wochenschrift in 1905, nos.
12 and 14. See: Deycke, G. “Zur Theorie une Praxis der immunisierenden Behandlung der Lepra mit Nastin.”
Lepra Bibliotheca Internationalis. 1907, Fasc 1.
276
Deycke, G. “A Lecture on a Specific Treatment of Leprosy”. The British Medical Journal. April 4, 1908:
802-806.
277
In the years that followed, several physicians referred to Kedrowsky’s model of the leprosy bacillus having its
own morphology, and argued that the streptothrix was in fact the leprosy bacillus proper but in a different stage
of its growth. As A. G. Foulerton put it in a discussion following Deycke’s presentation of Nastin in London in
1912; “the acid-fast forms of a streptothrix represent only a single phase in the life of the organism. Young
cultures are not acid-fast; the property is one which is acquired in later growth, and even then is, under the
conditions of culture on artificial media, of very variable occurence. In a sense, the acid-fast phase of a
streptothrix is an accidental one; the acid-fast type probably representing more resistent forms of the organism.”
(“Discussion”. Transactions of the Royal Society of Tropical Medicine and Hygiene. March, 1912: 196.)
 112

considered himself to be thoroughly cured and left the hospital. Seeing that similar results
were also obtained in other cases of leprosy, we naturally made it our task to discover the
curative principle contained in the cultures.278


The unexplained success meant taking the substance back into the laboratory for
further investigations: Testing, filtering and chemical experimentation. The outcome
was a substance Deycke named ‘Nastin’, a fatty acid in a state suitable for injections
just beneath the skin (hypodermic injections). Further tests on patients revealed that
the responses differed. Some had violent reactions ‘dangerous to life’; others showed
no reaction at all. Applying the drug to a culture of tuberculosis under the microscope
did however give insights into how the drug worked: The Nastin would mix with the
fat contained in the bacillus, dissolve it and then leave the bacillus vulnerable. This
could also explain why the drug did not work in all cases: It needed a substance to
activate the fat-dissolving reaction. After testing several benzoic acids in vitero, again
using cultures of the tubercle bacillus to see what best dissolved the fat surrounding
the bacteria, he settled on benzoylchloride.


The nastin is carried to the lepra bacilli, to which, owing to its near chemical and physical
relation, it attaches itself, and then benzoyl can fully display its antibacterial action in the
fat-removing sense. When deprived of fat the lepra bacilli seem to be doomed; the human
organism then effects with comparative ease the further dissolution and ultimately the
complete destruction of the bacteria nuclei.279



The drug was put up for sale in three varieties containing different mixtures of
benzoyl and Nastin, named Nastin-B0, Nastin-B1 and Nastin-B2, in addition to the
drug “Lösnung K” which contained pure Benzoylchlorid. The drug was administered
by injecting it under the skin of the arms, the hips and the back, producing a burning
but passing pain. The injections were initially to be given once a week, gradually
increasing to five injections per week. In direct contrast with Rost’s Leprolin, a strong




278
Deycke 1908: 802.
279
Deycke 1908: 805.
 113

fever reaction was perceived to be a bad sign, and the proscribed procedure was to
replace the injections with Lösnung K.
Due to increased availability, Deycke avoiding the controversies regarding
culture, positive reports from the first independent trials, being relatively free from ill
effects, and the modest insistence that Nastin was not a magical remedy that always
worked but that it frequently produced very good results, the drug was tested in
numerous locations. In Lepra Bibliotheca Internationalis between 1907 and 1915,
Nastin was the topic of twenty papers. When including all research on treatment from
1900 to 1915, this made up about a fifth of the total number of papers and almost four
times as many as Rost’s Leprolin. That failed treatments could be ascribed to the
physician neglecting to individualize the drugs correctly, and not a failure of the drug
itself, probably also played part in the initial optimism.
In the invitation to the second International Leprosy Conference in Bergen in

1909, Nastin was highlighted as one of the new means which science could offer
governments in order to achieve the goal of exterminating leprosy, much like
Carrasquilla’s serum had been a topic in Berlin twelve years earlier.280 The session on
treatment was opened by Deycke himself, who claimed that Nastin was a specific
drug that targeted the pathogen directly; “a significant weapon in the battle against the
leprosy epidemic”.281
Among the first to send in an order for Nastin was Captain T. S. B. Williams of
the Indian Medical Service, who worked with leprosy sufferers in Bushire by the
Persian Gulf (now Bushehr, Iran). After testing Nastin on twelve cases for up to a
year, he reported that seven of the patients had improved dramatically, while the rest
had no relapses. In all but one case, ulcers and lepromata (leprous nodules) had
steadily improved and the number of leprosy bacillus in skin and nose samples had




280
“Programme provisoire de la Deuxième Conférence Internationale Scientifique contre la Lèpre devant avoir
lieu du 16 au 19 Août 1909 à Bergen, Norvège.” Lepra bibliotheca Internationalis. 1908, Fasc 2: 125.
281
“Das Nastin B ist ein spezifisches, d. h. direct die Leprarreger angreifendes Mittel. (…) Mit einem so
gearteten Mittel ist uns aber, wie ich überzeugt bin, eine nicht zu verachtende waffe im kampf gegen die lepra
als volksseuche in die hand gegeben.” . Deycke, G. “Über die Therapie der Lepra”. Lepra Bibliotheca
Internationalis. 1910: 211-222, quote on p. 222. For Deycke, Nastin did not substitute the need for forced
 114

diminished. “Deycke’s brilliant researches have, I am sure, given us at last a specific
foundation on which to base our treatment.”282
Despite some reservations voiced in the discussion, the final resolution of the
Bergen conference rejected the conclusion from Berlin that the disease was
incurable.283 Reflecting the cautious optimism regarding the new drugs, from 1909
the official consensus among the leprologists was that: “The clinical study of Leprosy
induces the belief that it is not incurable. We do not at present possess a certain
remedy. It is desirable, therefore, to continue the search for a specific remedy.”284 A
winning argument was what the German dermatologist Paul Gerson Unna first had
voiced at the Fifteenth International Medical Congress in Lisbon in 1906: If leprosy
was considered incurable, further research into finding a cure was per definition
meaningless.285
Further tests with Nastin, however, produced confusing and conflicting results.
In the capital of German East Africa, Bagamojo (in what is now Tanzania), physician
Lenz tested Nastin on five patients in 1907, and then twelve more in 1908. Failing to
obtain any results led him to the conclusion that the drug might have been damaged
during transportation.286 Likewise, after one year of testing the drug on six patients at
the leprosy investigation station at Honolulu and seeing only slight improvement in
two of them, Walter R. Brunckerhoff and James T. Wayson sent the drug back to the
manufacturer in Europe, asking them if the drug was inactive. The drug was returned






isolation, but being able to offer treatment and the hope of a cure, he argued, would make such policies easier to
implement.
282
Williams, T. S. B. “Nastin treatment of Leprosy”. Lepra Bibliotheca Internationalis. 1910: 261. The paper
was submitted to the Bergen Conference, but was not read as Williams was unable to attend.
283
See Appendix 2.
284
Lie, H. P. “Internationale Wissenschaftlige Lepra-Konferenz. Abgehalten vom 16. bis 19. August 1909 in
Bergen (Norwegen). Mitteilung und Verhandlungen.” Lepra Bibliotheca Internationalis. 1910, Fasc 3: 418-
419. In addition to Nastin and Leprolin, the German physician Franz Engel-Bey working in Cairo presented his
drug Antileprol, a derivate of chaulmoogra oil which from 1908 sold via the German company Beyer & Co
from 1908. (Engel-Bey. “Zur Behandlung der Lepra mit Antileprol”. Lepra Bibliotheca Internationalis. 1910:
274-290.) More on chaulmoogra and its derivates later in this chapter.
285
Unna, P. G. “Sur la pathologie et la thérapeutique de la lèpre”. Lepra Bibliotheca Internationalis. 1906:
Fasc. 3. According to Unna, the prevalent view that leprosy was incurable created a self-fulfilling prophecy
which needed to be rejected.
286
Lenz. “Berich über die Behandlung Aussätziger mit Nastin und Chaulmoograöl”. Lepra Bibliotheca
Internationalis. 1910: Fasc. 1. In comparison he found chaulmoogra oil to be more efficient.
 115

with a note saying that the Nastin was indeed active and ought to work – given the
right doses.287 At the leprosarium in Kuuda in Estonia, physician Arthur Kupffer
recommended using Nastin injections as a supplement only if chaulmoogra oil alone
did not produce results.288
In many cases the initial impressions were positive, but faith in the drug
declined as the trials progressed. Visiting medical officer to the Pretoria Leper
Asylum in Transvaal (now South Africa), Gordon B. Messum, put in an order for
monthly shipments of Nastin in 1908 and tested it on twenty patients for between six
and eighteen months. Initially the results were promising, but after a while doubt set
in. Messum’s report was one of few occasions where also statements made by the
patients themselves were part of the argument:


It is curious to note that after the first 10 or 12 injections, so many of the patients declared
themselves much benefited, and greatly improved in general health. Expressions were used,
such as “I now feel much stronger”, “I can now use my hands with more grasping power”, “I
can now walk without getting so easily tired”. Whether these feelings were due or suggested
by anticipatory expectations of the reputed curative property of Nastin or not, is a question,
because many of the patients had been told and had read of some wonderful cures as the
result of this treatment, and they may thus have been impressed suggestively. It was clearly
noticeable that there was much more cheerfulness amongst them, due to hopeful
anticipations, and they were so positive in their statements that I was myself at first carried
away on the wave of optimism. In order to test the improvements thus reported, they were at
this time thoroughly examined, and I was myself somewhat astonished and taken back to
find no definite difference or improvement in them. I did not let them know, however, that
such had been my finding, but I was beginning to feel that most were inclined to be
impressionists, whose imagination created more than I could discover.289








287
Brinckerhoff and Wayson. “Report upon the treatment of six cases of leprosy with Nastin (Deycke)”. Lepra
Bibliotheca Internationalis. 1910: 228.
288
Kupffer, A. “Ein Beitrag zur Behandlung der Lepra mit Chaulmoograöl und Nastin”. Lepra Bibliotheca
Internationalis. 1909: Fasc. 3.
289
Messum, Gordon. “Twenty cases of Leprosy treated simultaneously with Deycke’s Nastin”. Lepra Bibliotheca
Internationalis. 1910: 239-240, originally published in The Transvaal Medical Journal. May. 1910. See also:
Editorial. “The treatment of leprosy by Nastin.” The Lancet. July 30. 1910: 325-326.
 116

Messum’s misgivings only grew stronger when one patient who secretly received
saline injections instead of Nastin reported that he too benefitted from the cure. As
months went by the early confidence in the cure was replaced by indignation and
anger that the drug had left them worse off than before. After a year and a half
Messum concluded: “In the treatment of the cases which I have here recorded, I am
sorry to say that Nastin has not shown itself capable of producing any definite
remarkable results.”290

Interestingly, the interpretations of a single trial could also differ, such as in the
Nastin trial at the Public Leper Asylum at Mahaica in British Guiana between 1908
and 1912 where 135 voluntary patients received injections. The first six months of the
trials were done in collaboration with Deycke, who had been invited by the Governor,
Sir Frederick Mitchell Hodgson. While Deycke concluded that the injections in
almost all cases arrested the progress of the disease, the local physician K. S. Wise
concluded that only three were cured, some had gotten worse, and the majority
remained in status quo. Finally, in the letter accompanying Wise’s report Governor
Hodgson claimed that


(…) there are 56 cases in which no leprosy bacilli can be found, and of this number it is
hoped that 75 percent will be fit to be discharged within the next three months. Never before
in the history of the Leper Asylum of the British Guiana has leprosy been successful fought,
and the results now obtained will doubtless lead to further research and to a more complete
conquest of this most terrible of diseases.291

After Deycke had left, Wise in collaboration with E. P. Minett continued the trial.
Over four years, 244 individuals suffering from leprosy received injections. At first
the results were encouraging, but by September 1912 they concluded that Nastin, at
best, only offered a slight temporary check to the course of the disease. Ultimately, a








290
Messum 1910: 240.
291
Editorial. “The Nastin Treatment of Leprosy”. The Lancet. July 22. 1911: 237.
 117

control group was given injections of only benzoyl-chloride (Lösnung K designed to
activating the Nastin) and ended up producing identical results.292
Only months earlier, at the February meeting of the Society of Tropical
Medicine in London in 1912, Deycke had enthusiastically referred to the drug being
tested on 529 cases in 69 different locations, not mentioning the results from British
Guiana as he had been personally involved: 13 were reported as cured, 34 as nearly
cured, 131 considerably improved and 154 as improved. Instead of highlighting that
only 13 out of 529 cases had resulted in a cure, Deycke stressed that beneficial results
were attributed to the treatment in 332 cases (62.76 %).293 By then, however, Deycke

was fighting a losing battle. The Lancet, which followed the Nastin-trials closely,
concluded in an editorial in July 1910 that the jury was still out: “In our opinion
further experience of its use on a large and extended scale in leper establishments is
needed in order to supply the evidence on which its acceptance or rejection by the
medical profession must ultimately depend.”294 Two years later, they were not
convinced: “With all this conflicting evidence before us it is not easy to arrive at a
definite conclusion, but in the circumstances we think we are justified in saying that
up to the present the evidence put forward in favour of Nastin is hardly convincing
enough to lead to its general acceptance.”295
Nastin did remain in use in certain locations, depending on the local
experiences, but most physicians were deterred by the dubious results and high
cost.296 Like Beauperthy’s cure, Tuberculin, Carrasquilla’s serum and Leprolin before
it, the general consensus was that Nastin did not live up to the expectations. Instead, it







292
Wise, K. S. and E. P. Minett. “Treatment of Leprosy by Nastin”. Journal of Tropical Medicine and Hygiene.
September 2. 1912: 259.
293
Deycke, Georg. “Treatment of leprosy by nastin, and results so far obtained by this treatment.” Transactions
of the Royal Society of Tropical Medicine and Hygiene. March. 1912: 168-174, 195-204; Editorial. “The
treatment of leprosy by nastin.” The Lancet. March 30. 1912: 881-883.
294
Editorial. “The treatment of leprosy by nastin.” The Lancet. July 30. 1910: 325.
295
Editorial. “The treatment of leprosy by nastin.” The Lancet. March 30. 1912: 883.
296
H. P. Lie, who tested the drug on six patients in Bergen between 1907 and 1911, seems representative when
he concluded that Nastin might be of some use in isolated cases, and this made it interesting, but that the drug
was too unpredictable to in any way revolutionize the campaign against the disease. (Lie, H. P. “Om nastin og
nastinbehandling i lepra.” Medicinsk Revue. 1911: 353-362.)
 118

was an old herbal medicine that from the 1920s dominated discussions on treatment
of leprosy worldwide.





Did the treatments work?


Before investigating the chaulmoogra treatment, it is necessary to take a step
back and discuss whether the treatments worked. In the strictest sense, all the drugs
mentioned so far failed to achieve consistent cures in other locations than the one
where it was first tried. On the other hand, there were several reports of at least initial
improvements in those treated. In the following I will show how the criteria for
answering the question ‘did the treatments work?’ depended on the yardstick used,
and that the measure for success changed between the 1850s and the 1930s. I will also
discuss to what extent these medical trials reflected actual local practices.
Up to the 1870s, a common explanation for why the occasional report of
successful leprosy-cures proved impossible to reproduce was that the label ‘leprosy’
was used on a variety of skin diseases. If a treatment succeeded, it was often
dismissed as a case of initial misdiagnosis. And even if the diagnosis was accepted as
‘correct’, each individual case was unique. Leprosy, like any other diseases, was the
result of multiple causes working together, and many argued that attempts at finding a
single drug or a standardized treatment plan which would work equally well in all
cases was doomed to fail. In 1871, Robert Welbank Macaulay with the Bengal
Medical Service summarized in a medical dictionary aimed at a wider audience:


The insignificant remedies which have been recommended for the cure of leprosy are very
numerous, probably arising from the circumstance, that there is no single application or plan
of treatment that will be uniformly successful, even where we are attentive to the nature of
the disease, and the circumstances of each case; but where we merely take up the name, and
 119

indiscriminately apply to every case we call leprosy, some one medicine or plan, we may be
certain of being repeatedly altogether disappointed.297

Many of the treatments did reportedly do some good. Explaining why the effects of
the treatments differed was a recurring topic for debate. Gordon Messum in Pretoria
was but one of many who argued that every treatment initially did some good based
on anticipation alone. Another often used explanation was that each individual
differed in their resistance to the disease and that this inherent resistance could
overcome the disease, regardless of any medication. In the case of a British soldier
successfully treated with strychnine, gurjon and chaulmoogra in Sydney, for instance,
John Ashburton Thompson explained that the drugs probably had been of little
consequence: “on the whole I feel obliged to express the opinion that it would not
have produced the excellent results recorded in this case, unless the patient had
possessed an unusual inherent power of combating the infection.”298 Yet others
argued that the drugs worked, but that a successful treatment required a persistence
that most ‘lepers’ lacked.

In general, the smaller trials were reportedly more successful than the larger
ones. In the discussions on treatments, several pointed out that even Danielssen had
occasionally discharged patients as cured, and it was well accepted that a small
proportion of those affected by the disease spontaneously recovered, independent of
any treatment. This undermined the confidence in the value of the smaller trials. Was
reporting a success simply more attractive than describing treatments that failed? Did
this create a bias? Was the initial diagnosis wrong?
Taking stock of the state of leprosy treatments at The Fifteenth International
Medical Congress in Lisbon in 1906, German dermatologist Paul Gerson Unna
pointed out that many of the reported successes were made by physicians with only




297
Macaulay, Robert Welbank. A dictionary of medicine and surgery designed for popular use containing an
account of diseases and their treatment, including those most frequent in warm climates. 1871: 437. This was,
in turn, a direct quote from the first edition by his father, Alexander Macaulay, published in 1828. My thanks to
Åsne Hagen for this.
298
Thompson, J. Ashburton. “A Case of Lepra Tuberosa; Approximate Recovery.” Lepra Bibliotheca
Internationalis. 1907: 23.
 120

limited experience with the disease. Judged for instance by the number of different
authors publishing in Lepra Bibliotheca Interationalis, it seems there was some merit
to this criticism: Of 104 papers on treatment published in the journal’s fifteen years of
existence, 92 authors published only once. According to Unna, papers presenting
single cases were naïve, misleading and contributed to the difficulties in getting an
overview. Instead, large studies conducted by experts with extensive experience
should be the norm.299 Large studies required access to large numbers of cases and the

ability to monitor the patients over time. This meant excluding the general physician
meeting occasional patients on the bedside, in favor of those working in leprosaria
and other specialist institutions with hospital wards.
However, measuring the efficacy of a drug in larger groups instead of in
individuals was not enough to avoid bias. In a discussion in London in 1912,
Messum’s predecessor as medical Medical Superintendent at the Pretoria Leper
Asylum, George Turner, suggested giving half the patients a mixture of lime juice,
syrup and tincture of ginger.300 In his experience, “the glorified ginger beer” always
produced equally good results when compared to proposed cures, proving that the
drugs used were in themselves insignificant: “Unless, as I said before, the cures or
arrests very greatly exceed 2 or 3 per cent., the figures obtained without control mean
absolutely nothing.”301 In the 1920s, some argued that the percentages of expected
cures produced independent of any treatments could be as high as 20 percent.
While Unna simply argued that the experts working with groups of patients
would produce better knowledge than general practitioners seeing at most a handful
of cases, it is important to note that they also produced a different kind of knowledge.




299
Unna, P. G. “Sur la pathologie et la thérapeutique de la lèpre”. Lepra Bibliotheca Internationalis. 1906:
Fasc. 3.
300
George Turner worked as Medical Officer of Health in the Cape Colony from 1895, and was Medical
Officer at the Pretoria Leper Asylum from the early 1900s until retiring and returning to England in 1908. In
1913 he was knighted, and it became publicly known that he himself was a victim of leprosy. In the popular
press, he was immediately portrayed as the “Father Damien of the British Empire”, a term that was repeated in
the obituaries when he died two years later. See i.e. “Doctor, Knighted, A Leprosy Victim. Story of Turner’s
Self-Sacrifice among Lepers at Pretoria Moved the King.” The New York Times. January 19, 1913. “England’s
Father Damien. A Victim of Leprosy.” The Advertiser. Adelaide. February 24, 1913: 16; “Sir George Turner
Dies From Leprosy. Sacrificed His Life in His Efforts to Find a Cure for the Dread Disease.” The New York
Times. March 14, 1915.
 121

In Pickstone’s vocabulary, walking the wards was a different way of working than
meeting single patients, and this was entangled with a different way of knowing. This
is reflected in the reports produced: The case-stories generally contained far more
information that only the person suffering from the disease could provide compared to
the quantitative studies produced in institutions, such as details of the life the (often
named) sufferer led prior to being diagnosed. In some cases, they contained details of
where, how and why the physician and leprosy sufferer met. The descriptions of
lesions and the rationale for the diagnosis were also much more elaborate. Although
reports on relatively large trials could emphasize the individual patients taking part,
such as Danielssen’s tuberculin trial, and while working in institutions generally
meant having the sufferers under continuous scrutiny over longer periods of time,
increasingly the individualizing details were seen as less important. After all, when
referred to by others these details were almost consistently ignored.
By the 1920s, studies of individuals had not completely disappeared, but the
genre of case studies was mainly withheld for cases explicitly out of the ordinary.
Increasingly, studies that produced conclusions which could be presented in numeric
ratios took over. In the interwar period the large scale trials, where the success of
treatments could be measured in numbers and proportions rather than minute
descriptions, began to dominate. When Solis and Wade examined several hundred
children in Manila in the mid-1920s, for instance, it is obvious that any details on the
individuals had to be omitted.302 Textual elaborations on what changes had occurred
in the individual patients were slowly replaced by statistics separating the patients into
groups. Producing knowledge that could be quantified became a goal in itself. When
Etienne Burnet in the late 1920s argued on behalf of the League of Nations Leprosy
Commission that time was ripe for coordinated large-scale experiments, this was a






301
Discussion. Transactions of the Royal Society of Tropical Medicine and Hygiene. March, 1912: 200.
302
Solis and Wade’s study of Philippine children was published in Journal of the Philippine Island Medical
Association (vol. 5, December 1925), the follow-up in the same journal in 1927 (vol. 1). Referred to in: Burnet,
Et. “Provisional report presented at the Leprosy Commission at its meeting at Tokyo in April 1930:
Consideration of urgent matters to which the commission drew attention at its May session, 1928”. League of
Nations, C. H./Leprosy/7a, Geneva, January 1930: 5.
 122

reflection both of the ideology of the League, and new emerging medical virtues
which put emphasis on the production of comparable results. 303
According to historian Theodore M. Porter, quantitative and procedural forms
of accountability must be understood as ‘technologies of distance’, developed to
provide a check on subjectivity and combat distrust. Quantification, Porter has
argued, is a communication strategy that goes beyond the boundaries of locality and
community, and helps produce knowledge independent of the particular people who
made it. Calls for quantification came mainly from outside pressure on weak research
communities and was employed as a way to increase authority.


The advances of statistics in medicine must be understood as responses to problems of trust,
which have been most acute in the context of regulatory and disciplinary confrontations.
This, and not any inherently statistical character of clinical medicine, explains why
inferential statistics entered medicine through therapeutics.304

While the international leprosy research community can be perceived as relatively
weak, the rationale for quantification was not a response to demands from ‘outside’
forces. Instead, it reflected the assumption that leprosy was the same disease
regardless of location, and that the disease was governed by the same general laws.
These laws were not deterministic on an individual level; instead they were made
visible only in larger numbers. Hansen’s argument for contagion in the early 1870s, as
I will return to in the following chapters, was based on a quantitative comparison of
prevalence in different districts in Norway. The statistics showed that the number of
new cases declined proportional to those already having the disease being ‘evacuated’






303
“Time has come to organize large-scale experiments; the comparative study, on groups of similar cases (…)
These experiments should be world-wide; they call for universal co-operation, that is to say, continual
exchange between all leprosy countries. This appears to be one of the most important items of the
Commission’s programme.” (Burnet 1930: 8-9.) The ensuing attempts at creating a global system for
classifying cases (see Chapter 5) were a seen as a necessity to facilitate globally comparative large-scale trials.
304
Porter, Theodore M. Trust in Numbers. The Pursuit of Objectivity in Science and Public Life. 1995: 208-
209. For a review discussing the reception of the book, see: Hagendijk, Rob. “An Agenda for STS: Porter on
Trust and Quantification in Science, Politics and Society.” Social Studies of Science. Vol. 29, No. 4. 1999: 629-
637.
 123


to institutions.305 The same rationale applied to testing the efficacy of treatments.

Quantification was not a matter of distrust, but a tool to go beyond the local
particularities and to make a general argument applicable to other contexts than where
the numbers were first produced.
The question of what was to be observed, whether counted or described, was
contested. This was connected to competing disease models. In the late 1860s,
summarizing his experiences of treating sixteen lepers at the Hospital of San Lazaro
in Lisbon, James J. L. Donnet argued that “In the treatment of this disease the
hygienic, the dietetic, and the palliative had more influence than the therapeutic.”306
Later, especially British physicians would hold on to the argument that improved diet

and a change in climate would produce better results than any drugs. The prominent
physician Jonathan Hutchinson, for instance, argued that the disease was caused by
eating badly cured fish, and was cured by moving sufferers to a different climate,
making them do physical exercise, administering small doses of arsenic, “and a
resolute abstinence from all fish.”307 While I have focused on observations of
patients, many argued that observations on climate and diet were equally relevant to a
discussion on treatment. Only in the 1920s, climate and diet were displaced by
attention to hygienic conditions.
Making the bacillus the target for medications did not put an end to yet another
rationale for treatment strategies: Analogies with other diseases. Following The
Danish physician Niels Ryberg Finsen’s Nobel Prize in Medicine in 1903, for
instance, the light radiation treatment developed especially for lupus vulgaris
(tubercular skin infections) was employed extensively on leprosy patients. This was
but one of many analogies. The de facto main editor of Lepra Bibliotheca
Internationalis, Danish physician Edvard Ehlers, argued for instance that leprosy,







305
For more details on the Norwegian debates, see Chapter 5.
306
Donnet, James J. L. “Clinical Notes on Leprosy.” British Medical Journal. August 10, 1889: 301-304.
Donnet saw the disease as ultimately incurable; “it is one that follows a determined course, rapid in some, more
dilatory and seemingly stationary in others, but never retrogressing, always advancing.” (op.cit.)
307
Hutchinson, Jonathan. “On cases of recovery from leprosy.” Lepra Bibliotheca Internationalis. 1901: 53.
 124

tuberculosis and syphilis belonged to the same family of diseases.308 Others argued
that leprosy was the fourth stage of syphilis, yet others that it was an expression of
Morvan’s disease (syringomyelia), linked to racial degeneration, goitre (struma), and
dwarfism. While making analogies to other diseases was an important rationale for
trying drugs such as mercury and salvarsan (both known to work against syphilis),
this did not invite to debates on finding a common ground for assessing results.
Analogies remained important for justifying new and creative treatments, but also
added to the complexity of the debates.
Agreeing that the disease was connected to the leprosy bacillus was a step in
the direction of global convergence of treatment regimes, but the exact nature of the
bacillus remained contested. The research aimed at cultivating the leprosy bacillus
outside the human body did not succeed in producing an entity which was identical in
different parts of the world. Strains of both Kedrowsky’s lepra-cultures from Moscow
and Deycke’s Streptothrix leproides from Hamburg were shipped and cultivated
elsewhere, but problems reproducing the results, not to mention interpreting the
outcomes of the procedures, made it difficult to stabilize the leprosy bacillus as a
unifying entity outside its mere presence in skin samples. By the 1920s most agreed
that the attempts at demonstrating the bacillus in the same way as Koch had
demonstrated the pathogen of tuberculosis had all failed. With a possible exception of
studies into ‘rat leprosy’, there were no animal models. Medical trials testing new
treatments had to be conducted on those suffering from leprosy directly.
Finally, there were different standards for measuring success. For some
increased energy, the ability to work, increased sex drive and a feeling of optimism
among the patients was in itself enough to justify declaring the treatment a success.
Others seem to have been content if treatment introduced cleanliness or order. Some
focused on improvements in the clinical signs of the disease, mainly ulcers healing
and anesthetic spots regaining sensation; some focused on stopping the progress of
the disease. From around the First World War, demanding that no bacilli were found





308
See i.e. Ehlers, Edvard. “Le traitement mercureil de la lepre.” Lepra Bibliotheca Internationalis. 1900: 45.
 125

in tissue samples over a period of several years was increasingly adapted as a
standard, but some still withheld that a cure meant that all symptoms of the disease
ever having been present must disappear.





The best case scenario


In 1893, the Leprosy Commission to India concluded that leprosy was incurable, at
least with the drugs available. This was also the consensus at the first international
leprosy conference in Berlin. But incurable did not mean untreatable. The
Commission to India, for instance, still recommended ointment and other treatments,
as the palliatives made the disease progress more slowly. While the progress of the
disease could never be stopped completely, it could be slowed down.
At the second international leprosy congress in Bergen in 1909, the final
resolutions stressed that despite science not possessing a specific remedy, the disease
was not incurable.309 After all, occasionally some patients did get well. But although
the increasingly dominant goal of finding a specific cure led to even more attention to
developing and testing new drugs, only a minority of the physicians working with
leprosy on a daily basis seems to have been very optimistic. Etienne Burnet’s report
on behalf of the League of Nations on the status of treatment in 1928 also applies to
the preceding decades. The report opened as follows:

For a long time, lepers were left to themselves; this is true at any rate of leprosy if not of
lepers. Leprosaria were homes for incurables. Intercurrent diseases were treated, and
symptomatic treatment was applied if the means were available. There was no idea of curing
leprosy. The enquiry shows that the cause of treatment has not yet completely triumphed.
Treatment is frequently given from a sense of duty to do something.310







309
Lie, H. P. Internationale Wissenschaftlige Lepra-Konferenz. Abgehalten vom 16. bis 19. August 1909 in
Bergen (Norwegen). Mitteilung und Verhandlungen. Bd. 3: 418-419. (Distributed in Lepra Bibibliotheca
Internationalis. 1910.)
310
Burnet 1930: 7.
 126

Generally, treatments for which the best case scenario was keeping the disease at bay,
or at least temporarily alleviating some of the suffering caused by the disease, were
not published in the medical journals. Palliative treatments were mentioned in
medical textbooks, but seldom much elaborated. To some extent, however, local
practices were reflected in reports and testimonies made by visitors. Souza-Arùja’s
Leprosy Survey made in Fourty Countries (1929) and Etienne Burnet’s Report on the
Study Tour of the Secretary of the Leprosy Commission in Europe, South America and
the Far East (1930) suggest that only when local practices could be compared and
differences in daily routines identified, local customs were seen as something worth
highlighting. In addition, some of the papers on the prevalence of leprosy in specific
countries presented at the international leprosy conferences discussed daily routines
within and outside the institutions. Together with the papers published in Lepra
Bibliotheca Internationalis under the heading ‘Geographia’, they often gave a very
different picture of the situation on the ground than the impression gathered from
reading just the presentations of proposed cures and medical trials. There seems to
have been a clear mismatch between the printed discussions on treatments, which
represented something new and out of the ordinary, and the most common local
practices, which mainly consisted of routines and palliative treatment.
The use of drugs was not the only strategy for pain relief. From the late 1870s,
nerve stretching was used as a palliative, especially in anesthetic cases.311 The
treatment consisted of cutting open the leg or lower back of patients to reach the main
nerve going into the lower limbs (the sciatic nerve), and then massage it using fingers
or the back of a surgical knife. One of the foremost proponents was the British
physician Beaven Neave Rake, medical superintendent at the leprosy asylum in
Trinidad. In 1888, after one hundred operations on sixty patients, he concluded in the
columns of The British Medical Journal that the procedure had led to “more or less
relief in forty-seven cases, no relief in forty-nine cases, and a doubtful result in four






311
According to historian Jane Buckingham, the first procedure of nerve stretching was reported in the Indian
Medical Gazette in July 1877. (Buckingham 2002: 87-88).
 127


cases.”312 Nerve stretching, he argued, provided relief and was in many cases an
alternative to amputations.313 While it is unclear how widespread this procedure
actually was, general palliative treatments and daily care received little attention in
medical journals such as Lepra Bibliotheca Internationalis (1900-1915). Despite
being relatively easy to administer, nerve stretching was only mentioned once in a
summary paper throughout the journal’s fifteen years existence.314 In comparison,
despite demanding expensive equipment and a steady electrical supply, seven papers
discussed the use of X-rays at length.315 As late as 1940, Rogers and Muir explicitly
warned against the ill effects of nerve-stretching, which suggests that the procedure
was still being practiced.316 This, again, indicates that not all medical practices were
reflected in the circulation of knowledge. The production of new knowledge was
more interesting than routines; the search for a cure was perceived to be more







312
Rake, Beaven. “The value of nerve stretching in leprosy: based on one hundred cases.” The British Medical
Journal. December 22. 1888: 1373-1378, quote on p. 1378.
313
For tubercular cases, Rake recommended surgery. To treat an ulcer under the foot, he recommended using a
surgical knife (bistoury) and cutting through the foot, starting with the ulcer, and cutting straight forwards until
the knife could be brought out between the toes of the patient. The foot was then stuffed to arrest hemorrhage.
(Rake, Beaven. “The treatment of perforating ulcer in leprosy”. The British Medical Journal. November 8,
1890: 1059-1060. See also: Rake, Beaven. “On the treatment of tubercular leprosy by excision”. The British
Medical Journal. June 9, 1888: 1214-1215.) Surgical interventions were widespread. In Bergen, for instance,
Eduard Boeckmann used surgery to create scars in an attempt to contain the disease and stop blindness.
(Boeckmann, Eduard. “Om de Spedalskes Øienlidelser.” Medicinsk Revue. 1886: 257-267, 289-296.)
314
“Arsenic internally, guryonoil externally and internally, carbolic acid externally and internally, appeared to
do the most good. Among other remedies employed were perchloride of mercury, ichtyol, resorcin, thyroid
extract, zinc sulphate etc etc. In some cases nerve stretching was practiced.” (Simpson. “410 Cases of Leprosy
treated in the North-West Province and Oudh in India.” The Polyclinic. March 1902: 159ff; Lepra Bibliotheca
Internationalis. Vol. 3, Fasc. 3. 1902: 184.)
315
Oudin. “Lèpre tuberculeuse traitée par les rayons X”. Annales d’électrobiologie et de radiologie 1903: No.
1, in Lepra Bibliotheca Internationalis, 1903; Belot. “Les rayons-X dans la lèpre.” (Extract from: “La
Radiothérapie dans les affections cutanées”. Lepra Bibliotheca Internationalis. 1904, originally published in
Annales de Dermatologie et de Syphiligraphie. 1904: 533; Wilkinson, H. B. “Leprosy in the Philippines with an
Account of its Treatment with the X-rays.” Lepra Bibliotheca Internationalis, 1906: Fasc 3, originally
published in The Journal of the American Medical Association. February 3, 1906; O. Lassar, A. Siegfried and
Urbanowitz. “Versuche mit der Behandlung Leprakranker mit Röntgenstrahlen.” Lepra Bibliotheca
Internationalis 1907, originally published in Klinische Jahrbuch, 1905: Heft 1; Matthews. “Treatment of
Leprosy with X-rays and high Frequency.” Lepra Bibliotheca Internationalis. 1908: Fasc 3, originally
published in Indian Medical Gazette, August 1908; Heiser, Victor. “Leprosy in the Philippine Islands”. Lepra
Bibliotheca Internationalis. 1910: 38-39, originally published in Treasury Department Public Health Report.
No. 35, 13. August. 1909; Heiser, Victor. “Case of Leprosy apparently cured with the X-rays.” Lepra
Bibliotheca Internationalis. 1910: Fasc. 1, originally published in Medical Record. New York, October 31.
1908.
316
“Nerve-stretching is always harmful.” (Rogers and Muir 1940: 243)
 128

interesting than daily care. In other words: Although routines differed from place to
place, this was generally not reflected in the papers that were circulated.
Despite impressive numbers, such as Nastin over a five year period being
tested on close to a thousand individuals in more than seventy different locations, this
was but a fraction of the ‘lepers’ that met with physicians globally. And this number
was in turn but a fraction of the ‘lepers’ reported in the statistics presented for
instance at the international leprosy conferences. For the vast majority of those
affected by the disease, the medical trials – or Westernized medical treatment at all –
was never part of the experience.
The answer to the question ‘did the treatments work?’ depended on who was
asked, their own personal experiences and what reports they had access to. Both
language skills and access to reports from afar differed. With the advent of medical
trials, several journals published review-articles aimed at giving a comprehensive and
updated picture of the status of the possible cures. But despite editorials and
numerous new and specialized medical journals aimed at improved communication,
which I will discuss in Chapter 6, not everything was published in more languages
than one, or in more places that one. Not everyone read every language, had access to
every report, read every issue of every medical journal, attended every meeting or
read every proceeding.
There were dominating trends, though. Until the first decade of the 20th

century, leprosy was widely believed to be incurable. What medicine could offer was
palliative at best. From the second international leprosy conference in Bergen, the
occasional cases of individuals’ spontaneously healing disease convincingly proved
the disease was curable, although the mechanisms involved were not known, nor how
they could be reproduced. Various remedies were proposed, and in general the
physicians (at least those who actively published) agreed that new drugs would
eventually offer a medical solution.
The introductions of new remedies were all surrounded by optimism and
reports of success. The news was spread at conferences and through medical journals,
increasingly containing explanations for why the suggested treatments ought to work.
 129

The new drugs were then tested in various locations, and the results of the trials were
also circulated mainly through journals and conferences. Although some reported that
the trials were successful, compiling the results showed that the few glimmers of hope
were overshadowed by numerous reports of the treatments having failed.
Over time the standards for success changed. Despite most experience pointing
to the opposite, the faith that medical research eventually would produce a solution in
terms of a drug which could cure leprosy only grew. Linking the disease to the
bacillus probably contributed: Instead of expecting the clinical signs of the disease
(mainly ulcers and anesthesia) to disappear, the lack of bacillus was slowly introduced
a new standard for success. The best case scenario changed from providing palliatives
which could slow the unstoppable progress of the disease, to the eradication of the
bacillus in the body being introduced as proof that a cure had indeed taken place.




Reinventing Chaulmoogra


In the medical discussions there were frequent references to the long list of
medications used to treat leprosy, which in the words of Gerhard Armauer Hansen
included “all possible and, we may say, impossible remedies”.317 Such lists included
potassium iodide, arsenic, antimony, copper, vaccines, aniline dyes, mercury, gold,
iodine, thymol, trychnine, sodium salicylate, carbolic acid, collargol, creosote,
phosphorus, ichthyol, and surgical procedures such as nerve-stretching, bleeding and
surgical removal of ulcers; baths and steam baths of various kinds, X-rays, radium,
electrical currents, snake-poison and other venoms, proteins, serum, various herbs,
plants and derivates; rest, exercise, change of climate, diet, prayer, ivory, and other
parts of exotic animals. All were reportedly employed in more places than one for
shorter or longer periods of time, but were seldom, if at all, the subjects of organized
research like the medical trials detailed earlier in this chapter. From the 1870s,






317
Hansen and Looft 1895: 105.
 130

chaulmoogra would be at the top of this list: Extensively used but never the subject of
coordinated medical trials.
When chaulmoogra was introduced to Western medicine in the middle of the


19th century, it had been in use in parts of Asia for half a millennium or more.318 In

1854 the British physician Fredric John Mouat, working in Calcutta, reported that he
had had ‘remarkable and indisputable’ success on one case and encouraged others to
test it.319 Based on oil from seeds in the fruits of trees locally available in India and
other parts of Asia, its use slowly proliferated, first in Asia and later in Europe. The
honor for introducing chaulmoogra to French and German-speaking audiences,
respectively, was usually attributed to Ernest Henri Besnier and Paul Gerson Unna
who made chaulmoogra part of the leprosy treatment at their hospitals in Paris and
Hamburg.
While some physicians saw improvements in their patients and recommended
it to others, chaulmoogra was until the first decade of the 20th century generally
considered belonging in the category of palliatives. In 1894, the Leprosy Commission
to India compared it favorably to gurjon oil, but did not go as far as considering it a
cure. The expectation of the drugs was relief, at least temporarily:


(…) it seems that the action of chaulmoogra oil in leprosy, though at the best palliative, is
nevertheless more marked than that of gurjun oil. Indeed it is probable that a prolonged and
regular use of this oil may in some cases arrest the progress of the disease, though for how
long must still be doubtful.320


Since chaulmoogra was mainly perceived to be an additive to other treatments, and since the
friction produced through rubbing it on the skin was considered more important than the
drug itself, the actual content was for decades deemed of little importance. ‘Chaulmoogra’
was a catch-all category of oils produced from a range of plants. In 1879, testing
chaulmoogra at Blackfriars hospital for diseases of the skin in London physician Wyndham




318
Parascandola, John. “Chaulmoogra Oil and the Treatment of Leprosy.” Pharmacy in History. Vol. 45, No. 2,
2003: 47-48. In China it was introduced in the thirteenth century under the name Ta Feng Tzu, see: Leung 2009:
56.
319
Parascandola 2003: 48-49.
 131

Cottle explained that “Chaulmoogra is the oil expressed from the seeds of the Gynocardia
odorata.”321 Others highlighted Taraktogenos kurzii and other evergreen trees from the
Hydnocarpus family found in central Asia. Most referred to it simply as what they got when
buying ‘chaulmoogra’ at the local market and gave no further details. In 1900 the French
botanist Georges Desprez tried to clear up some of the vagueness in the monograph Le
Chaulmoogra, Huile de Chaulmoogra, Acide Gynocardique (1900) by describing and
differentiating plant species and their oils. At the beginning of the 20th century Frederick B.
Power and his colleagues at the Wellcome Chemical Research Laboratory in London tested
the content of the various oils chemically, and concluded that proper chaulmoogra oil could
only be produced from three species of the Hydnocarpus family and not Gynocardia
odorata.322 It did however take several years before there was any common agreement on the
actual content of chaulmoogra. While chaulmoogra was mentioned as part of the treatment in
almost two out of five papers on treatment (37 out of 106) published in Lepra Bibliotheca
Internationalis, the compounds making up the content of chaulmoogra was never discussed.
Still, transforming chaulmoogra from a generic to a distinct substance was the first step in
redefining chaulmoogra into a specific medication for leprosy.
Chaulmoogra was not only administered as oil to be massaged, it was also
given orally as drops or in capsules mixed with Vaseline. This was not unproblematic.
Chaulmoogra was frequently referred to as having a distinct and unpleasant bitter
taste, and it had severe side effects. For some it produced nausea, for most severe
indigestion. In order to have an effect when taken orally, resistance had to be built up
over time to reach the necessary high doses. Then treatment had to be continued for
so long that most patients gave up. Failure to produce cures was in many instances
blamed on patients’ lack of determination to get well. Apparent cures were often
explained by unprecedented resolution in those who managed to follow through with
the chaulmoogra-treatment. What should be considered proper dosage, the use of









320
Report of the Leprosy Commission in India, 1890-91. Calcutta. 1893: 340.
321
Cottle, Wyndham. “Chaulmoogra oil in leprosy”. The British Medical Journal. June 28, 1879: 969.
322
Parascandola 2003: 50; Editorial. “Chaulmoogra Oil Therapy in Leprosy”. California State Journal of
Medicine. February 1922: 64-65.
 132

additives and different regimes to develop resistance in the patients was an ongoing
and lasting discussion.323
Finally, chaulmoogra was given by subcutaneous and intramuscular injections.
This method was pioneered by Tourtoulis-Bey in Cairo, who in 1899 reported on four
years of experiments. But also the injections were problematic. When demonstrating
the procedure at the Academy of medicine in Paris in 1901, François Henri Hallopeau
summarized some of the drawbacks:


Subcutaneous injections of Chaulmoogra Oil give rise to marked inflammatory reaction of
the cellular tissues. They lead to obstinate indurations. The injections are painful and in
nearly all cases, it is impossible to administer them in a continuous manner. Moreover, they
give rise to pulmonary fatty emboli. (…) On the whole, the treatment must be employed
only in exceptional cases, and not in a routine manner.324


In addition to causing inflammation and blocking the blood flow, the oil solidified at
room temperatures and needed to be heated before injections. This made the
injections even more painful to endure.
The numerous drawbacks led to several reports of chaulmoogra treatment
being given up. In Algerie, J. Brault concluded in 1908 that the disadvantages
outweighed any alleged benefit, and concluded that the best a physician could do was
to ensure hygienic surroundings and care.325 In the German colony of Kamerun
(Cameroon), Hans Ziemann gave up on chaulmoogra in 1909, the moment he




323
See i.e.: Brousse, A. and Vires. “Sur un cas de Lèpre tuberculeuse. Traitement par l’huile de Chaulmoogra.
Amélioration trés rapide.” Lepra Bibliotheca Internationalis. 1900: Fasc. 4; Crocker, Radcliffe. “On Leprosy as
seen in London”. Lepra Bibliotheca Internationalis. 1901: 49, originally published in The Polyclinic. October
1900: 243; Espanda, Joaquin Petron. “Quelques considérations sur la lèpre, son traitement curatif.” Lepra
Bibliotheca Internationalis. 1901: 185; Danlos. “Lèpre anestésique, relief considérable des taches, dyspepsie,
traitement par l’huile de chaulmoogra en lavements.” Lepra Bibliotheca Internationalis. 1904: Fasc 1; Alfonso,
Manuel F. “Les traitements de la lèpre”. Lepra Bibliotheca Internationalis. 1904: Fasc 1, originally published
in Revisita medica Cubana. July. 1903, La Caducée. September 26. 1903; Lie, H. P. “Die Therapie der Lepra”.
Lepra Bibliotheca Internationalis. 1905: Fasc 4, originally published in Deutsche Medizinsche Wochenschrift.
No. 38, 1903.
324
Hallopeau, François Henri. “Traitement de la lèpre par l’injection sous-cutanée d’huile de chaulmoogra”.
Lepra Bibliotheca Internationalis. 1901: 115. ‘Obstinate indurations’ meant untreatable hardening of the tissue;
pulmonary fatty emboli meant that lumps of chaulmoogra entered the bloodstream and could block the
circulation.
 133


acquired a batch of Nastin.326 With frequent reports on at least moderate results

through the use of chaulmoogra, ‘conversion’ could also go the other way. When
Ziemann changed from chaulmoogra to Nastin, his colleague Dr. Lenz in Bagamojo,
the capital of neighboring German East Africa (now Tanzania), gave up on Nastin and
switched to chaulmoogra.327 In Lazaretto Tracadie in New Brunswick, Canada,
physician A. C. Smith justified testing chaulmoogra on his patients with “favourable
reports on the use of chaulmoogra oil and creolin in foreign leper hospitals.”328 In his
summary of treatments presented at the international medical congress in Lisbon in
1906, Paul Gerson Unna listed 35 researchers who had tested chaulmoogra, situated
in North, Central and South America, Russia, Japan, England, Germany, Austria,
Egypt and Greece.329
As the uses of chaulmoogra proliferated, so did the attempts at overcoming its
drawbacks. The easiest and initially most widespread methods was mixing it with
olive oil or, as Lenz did, have the patients wash it down with palm wine or other
alcohols. A less common, but eventually more influential, solution was creating
derivatives in collaboration with chemists. The medical superintendent at Robben
Island, Robert Sinclair Black, was among the first to collaborate with Burroughs,
Wellcome & Co in London. From 1903 he started testing capsules and injections of
various mixtures of fatty acids produced by Power and colleagues in London.330 Two
years later, Isadore Dyer started collaborating with Parke, Davis & Company, then the
world’s largest pharmaceutical company situated in Detroit, Michigan. Parke-Davis
produced acids based on crude chaulmoogra, and Dyer tested them on patients at the




325
Brault, J. “Les lépreux en Algerie”. Lepra Bibliotheca Internationalis. 1908: 107, originally published in
Archiv für Schiffs- und Tropenhygiene. 1908: No. 7.
326
Ziemann, H. “Berichte über den gegenwärtigen Stand der Lepra in Kamerun, Westafrika, mit Beitrag zur
Nastintherapie.” Lepra Bibliotheca Internationalis. 1909: Fasc. 1.
327
Lenz. “Bericht über die Behandlung Aussätziger mit Nastin und Chaulmoograöl.” Lepra Bibliotheca
Internationalis. 1909: Fasc. 1.
328
Smith, A. C. “Report of the Lazaretto Tracadie, New Brunswick”. Lepra Bibliotheca Internationalis. 1900:
324.
329
Unna, P. G. “Sur la pathologie et la thérapeutique de la lèpre”. Lepra Bibliotheca Internationalis. 1906:
Fasc. 3.
330
Black, R. Sinclair. “Leprosy and its treatment by Claulmoogra Oil.” Lepra Bibliotheca Internationalis. 1904:
140, originally published in South African Medical Record. June 15. 1903 and Journal of Tropical Medicine.
September 15. 1903.
 134

Louisiana Leper Home in Carville, Louisiana.331 The first commercially available
derivate was developed by the German physician Friedrich Engel Bey working in
Cairo, Egypt, in collaboration with the pharmaceutical Bayer & Co in Elberfeld,
Germany. “Antileprol” was put on the market in 1908.332
The formula that would do the most to inspire new research into chaulmoogra
treatments was developed in the Philippines by Victor Heiser and Eliodoro Mercado
between 1909 and 1914. Chaulmoogra had been in use in Manila since the 1890s, but
after the US occupation in 1899 it was abandoned due to severe side effects and
limited success. The use was resumed after Heiser visited Louisiana Leper home in
1908 and was impressed by Isadore Dyer’s experimental results. Back in Manila, oral
administration led to nausea, indigestion and consequent patient resistance. Heiser
and Mercado therefore started experimenting with injections. In an attempt at finding
a formula which would lead to increased absorption of the injections, Heiser
contacted the pharmasutical and chemical company Merck & Co in New York.
Among their suggestions was the use of camphor or ether. The final recipe, which
was initially named the ‘Heiser-Mercado-formula’ and later just ‘Mercado-formula’,
consisted of equal proportions of chaulmoogra and camphor with 4 percent resorcin
as a disinfectant.333 The drug was to be injected weekly, and in 1913 and 1914 Heiser

reported that treatment “produces apparent cures in some cases, causes great
improvement in many others, and arrests the progress of the disease in almost every
instance.”334
The advantages of the Heiser-Mercado-formula were that it was easy to

produce using standard laboratory equipment and had fewer side effects than pure








331
Dyer, Isadore. “The cure of leprosy”. Lepra Bibliotheca Internationalis. 1906: 51-55, originally published in
The Medical News. July 29. 1905.
332
Engel-Bey, Franz. “Zur Behandlung der Lepra mit Antileprol.” Monatshefte für praktische Dermatologie.
1909: 290-293. An extended version of the paper was distributed at the conference in Bergen in 1909 and
translated to English in 1911 under the title The treatment of Leprosy Especially by Antileprol.
333
Parascandola 2003: 51-52.
334
Heiser, Victor. “Leprosy. Its treatment in the Philippine Islands By the Hypodermic use of a Chaulmoogra
Oil Mixture.” Public Health Report. Vol. 29, suppl. 20, 1914: 25; as quoted in Parascandola 2003: 52.
 135


chaulmoogra.335 Among those who tested the recipe was the Brazilian physician and
leprologist Heráclides César de Souza-Araújo, who after treating 900 patients
reported that 11.1 % of the cases had achieved radical cures. In further 44.4 % of the
patients, the signs of the disease had retracted (‘clinical cure’), while 33.3 % had
experienced considerable improvements.336 On his three year trip around the world in
the mid-1920s, which I will return to in Chapter 7, de Souza-Araújo documented the
use of chaulmoogra also in the United States, Japan, Korea, China, Philippines,
Federated Malay States, India, Burma, Iraq and Palestine.
But more than being useful in itself the research at Manila inspired others.
From 1915, chemistry teacher Alice Ball at Hawaii College’s chemistry department in
Honolulu pioneered a method of producing a fluid of the fatty acids found in
chaulmoogra oil that was thinner, easier to absorb and thus more suitable for
intramuscular injections. After Ball’s death at the end of 1916, the head of the
department, Arthur Dean, continued the work. In the 1920s ‘Dean’s derivatives’ was
widely used around the world.337 When the leprosy workers at Culion on the

Philippines in 1921 extended the treatment from voluntary experiments on selected
cases to a routine procedure, they used the esters and not the Mercado-Heiser formula,
which by then had proved both painful and prone to produce tissue damage.338
Honolulu was not the only site for developing new drugs based on
chaulmoogra. Just before Heiser in 1915 retired from his position as Director of
Health in the Philippines to begin working for the Rockefeller Foundation, he visited
Leonard Rogers in Calcutta and convinced him to continue this line of research.339 In




335
For instructions on the production of the most commonly used derivates, see i.e. de Souza-Araújo 1929: 192-
198; Muir 1924: 12-14; Rogers and Muir 1940: 246-247.
336
De Souza-Araújo 1929: 31.
337
Parascandola 2003: 53.
338
In 1921, the treatment was expanded first to 500 cases, and then doubled by the end of the year. By the end
of 1922, 4,458 lepers received treatment with chaulmoogra products at Culion. (Lara, C. B. Progress of Leprosy
Treatment at the Culion Leper Colony. 1929: 5; Rodrigues, Jose N. “Brief Review of the Medical Work at
Culion Leper Colony”. Journal of the Philippine Islands Medical Asociation, February, 1926; Wade, W. and J.
N. Rodriguez. A Description of Leprosy. Its etiology, pathology, diagnosis and treatment. 1928: 61)
339
Power, Helen Joy. Sir Leonard Rogers Frs. (1868-1962): Tropical Medicine in the Indian Medical Service.
PhD Thesis, University College London. 1993: 195; Rogers, Leonard. “Recent Advances in the Treatment and
Prophylaxis of Leprosy”. Edinburgh Medical Journal. 1930: 11. The paper was a reprint of the Cameron Prize
Lectured delivered at the University of Edinburgh on October 18, 1929.
 136

the years that followed Rogers collaborated with chemists at Calcutta Medical
College and, after moving to London in 1920, with Burroughs, Wellcome & Co.
Wellcome quickly launched a derivate similar to Bayer’s Antileprol, branded
‘Moogrol’. This was followed by ‘Alepol’, a compound of sodium salts of selected
fractions of hydnocarpus oil.340 In 1926 they devised a formulation of mercury in
hydnocarpus oil marketed as ‘Avenyl’, soon followed by compound ‘Avenyl-
Moogrol’.341
The main differences between esters and hydnocarpus oil were price and
consistency. The esters were less viscid and thus easier to inject and more rapidly
absorbed in the tissue; the hydnocarpus oils were thicker, cheaper to produce and
more stable for long-term storage. Having a slower absorption rate was occasionally
highlighted as a selling point for the hydnocarpus oils, but whether this actually was
beneficial to the patients was contested. Most institutions that could afford it used
multiple chaulmoogra varieties. Throughout the 1920s, the different formulas were
discussed under the same heading: Chaulmoogra. When Muir’s continued
experiments at refining chaulmoogra at the end of the 1920s led to the compound
‘ECCO’, consisting of ethyl ester chaulmoogra, olive oil free from fatty acids and
creosote, the division between the hydnocarpus oil and the esters was in effect
bridged.342
One reason why the use of chaulmoogra spread in the 1920s was organized
distribution. Rogers, himself a devote Christian, collaborated especially close with
medical missionaries. In February 1920 he represented the Indian government in a
conference of missionary superintendents of leper asylums arranged by the Mission to
Lepers.343 When Rogers left India for England a month later, he appointed Ernest
Muir, former medical missionary to Bengal, to be his successor as head of the





340
All the chaulmoogra derivatives stemmed from the fatty acids, and were differentiated by their melting
points. Those with a low melting point were termed gynocardic acid, those with highest melting point
chaulmoogric acid – with hydnocarpic acid in between. (Power 1993: 197)
341
Greenwood, David. Antimicrobial Drugs: Chronicle of a twentieth century medical triumph. 2008: 192-193.
342
Power 1993: 221.
343
Oldrieve, Frank. Report of a Conference of Leper Asylum Superintendents and others on the Leper Problem
in India. 1920.
 137

Leprosy Section at the Calcutta School of Tropical Medicine. In 1924, Rogers formed
the British Empire Leprosy Relief Organization (BELRA) in collaboration with Frank
Oldrieve, who went from the position as Mission to Lepers’ secretary in India to
being secretary for the new organization.
BELRA’s main objective was to “stamp out leprosy”; their method was to
spread the gospel of chaulmoogra treatment, both through education and through the
distribution of drugs. From 1924 BELRA sponsored four courses on leprosy in
Calcutta every year, and by the end of 1928 the courses had been attended by 404
doctors who in turn had trained at least 600 more.344 In 1928 alone, the organization
distributed 500,000 doses of Alepol to various clinics and colonies throughout the
British Empire.345 By 1930, their medical journal Leprosy Review had reached a
circulation of 2000,346 and Mission to Lepers had adapted the slogan “Faith, Oil and
Work”.347
Even for BELRA, chaulmoogra medication was never more than part of the
treatment. As Ernest Muir put it in 1924; “No drug has yet been discovered which can
be relied upon of itself alone to cure leprosy.”348 In addition to the injections, efforts
should be made at improving the sanitary surroundings where leprosy occurred. Also,
the patients’ natural resistance needed to be restored through a strict diet of fresh
food, especially vegetables, fruits and dairy products. Alcohol, milled rice and grains
should be absolutely avoided, and tea, coffee and tobacco should be taken only in
moderation. Furthermore, the patients should exercise, preferably through walking or
working in the fields, and bathe every day. Other diseases should be tended to.
Finally, “The mind should always be kept fully occupied and all brooding on his own






344
Burnet, Et. League of Nations Health Organisation. Report on the Study Tour of the Secretary of the Leprosy
Commission in Europe, South America and the Far East. January 1929-June 1930. LNHO: C. H. 887. Geneva,
1930: 11.
345
Rogers, Sir Leonard. “Recent Advances in the Treatment and Prophylaxis of Leprosy”. Edinburgh Medical
Journal. 1930: 24.
346
Leprosy Review was first published as the quarterly Leprosy Notes in 1928, and was renamed in 1930.
(Rogers 1930: 10.)
347
A report of the fifty-seventh year’s work in India of The Mission to Lepers. September 1930-August 1931: 4.
348
Muir, Ernest. Leprosy. Diagnosis, Treatment and Prevention. 1924: 22. See also: Muir, Ernest. Popular
lecture on leprosy, illustrated with lantern slides. Lahore. 1925.
 138

condition should be carefully avoided by the patient.”349 The result of the treatment
program ranged from 10 to 40 percent cures, and up to 60 percent in new cases.350
Not everyone agreed that chaulmoogra worked. In Hawaii chaulmoogra was
used systematically from 1914, changing to Dean’s ethyl esters in 1918. By 1925, 414
patients were paroled as cured, but in 104 of them the disease returned. “Spontaneous
improvement or quiescence and even the arrest of the disease, are observed in 8 to 10
per cent of clinically diagnosed cases – i.e., precisely the proportion of released
patients who remain negative for some years after their discharge.”351 According to
James Thomas Wayson of the Board of Health at Hawaii, chaulmoogra could be used
to hold leprosy in check, but the disease could never be cured. Therefore, all
registered lepers should remain under medical supervision indefinitely. In Japan,
chaulmoogra was given to three-fourths of the patients, but even their foremost
expert, Kensuke Mitsuda, argued that “all lepers who are rendered negative are bound
to be positive again.”352 Secretary of the League of Nations Leprosy Commission,
Etienne Burnet, fittingly termed this position “Once a leper, always a leper.”353
In 1930 Burnet, published a report from his travels in Europe, South America
and Asia. The use of chaulmoogra was his main focus.

Is it really efficacious? (…) The technical reviews give no idea of the spirit with which the
question is being discussed by enthusiasts and sceptics alike. Some go so far as to say that
all this excitement about cure is mere humbug, while others declare that to be lukewarm
about treatment is as great a crime as to refuse quinine to a malaria patient or arsenobenzol
to a person suffering from syphilis.354









349
Muir 1924: 24.
350
Rogers 1930: 18-20.
351
Burnet, E. “League of Nations Health Organisation. Report on the Study Tour of the Secretary of the
Leprosy Commission in Europe, South America and the Far East. January 1929 - June 1930.” (C. H. 887).
Geneva, 1930: 24.
352
“Rendered negative” meant that no bacilli were detected in any tissue samples. (Burnet 1930: 13-14, italics
in the original.)
353
Burnet 1930: 24; Wayson, N. E. Public Health Reports. Vol, 44, No. 51, December 20. 1929.
354
Burnet 1930: 39.
 139

The actual value of the drug was impossible to ascertain, as even those most skeptical
offered chaulmoogra as part of their treatment due to pressure from the patients.355
Especially the American Surgeon General Hugh Cumming repeatedly called for the
League of Nations to coordinate comparative studies so that what he considered
myths surrounding the alleged efficacy of chaulmoogra could be debunked.356 Even
Burnet, who held chaulmoogra in high regards, had to admit that “No conclusive
evidence exists of the efficacy of chaulmoogra as such. The crucial test of a
comparison of two like groups of patients – one being treated by chaulmoogra and the
other not – has, it seems, never been carried out.”357
The peak of chaulmoogra was in the 1920s and early 1930s. By the end of the

1930s, however, even the medical advisors to the League of Nations, such as Earl
Baldwin McKinley from Leonard Wood Memorial, reported that “those who advocate
chemotherapy [using chaulmoogra] in leprosy have the burden of proof upon
them”.358 If chaulmoogra did not work in for tuberculosis, which was also caused by
an acid-fast bacillus, there was no reason why it should work on leprosy, he argued. In
McKinley’s view, the institutional care alone was enough to explain the apparent
cures: Chaulmoogra had no effect.
The core of the debate was not only the dubious efficacy of chaulmoogra, but
also disagreements regarding how treatment should be organized. The foremost
proponents of chaulmoogra, namely BELRA and the Calcutta-school, argued that
having a treatment available meant that the whole treatment regime should be
revolutionized. Chaulmoogra was a carrot that would attract people looking for a
cure. Therefore, compulsory segregation should be abandoned in favor of voluntary
treatment. Compulsion only led to the hiding of cases, Rogers and Muir argued,




355
Burnet 1930: 43.
356
In a letter to the Director of the Health Section of the League of Nations, Ludwik Rajchman, dated September
25, 1931, for instance, Cumming argued that “chaulmoogra oil is being stressed too greatly as a therapeutic
specific and that too little attention is being given by leprologists to other factors of perhaps equal or greater
importance.” He therefore suggested “that a selected group of patients in an existing institution or in an area
where leprosy is prevalent might be subjected to a modified sanitarium regime without chaulmoogra oil,
and be productive of suggestive, and perhaps startling, results.” (LNHO: 8A/R5892/32219-6651).
357
Burnet 1930: 40.
 140

ensuring that the disease was spread before the lepers were segregated.359 While
chaulmoogra did not cure all cases, it provided hope and could be used in prevention.
The treatment was most efficient in the early stages of the disease, but this was also
when they considered the disease to be most contagious.
The strategy BELRA promoted consisted of propaganda, treatment and survey
(the ‘PTS-model’), and was aimed at winning the confidence and cooperation of
villages through offering voluntary out-patient treatment. First, a survey was carried
out and the results used as “special propaganda” in explaining the prevalence of the
disease, how it had spread and what signs to look for. Then, the public was informed
what measures should be taken to avoid contagion, and that leprosy could be cured.
Treatment was administered in out-patient clinics where the lepers were free to come
and go as they pleased. While the treatment admittedly was of limited curative value,
out-patient treatment would encourage the lepers to volunteer for proper institutional
care. Releasing and returning those who were cured would in turn encourage other
sufferers to seek institutional treatment at an early stage.360 The primary goal of

treatment was thus not necessarily to cure all lepers, but to fight new infections.
Spreading the PTS-model was an integral part BELRA’s training program and
publications.
While BELRA in the 1920s became the foremost proponents of the voluntary
model, they did not invent this. In 1919, Dr. Léon Stevenel in French Guiana was the
first to argue that chaulmoogra treatment was the key to solving ‘the leprosy
problem’:

“For many reasons there can no longer be any question of isolating every leper of the
colony. The public authorities are mistaken if they think the spread of leprosy can be




358
McKinley, E. B. “Note on LEPROSY”. Report to the League of Nations. Geneva, November 10, 1937.
(LNHO: 8A-R6071/31395/1681).
359
“Before we had any effective treatment even of early cases, compulsory segregation was the most generally
recognized method for reducing leprosy, but it has the serious drawback that it inevitably leads to all early cases
being hidden until past the most curable stage, and usually until they have infected others.” Rogers 1930: 22.
See also: Rogers and Muir 1940: 121.
 141

prevented by sequestrating a small number of sufferers while thousands of lepers are left
free to carry on trades of all kinds in various parts of the colonies. (…) I am in favor of the
establishment in the more populous centers of anti-leprosy or preferably mixed preventoria
to prevent ‘free’ lepers. (…) would come with their families for treatment, medicaments and
advice on how to prevent the disease from spreading.”361

An important advantage of the out-patient treatment model was that it was cheap.
While the official census for 1921 showed 102,513 lepers in India, Muir believed the
actual numbers to be at least seven times as high.362 Rogers estimated in 1930 that
there were at least three million lepers globally.363 The scale of the problem made
wholesale segregation unattainable, it was simply too costly. Economically, out-
patient treatment was far more efficient: “The cost of the drug for a year’s treatment
per patient is one-sixtieth of that of isolating a single leper in India, while the sum of

£200 expended in New South Wales for each segregated leper will supply the drugs
for treating 1600 lepers for a year.”364
The faith in chaulmoogra was closely correlated with the faith in the out-
patient treatment model. Japan and the United States both justified compulsory
segregation by pointing out that treatment did not provide reliable cures. In Bergen,
chaulmoogra was hardly used at all, because the system of home-segregation alone
made it possible to stamp out the disease.365 The Philippines adapted a middle way by
retaining Culion as an ‘in-patient’ leprosy colony for segregation, and adding
outpatient clinics. According to Herbert Windsor Wade, in charge of research at the
Culion leper colony and first Medical Director of the Leonard Wood Memorial,
treatment was an addition – not a replacement for segregation. “To eliminate all
segregation would be as dangerous as to employ this system alone. (…) Thanks to





360
Rogers and Muir 1940: 135. See also: Rogers, Leonard. “Memorandum on the prevalence and prophylaxis
against leprosy in the British Empire, based on replies to the questionnaire of the British Empire Leprosy Relief
Association; with suggestions for dealing with the problem”. 1925: 19-22. (LNHO: 12B-R898/4264/29272.)
361
Quoted in Burnet 1930: 9-10.
362
Burnet 1930: 15-16.
363
Rogers 1930: 1.
364
Rogers 1930: 22.
365
Burnet 1930: 8, 12-14, 24.
 142

treatment, the utility of segregation is increased.”366 The first outpatient clinics
opened at Pilapilan and Baldad in 1922.367
Also Rogers stressed that in countries where much money had been spent on
segregation, out-patient treatments should be an addition, not a replacement for
already existing institutions.368 This did little to convince the segregationists. After
all, why offer out-patient treatment when the treatments did not work? In the next
chapter I will adress the question of prevention.





Conclusion


“The number of drugs which have been used in the treatment of leprosy almost
embraces the whole pharmacopædia.”369 While this exact expression was coined in
1903 by the medical superintendent at Robben Island, Robert Sinclair Black, similar
statements were repeated in almost all surveys of treatments published in the period I
have studied. It reflected both a hope that leprosy could be cured given the correct
drug and a disappointment that no cure had yet been found.
Whether it actually was possible to cure a ‘leper’ remained contested. Until
around the turn of the 20th century, a majority of the leprologists believed the disease
was incurable. At best, the progress of the disease could be slowed down, and some of
the pain alleviated. This changed at the second international leprosy conference in
Bergen in 1909. Based on the observation that some people did in fact get well, a
majority of the attendees agreed that the disease in theory could be treated but that no




366
Wade, quoted in Burnet 1930: 21.
367
Rodrigues, Jose N. “Brief Review of the Medical Work at Culion Leper Colony”. Journal of the Philippine
Islands Medical Association. February. 1926: 5. (reprint)
368
As Rogers put it in The Practitioner in April 1928: “In countries where much money has been expended in
segregating lepers compulsory, I do not advise that this plan should be abandoned for the present, but that it
should be modified (…) to prevent it doing great harm by preventing the patients coming forward for treatment
in the earliest stages.” (Quoted in Burnet 1930: 16.)
369
Black, R. Sinclair. “Leprosy and its treatment by Claulmoogra Oil.” Lepra Bibliotheca Internationalis. 1904:
140, originally published in South African Medical Record. June 15. 1903 and Journal of Tropical Medicine.
September 15. 1903. The same sentiment was expressed both earlier and later in time. See i.e. Parascandola
2003: 47; Rogers and Muir 1925: 245-254; Rogers and Muir 1940: 226-245; Hansen and Looft 1895: 105-125;
Danielssen and Boeck 1847: 115-133.
 143

specific cure yet existed. In the 1920s and 1930s, however, several influential experts
still argued that ‘once a leper, always a leper’.
From the 1880s, numerous new medical journals, and the increasingly
widespread practice of publishing abstracts of reports printed elsewhere, provided a
fundament for increased coordination in the testing of new treatments. The tuberculin-
experiments exemplify how medical trials no longer were a matter of individual or
local experience. Instead, treatments were tested in numerous locations and the results
compiled and compared before any definite conclusions could be drawn. In general,
the numerous drugs developed and tested to cure leprosy all suffered the same fate:
Initial optimism, distribution of the active ingredient (or the methods for producing
it), extensive testing, publishing results, compilation and comparison of various
studies – and finally a declaration of defeat as the drugs failed to live up to the hype.
If a drug was perceived to be successful in one place, however, reports from other
places were not alone enough for a treatment regime to be discontinued. Just as with
diagnosis, treatment regimes were never identical around the world.
Increasingly, it was not enough to present the method for producing a
compound, or anecdotal claims that the drug had worked in specific cases. Reports
that could be quantified were progressively given more weight than reports on
treatments of individual cases. This was both an effect of journals and conferences
leading to an increased globalization of the medical community, and a reflection of
the increasingly shared assumption that the disease was governed by the same general
laws regardless of location. These laws were not deterministic on an individual level,
but could be observed as statistical proportions in larger groups. While collaboration
with chemists and professional manufacturers from around 1900 led to increasing
standardization of the compounds used, quantification led to a standardization of the
collective leper body. The rationalization for medical statistics was that they enabled
the physicians to see beyond individual particularities and thus get unbiased access to
the underlying regularities governing the disease and the efficacy of any given
medical treatment.
 144

From around the turn of the 20th century, new proposed treatments also
required a rationalization justifying the claims to an effect based on previous
scientific medical knowledge. Possibly, the belief in incremental steps instead of
radical breakthroughs was due to the numerous sensationalist announcements of
radical cures that all turned out to be impossible to reproduce. A consequence of the
increased desire for quantification and theoretical medico-scientific contextualization,
however, was that the general practitioners who encountered only a handful of cases
were excluded in favor of experts working in specialized leprosy institutions.
As the chapter on diagnosis showed, more and more leprosy meant the leprosy
bacillus acting in the body, not the presence of clinical signs. Also when it came to
treatments, the bacillus was increasingly singled out as a target. The first medical trial
that used the leprosy bacillus as part of the rationale was the tuberculin trials in the
early 1890s. The failure to cultivate the bacillus in artificial media was a problem.
Despite numerous claims that the bacillus had been cultivated, these were all
surrounded by controversy and proved hard to reproduce or interpret.
With no animal models, the treatments had to be tested on those affected by the
disease directly. Danielssen’s patients taking part in the tuberculin trial in Bergen is
but one of numerous examples of leprosy sufferers asking or being asked to take part
in the medical trials. There are also several reports of leprosy sufferers who after
failing to experience any benefit from the drugs refused to take part in further
experiments.
Some of the treatments were explicitly intrusive. For Leprolin, for instance,
provoking fever, nausea and pain was seen as proof that the drug was efficient. For
Nastin, in comparison, a fever was seen as a sign of deterioration in health and the
treatment therefore should be suspended. However, this did not change the fact that
also Nastin in the great majority of cases failed to produce lasting benefits.
Chaulmoogra was an exception to the rule of breakthroughs and subsequent
failures. For the critics, the lack of a specific effect on other acid fast bacilli and the
fact that chaulmoogra had never been subject of coordinated medical trials proved the
 145

drug to be nothing but a placebo. For the proponents, its efficacy was based on
experience.
By the time chaulmoogra was made known in Europe from the 1850s, it had
been in use in Asia for centuries. The redefinition of chaulmoogra from a palliative to
a specific (but highly contested) drug against leprosy underwent several phases.
Around the turn of the 20th century, the chemical content of ‘chaulmoogra’ was
defined. Some ten years later, experiments with derivatives began, consisting of
chemically removing impurities from the herbal remedy and mixing it with other
substances in order to dampen its severe side effects. Methods for producing
treatments according to well-defined formulas were distributed widely, and
chaulmoogra products were rebranded and put up for sale by medical companies.
The primary advocate of chaulmoogra was The British Empire Leprosy Relief
Association (BELRA). The drug admittedly did not cure everyone, but it was good
enough to provide a carrot to get leprosy sufferers to seek early treatment and thus
avoid spreading the contagion. The stick offered by compulsory segregation, BELRA
argued, only led to people hiding their disease. While some physicians firmly believed
chaulmoogra would produce consistent cures, given that the treatment started early
enough and the patients had the necessary determination to go through with the
prolonged and often painful treatment, others saw it as a mostly harmless drug that
could be used in order to have at least something to offer the patients. Yet others
pointed out that the chaulmoogra derivates were essentially the same drug that for
decades had been perceived to be a mere palliative, and called out for comparative
large-scale trials.
Finally, the coordinated medical trials expose the discrepancy that existed
between the publications and the actual local practices. Instead of describing daily
routines and day-to-day care, the published medical trials focused on what was new
and out of the ordinary. Reports by visitors who could compare local practices in
different locations provide glimpses into how the daily routines differed, but studying
the circulation of knowledge certainly does not replace the need for local studies. The
published reports only tell part of the story.
 146

It was not the ability to provide a cure for the individuals suffering from
leprosy that gave the medical experts their authority. But although the individual
sufferer could not be cured, leprosy could be stopped by protecting the healthy
majority through segregation. The following chapter will investigate the medical
discussions on prevention of leprosy (prophylaxis). There, too, quantification and
arguments based not on individual experiences but on producing numbers that could
be used to manage populations would play a pivotal role.
 147



4. The question of prevention


On September 20, 1852, after visiting the recently opened Lungegaardshospitalet in
Bergen, the American Episcopalian Reverend James C. Richmond wrote an alarmed
letter to his friend Bishop Jonathan Mayhew Wainwright in New York. “It will
probably surprise you to learn that the Oriental leprosy, as described by Moses and
healed by our Saviour, exists at this moment in Norway. It is not an hour since I have
seen over a hundred cases of this frightful and loathsome disease, which is here
exactly the same that you found at Nablous and elsewhere in Palestine.” While
impressed by Danielssen’s recently opened leprosy research hospital, the main
purpose of the letter was to sound the alarm: Among the increasing number of
Norwegian emigrants arriving in the United States there were lepers, and unless
something was done the dreaded disease was bound to become permanent also in the
United States. The solution, Richmond argued, was to stop the lepers at the border
and send them back.


Many vessels with emigrants now sail annually from Norway to the United States. They land
chiefly in New York. Let the City or the State enact a law, and make it known in Norway,
appointing a physician to enquire if the disease exists among the emigrants who arrive, and
if such be found, let them have their choice between being transferred to a hospital or
returned to their own country. The remedy may act harshly in some individual cases, but it is
by no means more tyrannical than the Quarantine laws that already exist. It will tend to
secure future generations against one of the most fearful calamities that can become
permanent among a people.370

As I showed in the previous chapter, medicine could not offer a cure to those affected
by the disease. With the exception of those who from the 1920s had faith in
chaulmoogra, this was as true in 1850 as in 1930. Increasingly throughout this period,
leprosy was perceived as a problem not only to the sick but also to the healthy. In a





370
Richmond, James C. “Norwegian Leprosy”. The New York Times. December 27, 1852 (Appendix 4).
 148

context where the health of the population was increasingly seen as a state matter in
the West, this brought the question of prevention to the forefront. Instead of curing
those already affected, prevention was about stopping new individuals from catching
the disease. Prevention was an integral part of the medical debate, and more and more
a matter for medical experts alone. Stopping those affected by leprosy at the border
was but one of several strategies.
In this chapter I will first present the debate on quarantine. Next, I will
investigate the debates on etiology and prevention leading up to the recommendations
from 1897 which stressed the need for segregation. Then I will inspect the actual
preventive measures taken, with a focus on on the period between the late 1890s and
early 1920s, and present the three main strategies for prevention pursued around the
world. Finally, I will expand upon the Calcutta-school’s new rationale for prevention.
As numerous studies into the history of leprosy have shown, the immediate
context for prevention of leprosy being raised to the national agenda differed from
country to country. My intention in this chapter is not to pursue all local specificities,
but to focus primarily on the rationales presented in the most widely distributed
reports, medical textbooks, Lepra Bibliotheca Internationalis and the international
medical conferences. These sources reflect perceptions of the situation on the ground
and the preventive measures taken, and were used by others looking for advice. What
arguments were available to those looking for advice on leprosy prevention in the
transnational medical debates? Which strategies were suggested and how did the
dominant positions change over time? What was the role of the bacillus when it came
to prevention?
 149

Quarantine: Stopping leprosy at the border


Reverend James C. Richmond’s letter in the fall of 1852 was reprinted in numerous
newspapers and periodicals, and provoked several responses.371 Some argued that to
be on the safe side all Norwegians should be barred from entering the United States,
others pointed out that since the disease was hereditary it posed no danger to anyone
but the unfortunate sufferers and their families. The Norwegian businessman Peder
Anderson in Boston, who had left Bergen in 1830 and was among the first promoters
of Norwegian emigration, argued that given the improved diet and milder climate in
the United States, the disease would probably completely die out. Therefore, there
was no need to take any action.372
When Richmond wrote his letter, quarantine was already discussed in relation
to other diseases, primarily cholera, plague and yellow fever. Accelerating
transportation, with steam engines in trains and ships, exploding international trade
and the increasing scale of colonialism was perceived not just as progress, but as
opening up to diseases originating outside the Western hemisphere. In 1851 the first in
a series of International Sanitary Conferences was held in Paris, the impetus being the
cholera epidemics that haunted Europe from the 1830s. Arguably, these conferences
were the first effort to regulate health on an international scale.373

For leprosy, quarantine measures can be traced back to the Bible and Leviticus’








371
The letter was first published in the monthly Evangelical Catholic (1851-1853) in New York, edited by
William Augustus Muhlenberg, an early leader in the Angelical Christian community in the United States. In
addition to The New York Times, re-prints made the front pages of The Daily Times (December 22, 1852), New
York Evening Express (December 24, 1852), New York daily Tribune (December 24, 1852) and The Daily
Gazette (Thursday January 6, 1853, adding a report on leprosy in Jerusalem). In addition, the report on
Norwegian leprosy was reprinted in The Religious Observer and Northern Christian Advocate, indicating the
wide interest produced by the report.
372
Haugen, Eva L. “The Story of Peder Anderson. Anderson’s autobiography translated and edited.” Studies
and Records. The Norwegian-American Historical Association. Vol. 26, 1974: 43. (Available online: http:
//www.naha.stolaf.edu/pubs/nas/volume26/vol26_2.htm). Between 1836 and 1930, 852,142 Norwegians
emigrated to the United States - no country except Ireland had a higher rate of emigration. Haugen, Einar.
“Norwegian Migration to America”. Studies and Records. The Norwegian-American Historical Association.
Vol. 18, 1966: 1-23. (Available online: http: //www.naha.stolaf.edu/pubs/nas/volume18/vol18_1.htm).
373
Huber, Valeska. “The Unification of the globe by disease? The International Sanitary Conferences on
Cholera, 1851-1894”. The Historical Journal. Vol. 49, No. 2. 2006: 454-476.
 150

instructions for declaring lepers ‘unclean’ and belonging outside the camp.374 Experts
such as Danielssen and Boeck, who firmly believed that the disease they saw
concurrently was the same as the Biblical disease, warned that this exact line of
reasoning had led to inhumane prosecution in Medieval Europe.375 As medical
historian Erwin H. Ackerknecht has pointed out: The mechanisms of how a disease
originated determined the principles for how it could be stopped. Whether etiology or
policies were the prime mover was seldom easy to untangle. Rather, cause and
prevention were always connected, making etiology an inherently ideological
question.376 No disease model fully explained why some persons developed leprosy
and others not, and different schools of thought disagreed both on what observations
should be given weight, how these should be interpreted and what preventive
measures they prompted.
Despite widespread attention, Richmond’s report had no practical
consequences. When the first big surge of Norwegian emigration hit the United States
between 1866 and 1873, the worry that Norwegians could bring leprosy seems to have
faded from public attention.377 This is fairly representative also for the debate among




374
“And the leper in whom the plague is, his clothes shall be rent, and his head bare, and he shall put a covering
upon his upper lip, and shall cry, Unclean, unclean. All the days wherein the plague shall be in him he shall be
defiled; he is unclean: he shall dwell alone; without the camp shall his habitation be.” (Leviticus 13: 45-46,
King James Version)
375
Danielssen and Boeck. 1847: 90-92.
376
Ackerknecht, Erwin H. “Anticontagionism between 1821 and 1867. The Fielding H. Garrison Lecture”.
Bulletin of the History of Medicine. 1948: 562-593, reprinted in International Journal of Epidemiology. 2009:
7-21. As Chrostopher Hamlin summarized in a commentary: “This is not a world in which the enterprise of
etiological hypothesis-testing is suddenly and surprisingly found to be rife with political implications and
complications, which, in the absence of adequate data and analytical methodologies come to dominate. On the
contrary, the medical was inherent to the political.” Hamlin, Christopher. “Commentary: Ackerkecht and
‘Anticontagionism’: a tale of two dichotomies.” International Journal of Epidemiology. 2009: 22-27, quote on
page 23. See also: Baldwin, Peter. Contagion and the State in Europe, 1830-1930. 1999.
377
About 110,000 Norwegians emigrated during the eight-year period. In Iowa it was not until the Swedish
physician Fredrik Eklund contacted the State Board of Health in 1883 asking for information on their number of
lepers that they were made aware that the disease existed in the State at all. (Kennedy, J. F. “Extract of the State
Board of Health of Iowa on Leprosy”. Leprosy in Foreign Countries. Honolulu, 1886: 198ff). Further, Eklund
informed the Board of Health of the two previous expeditions made by Norwegian physicians investigating
leprosy among Norwegian emigrants: Jens Andreas Holmboe in 1863 and Carl Wilhelm Boeck in 1869-70. In
1889 Gerhard Armauer Hansen would argue that 160 Scandinavians with leprosy had immigrated to the United
States, that only 13 had survived until the time of his survey, and that these had not infected any new cases. This
confirmed, Hansen argued, that the disease was contagious (and not hereditary) but that hygiene and improved
living conditions had stopped its spread. In a letter to state public health officials he therefore recommended
that proposed rigid segregation would be unnecessary. Moran 2007: 20; Hansen, G. Armauer. “Spedalskhedens
arvelighed”. Nordiskt Medicinskt Arkiv. No. 4, 1889: 1-13. See also: Lie, H. P. “Norwegian Lepers in the
 151

physicians: As long as the disease mainly was framed as a disaster to individuals or
families, leprosy remained a matter for the individual sufferer, their families and
philanthropy. This changed in the 1890s, when leprosy increasingly was believed to
be contagious. More and more frequently, the presence of the bacillus was used as
proof that the disease was contagious, and that prevention meant interrupting the path
of infection.378
The rationale for quarantine was that disease could be stopped at a
geographical border. Quarantine was especially relevant where leprosy was seen as a
foreign disease imported through migration. In the United States, leprosy was made
part of the federal quarantine regulations in 1894: “Vessels arriving at quarantine with
leprosy on board shall not be granted pratique until the leper with his or her baggage
has been removed from the vessel to the quarantine station.”379 Persons affected by
leprosy were to be detained until the ship was outbound, and returned at the expense
of the vessel.380 This was an extention of the National Quarantine Act passed one year
earlier, initially aimed at cholera, yellow fever, smallpox, plague and typhoid fever.
Letting the shipping companies take the financial burden of harboring lepers was to
serve as an incentive for them to screen their passengers at departure. Canada




United States: The investigations of Holmboe, Boeck and Hansen”. International Journal of Leprosy. No. 3.
1938: 351-356; Gussow 1989: 81-82; Davidsen, Bjørn. “"Forskerstafett" til Amerika 1863-1888.”
Bergensposten, no. 4. 2001: 29-39.
378
The bacillus was not a required component for this line of reasoning. As I will return to later in this chapter,
Hawaii pursued segregation from 1866, based on the observation that the prevalence of the disease was
increasing.
379
White, James C. “Leprosy in the United States and Canada”. Mittheilungen 1897. Bd. 1, Abt. IV. 1897: 29;
Kerr, J. W. “Communicable diseases: An analysis of the laws and regulations for the control thereof in force in
the United States.” Public Health Bulletin No. 62. 1914: 22-23. See also: Moran 2007: 22. Some states had
established quarantine-regulations prior to the federalisation of the US quarantine system in 1890. From August
1883, for instance, any vessels carrying persons affected with leprosy or elephantiasis within the Bay of San
Francisco, were to deliver them to the local lazaretto. (Meares, J. L. “San Francisco, California”. Leprosy in
Foreign Countries. Honolulu, 1886: 216). For a discussion arguing that the discourse linking leprosy with fear
of immigration has lately reignited in the United States, see: White, Cassandra. “Déjà Vu: Leprosy and
Immigration Discourse in the Twenty-First Century United States”. Leprosy Reveiw. 2010: 17-26.
380
For more on the role of shipping interests in US migration policies, see: Feys, Torsten. “The visible hand of
shipping interests in American migration policies 1815-1914”. Tijdschrift voor sociale en economische
geschiedenis, vol 7, nr 1, 2010: 38-62, and Sebak, Per Kristian: A Transatlantic Migratory Bypass –
Scandinavian shipping companies and transmigration through Scandinavia, 1898-1929. PhD-thesis, University
of Bergen, 2012. Feys focuses on Holland America Line as middleman and active policy agent in the period
before the First World War, while Sebak’s focus is on DFDS and the Norwegian America Line in the interwar
period. See also: Zolberg, Aristide R. A Nation by Design – Immigration Policy in the Fashioning of America.
2006.
 152

followed suit in 1896,381 and some years later the legislations led to calls from
physicians in Latin America that similar precautions must be put in place also there.382
Despite the participants at the first international leprosy conference in Berlin in


1897 agreeing that “Every leper is a danger to his surroundings”,383 only two
physicians advocated quarantine measures: François Henri Hallopeau from Paris and
Eduard Arning from Hamburg.384 Both saw leprosy as an imported disease originating
outside the European continent, and just as they believed that the disease had been
brought to Europe by the first Christian crusaders, they held the advent of mass
migration in the second half of the 19th century responsible for the disease
reappearing. According to Arning, most immigrants came from countries where
leprosy was endemic (identified as South China and Japan, followed by British India,
Russia, Scandinavia and Portugal). While importing foreign labor was in itself
justified, the migrants stuck to the way of life they were used to from their home
countries, and imprinting that they ought to take proper precautions to avoid
spreading their disease was impossible. Hallopeau emphasized that since leprosy was
contagious and maritime quarantine had protected France against the other contagious
diseases, the lessons learned should be applied also for leprosy.385
What Arning and Hallopeau called for at the Berlin conference was inspired by

the US Quarantine system: Refusing the landing of lepers, and making the states

‘exporting leprosy’ responsible for controls at departure. This, they argued, was safer




381
Pernet, George. “Leprosy in the British Empire (South Africa and Australia excepted)”. V. Internationaler
Dermatologen-Kongress abgehalten in Berlin vom 12-17.September 1904. Verhandlungen und Berichte. 1904:
46.
382
The question of preventing leprosy through quarantine was a topic at the Third Pan-American Medical
Congress held at Havana, Cuba, in February 1901. The Cuban physician Manuel f. Alfonso, especially, argued
that: “Any immigration on a large scale from leprous foci is an important matter as far as the spread of leprosy
is concerned.” Alfonso, Manuel F. “Leprosy in Cuba”. Lepra Bibliotheca Internationalis. 1902: 52. See also:
Robelin. “La lèpre en Cuba: Algunos datos referentes à la lepra en Cuba.” Lepra Bibliotheca Internationalis.
1902: Fasc 3; Revisita de medicina tropical. March, 1902.
383
Abraham, Phin. S, Edward Arning, E. von Bergman, Dubois-Havenith, J. J. Kinyoun and G. Thibierge. “The
Honorary Secretaries’ report from the First International Leprosy Conference” Mitteilungen 1897. Bd 2. Abt.
IV: 191-192.
384
Arning, Edmund. “Lepra und Immigration”. Mittheilungen 1897. Bd 1. 1897: 8-13; Hallopeau. ”Die
Isolirung der Aussätzigen und die dazu erforderlichen Massregeln”. Mittheilungen 1897. Bd. 2. 1897: 163.
385
Quarantine was not a uniform intervention. For a detailed comparison of quarantine measures against
cholera, smallpox and syphilis in Britain, France, the German states and Sweden, see: Baldwin, Peter.
Contagion and the State in Europe, 1830-1930. 1999.
 153

and more practical than controls at arrival, as it was much more difficult to return
those who have already arrived. But while none of the delegates explicitly disagreed,
none signed up when the question of immigration and emigration was put up for
debate under its own heading.386 Possibly, quarantine regulations were seen as
questions for inter-state diplomacy – not a matter for a scientific conference. More
likely, quarantine was seen as a derailing from the more important issue, that of
segregation. Besides, was quarantine really applicable to a disease such as leprosy?
To stop leprosy at the border was easier on paper than in practice. At the Berlin
conference, dermatologist Georges Thibierge from Paris pointed out that health
inspection of all subjects from ‘contaminated countries’ was impractical. Instead, he
suggested targeted inspections of those most exposed to the danger of infection:
Soldiers returning from military campaigns in leprous countries, sailors, and
employees of the colonial- and penitentiary services.387 His colleague Ernest Henri
Besnier agreed: “In most cities it is impossible to stop the leper on arrival, unless they
are filthy with evident facial lesions.”388 Instead, he recommended that municipalities
should register all foreign residents originating in countries with leprosy, and
monitored their health over time.
At the annual meeting of the American Dermatological Association in 1900,
physician Prince A. Morrow from New York summarized the three main arguments
against quarantine: First, leprosy had an incubation period which could last for years
in which not even the person affected was aware of the disease.389 In comparison, the
incubation period of yellow fever and cholera was five days, smallpox two weeks and
typhoid fever up to twenty days.390 Second, the disease was hard to diagnose,
especially in its early stages, and the consequences of a mistaken diagnosis were




386
Mittheilungen 1897. Bd 2. 1897: 121.
387
Thibierge, G. “Die Isolirung der Aussätzigen und die dazu erforderlichen Massregeln”. Mittheilungen 1897.
Bd. 2. 1897: 180.
388
“Dans la plupart des villes, il est impossible d’arrèter le lépreux à l’arrivée, à moins qu’il ne soient des
lépreux sordides avec les lésions faciales manifestes.” Besnier, Ernest Henri. “Die Isolirung der Aussätzigen
und die dazu erforderlichen Massregeln”. Mittheilungen 1897. Bd 2. 1897: 171.
389
“No system of quarantine has ever been devised that will effectually prevent the importation of a disease so
prolonged in its incubation and so little manifest on ordinary inspection as leprosy.” (Morrow, Prince A. “The
Prophylaxis and Control of Leprosy in this Country.” Lepra Bibliotheca Internationalis 1901: 171.)
 154

grave. Finally, as by then had been argued at the International Sanitary Conferences
for half a century, rigid border control would interfere with commerce. “There can be
no commerce or free intercourse between nations or races without an interchange of
infectious diseases as well as commercial commodities.”391 In the columns of Lepra
Bibliotheca Internationalis, Hansen concurred: “I think it is impossible to prevent the
emigration and immigration of lepers, because, the disease develops so slowly, that
even a physician knowing the disease very well cannot diagnose leprosy for many
years, how many, nobody knows, in its beginning.”392 The difficulties of early
diagnosis, combined with leprosy having an incubation period lasting years not days,
were strong arguments against adapting quarantine measures developed for other
contagious diseases: Quarantine might be desirable, but in practice it was impossible
to implement.
When the Fifth International Congress of Dermatology convened in Berlin in
September 1904 and dedicated the whole first volume of the proceedings to follow-up
on what actions had been taken since the leprosy conference in 1897, quarantine
measures were hardly mentioned.393 Nor was it a central topic at the Second
International Leprosy Conference in Bergen in 1909.







390
Treasury Department. United States Quarantine Laws and Regulations. February 24. 1893: 17.
391
Morrow, Prince A. “The Prophylaxis and Control of Leprosy in this Country.” Lepra Bibliotheca
Internationalis 1901: 170. Morrow did however argue for selective border controls aimed at the Chinese:
“Before dismissing this part of the subject it may be said that the Chinese have been the most active
disseminators of leprosy in modern times. These pig-tailed Argonauts of the Orient in their world-wide
migrations in quest of the Golden Dollar have invaded many lands and almost every land they have touched
they have tainted with leprosy.” (Op. cit.) Morrow’s sentiment against the ‘yellow peril’ was undoubtedly
shaped by the recent US annexation of Hawaii, where Chinese immigrants had been identified as likely culprits
already in William Hillebrand’s report from 1865, and the locals named the disease “mai pake” (“Chinese
disease”). The Chinese Exclusion Act passed in 1882, excluding “skilled and unskilled laborers and Chinese
employed in mining” from entering the country shows how Chinese “coolies” as carriers of leprosy was but a
part of a more widespread prejudice. (Chinese Exclusion Act, 1882).
392
Hansen, G. Armauer. “On the prevention of emigration and immigration of lepers.” Lepra Bibliotheca
Internationalis. 1900: 88.
393
The only exception was French dermatologist Eduardo Jeanselme, who argued that the most important action
to be taken by the European colonial powers to stop the spread of leprosy was prohibiting lepers from the
colonies travelling to Europe. (Jeanselme, M. E. “Frankreich und Kolonien. Bericht”. V. Internationaler
Dermatologen-Kongress. 1905: 227.). Also Wellesley C. Bailey from Mission to Lepers tangented on the topic
in his lecture on “How Lepers Travel”, which concerned how ‘lepers’ moved about within India. (Bailey,
Wellesley C. “British India.” In: Rosenthal, O. V. Internationaler Dermatologen-Kongress abgehalten in Berlin
vom 12.-17. September 1904. 1. Band. 1904: 98-99.)
 155

Despite several physicians questioning the viability of stopping leprosy at the
borders, and no international resolutions to give weight to the arguments, the debate
continued. In the spring of 1901, the German government announced that they had
reached an agreement with the Persian, Romanian, Russian and Turkish governments
aimed at preventing the movement of leprosy patients between the four countries. “To
this end it was decided that the authorities of the country interested do not deliver
passport to lepers, or even ID-cards.”394

In France in 1905, the section for medicine and hygiene at The Colonial
Congress in Paris unanimously recommended that lepers in the French colonies
should be prohibited from crossing state borders.395 When founding editor of the
medical journal Annales d’Hygiène et de Médecine Colonial (1898), Alexandre
Kermorgant, was made Inspector General of the colonial health service in 1906, he
quickly made leprosy one of his top priorities.396 Pointing at the resolutions passed at
the international congress in Berlin in 1897, which concluded that the disease was
contagious, he strongly argued that due to increased traveling leprosy in the colonies
was a growing threat to the colonizers. France desperately needed to build institutions
for the isolation of lepers arriving from abroad so that proper quarantine measures
could be put in place.


We have noted the danger and it is growing every day following the expansion of all colonial
peoples, the growing number of relationships with other countries, and facilities provided to
passengers to travel the world. In these circumstances would it not be prudent to consider,
not the leper colony – that would be medieval – but sanatoriums or nursing homes to isolate
lepers who come to us from beyond the sea. (…) Remember, in any case, nothing is more




394
“Mesures internationales contre la propagation de la lèpre” Lepra Bibliotheca Internationalis. 1901: 120,
originally published in La Semaine médicale, April 10. 1901.
395
“Voeu du Congrès colonial de Paris de 1905”. Lepra Bibliotheca Internationalis. 1906. Further, the
congress recommended isolating all lepers with open wounds or virulent forms of the disease; banning lepers
from trades where they might spread their contagion; and establishing ‘maritime leprosaria’ – islands where
especially vagabond lepers should be deported. Instead of prison-like institutions, they recommended
establishing agricultural colonies, where lepers could enjoy relative freedom in collaboration with other
sufferers.
396
Kermorgant had a long career in the navy, first as a surgeon and later as a medical doctor, before being put
in charge of the French colonial health services in 1906. For more, see: Weiner, Bernadette and Jean Flahaut.
 156

dangerous than the failure of any prophylactic measure vis-à-vis a scourge that threatens us.
Caveant consules!397


Kermorgant seems to have had little immediate success in convincing the French
government that the precautions were necessary. In 1909, as vice-president of Société
de Pathologie Exotique, he set down a commission on leprosy in the colonies
consisting of himself and three other physicians. After months of discussions they
jointly sent their recommendations to the colonial minister. The main message was
that leprosy existed in almost all colonies, and that once introduced to a virgin
population, the disease proliferated at an alarming rate.398 Norway was presented as
the primary example proving that with proper precautions, the trend could be
reversed, but that getting rid of leprosy was both more expensive and more time-
consuming than preventing it in the first place. However, to stop leprosy at the
borders was but one of eleven recommendations for preventive measures suggested
by Kermogrant’s commission. Faced with leprosy, quarantine alone was simply not
enough.399
While the report itself did not dictate action, it shows how physicians

increasingly were the driving force in putting prevention on the political agenda.




“Alexandre Kermorgant (1843-1921) témoin de l’état sanitaire des anciennes colonies françaises”. Histoire des
Sciences Médicales. Vol. 33, No. 3, 1999: 267-274.
397
Kermorgant, M. A. ”Des dangers que nous fait courir la lèpre.” Inspecteur général du service santé des
colonies.” Lepra Bibliotheca Internationalis. 1902: 43-44.
398
From the mid 1890s, this line of reasoning was widespread. Physician Isodore Dyer at Hawaii, for instance,
argued that: “Leprosy has spread whenever it has been introduced, notably in the West Indies, Sandwich Islands,
South America, Mexico and in Louisiana. (…) The Conference of 1897, in Berlin, was held because of the
recognition of the appalling proportions of leprous inhabitants on the face of the earth, suddenly realized in all
the awfulness of the danger threatening.” Dyer, Isodore. “Investigation of Leprosy (from Report of Marine
Hospital Service for 1898).” Lepra Bibliotheca Internationalis. 1900: 91.
399
In addition to stopping leprosy through quarantine, the committee recommended spreading propaganda of the
dangers of leprosy; preventing lepers from trades where they would be in direct or indirect contact with healthy;
surveillance of schools and public places to detect lepers; disinfection of lepers’ homes; segregation of leper
vagabonds, and denying foreign lepers at the borders. In addition they recommended erecting leprosy camps in
the colonies. These should be put under the administration of a physician and surrounded by a 200- meter safety
zone. Inside the camps the sexes should be segregated, there should be a hospital for treatment, a separate area
for suspected cases, a graveyard, and a system of punishments and rewards (such as permits to visit family
members) to ensure proper discipline. Finally, children of leprous parents should be sent to orphanages.
(Delrieu, Grall, Jeanselme and Kermogrant. “Rapport de la Commission de la Lèpre de la Société de Pathologie
Exotique”. Lepra Bibliotheca Internationalis. 1909: Fasc 4, originally published in Bulletin de la Société de
Pathologie Exotique, 1909: 67; “Prophylaxie de la lèpre dans les Colonies Françaises” Société de
 157

Among the results were new legislations in the French protectorate of Tonkin, which
from December 1909 prohibited lepers from entering the area by law. Lepers were
also banned from certain professions, and – explicitly inspired by the Norwegian
legislations – those who could not be safely isolated at home were to be forced into an
institution.400
Quarantine was never a big debate in the columns of Lepra Bibliotheca

Internationalis, but notifications that similar legislations were put in place in other
parts of the world kept accumulating. In September 1909, for instance, the maritime
quarantine department in Australia clarified that the 1908 Quarantine Act (Regulation
No. 49) also applied to lepers and that lepers arriving in one of the ports should
immediately be isolated and returned.401
It was not until the third conference in Strasbourg in 1923, where segregation
was downplayed in favor of more emphasis on country-specific interventions, that the
question of immigration made it to the closing resolution: “1) Laws governing the
anti-leprosy campaign should vary according to the country in which they are applied,
but in all cases foreign lepers should be barred from entering a country.”402 Calls for
international quarantine measures addressing lepers were in turn repeated in the
League of Nations’ first prophylaxis report published in 1931: “International
agreements should be arranged to regulate the movements of lepers from one country
to another.”403 Apart from the general encouragement, however, it seems the League’s
leprosy commission did not see brokering an international agreement as part of their
mandate. Nor was leprosy part of the agreements reached at the international sanitary




Pathologique exotique, Meetings February 10, March 10 and April 14, 1909) ; “Discussion du Rapport de la
Commission de la Lèpre”. Lepra Bibliotheca Internationalis. 1910: Fasc 3.)
400
Audian. “Prophylaxie de la lèpre au Tonkin”. Lepra Bibliotheca Internationalis. 1910: Fasc. 4, originally
published in Annales D’hygiène et de médecine colonial. July-September. 1910.
401
“Commonwealth of Australia – Law as to leprosy”. Lepra Bibliotheca Internationalis. 1910: Fasc. 4. Prior to
the unification of the Commonwealth of Australia in 1901 the different territories had different laws. In New
South Wales, for instance, the notification and detention of lepers was made compulsory by law already in
1890: If two medical practitioners agreed the person suffered from leprosy, they were given the choice of
confinement for life in the Leper Asylum at Little Bays, or leave the country. (Thompson, Ashburton. “Report
on Leprosy in New South Wales for the year 1899.” Lepra Bibliotheca Internationalis. 1902: 221. See also:
Robertson 1997.)
402
See: Appendix 2c.
 158

conferences. While several countries ended up including leprosy in already existing
quarantine regulations, either explicitly or through defining leprosy as a contagious
disease, it was never universally adapted.





The rise of segregation: Towards Berlin 1897


Denying lepers from crossing state borders did not stop the disease where it was
endemic or had already been introduced, and quarantine was not the only way leprosy
became a concern for governments. From the mid 1890s to the early 1920s, the
preventive measure that dominated the international medical debates was segregation.
As the League of Nations’ Leprosy Commission put it their first general report, The
Principles of the Prophylaxis of Leprosy (1931): “Until recently, the compulsory
segregation of lepers in special leprosaria has been the chief - almost the only -
measure of prophylaxis”.404 Segregation was not about stopping lepers from entering
into an area, but isolating those already present.
As Dorothy Porter and others have shown, in Western countries the health of
the population was increagingly seen as a matter for the state.405 For leprosy, the
breakthrough of segregation as an international recommendation can be traced to the
first international leprosy conference in Berlin in 1897. The delegates concluded that
leprosy was contagious: “Every leper is a danger to his surroundings, the danger
varying with the nature and extent of his relations therewith, and also with the
sanitary conditions under which he lives.”406 Since leprosy was considered incurable
to the individual and detrimental to the society as a whole, adapting legal measures





403
League of Nations Health Organisation. The Principles of the Prophylaxis of Leprosy. First General Report
of the Leprosy Commission. (Official No. C. H. 970). Geneva, April 1931: 7.
404
League of Nations Health Organisation. The Principles of the Prophylaxis of Leprosy. First General Report
of the Leprosy Commission. (Official No. C. H. 970) Geneva, April 1931: 6.
405
Porter, Dorothy. Health, Civilization and the State. A history of public health from ancient to modern times.
[1999] 2005: Part 2.
406
Abraham, Phin. S, Edward Arning, E. von Bergman, Dubois-Havenith, J. J. Kinyoun and G. Thibierge. “The
Honorary Secretaries’ report from the First International Leprosy Conference” Mitteilungen 1897. Bd. 2: 191-
192.
 159

for isolation was seen as a logical consequence: The healthy population needed to be
protected. Striking a balance between the rights to liberty of those suffering from the
disease and the rights of the healthy majority, the preventive measures put in place in
Norway were held up as a golden standard.
Before examining the consequences of these recommendations, I will in the
following investigate the medical debates that led up to the Berlin resolutions. My
argument is that the resolution was a compromise in the dispute regarding etiology
and prevention. On the one hand it was sufficiently severe to satisfy even the most
hardline contagionists, on the other it put adequate emphasis on the need for
adaptation based on local social conditions to persuade those not convinced the
disease was contagious. Most importantly, it established local medical authorities as
the ultimate policy experts.
For physicians interested in leprosy in the last decades of the 19th century there

were numerous explanations for how leprosy proliferated. The debates illustrate how
practical measures towards the disease were entangled with the mechanisms for how
the disease spread, but also with what preventive measures were considered
practically possible, as well as different interpretations of the outcomes of measures
put in place. I will begin with the ‘leprosy epidemic’ on Hawaii, which in the 1880s
and 1890s became a reference point for proponents of several different disease
models.
Thirteen years before the Berlin conference, in 1884, president of the Board of
Health and Minister of Foreign Affairs on Hawaii, Walter Murray Gibson, sent an
enquiry to diplomats in various parts of the world asking for “information as to
Leprosy and the social and medical treatment of lepers in other countries.”407 The





407
Gibson, Walter M. “Introduction to Reports on Leprosy by the Government of British India and Other
Foreign Powers”. Leprosy in Foreign Countries. 1886: 3. Asking for advice in other countries was not the only
strategy Gibson pursued. In 1884 he invited the German physician Eduard Arning to investigate the ‘leprosy
epidemic’. In the fall of 1885 Arning inoculated the convicted murderer Keanu, and two years later he was
diagnosed with the disease. When Arning announced his experiment in 1889, this led to huge debates both of
the ethics of the experiment and how the outcome should be interpreted. The contagionists withheld that
Arning’s experiment proved the disease to be contagious, others disagreed. Jonathan Hutchinson, for instance,
argued that since the man had been living under the same conditions as others who had developed the disease,
and that his son, nephew and brother-in-law were also victims of the disease, the experiment proved nothing.
 160

background for the request was that despite almost twenty years with compulsory
segregation, there was little indication that the disease was in decline.
The Kingdom of Hawaii had begun its attempt to “stamp out the scourge by
segregation” in 1865.408 This was a response to physician William Hillebrand’s report
that leprosy had recently been introduced by Chinese immigrants, and that the disease
was proliferating at an alarming rate.409 The “Act to Prevent the Spread of Leprosy”
made it mandatory to report every case of the disease to the sanitary authorities. The
police was required to arrest and deliver any person alleged to have leprosy to the
Board of Health for a medical inspection, and a remote peninsula on the island of
Molokai was set aside for a leprosy settlement. The first seven years, 1.288 persons
were examined by the board, and 529 were sent to Molokai. By the early 1880s,
approximately ten percent of government revenues were going to the Board of Health,
between 50 and 65 percent of which was allocated to leprosy.410 On average about
140 new cases were admitted to Molokai every year; reaching a peak of 571 new
cases in 1888.411
Gibson’s request resulted in a report with replies from British India, Ceylon,
Hong Kong, Siam, the Netherlands and their colonies, the Canary Islands, Norway,
Spain, Mexico, Chile, Japan, Guatemala, several states in the United States, and the
leprosy institution Tracadie in New Brunswick, Canada. The replies described
prevalence, diagnosis, etiology, measures put in place to check the spread of the






(Hutchinson, Jonathan. “Remarks on some facts illustrating the early stages of leprosy”. The British Medical
Journal. March 8, 1890: 529-531; “The Contagious nature of leprosy”. The British Medical Journal. April 19,
1890: 909.) For more on this well-documented dispute, see: Edmond 2006: 91; Inglis, Kerri A. “‘Cure the dread
disease’: 19th Century Attempts to Treat Leprosy in the Hawaiian Islands”. The Hawaiian Journal of History,
Vol. 43. 2009: 109-124; Gould 2005: 80-83.
408
Gibson, Walter M. Leprosy in Foreign Countries. Hawaii 1886: 1.
409
Classifying leprosy as a threat based on race was very much in line with what historian Michelle T. Moran
has identified as typical for the US approach to leprosy and public health. (Moran 2007). For similar arguments
in Australia, see: Robertson 1999; Bashford, Alison and Maria Nugent. “Leprosy and the management of race,
sexuality and nation in tropical Australia”. In: Bashford, Alison and Claire Hooker (eds.) Contagion. Historical
and cultural studies. 2001: 106-128.
410
Inglis, Kerri A. “‘Cure the dread disease’: 19th Century Attempts to Treat Leprosy in the Hawaiian Islands.
The Hawaiian Journal of History, Vol. 43. 2009: 101-124; Gould 2005: 59-109; Edmond 2006: 145-156. See
also: Leprosy in Foreign Countries. 1886.
411
Report of the Board of Health of Hawaii, 1909: 186, reproduced in: Hoffman, Fredrick L. Is Leprosy
Increasing? 1920: 49-50. Between 1866 and 1906, 5.876 ‘lepers’ were sent to Molokai.
 161

disease, as well as direct policy recommendations. The answers varied widely and
illustrate the wide range of coexisting etiological explanations for leprosy.
Dr. J. L. Meares, Health officer of the San Francisco Board of Health, saw
leprosy as highly contagious and argued that “The isolation of lepers is so important
and its necessity so self-evident, that I scarcely think the subject worthy of
discussion.”412 Boston physician John C. White agreed: “Lepers belong to the
dangerous classes of the community which require perpetual confinement, and the
sooner this remedy is applied the less seemingly cruelty will attach to it.”413 The
report also included Henry Vandyke Carter’s Prevention of leprosy by segregation
(1884) which argued the necessity of registration and isolation based on the results
achieved in Norway,414 as well as two papers from American medical journals
arguing that the leprosy bacillus was proof that leprosy was a specific and contagious
disease.415
Despite contagion being the ruling paradigm on Hawaii, contagionists arguing
for segregation were in a minority in the replies. The largest report came from India,
where Alexander Mackenzie, Secretary to the Government, summarized that there
was no need for direct action since the disease was not contagious: “In support of this
view it may be mentioned that not a single servant of the asylum at Almora in the
Kumaun District of the Northwestern Provinces appears to have contracted the
disease during the thirty-one years for which there is information.”416 Surgeon
General with the Government of Bombay, W. J. Moore, withheld that leprosy was “a
latent syphilitic inherited constitutional taint” and that “the means of preventing
leprosy is not in reviving the antiquated system of leper asylums, but by measures
against the spread of syphilis and by sanitation in the fullest sense of the term. (…) In




412
Meares, Dr. J. L. “San Francisco, California”. Leprosy in Foreign Countries. 1886: 214.
413
White. “The Question of Contagion in Leprosy”. American Journal of the Medical Sciences. October, 1882.
Reprinted in: Leprosy in Foreign Countries. 1886: 222.
414
Carter, H. V. “Prevention of Leprosy by Segregation” . Leprosy in Foreign Countries. 1886: 82-101. More
on Carter in the following chapter.
415
White, Dr. “The Question of Contagion in Leprosy”. American Journal of the Medical Sciences. October
1882, reprinted in: Leprosy in Foreign Countries. 1886: 219-222; Belfield, Wm. T. “The Bacillus of Leprosy.”
Journal of Cutaneous and Venereal Diseases. July, 1883. Reprinted in: Leprosy in Foreign Countries. 1886:
223-226.
 162

sanitation I include the prevention as much as possible of whatever entails a state of
human system below par.”417 In Moore’s view, the disease would decline if the
government provided a robust economy, affordable and nutritious food and clothing,
improved housing conditions, drainage, “in short, everything tending to improve the
condition of the population of a country.”418 T. R. Lewis and D. D. Cunningham, who
in 1877 published the conclusions of a sanitary investigation regarding leprosy in
India, concluded that the disease was hereditary. Since lepers tended to develop
sterility, the disease would gradually disappear without any intervention.419 While
sanitary explanations dominated, the report from India was the one with the largest
variety in the explanations of the mechanisms which determined the outbreak of the
disease. The vast majority did however have the conclusion in common: There was no
need to intervene against leprosy specifically, but improved sanitary conditions would
get rid of this and other diseases.
As I will return to in the following chapter, the hands-off approach was the
dominant line of reasoning in India from Gavin Milroy’s report on leprosy in the
British Empire in 1867 to the end of the century. As Dyce Duckworth, the appointed
representative of the Royal College of Physicians to the Leprosy Commission to India
would argue in 1893: The arguments for contagion were circumstantial at best, and
much clearer for other diseases. As long as there were no policies for segregating
people with tuberculosis or syphilis, the whole idea of segregating lepers was absurd.

I know of no trustworthy evidence to prove that a leper in any community is a source of
greater danger than is a consumptive patient, and I know that a person suffering from
Syphilis is a real and very positive source of danger anywhere. It would therefore be absurd








416
Mackenzie, A. “Leprosy in India”. Leprosy in Foreign Countries. 1886: 11.
417
Moore, W. J. “Extracts from report of August 12, 1885”. Leprosy in Foreign Countries. 1886: 13
418
Op. cit.
419
For a summary of the different anti-contagionist positions (the hereditarian, the dietary, and the sanitarian),
see: Pandya, Shubhada S. “Anti-Contationism in Leprosy, 1844-1897”. International Journal of Leprosy and
other Mycobacterial Diseases. Vol 66, No. 3. 1998: 374-384. More on the reports on leprosy in India in the
following chapter.
 163

on the face of it to adopt stringent laws for the leper, and to let the Syphilitic person go
free.420


While Carter’s report argued that the disease in Norway was considered to be
contagious, Consul-General for Salvador in Norway, Søren Caspersen, held
hereditarism to be the ruling paradigm. When Carter pointed at isolation, Caspersen
attributed the reduction of new cases to “The higher civilization, better sanitary
habits, and the public asylums”.421 Heredity was also the ruling paradigm in Japan.
Surgeon K. Yamamoto reported that the disease was “highly inheritable (…) so those
who have leprosy, or its tendency, among their families or relatives, are strongly
refused to marry with other healthy families.”422 The shame the disease brought on
the whole family led the lepers to be confined at home and isolated from social
relations with others. In Mexico, the disease was regarded as hereditary but only
through the maternal line; in Canada and the Canary Islands the physicians withheld
that heredity did not cause leprosy in itself, but was a necessary predisposition for
contagion to take place. There were also those who argued that leprosy spread
through sexual intercourse; while others echoed the arguments from India that
climate, poverty and sanitary conditions were either directly or indirectly responsible.
Especially in Britain, where the variety of etiologies was greater than anywhere
else, Hawaii was highlighted as proof that segregation was futile. Prominent anti-
vaccinationist William Tebb, for instance, argued in 1893 that the law of enforcing
segregation of lepers at Molokai was “an admitted failure (...) the most heart-rending
and painful experience, in a tolerably long life, I have ever witnessed.”423 Since the
only way the disease could spread was through inoculation, the primary means of
prevention was to ban vaccination: Segregation was unnecessary, cruel and








420
Leprosy in India, Report of the Leprosy Commission in India, 1890-91. 1893: 9.
421
Caspersen, Soren. “Norway.” Leprosy in Foreign Countries. 1886: 192. According to Caspersen, a rationale
for the public asylums was that they segregated the sexes and therefore stopped the new cases from being born.
422
Yamamoto, K. “Leprosy in Japan”. Leprosy in Foreign Countries. 1886: 217. Italics in the original.
423
Tebb, William. The Recrudescence of Leprosy and its Causation. A Popular Treatise. 1893: 282.
 164

inhumane.424 Jonathan Hutchinson agreed, but on radically different grounds: The
disease was caused by the consumption of badly cured fish, and claims that the
Chinese spread the disease was merely a consequence of them introducing fish to the
local diet.425 In order to solve the problem of leprosy, one simply had to promote an
enhanced diet. Compulsory segregation was not just cruel, it was beside the point.426
Contagionists, on the other hand, held Hawaii as proof in opposition to theories of
climate, soil, diet and habits of life, and pointed out that “All these causes acting
together for centuries did not produce the disease in the Hawaiian Islands, nor was it
known there until some time after the islands were open to foreign trade and
commerce with other nations. Hence it is reasonable to suppose that it was imported
from other places.”427







424
According to Tebb, only way the disease could spread was through inoculation, “both accidental, as in a cut
or a sore, and by design as in vaccination. I believe that the instances of communication apart from inoculation
of this disease (if they exist at all) are extremely rare.” (Tebb 1893: 81). Proper clothing and personal hygiene
was in itself enough to prevent accidental inoculation, and thus the theory explained the correlations between
prevalence of the disease, culture and climate. Tebb’s arguments were well known, but contested. A year before
the publication of Leprosy and Vaccination, Beaven Rake and George Alfred Buckmaster, physicians and
members of the British Leprosy Committee, concluded after comparing the number of people being vaccinated
and the number of people with leprosy that “the risk of transmission of leprosy by vaccination is so small, that,
for all practical purposes, it may be disregarded.” (Rake, Beaven and George Alfred Buckmaster. “An inquiry
into the question of communicability of leprosy by vaccination.” Journal of the Leprosy Investigation
Committee. No. 4, 1892: 35.) When the Leprosy Commission in India published their report later in 1893, they
too rejected Tebbs theory after a long discussion. (Leprosy in India. Report of the Leprosy Commission in
India. 1890-91. 1893: 127-135).
425
“Gardening, poultry-rearing, and fishing are a Chinaman’s natural vocations, and he will cook and eat almost
everything that has had life. There is no improbability in the supposition that the Chinese may have introduced
into the Sandwich Islands novelties in the way of food, and especially in reference to shell-fish and fish. This
hypothesis would explain how it is that the Chinese introduce the disease only into certain places and fail entirely
in others.” (Hutchinson, Jonathan. “Memoranda for Future Investigations as to the Cause of Leprosy”. Journal of
the Leprosy Investigation Committee. No. 1. 1890: 87.) According to Hutchinson, the dietary model also
explained how the disease had proliferated in early Medieval Europe: Leprosy was not imported by Crusaders
like the contagionists argued, but spread through the advance of Christianity and its promotion of eating fish at
least once a week. And it was not segregation, but improved diet that explained why the
prevalence later had declined: “I believe that the advance of Christianity, with its salt-fish feasts, and not the
Crusades, was mainly conducive to the general prevalence of the disease in Europe during the Middle Ages,
that its spreading is always due to food and never to contagion, and its disappearance to an improved diet, and
not in the least to enforced isolation.” (Hutchinson, Jonathan. “Memoranda for Future Investigations as to the
Cause of Leprosy”. Journal of the Leprosy Investigation Committee. No. 1, 1890: 68.)
426
“Compulsory segregation would I think involve injustice, and entail much social misery.” (Hutchinson in:
Leprosy in India, Report of the Leprosy Commission in India, 1890-91. 1893: 10.) The British physician was,
however, not adverse to voluntary segregation in philanthropic institutions.
427
Abbott, Samuel W. “Massachusetts: Extracts from the Fourth Annual Report of the State Board of Health”.
Leprosy in Foreign Countries. 1886: 209.
 165

For Gibson, the continued detection and confinement of cases did not indicate
that segregation was futile. It merely proved that the disease on the island was
especially contagious. “To judge by the number of cases in proportion to the
population, the disease appears to be more virulent and malignant in the Hawaiian
Archipelago than elsewhere on the face of the globe.”428 Samuel W. Abbott from
Massachusetts, in contrast, argued that the problem was not in the legislations, but
that the implementation was not sufficiently strict: “If it be urged that isolation and
other sanitary measures have not succeeded in controlling the spread of leprosy in the
Sandwich Islands, it should also be stated that in the earlier years of sanitary control
the execution of the law was opposed very generally, especially by concealment and
deceit.”429
While the Kingdom of Hawaii was one of the first modern countries to
legislate compulsory segregation for the prevention of leprosy, the dubious outcomes
made it a case in point for the defenders of numerous different etiologies. But Hawaii
was not the only country to legislate segregation.
At the conference in Berlin in 1897, Gerhard Armauer Hansen made a more
compelling argument for segregation: Statistics which showed that since the practice
of sending ‘lepers’ to state institutions had begun in Norway in 1856, the number of
new cases had declined every year. When compulsory registration began in 1856,
there were 2870 registered lepers. By 1895, the official statistics showed only 321
known cases. The decline was sharpest in the municipalities where lepers were sent to
institutions. According to Hansen, the decline was therefore explained by Norway’s
increasingly strict practice of isolation, especially the legislations from 1877 and 1885
which he himself had designed.430 “These results, which we in Norway have achieved





428
Gibson, Walter M. Leprosy in Foreign Countries. Hawaii 1886: 1. The report had little or no practical
consequences. The Bayonet Constitution enforced in 1887 stripped Gibson (who by then held the posts of
Prime Minister, Minister of Interior and Secretary of War and Navy) of all his powers.
429
Abbott, Samuel W. “Massachusetts: Extracts from the Fourth Annual Report of the State Board of Health”.
Leprosy in Foreign Countries. 1886: 212. Likewise, at the first leprosy conference in Berlin in 1897, German
consul Henry F. Glade argued that it was first in the 1890s, when segregation was more rigorously enforced,
that the ‘leprosy epidemic’ was finally brought under control. (Glade, H. F. “Die Isolirung der Aussätzigen und
die dazu erforderlichen Massregeln”. Mittheilungen 1897. Bd. 2. 1897: 182-183.
430
Already at the International Medical Congress in Copenhagen in 1884, Hansen had in the paper “The
 166

through the isolation of lepers, show the benefit of the policies.”431

In addition to surveillance of those affected by the disease, and voluntary
institutions from the mid-1850s, the Norwegian laws had since 1885 demanded
compulsory isolation of those affected, either at home or in special institutions. Those
who had a private bed (preferably in a private bedroom), their own cutlery (which was
not to be washed with the cutlery of others), were cleanly and showed caution in
associating with others could remain in home segregation, the rest were to be arrested
and sent to one of three state institutions.432 The power to decide if the proper
precautions were taken was granted to the local health committee, headed by the
physician responsible for visiting the lepers in the area. As Hansen put it: “This is
very democratic, in that it is left to the local community to decide whether they want
to protect themselves against the disease or not.”433
The lessons from Norway were disputed. When the British Leprosy
Commission to India published their report in 1893, Hawaii and Norway were both
highlighted as examples to prove that segregation had failed.434 In support of this,
they quoted physician W. J. Collins who visited Norway in 1889 and found
segregation to be only partial:








Etiology and Pathology of Lepra” presented a similar argument: “Isolation was necessary; for, although the
disease was spontaneously curable, they could not cure it; and the practice of isolating the Norway had been
effective in reducing the number of lepers in twenty years by nearly one-half.” (Editorial. “International Medical
Congress: Section of Dermatology and Syphilis”. The British Medical Journal, August 30, 1884: 426). More
on the Norwegian debates on the leprosy legislations in the following chapter.
431
“Es kann nach den Resultaten, die in Norwegen durch die Isolation der Leprösen gewonnen sind, kaum
Zweifel an dem Nutzen derselben erhoben werden.” (Hansen, G. Armauer. “Facultative oder obligatorische
Isolation der Leprösen.” Mittheilungen 1897. Bd. 1, Abt. 3. 1897: 4.) In Norway, the legislations against
leprosy were considered so successful that they in 1900 were used as a model for a national campaign against
tuberculosis. The legislations were designed by Klaus Hanssen, Armauer Hansen’s brother. See: Ryymin,
Teemu Sakari. Smitte, språk og kultur. Tuberkulosearbeidet i Finnmark. 2009: 32-36; Schiøtz, Aina. Det
offentlige helsevesen i Norge 1603-2003, Bd 2: Folkets helse – landets styrke, 1850-2003. 2003: 63-69; Blom,
Ida. Feberens ville rose. Tre omsorgssystemer I tuberkulosearbeidet. 1900-1960. 1998: Chapter 3.
432
Hansen, Gerhard Armauer. “Die Isolirung der Aussätzigen und die dazu erforderlichen Massregeln”.
Mittheilungen 1897. Bd. 2. 1897: 163-165.
433
“Dies ist also ein sehr demokratisches Gesetz, indem es dem Volke selbst freigestellt wird, ob dasselbe sich
gegen die Lepra wehren will oder nicht.“ Hansen, Armauer. “Facultative oder obligatorische Isolation der
Leprösen.” Mittheilungen 1897. Bd. 1, III. Abtheilung. 1897: 4.
434
“Complete segregation has never been possible. Both in the Sandwich Islands and in Norway it has failed.”
Leprosy in India, Report of the Leprosy Commission in India, 1890-91. 1893: 385.
 167

To attribute the decline of leprosy in Norway to compulsory isolation is entirely erroneous.
In the first place no such powers exist or are likely to be sanctioned by the Norse democracy;
if they did exist, it would be impossible without further accommodation to segregate even
the reduced number of lepers in Norway at the present time. Indeed, I met many lepers in the
streets of Bergen and on the quay, going about their usual vocations.435


Collins supported Hutchinsons’s dietary theory (that leprosy was caused by eating
badly cured fish), and in line with what Milroy had argued in 1867, he believed that
“the exaggerated notion of its communicability in the lay man” was due to “the
repulsiveness of the disease”. It was not segregation that was stamping out leprosy in
Norway, “but the increased material prosperity of the people, the growth of foreign
trade, the inter-communication with town life, and the opportunities these give for
better and more varied subsistence.”436 In other words: Segregation did not address
the real cause of the disease, and was therefore unnecessary.
No strong defenders of the sanitary model of leprosy attended the conference
in Berlin in 1897, but both the dietary theory and the theory of heredity had their
champions. Jonathan Hutchinson pointed out that the theory of contagion did not fit
all observations: “The suggestion that it spreads by contagion might well fit some of
the facts but it is absolutely incompatible with many others.” In some places (such as
Hawaii) the disease spread despite precautions, in others it died out entirely “in spite
of the utter neglect of precautions against contagion.”437 Further, even direct
inoculation experiments had failed to prove that this could cause the disease. The only
common feature in places with leprosy around the globe, Hutchinson repeatedly






435
Collins, W. J. “Note on the Leprosy Revival”. The Lancet. May 17, 1890: 1064. Quoted in: Leprosy in
India, Report of the Leprosy Commission in India, 1890-91. 1893: 386. This interpretation of the Norwegian
leprosy system seems widespread among British physicians. But “lepers in the streets of Bergen (…) going
about their usual vocations” was representative only of the privately run St. Jørgens Hospital, not the State
institutions. (Andresen 2004). The lax segregation at St. Jørgens was a constant concern for contagionists such
as Hansen, and in 1891 the lepers were banned from trading their goods at the public market in Bergen. For
more on the conflict between the two institutions, see: Vollset, Magnus “Ett år på St. Jørgen – 1885 i
dokumenter”. In: Irgens, Lorentz M., Yngve Nedrebø, Sigurd Sandmo and Arne Skivenes (eds.) Lepra. 2006:
65-70).
436
Collins, W. J. “Note on the Leprosy Revival”. The Lancet. May 17, 1890: 1064-1065.
437
Hutchinson, Jonathan. “Erste Sitzung, Einleitung”. Mittheilungen 1897. Bd. 2. 1897: 21.
 168

insisted, was the consumption of fish.438 However, at the conference Hutchinson was
indisposed, and when his paper was read by his countryman Phineas S. Abraham it
was simply ignored by the rest of the delegates. Zambaco Pacha from Constantinople
suffered the same fate when he argued that the disease was hereditary, and that the
best prophylaxis was to ban lepers from entering into marriage.439
The different etiologies were not mutually exclusive. Physician Julius
Goldschmidt from Madeira, for instance, saw leprosy as contagious with a hereditary
taint. In 1891 he therefore argued that: “Complete isolation of all lepers and their
families is the only reliable measure in order to quickly and totally eradicate the
contagium.”440 Furthermore, this should be combined with sanitary measures aimed at
alleviating the power of resistance in the rest of the population through abundant
food, a moderate quantity of sound alcoholic drinks and cleanliness. At the
conference in Berlin he still held predisposition as a possibility, but argued that the
policies put in place in Norway had produced the best effects in that the number of
lepers had declined.441 Also the official delegate from the Government of Hawaii,
Superintendent Luis F. Alvarez from the newly opened Hospital for the Treatment of
Leprosy in Honolulu, concluded that matters would have been worse had segregation
not been put in place: “The results have been disappointing to those who had








438
“...if the food-hypothesis be the true one all measures for the compulsory segregation of lepers are useless
and cruel. It is the disuse of all forms of half-cured or uncooked fish is I feel convinced the simple measure
which ought to be enforced in districts in which leprosy is prevalent.” Hutchinson, Jonathan. “Erste Sitzung,
Einleitung”. Mittheilungen 1897. Bd. 2. 1897: 23.
439
Pacha, Zambaco. “Des rapports qui existent entre la maladie de Morvan, la Sytingomyélie, la Sclérodermie,
la Sclérodactylie, la Maladie de Rayunaud, la Morphée des Contemporains, l’Aïnbum, l’Atrophie musculaire
progressive Aran-Duchenne et la Lèpre”. Mittheilungen 1897. Bd. 1, III Abtheulung. 1897: 21-81. Both would
continue to defend their theories in the columns of Lepra Bibliotheca Internationalis, but were met with strong
criticism. In 1907, for instance, Zambaco Pacha argued that the best way to promote the extinction of leprosy
was that a certificate from a physician should be made mandatory in order to enter into marriage, and that lepers
should be disqualified. (Pacha, Zambaco. “La contagion de la lèpre en l’etat de la science.” Lepra Bibliotheca
Internationalis, 1907: 129) Pacha was not the only one to connect hereditary with marriage prohibition as a
suitable response. In Norway in 1850 when the disease was thought to be hereditary, for instance, a committee
suggested that people from ‘leprous families’ should be banned from marriage. (Vollset 2005: 44-47).
440
Goldschmidt, Julius. “The Madeira Leprosy”. Journal of the Leprosy Investigation Committee. No. 4. 1891:
31.
441
Goldschmidt, Julius. “Vorschläge zur Verhütung und Unterdrückung der Lepra”. Mittheilungen 1897. Bd. 1,
II Abtheilung. 1897: 14-17.
 169

predicted that this law would be the means to stamp out the disease. However the law
has been very useful in keeping the disease in check.”442
The contagionists dominated the Berlin conference. Despite admitting that the
precise mechanisms for contagion were unknown, the vast majority of those attending
agreed that the disease was caused by a bacillus, that the bacillus was found in every
leper and that therefore every leper was a danger to others. As for other pathogenic
diseases, the bacillus shifted the focus of disease prevention from a range of
environmental and hereditary factors to a focus on humans as carriers of disease. But
not everyone agreed, and the bacillus did not entail complete agreement when it came
to prevention. What was at stake was finding the right balance between the liberty of
those suffering from the disease, and the need to protect those not yet infected. As
Hansen argued in the debate the first day, it was a question of rights:


A sick person has not only rights but also duties, and the primary and most sacred duty must
be to not jeopardize the health of his fellow man. The healthy too have human rights, and this
obviously includes protection from disease. Fortunately, the healthy are in the majority, and it
would be foolish to turn that majority into a minority. (…) I find it more humane to protect
people from leprosy than to grant lepers the right and opportunity to spread their disease. I
have no doubt that we do mankind a great service if we could free the world from leprosy, and
this is indeed possible.443

What Hansen argued was necessary, was a system of surveillance and isolation, as
well as educating the population that lepers were dangerous. But since the
contagiousness of the disease was probably quite limited, Hansen stressed that the
requirements for home segregation were not very strict. This position was more




442
Alvares. ”Die Isolirung der Aussätzigen und die dazu erforderlichen Massregeln”. Mittheilungen 1897. Bd.
2. 1897: 182.
443
“Ein kranker Mensch hat neben seinem Rechte auch Pflichten, und die grösste und heiligste Pflicht muss
sein, seine Mitmenschen nicht zu gefährden. Ferner haben die Gesunden auch ihre Menschenrechte, und zu
diesen gehört offenbar auch, sich gegen die Krankheit zu wehren. Glückweise aber sind die Gesunden in der
Majorität, und es wäre unzweifelhaft thöricht, diese Majorität, wenn möglicht, in eine minorität zu verwandeln.
(…) Ich finde es dagen viel humaner, die Menschen gegen Lepra zu schützen, als den Leprösen das Recht und
die Gelegenheit zu geben, auch andere leprös zu machen, und ich zweifle nicht, dass wir der Menschheit einen
 170

moderate than the legislations in Hawaii, and too moderate in the eyes of some
contagionists.
In the months before the conference, the most vocal critic of the Norwegian
system was the American physician Albert S. Ashmead, who believed the lepers in
Norway were granted too much freedom to spread their disease. He called for “perfect
isolation; not isolation as it exists in private houses of Norway to-day (for Norwegian
isolation is far from being complete), but real, complete isolation in separated
colonies, by decrees enforced by government.”444 His argument was simple: Given
that the disease was incurable, those already affected by the disease were beyond
hope. The most humane approach was strict isolation, not for the benefit of the sick,
but to protect the healthy: “if we take care only of one generation of lepers, and
prevent inoculation of children, the disease will be eradicated. Is this not worth
fighting for?”445
The more highly contagious the disease was perceived to be, the stricter the
advice for segregation. While the bacillus was not necessary to the argument, as the
case of Hawaii shows, the bacillus was increasingly referred to as decisive proof that
contagion was beyond dispute and that this dictated isolation. In 1879, the Swedish
physician Fredrik Eklund was the first to use the presence of a bacillus as proof that
leprosy must necessarily be highly contagious. Therefore, he argued, lepers should be
confined in a separate room, everything they touched should be considered
contaminated, and the population should be constantly reminded that those suffering
from the disease were dangerous: “There should be a white, oil painted plate above





grossen Dienst leisten würden, wenn wir dieselbe von Lepra befreien könnten; das aber ist unzweifelhaft
möglich.” Hansen, Gerhard Armauer. “Erste Sitzung, Einleitung”. Mittheilungen 1897. Bd. 2. 1897: 17.
444
Ashmead, Albert S. Suppression and Prevention of Leprosy. 1897: 75-76. Also later physicians, such as
bacteriologist H. Bayon of South Africa, argued that the leprosy campaign in Norway had been unnecessarily
prolonged due to being too lenient: “Norway has also successfully dealt with the disease; but laxity there in
methods of segregation, notwithstanding a very complete record of all cases, has made it a very much longer
process than was necessary. (…) Leprosy is an unmitigated evil in any country, and if experience or scientific
research tells us that the scourge can be stamped out even the most causistic ingenuity cannot find an argument
in favour of allowing the cause of so much misery to continue to exist.” (Bayon, H. “On the necessity or
advisability of segregation in relation to the conditions and spread of Leprosy in South Africa at the present
time; the measures to be provided for the prevention and cure of Leprosy; and the suitability of Robben Island
as a place of detention for Lepers.” Lepra Bibliotheca Internationalis. 1914: 134-135.)
445
Ashmead, Albert S. Suppression and Prevention of Leprosy. 1897: 76-77.
 171

the entrance of the lepers home, on which the words ‘leper infected’ is written with so
big large letters that they can be read by a person with normal vision from at least 50
cubits distance [~30 meters].”446 Finally, the leper should be provided with a Bible
promising hope for the afterlife.
Others attending the Berlin conference argued that to the contrary, compulsory
segregation went too far. Alvarez, the American physician who pioneered the method
for boiling and grinding tissue samples to ensure that no bacilli hid inside them,
warned that what the experiences from Hawaii really showed was that treating lepers
as criminals destined for exclusion only led people to conceal their disease.447 The
same was reported from South Africa, the British representative Phineas S. Abraham
added:


(…) it appears to me that attempts at the absolute isolation of lepers must in many places be
quite futile. Where the lepers are few and public opinion unanimous as to the necessity for
their exclusion, such measures might be possible, but where the cases are numerous and not
desirous of being seperated from them, harsh measures of isolation and segregation become
impossible – their chief result being the concealment of cases.448

A third line of reasoning was that the contagiousness of leprosy differed from place to
place. This was heralded by Ernest Besnier, medical director of the Hôpital Saint-
Louis in Paris, who pointed out that despite 150 to 200 known lepers in Paris alone,
the prevalence did not seem to increase. The same had been observed in Britain,




446
“Öfver ingången till den spetelskes bostad skall ständigt finnas uppsat en oljemålad, hvit tafla, å hvilken
orden «spetelsk smitta» äro anbragta med så store, svarte bokstäfver, att de kunna läsas af en normalseende på
minst femtio alnars afstånd.” Eklund, Fr. Om Spetelska (Elefantiasis Græcorum vel Lepra Arabum). 1879: 87-
90, quote om page 89-90.
447
“I am opposed to the adoption of rigorous or cruel measures against the lepers, because they lead to
concealment of cases and thus defect the object for which they were adopted, and, above all, because we ought
to adhere to principles of justice and humanity and must not treat the lepers as if they were criminals. The
Hawaiians are the most peaceful and law-abiding people in the world, and yeat at times they resist the officers
of the law when they attempt to arrest a membef of their family.” (Alvarez. ”Die Isolirung der Aussätzigen und
die dazu erforderlichen Massregeln”. Mittheilungen 1897. Bd. 2. 1897: 182.) Some six years later, however,
after Hawaii had been annexed by the United States, Governor Sanford B. Dole argued to the contrary: The
recent decline in new cases being sent to Molokai was due to introducing more rigorous segregation: “From
these figures it would appear that with strict segregation the disease has steadily diminished, while, without
strict segregation, it shows a tendency to spread.” (“Leprosy in Hawaii. Report of Governor of the Territory of
Hawaii.” Lepra Bibliotheca Internationalis. 1903: 98.)
 172

where all but a few of the twenty or so known cases had caught the disease in the
colonies where the disease was endemic. With proper hygiene and cleanliness, and an
administration set up to supervise this, segregation was not necessary, Besnier
withheld – at least not in Europe.449
Despite objections, the conference agreed to pass resolutions which

highlighted leprosy policies in Norway as the golden standard for others to mimic.
The reason was not just that Norway had succeeded in reducing the number of cases,
or that it was the discoverer Hansen that had come with the suggestion. Rather,
recommending Norwegian-style segregation was sufficiently strict to satisfy those
who saw the disease as highly contagious, at the same time the comparatively lax
rules for home segregation made the Norwegian ideal acceptable also to those who
saw compulsion as counter-productive. Finally the emphasis that ‘local conditions’
differed, meaning both the capacities of the health system and the relative
contagiousness of the disease, and that decisions regarding prevention therefore
should be taken by medical experts as close to the problem as possible, made the
recommendations universally acceptable. In effect, references to the successful
campaign in Norway could be used to justify compulsory segregation one place, and
as an argument against compulsion in another.
The final resolution read as follows:



In view of the virtual incurability of Leprosy and the serious and detrimental effects which
its existence in a community causes, and considering the good results which have followed
the adoption of legal measures of isolation in Norway, the Leprosy Conference, as a logical
issue of the theory that the disease is contagious, has adopted the following resolution
proposed by Dr. Hansen and amended by Dr. Besnier.

1) In such countries, where leprosy forms foci or has a great extension, we have in isolating the
best means of preventing the spread of the disease.






448
Abraham. “Sechste Sitzung.“ Mittheilungen 1897. Bd. 2. 1897: 195.
449
Besnier. “Sechste Sitzung.“ Mittheilungen 1897. Bd. 2. 1897: 171.
 173

2) The system of obligatory notification of observation and isolation as carried out in Norway
is recommended to all nations with local self-government and a sufficient number of
physicians.
3) It should be left to the legal authorities after consultation with the medical authorities to take
the special measures applicable to the special social conditions of the districts.450







Push, pull, restrict


The primary goal of all strategies for prevention was to protect the healthy majority
from contagion, not to benefit those suffering from disease. Given that leprosy was
contagious and incurable, and isolation was the best, if not only, means of prevention,
how was this to be achieved? While the local specificities differed, in the first two
decades after the Berlin conference three main strategies were pursued: ‘Pull’, ‘push’
and ‘restrict’.451
Hansen and most other physicians who advocated segregation leaned towards

push-strategies. This meant employing legislation aimed at forcing lepers into
isolation. In practical terms, this required a system for the detection of cases, areas set
aside where the lepers were to be isolated from the healthy, either institutions, leper
colonies or home segregation, and propaganda aimed at educating the population that
lepers were dangerous so that they would be pressured into seeing isolation as a
refuge. Push-strategies dominated the medical debates between 1890s and the 1920s.
The pull-strategies relied on making segregation attractive, so that the lepers

would seek institutionalization voluntarily. Initially this was advocated by those who





450
Abraham, Phineas S, Edward Arning, E. von Bergman, Dubois-Havenith, J. J. Kinyoun and G. Thibierge.
“The Honorary Secretaries’ report from the First International Leprosy Conference” Mitteilungen 1897. Bd. 2.
1897: 191-192.
451
The terms ‘pull’ and ‘push’ are adapted from migration research, where the expressions have been used to
describe the factors leding people to leave their original homes (‘push’) and the factors attracting people to a
specific destination (‘pull’). The origin of the terminology is Everett S. Lee’s theory of migration, which
presents pull and push as the first of four factors determining migration: “1. Factors associated with the area of
origin. 2. Factors associated with the area of destination. 3. Intervening obstacles. 4. Personal factors.” Lee,
Everett S. “A Theory of Migration” Demography. Vol. 3, No. 1. 1966: 47-57; quote on page 50.
 174

saw segregation as unnecessary due to the limited contagiousness of the disease, but
increasingly this line of reasoning was adapted also by contagionists who came to the
conclusion that the promise of forced and indefinite detention only led those affected
by the disease to hide their disease for as long as possible.
The third dominant strategy was aimed at reducing the chances of contagion
not through isolation, but through placing restrictions on those suffering from the
disease. Especially in India, but also in French colonies and elsewhere, lepers were
banned from certain trades, from the use of public transport and from begging in
public places. This strategy was more affordable than wholesale segregation, it
educated the population that leprosy was contagious, and was an easily administered
response to local calls for legislative action.
There were also ‘minor’ strategies, such as separating the children of lepers
from their parents, first proposed in 1879 by William Munro and later propagated by
missionaries.452 This was not part of the first set of recommendations from 1897, but
made part of the conclusion in Bergen in 1909 and repeated in Strasbourg in 1923.
When BELRA surveyed the prevalence and prophylaxis against leprosy in 1924, they
found that early separation of children born to lepers was almost uniformly pursued in
the British Empire.453
The strategies were not mutually exclusive, and in practice most national





452
Munro 1879: 95. In a letter to the leprosy conference in Berlin, the founding head of Mission to Lepers,
Wellesley C. Bailey, underlined that “if the children of leprous parents can be separated from their leprous
relatives and all leprous surroundings, they will in most cases never contract the disease. (…) The Society
which I represent has now several Homes for the untainted children of lepers.” (Mittheilungen 1897. Bd. 2.
1897: 77.) In general, the missionaries appears to have contested conclusions, such as from the Leprosy
Commission to India, which claimed the contagiousness of leprosy to be relatively limited. As John Jackson put
it in 1900 in one of the first in a series of biographies describing the life and hardships of a missionary to lepers:
“it may be fairly inferred that the danger of contagion is by no means, so ‘exceedingly small’ as the
Commissioners suppose. (…) the Committee and their Commissioners were unanimous on one point, viz, that
of incurability.” (Jackson, John. Mary Reed. Missionary to the Lepers. 1900: 49.) In February 1902 the Mission
to Lepers arranged a Conference of Superintendents of Leper Asylums in Wardha in central India, which
concluded that “The Conference as a body and as individuals is convinced of the contagious character of leprosy.
(…) in view of the extremely serious nature of the disease, lepers should be segregated.” (Bailey, Wellesley C.
“British India”. In: Rosenthal, O. V. Internationaler Dermatologen-Kongress abgehalten in Berlin vom 12.-17.
September 1904. Bd. 1. 1904: 96.)
453
Rogers, Leonard. “Memorandum on the prevalence of and prophylaxis against leprosy in the British Empire,
based on replies to the questionnaire of the British Empire Leprosy Relief Association; with suggestions for
dealing with the problem.” (LNHO: 12B/42641/29272). 1925: 12.
 175

leprosy campaigns consisted of combinations of these tactics. Emphasis differed and
could change over time. Regardless of strategy, more often than not the
recommendations from the international conferences were made part of the local
argument.
The push-strategies emphasized teaching the population that lepers were
dangerous, to add social pressure so that the lepers would seek refuge in the
institutions. As Hansen put it at the conference in Berlin; the lepers never
acknowledged that they posed a danger to the healthy, and naturally did not want their
freedom restricted. Part of the Norwegian success, he explained, was public lectures
reserved for the healthy, explaining the virtues of cleanliness, promoting the necessity
of isolation, and educating them that lepers were dangerous. “The healthy listen and
the main message is that the healthy do not want to have dealings with the lepers. This
is my goal. In Norway we have achieved that a leper who wants to hire a servant does
not find one.”454

There was never a universal stigma connected with leprosy. Especially where
the disease was endemic, many saw leprosy as an unpleasant but fairly ordinary way
of growing old. As Medical Officer to the Hausa Association’s Central Sudan
Expedition in 1893-95, T. J. Tonkin, presented in a paper in London in 1902:


The disease is so common that in spite of the repulsive appearance of the sufferers, the
general public have, as far as I could make out, no objection to it. They are accustomed to it,
and regard it as one of the stable things of the world, and the chance of catching it as one of
the ills to which human flesh is inevitably heir. They do nothing so far as I know to limit the
chance of contagion.455





454
“Die Gesunden beachten die Ausführungen, und das ist ja die Hauptsache, dass die Gesunden nicht mit
Leprösen Umgang haben wollen. Wenn ich das durchgesetzt habe, ist mein Ziel erreicht. Wir sind jetzt in
Norwegen so weit gekommen, dass ein Lepröser, der einen Diener haben will, keinen bekommt.” “Die Isolirung
der Aussätzigen und die dazu erforderlichen Massregeln”. Mittheilungen 1897. Bd. 2. 1897: 163. See also:
Hansen, Armauer. “Facultative oder obligatorische Isolation der Leprösen.” Mittheilungen 1897. Bd. 1, III
Abtheilung. 1897: 1-6; Pandya 2003: 172.
455
Tonkin, T. J. “Some general and atiological details concerning Leprosy in the Sudan.” Lepra Bibliotheca
Internationalis. 1902: 135, first read before The Royal Medical and Chirurgical Society of London. May 27,
1902.Tonkin himself believed that the disease was contagious, with a diet “wanting in nitrogenous elements”
(141) as a contributing cause. See also: Tonkin, T. J. “An Analysis of 220 Cases of Sudanese Leprosy”. The
Lancet. April 16. 1903: 1077-1083.
 176

Hansen, in his autobiography from 1910, noted that similar attitudes were prevalent
on the Norwegian countryside. “When I asked them how they had acquired leprosy,
the common answer was that ‘it’s probably destined’, or that Our Lord had brought
it.”456 Likewise, the Swedish physician Fredrik Eklund pointed out after visiting
Norway in 1878: “In my travels I have found that people are not sufficiently
frightened by the thought of contagion.”457
As contagionism gained momentum, the physicians increasingly saw it as their
task to teach the population that lepers ought to be shunned. But the chronic nature of
the disease made the danger of contagion difficult to convey. Without public fear of
the disease, forcing people into the institutions was almost impossible, as Edward C.
Long noted in a report from Basutoland (now Lesotho) at the beginning of the 20th
century.

It is in one sense unfortunate that leprosy is such a very chronic and in its early stages a non-
disabling, complaint; were it more rapidly fatal the people would soon learn to dread it and
easily co-operate in any means decided upon to stamp it out. As things are at present, any
attempt to stamp out the disease by forcible segregation, would as I have already stated
inevitably lead to concealment.458


Where public fear of the disease was strong, push-strategies were easier to implement.
Sometimes the precautions taken went further than the physician recommended, such
as in New Zealand where the public opinion bordered on lepraphobia. In 1903, Chief
Health Officer J. Malcom Mason reported on a Chinese gold digger who was
diagnosed with the disease. Despite Mason declaring that the man had no erosion in
the surface tissues, and therefore presented little to no danger from a public-health





456
“Naar jeg spurte om de hadde nogen greie paa hvorledes de hadde faat spedalskhet, saa var det jevnlige svar
at ‘de va vel so laga’, eller at Vorherre hadde lagt det paa dem.” Hansen, Gerhard Armauer. Livserindringer og
Betragtninger. 1910: Chapter 5.
457
“Öfverhufvod har jag under min resa funnit, att folk är alldeles för litet uppskråamdt med hänsyn till smitta.”
Eklund 1879: 42.
458
Long, Edward C. “Report to the Colonial Office on an investigation of the prevalence and distribution of
Leprosy in Basutoland.” Lepra Bibliotheca Internationalis. 1905: 234-241, quote on p. 241. Long explicitly
argued that mapping the prevalence of the disease should be combined with spreading knowledge about its
contagiousness, and that this would pave the way for more dramatic measures at a later point in time.
 177

point of view, the local county council put his hut under quarantine. A special box
was set up, where the man could deposit gold, in return for food. “The food is placed
in a box about a quarter of a mile from his hut; the gold is boiled before being handled
by the bank, and in this way all possible source of infection is destroyed. The police
authorities have been asked to keep an eye upon the man to see he does not break
bounds.”459
The specifics of the push-strategies differed from country to country. In Japan,

where leprosy already was connected to family shame, the legislation of 1907
emphasized the responsibilities of the physicians. While a system of state leprosy
hospitals was established, it was made obligatory for physicians to notify the
government of all cases of leprosy, and disinfect and isolate the lepers and their
houses. If the physicians failed to fulfill their duties, they were punished with fines.460
From 1906 the Philippines sent more than a thousand lepers to the island of
Culion every year. Their campaign, too, was built on convincing the population that
leprosy was contagious and that Culion was where the lepers belonged. In 1909,
Director of Health Victor G. Heiser explained the strategy: “it was deemed advisable
to precede the collection of lepers by a campaign of education and thereby secure the
cooperation of the public rather than its opposition.”461 Taking advantage of the
archipelagos’ geography, a team of educators were to tour an island two or more
times, followed by rounding up cases, until the area was considered leprosy-free. Only
then would they move on to the next. “By the method persued, the greatest amount of








459
Mason, J. Malcom. “A case of a Chinese gold digger with leprosy”. Lepra Bibliotheca Internationalis. 1903:
107. This was not exceptional. One year later Mason told the story of a child developing leprosy being moved
200 metres away from the community. The proscription was “not to allow any one to sleep, eat or live with him.
This has been carried out. (…) It will be a blessing when these poor unfortunates are taken by the State and
isolated on some island.” (Mason, Malcom. “Maru Pomare: Leprosy among the Maories. Public Health
statement for New Zealand.” Lepra Bibliotheca Internationalis. 1904: 129.)
460
“Leprosy in Japan, report by the Central Sanitary Bureau of the Home Department in Tokyo, 1907.” Lepra
Bibliotheca Internationalis. 1910: Fasc 2. See also: Ohtani 1998: 49-54; Burns 2012:301-327: Sato, Hijame
and Minoru Narita. “Politics of leprosy segregation in Japan: the emergence, transformation and abolition of the
patient segregation policy”. Social Science & Medicine. Vol. 56. 2003: 2529-2539.
461
Heiser, V. “Leprosy in the Philippine Islands.” Lepra Bibliotheca Internationalis. 1910: 36-39, quote on p.
37. First published in Public Health Report. No. 35, 13. August 1909:
 178

territory was freed in the shortest possible time. In military phraseology, the outposts
were captured first and the lines gradually moved forward to the strongholds.”462
In contrast to what I call the push-strategies, the common denominator for the
various pull-strategies was that they were aimed at attracting lepers through having
something to offer. As Jonathan Hutchinson pointed out in the first issue of the
Journal of the Leprosy Investigation Committee in 1890, preventing contagion was
not the only rationale for establishing leprosy institutions. When Norway built its state
leprosy institutions in the 1850s, Hutchinson stressed, this was motivated by
preventing marriage and thus transmission of disease to future generations. A third
and final justification was offering comfort to the sufferers, providing a home with
food, amelioration and hope of cure through medical treatment.463 In other words:

You did not have to be a contagionist to argue that lepers belonged in an institution.
When the Leprosy Commission to India published their report in 1893, they
concluded that the minimal contagiousness of the disease made compulsory
segregation unjustifiable.464 Instead, the conclusion was that improving the sanitary
conditions alone would reduce the prevalence of leprosy as well as a range of other
diseases. Besides, the prospect of segregating more than 100,000 individuals made
compulsory segregation ‘impracticable’: “Voluntary isolation is, therefore, the only
measure left for consideration.”465 Since leprosy was not considered a major threat to
public health, singling out the disease did not justify colonial spending. Local
authorities were free to build or enlarge leper asylums through municipal funds or
private subscriptions, but in practice philanthropic organizations that justified their
activities by offering care in voluntary institutions would dominate the preventive
measures in the subcontinent. The largest organization was Mission to Lepers,
established in 1873. By 1920, 41 of the 92 leper asylums in India, Burma and Ceylon





462
Op. cit.
463
Hutchinson, Jonathan. “Memoranda for Future Investigations as to the Cause of Leprosy”. Journal of the
Leprosy Investigation Committee. No. 1. 1890: 87.
464
“In no case would the Commissioners suggest an Imperial Act, especially directed against lepers as such, for
these are far less dangerous to a community than insane or syphilitic people.” Leprosy in India, Report of the
Leprosy Commission in India, 1890-91. 1893: 388.
465
Leprosy in India, Report of the Leprosy Commission in India, 1890-91. 1893: 387.
 179

were run by Mission to Lepers alone, and ten more by their aid. The Indian
government and municipalities ran sixteen institutions, and the native states
fourteen.466
In addition to sanitary measures and voluntary segregation, the Leprosy
Commission to India agreed that if local governments wanted to take further action
they could prohibit lepers from occupations where the possibilities for accidental
contagion were greatest, such as serving or preparing food, prostitution, working as
barbers or washing. They could also prevent vagrant lepers from frequenting public
places, to beg, or use public transportation.467 This was made law in The Lepers Act
of 1898. Vagrant lepers that caused public nuisance in urban towns could be forced
into the institutions, but as Shubhada Pandya has pointed out, India had in reality no
colonial containment policy.468 The institutions were voluntary sanctuaries for the
destitute, places where missionaries could spread the gospel, and not tools for
segregation.
In the medical textbooks on tropical diseases and dermatology published after
the Berlin conference, the descriptions of leprosy almost consistently included a
section on segregation. In Tropical Diseases: A Manual of the Diseases of Warm
Climates (1898), Patrick Manson highlighted that “the most effectual way of
suppressing the disease is the thorough isolation of existing lepers.”469 Since the
disease was caused by a bacillus, it was contagious. And since the disease was
incurable, isolation was presented as logical consequence. But faced with the real
world, one needed to be pragmatic. Isolation was the ideal solution, but the practical
difficulties many;

(…) springing from the rights of the individual, finance difficulties, difficulties arising from
concealment or incorrect diagnosis, as well as from the continued introduction of fresh cases





466
The last eleven institutions were labeled ‘unclassified’, which likely meant other philanthropic organizations.
The numbers were compiled by Frank Oldrieve in: The Mission to Lepers. Conference on the Leper Problem.
Calcutta, February 1920. 1920: 151.
467
Leprosy in India, Report of the Leprosy Commission in India, 1890-91. 1893: 4-5; 385-390.
468
Pandya 2003: 151-154.
469
Manson, Patrick. Tropical Diseases. A Manual of the Diseases of Warm Climates. 1898: 417.
 180

from without. These and other obvious obstacles, incident to any attempt at a wholesale
system of thorough isolation are so great that the most that can be hoped for in the present
time, and in the present state of public opinion, is some modified system of segregation and
isolation, such as has worked so successfully in recent years in Norway.470


Reflecting how ‘copying the success of Norway’ was adapted into widely different
strategies, Sir Malcom Morris highlighted in Diseases of the Skin (1911) that “Strict
isolation is the only trustworthy means of checking the spread of leprosy, as is shown
by the experience of Norway.”471 But Morris too stressed that segregation would
benefit to the lepers, since institutionalization provided access to medical
treatments.472 Norman Walker’s An Introduction to Dermatology (1911), on the other
hand, argued that “The careful statistics of the leper department of the Norwegian
Government clearly shows that the number of new cases is directly proportional to the
number of patients at large in a district.”473 According to Walker, the term ‘patients at
large’ did not relate to segregation, but that those suffering from leprosy were put
under a strict sanitary regime. “According to Hansen, the most important thing both
for the patient and the community is to put the patient in as good circumstances as
possible, and to use all measures of personal cleanliness; and the remarkable
diminution in the number of lepers in Norway under this able and vigorous régime is
the very best proof of the value of these means.”474 In later medical textbooks,
segregation was presented as the default, but increasingly contested means of
prevention.475






470
Manson 1898: 418.
471
Morris, Sir Malcom. Diseases of the Skin. An Outline of the Principles and Practice of Dermatology. 5.
edition. Printed in London, New York, Toronto and Melbourne. 1911: 535.
472
“Segregation, if properly carried out, is not only a protection to the community at large, but is greatly to the
advantage of the lepers themselves, who thus enjoy far better treatment than they could otherwise, in the
majority of cases, command.” Morris 1911: 535.
473
Walker, Norman. An introduction to Dermatology. 5. edition. 1911: 290.
474
Walker 1911: 296.
475
“The management of leprosy naturally includes a consideration of the means of prevention. There are still
great differences of opinion as to the necessity of segregation, and each side of the question has much in its
support.” (Stelwagon, Henry W. Treatise on Diseases of the Skin. 7th edition. 1914: 935.); “While segregation
is generally considered the one proven prophylactic measure there are those who question its value.” (Stitt, E.
R. The Diagnostics and Treatment of Tropical Diseases. 3. edition. 1919: 216); “The financial burden of
isolating large numbers of lepers is very heavy. Hence the difficulty of carrying out this very necessary method
 181

The main cause for concern, as Alvarez had argued in Berlin in 1897, was that
compulsory segregation led to the concealment of cases. At the Fifth Livonian
Medical Assembly in Pernau in 1903, physician H. Koppel from Dorpat made the
case that the propaganda presenting lepers as dangerous must be coupled with
promoting the institutions as shelters offering work and fulfilling lives. The leprosaria
must “lose their deterrent character in the eyes of the sick and the healthy.”476 The
same argument was repeated in numerous places around the globe, which suggests
that this was easier said than done. At the sixth international dermatology congress in
New York in 1907, for instance, Walter Remsen Brinckerhoff of Honolulu,
recommended that instead of highlighting that the disease was incurable, the
physicians should emphasize the occasional spontaneous cures, that they actually
could alleviate some of the pain, and that they in some cases managed to keep the
disease at bay.


The popular concept that when a patient once entered a leprosarium, it was to die without
treatment; this caused much prejudice against these institutions. In communities where
leprosy was likely to occur, the people should be informed that proper treatment would
render them more comfortable, even if it will not cure them. In this way only would it be
possible to get control of the cases early in the disease.477


For diseases such as tuberculosis, which also was met with institutionalization of the
sick, you were either cured or dead after a few years. Leprosy, on the other hand,
could last for decades. This led physicians to argue that the institutions should differ
from other kinds of hospitals. In 1898, Memel began building a set of cottages for 12
persons each in order for life in the leprosy institution to resemble life in family units.
The rationale was that “The patients must have room enough to walk about freely and
to play, the more so, as they are not allowed to leave the premises. Large sitting




of protection completely and efficiently.” (Castellani, Aldo and Albert J. Chalmers. Manual of Tropical
Medicine. 3. edition. 1919: 1666.)
476
Koppel. “Über die Beschäftigung der Leprösen in den Leprosorien”. Lepra Bibliotheca Internationalis.
1906: 57, originally published in St. Petersburg Medizinische Wochenschrift. No. 36. 1903.
 182

rooms, gardens and workshops should never be omitted. For if the patients cannot
occupy themselves and so avoid feeling dull, they will never feel at home in the
hospital.”478 Of the three main policy approaches, the pull-strategies were the most
expensive.
More often than not, the responses to leprosy were a mix of push, pull and
restrictions, and emphasis could differ over time. In Estonia the first lepers were
accepted at a new leprosarium in Kuda in December 1896, where admittance was
voluntary. Under the directorship of Arthur Kupffer from 1901, explicitly inspired by
the compulsory elements of the Norwegian model, the policies were reorganized.
From 1902 reforms demanded that if those affected by the disease could not
document necessary facilities for home isolation, the lepers could forcibly be moved
to the institution. The reform culminated in 1905 with regulations deciding whom to
be held accountable if a leper broke the rules for home segregation. This soon led to a
new patient body in the institutions: Instead of attracting almost only incapacitated
cases, a majority of the inmates were relatively healthy and in need of meaningful
activities. The solution – weaving, spinning, sewing and gardening for the women,
and handicrafts for the men – was however acknowledged to be second rate. “From
the lepers’ point of view, the institutions should offer treatments or a cure.”479
As the experiments with various treatments proceeded, increasingly the
promise of treatment was held as the main argument for pull-strategies. As H. Bayon
in South Africa put it in 1914; “Segregation without treatment appears a harsh, if
justifiable measure to take. Once treatment is instituted the leper is not only
segregated for the benefit of others, but in his own interests, because any treatment
that can be suggested must necessarily last a long time and be regularly
administered.”480





477
Brinckerhoff, Walter Remsen. “Proposals for diminishing the diffusion of leprosy”. Sixth International
Dermatological Congress. 1908: 46.
478
Kirchner, Martin. “Lepra in Memel”. Berliner Klinische Worhenschrift. Nr. 2. 1900, as quoted by Kuznitsky
in Lepra Bibliotheca Internationalis. 1901: 52.
479
Kupffer, A. “Die Lepra in Estland.” Lepra Bibliotheca Internationalis. 1914: 26-29.
480
Bayon, H. “On the necessity or advisability of segregation in relation to the conditions and spread of Leprosy
in South Africa at the present time; the measures to be provided for the prevention and cure of Leprosy; and the
 183

A matter for the state


The invitations to the leprosy conferences, and later the requests from the League of
Nations’ Leprosy Commission, asked for the prevalence of leprosy in each country.
More often than not, mapping prevalence was both a goal in itself and a means to an
end. Producing the numbers meant documenting that action was necessary; this was
the necessary first step in asking for measures of prevention to be put in place.
Producing numbers was one of four main strategies for making leprosy a matter for
the state.
Both high and low prevalence were used as arguments for segregation. In
Japan, it was statistics showing that the number of lepers had increased from 23,000
in 1897 to 40,000 in 1905 that led the state to start its anti-leprosy campaign.481 In
Tunisia, director Charles Nicolle at the Pasteur Institute argued that since there were
only about 70 lepers in the colony, it was imperative to take action before the situation
got out of hand.482
Having begun a leprosy-campaign was often used as an argument to expand it.
In the Cape Colony in 1907, fifteen years after the introduction of a Leprosy
Repression Act, Medical Officer A. John Gregory stressed in his annual report that
accommodation at Robben Island (651 inmates) and Emjanya Asylum (473 inmates)
was insufficient. The new cases outnumbered the available accommodation. “Of
course, every Leper segregated is a source of infection removed, but it is open to
question whether it is altogether fair on those Lepers who are compulsory segregated







suitability of Robben Island as a place of detention for Lepers.” Lepra Bibliotheca Internationalis. 1914: 134.
Although increasingly common, this was not a new argument. Already in 1890, Robson Roose argued that
compulsory segregation was to the benefit of the lepers because physicians were the only ones to provide pain
relief: “Compulsory isolation in suitable buildings and under proper care is urgently demanded in the interests
not only of the general community, but of the sufferers themselves. If leprosy cannot be cured, some of the most
distressing symptoms can certainly be alleviated.” (Roose, Robson. Leprosy and its prevention as illustrated by
Norwegian experience. 1890: 96.)
481
“La lèpre au Japon”. Lepra Bibliotheca Internationalis. 1908: Fasc 3, originally published in Bulletin
general de therapeutique. July 15, 1905.
482
Nicole, C. “La lèpre en Tunisie”. Lepra Bibliotheca Internationalis. 1907: Fasc. 2. What Nicole asked for
was two modern leprosaria for the isolation of the sick, and that lepers should be banned from entering the
country.
 184

that their fellows should be allowed at large without restraint.”483 Three years after the
unification of South Africa in 1910 bacteriologist Harry Bayon repeated the
argument: “The whole matter lies in a nutshell: Either we can go on spending the
large sums that are allocated now for the maintenance and segregation of a certain
proportion of the leprous population for an indefinite number of years, or the decision
can be made manfully to grasp the problem, set aside a sufficient sum for the
accommodation of all lepers and get rid of the scourge in ten or fifteen years.”484 The
problem, according to Bayon, was not only that only a proportion of the lepers could
be accommodated, “and the other half or third remaining is quite sufficient to keep
the disease going on for ever”, but that the institutions were deeply disliked by the
lepers who therefore actively avoided detention.
Presenting leprosy as a danger to the healthy population was increasingly
successful. At the first international leprosy conference in Berlin in 1897, 22
governments were represented. In Bergen in 1909, the number had grown to 27. At
the third international leprosy conference in Strasbourg in 1923, 34 governments were
represented. But even more countries had campaigns to prevent leprosy. At the Fifth
International Dermatology Congress in 1904, where following up on actions taken
against leprosy in the past seven years was on top of the agenda, there were reports on
leprosy in 71 countries.485 The second international leprosy conference in Bergen in




483
Gregory, A. John. “Leprosy in Cape Colony for the year 1906.” Lepra Bibliotheca Internationalis, 1906:
226.
484
Bayon. H. “On the necessity or advisability of segregation in relation to the conditions and spread of Leprosy
in South Africa at the present time; the measures to be provided for the prevention and cure of Leprosy; and the
suitability of Robben Island as a place of detention for Lepers.” Report by the Gouvernment Research
Bacteriologist to the Department of the Interior, Robben Island. February, 18, 1913. Lepra Bibliotheca
Internationalis. 1914: 135.
485
In order of appearance: Belgium, Congo, Bulgaria, China, Chile, Egypt, The British Empire (England,
Ireland, Gibraltar, Malta, Cyprus, British India, Bengal, Burma, Mauritius, Seychelles, Ceylon, Federated Malay
States, The Gold Coast, Lagos, Sierra Leone, Nigeria, British Central-Africa, East-Africa and Uganda, Canada,
Bermuda, Jamaica, The Leeward Islands, Antigua, St. Kitts, Barbados, St. Vincent, Dominica, Bahamas,
Grenada, British Guiana, New Zealand), Australia, United States, Cuba, France and colonies (Algeria, Tunisia,
Morocco, Senegal, French Guiana, Madagascar, Reunion, French Antilles, French Guyana, New Caledonia,
Indo-China, Algeria), Holland and colonies (Dutch West-Indies, Dutch East Indies) Iceland, Danish Antilles,
Italy, Montenegro, Norway, Austria, Hungary, Romania, Russia, Sweden, Serbia, Siam, Spain, and Turkey. The
reports included a brief history of leprosy in each country focusing on how and when the
disease was introduced and what measures had been taken to prevent it. In some cases the reports included legal
texts. Further, there were statistics on registered lepers or estimates of concurrent prevalence, and reports on
institutions (number of beds, admissions and discharges, drawings of the premises, management and how the
 185


1909 had reports on leprosy in 89 countries and territories.486 In the opening

statement, Edvard Ehlers and Feliz Verdier stressed that the disease was found on all
continents, in all climates and among all races. What they all had in common was the
leprosy bacillus: Proof that the disease was contagious and that regardless of local
conditions, this was the basis for preventive measures.487
While producing numbers seems to have been a common first step in all
leprosy campaigns, the reports presented at the international conferences reflected
great differences in what to do next. Involving the state seems to have been a common
goal, but the physicians’ did not only disagreed on the necessity of segregation and
what strategies to pursue, their relationship within the various legislative frameworks
also differed. Physicians were seldom the only actors who had a say.488 Furthermore,
the situation on the ground was not the same everywhere, neither when it came to
leprosy prevalence and its relative importance in comparison with other diseases, the
capacity of the health systems and the willingness of governments to single out
leprosy as a target for an intervention. As George Pernet underlined in his presentation
of leprosy in the British Empire in 1904:



Reviewing the foregoing survey, one feature stands out prominently, viz: the enormous mass
of leprosy with which the British have to cope. The magnitude of the task needs no
emphasizing when we consider the number and variety of the native races, the hugeness of
the population, the vastness of the area under the sway of the English.489


Not every country had leprosy campaigns. Following the Berlin conference in 1897,





lepers were kept occupied). Rosenthal, O. V. Internationaler Dermatologen-Kongress abgehalten in Berlin vom
12.-17. September 1904. 1. Band. 1904.
486
Ehlers, E. and Feliz Verdier. “Géographie de la lepre”. Lepra Bibliotheca Internationalis. 1909: Fasc. 4.
487
Op. cit. For a critique arguing that the celebration of Hansen’s discovery the leprosy bacillus overshadowed
clinical findings and the question of what science could do to help those affected by the disease, see: Deycke,
G: “Nachklänge zur zweiten internationalen Leprakonferenz in Bergen”. Medizinische-kritische Blätter in
Hamburg. Bd. 1, Heft 1. 1910: 68-75; reprinted and rebutted by Ehlers in Lepra Bibliotheca Internationalis.
1910: 246-252.
488
For a study highlighting the importance of negotigations between various actors at a local level, see:
Buckingham 2002. For an overview of the organization of public health measures in Britain, United States,
France, Sweden and Germany, see: Porter 2005.
489
Pernet, George. “Leprosy in the British Empire”. V. Internationaler Dermatologen-Kongress. 1905: 62
 186

the Austria-Hungarian minister of Finance and administrator of Bosnia and
Herzegovina, Benjamin von Kállay (Béni Kállay de Nagy-Kálló), first commissioned
physicians Edvard Ehlers and Leopold Glück to write a report on leprosy in Bosnia.
Possibly due to realizing that having the prevalence mapped would trigger demands
for a costly state intervention, when the report was finished in 1900 it was banned
with an explanation that the findings would be bad for tourism.490 As I will return to
in the following chapter, in India the colonial government saw leprosy mainly as a
sanitary problem.
The second line of arguments in involving the state was by pointing at
interventions in other countries. While Norway was highlighted as a success to be
copied, this was by far the only inspiration. During its fifteen years of existence Lepra
Bibliotheca Internationalis (1900-1914) published 86 papers dealing primarily with
the question of prevention, almost a tenth of the total number of articles. This shows
how prevention was an integral part to the medical debate. In addition to numbers
from fact-finding missions both domestically and in the colonies, they included policy
advice, reports from institutions. 39 of the papers were published under the heading
Prophylaxis, Legislatio etc, and provided updates on proposed and passed legislations
around the world, often including the full legal texts.491 The medical journals, as well

as conference proceedings, created a shared reservoir that the readers to turn to in
order to find arguments and examples to use in local debates.
A third prominent line of reasoning was found in Lepra Bibliotheca
Internationalis’ section Historia. This consisted mainly of papers dealing with leprosy
in Medieval Europe and the reasons for its alleged decline. These papers served two
practical purposes: First, they more or less consistently argued that history proved that




490
Glück, Leopold. ”Die Lepra tubero-anaesthetica, vom klinischen Standpunkte geschildert”. Lepra
Bibliotheca Internationalis. 1908: 2.
491
Some examples: New South Wales (Thompson, Ashburton. “Report on leprosy in New South Wales, for the
year 1897.” Lepra Bibliotheca Internationlis. 1900: Fasc 1); Denmark (Ehlers, Edvard. “Législation danoise
contra la lèpre. Ordonnances Royales du 17. Janvier 1908, visant la lèpre aux Antilles danoises”. Lepra
Bibliotheca Internationalis. 1908 : 208.); Japan (Central Sanitary Bureau of the Home Department in Japan.
“Leprosy in Japan. (Tokyo, 1907)”. Lepra Bibliotheca Internationalis. 1910: Fasc. 2); Indochina (“Arrèté
concernant la prophylaxie de la lèpre en Indochine.” Lepra Bibliotheca Internationalis. 1910: Fasc. 3,
 187

segregation worked. While leprosy never completely disappeared from Europe,
consensus was that the prevalence had dropped dramatically. Most authors withheld
that this was due to segregation. Second, by emphasizing the worst-case scenarios,
concurrent segregation became less cruel in comparison.492
History was also used as an argument in several of the papers published in the

section for Geographia, which not only outlined the concurrent situation in the given
geographical area, but often explained how the current situation had developed. The
explanations often included legal measures taken, and what practical consequences
these had led to (if any). If leprosy was increasing, the standard explanation was in the
preventive measures. Either no policies were put in place, the enforcement was not
sufficiently strict, or strict policies without sufficient resources had led to
concealment.
Forth and finally, the institutional reports published under the heading
Annuaria Leprosarium explicitly discussed the steps taken in order to found specific
institutions, cost per inmate, rules and regulations and what the institution was meant
to achieve. While not included in my enumeration above, these reports also provided
relevant examples for those arguing that erecting special institutions was a
cornerstone in the prevention of leprosy. Institutions needed to be financed, and more
often than not the implicit argument was that this was a matter for the state.





Burnet’s compromise


The dominant stance until the 1920s was prevention through segregation, and the





originally published in Bulletin De la société de pathologique Exotique. 1910); Australia (“Commonwealth of
Australia – Law as to leprosy.” Lepra Bibliotheca Internationalis. 1910: Fasc. 3.)
492
Medievalist Carole Rawcliffe has convincingly argued that this narrative of medieval ‘lepers’ being excluded
and forced into isolation at the edges of society was based on willful misreading dating from the 19th century. In
Britain, at least, leprosaria had more in common with monasteries than tools of segregation. The closing of
‘leper houses’ had more to do with social and economic factors than the disease disappearing. Rawcliffe,
Carole. Leprosy in Medieval England. 2006. Rawcliffe’s interpretation of Medieval England differs
dramatically from what the physicians I have investigated took to be true, but pursing this argument further
would go beyond the scope of this thesis.
 188

conference in Strasbourg in 1923 still advocated isolation, banning lepers from certain
trades and removing children of lepers from their parents. Still, the era of push-
strategies was coming to an end. For the first time the recommendations stressed that
“isolation should be humane and allow the leper to be near his family if this is
compatible with efficacious treatment.”493 Every country needed an anti-leprosy
campaign, but this should be designed according to the circumstances in each country.
For those attending the Strasbourg conference, the lessons were clear: Segregation
was a necessary evil that should be restricted as far as possibly. Too much emphasis
on persecution and the detection of new cases would suffer. Emphasis was shifting
from push to pull.

According to Etienne Burnet, secretary of the League of Nations Leprosy
Commission, the conference constituted a watershed in that the consensus for the first
time was not only that people suffering from the disease had a duty to go into
isolation, but that society had obligations in return:


By that time society had recognized not only its right to defend itself against leprosy but also
its duties towards lepers; since it deprived them of a normal existence it realized the
obligation to make their life bearable by providing them with human surroundings, hygienic
conditions, amusement and occupation, as well as at least a hope of cure.494

As I showed in the previous chapter, Burnet saw the hope of a cure in chaulmoogra
derivatives, directly inspired by BELRA and the Calcutta-school. This was
controversial: As I will show in Chapter 7, most members of the Leagues’ Leprosy
Commission thought the efficacy of chaulmoogra was overrated and maintained
segregation as the best and only prevention. The conclusions reached at the
Strasbourg conference was thus more a reflection of the list of attendees more than a
dramatic shift in policies everywhere. When Burnet traveled to Europe, Latin America




493
Resolutions and recommendations from the Third International Conference on Leprosy, Strasbourg 1923.
See: Appendix 2.
494
Burnet, Et. Provisional Report presented to the Leprosy Commission at its meeting at Tokyo in April 1930.
Part III: General Conditions of Prophylaxis. (League of Nations Health Organisation. C. H./Leprosy/7b) 1930:
2
 189

and the Far East at the end of the 1920s, he found the world divided in two camps:



(…) the question of segregation still remains a subject of controversy between advocates of
freedom on the one hand, and of coercion on the other. The results of the enquiry, which
included the consultation of a large number of leprologists, show that any meeting of experts
would be divided into two camps; those who may be described – by analogy with another
problem of social hygiene – as partisans of abolition and those who are in favour of
regulation. The concessions which those two schools are obliged to make in the course of
practical work prove that they have some common ground and justify the hope that they
would come to an agreement upon a programme of work.495


Before arriving at Burnet’s compromise between the two schools of thought that in

1931 would herald a new strategy for prevention, I will explain the line of reasoning
that made up BELRA’s challenge to the segregationist strategy for prevention.
The confidence in the efficacy of early treatments was the first of three
distinguishing features of BELRA’s approach to leprosy prevention. The second was
building on the argument that push-strategies, while ideal in practice, led to the
concealment of cases.496 The vital novelty, however, was the emphasis on the
circumstances under which leprosy appeared. The problem was not the individuals
suffering from the disease, but the conditions under which leprosy appeared. As
Ernest Muir put it in the leaflet Leprosy: Diagnosis, Treatment and Prevention (1924):

It is necessary by propaganda, by teaching the medical profession and through them the rest
of the people and by co-operation with educational authorities to familiarize every one with
the signs and dangers of the disease till every one learns to abhor not the leper but leprosy
and the conditions under which it is likely to spread.497









495
Burnet, Et. ”Report on the Programme of work of the Leprosy Commission.” C.H.887 (a); LNHO:
8A/16680/6714. Dated Geneva, August 20, 1930: 1-2.
496
“The ideal method of prevention would be the hindering of all contact. This was attempted on an extensive
and expensive scale in the Philippine Islands and proved a failure as a means of stamping out the disease.”
Muir, E. Leprosy. Diagnosis, Treatment and Prevention. Illustrated. 1924: 28.
497
Muir 1924: 28-29.
 190

Like with all arguments for prevention, the starting point for the argument was the
etiology of the disease. Muir did not contest that leprosy was contagious, but stressed
that much was still unknown about the exact means of transmission. For some the
uncertainty led to carelessness, for others an irrational and overblown fear of
contagion. Both were equally detrimental to a leprosy campaign as they got in the way
of early diagnosis and treatment, either due to ignoring the early symptoms of the
disease or people hiding their disease to avoid detention.
According to Muir, six factors determined the transmission of the disease: 1)
The infectivity of the disease transmitter (“The larger the number of lepra bacilli in
the body the more there are to propagate the disease; and the nearer they are to the
surface of the body the more likely are they to be carried to other people.”); 2) The
closeness of contact (”the disease is most commonly communicated where people live
under insanitary conditions, crowding together in small dwellings, using the same
eating and cooking vessels, and even promiscuously using the same clothes”); 3) The
length of contact (“The longer the period of contact the greater the danger of
infection); 4) Health of the person exposed to infection. (“This is very important as on
it to a large extent depends the resisting power of those who are exposed to
infection”); 5) Immunity (“The effect of lack of immunity has been repeatedly seen
where leprosy has suddenly been introduced into an island or other isolated area
where it had not existed for many generations, with the result that the disease has
spread rapidly and in a virulent form”); and 6) general sanitary conditions (“The
better these are the less the danger of infection”).498 Undoubtedly shaped by having

the main seat in India where the sanitary approach had de facto dominated for more
than half a century, the hallmark of BELRA’s leprosy approach was that prevention
no longer was just a question of leper versus healthy; the conditions of society as a
whole must be part of the equation.
Initially, BELRA was not directly opposed to segregation. Around the time of

Muir’s leaflet, they sent a questionnaire through the British Foreign, Colonial and





498
Muir 1924: 26-28.
 191

India offices asking for information regarding leprosy. The returns found that
segregation had “had a very good effect in reducing the lepers where it has been
carried out for some time, while where neglected the known lepers had greatly
increased.”499 On the other hand: Not every country was ready for compulsory
segregation. Especially in central Africa, “any attempt to enforce such a law would
result in hopeless failure due to hiding of cases, quite apart from the greater urgency
of devoting most of the available medical grants to combating more important
diseases, such as sleeping sickness, syphilis and yaws.”500 There, voluntary isolation
was the only possible solution, “as any drastic measures leading to extensive hiding of
early cases are likely to do more harm than good.”501 Throughout the 1920s, however,
the head of the organization, Leonard Rogers, would be increasingly confident in the
efficacy of early treatment with chaulmoogra and in 1930 he argued that segregation
should be abandoned altogether.502
According to BELRA, prevention should no longer take individual lepers as
carriers of a contagious disease as its starting point. Furthermore, improving the
sanitary surroundings was important, but alone not sufficient. Instead emphasis
should be on identifying early and potential cases in communities where the disease
was already present. BELRA’s mechanism to achieve this was the dispensary;
outpatient clinics. The dispensary had three main goals. First, they should spread
information about the disease, especially the message that a cure was possible if
treatment started early enough. Second, they should offer voluntary treatment
(chaulmoogra). Third, the patients under treatment should be convinced to bring
family and friends and have them examined for the presence of the bacillus.
According to BELRA the disease was most infectious before clinical signs appeared,
but this was also the stage in which the disease was easiest to cure. “Effective




499
Rogers, Leonard. “Memorandum on the prevalence of and prophylaxis against leprosy in the British Empire,
based on replies to the questionnaire of the British Empire Leprosy Relief Association; with suggestions for
dealing with the problem.” (LNHO: 12B/42641/29272). 1925: 3.
500
Rogers 1925: 5.
501
Rogers 1925: 21.
 192

treatment in the earliest stage of the disease is thus the key to present day
prophylaxis.”503
In a Foucault-inspired study of medical knowledge in Britain, David
Armstrong has argued that the dispensary represented a new way of observing illness.
While the clinic saw disease as situated within individual bodies, the dispensary
identified disease in the spaces between people, that is, disease in society.504 Through
the dispensary the medical gaze shifted its attention from observing people with
disease to looking for the potentially ill, the healthy and the normal. Armstrong’s
observations fit well with BELRA's vision for the dispensaries in the 1920s: Through
early intervention was it possible to stop leprosy through identifying potential victims,
which could only be achieved in close collaboration with the local population.
Faced with the arguments from BELRA on the one hand, and segregationists
both in the Leprosy Commission and in leprosaria around the world on the other hand,
Burnet presented a compromise: Instead of seeing the two approaches as competing,
they must be understood as complimentary. The problem with the dispensaries was
that they did not provide necessary means to remove infection from the community;
the problem with the institutions was that they did not reach the communities in the
first place. Therefore, while neither leprosaria nor dispensaries were sufficient alone,
both institutions were necessary.

Formerly, the whole prophylaxis of leprosy consisted in segregation in leprosaria; to-day,
however, some are opposed to this segregation. It is best to avoid both extremes and
recognize that while leprosaria are still necessary they are not sufficient in themselves. (…)




502
See i.e. Rogers letter to the Bangkok conference on leprosy in December 1930, referenced in: “Extract from
the Report by the Medical Director to the Health Committee. Seventeenth Session, May 4-8, 1931.” (LNHO:
8A/30632/29090). 1931: 17.
503
Rogers 1925: 20.
504
“The clinical gaze within the hospital had outlined and sustained the passive and discrete body by localizing
illness within it. In a similar fashin the Dispensary gaze established the reality of the social by identifying
diseases of social spaces, of contacts and of relationship. Thus, as the social basis of the disease justified the
Dispensary as the appropriate mechanism to combat it, so too the Dispensary established, by its deployment in
the community, the social origins and character of the new health dangers.” (Armstrong, David. Political
anatomy of the body. Medical knowledge in Britain in the twentieth century. 1983: 7-13, quote on p. 11.)
Armstrong traces the dispensaries back to a tuberculosis dispensary in Edinburgh, which opened in 1887,
 193

At the present time, the dispensary (…) is an integral part of the ideal anti-leprosy
organization and is no less necessary than the colony; but of it also we can say, as of the
colony, that, though necessary, it is not sufficient in itself.505


The model Burnet envisioned was institutions for isolation of contagious cases, and
dispensaries to act as intermediates between leprosy institutions and the public. The
dispensaries were not just to be charged with distributing treatments, but with
constant monitoring of the the society to identify early and potential cases.


“The real object of permanent supervision of social conditions is to keep an eye on the large
number of relations and neighbours of lepers who are contacts and suspected cases, and are
as important from the point of view of theoretical study as from that of prophylaxis. Cases
found among such persons are at the same time the most difficult to diagnose and the easiest
to cure.”506

Burnet’s compromise was discussed at the Leprosy Commission’s meeting in
Bangkok in December 1930 and at the extended conference in Manila a month later.
In addition to deciding that the term “segregation” should be replaced by
“isolation”,507 the conclusion was that the preventive measures must depend on the
particularities of each country with respect to the number of cases, popular beliefs
about the disease, and the strength of the health systems. Third, the committee agreed,
isolation alone was “not sufficient as a prophylactic measure, but must be
supplemented by epidemiological control, treatment and education for patients and
public alike.”508 In other words, the goal of eradicating leprosy remained, but the
repertoire of prevention had to be expanded.





followed by a Central Fund for the Promotion of the Dispensaries System which started operating tuberculosis
dispensaries in London in 1911.
505
Burnet, Et. Provisional Report presented to the Leprosy Commission at its meeting at Tokyo in April 1930.
Part III: General Conditions of Prophylaxis. (League of Nations Health Organisation. C. H./Leprosy/7b) 1930:
1- 4.
506
Burnet 1930: 5.
507
The winning argument was that the term “segregation” had historical connotations a final destination, and
that this was part of the reason why lepers hid their disease as long as possible.
508
Extract from the Report by the Medical Director to the Health Committee, 17. Session, May 4-8 1931: 11.
(LNHO: 8A/R5930/30632).
 194

The debate resulted in the widely distributed first general report of the League
of Nations’ Leprosy Commission, The Principles of the Prophylaxis of Leprosy
(1931), which heralded a the new global consensus on prevention. The report
embraced treatment, propaganda, separating children from leprous parents,
quarantine, and sanitary measures alike. While the report included new standards for a
globally unified terminology of diagnosis, recordkeeping and epidemiological
examinations, ironically the premise for the conclusion on prevention was that
preventive measures must differ from place to place:


1. Prophylaxis of leprosy is not a problem that admits of solution by the syndication of any one
measure, since the means of dealing with it obviously vary with geographical, economic,
administrative, financial and social conditions and with the incidence of the disease.
2. There is no reliable system of prophylaxis without treatment, and it is generally accepted
that the earlier the treatment is instituted the better will be the results.
3. Leprosy resembles tuberculosis in being, in certain stages, a contagious but curable disease:
curable at least in the sense that bacteriological examination becomes negative and other
active signs disappear and remain absent permanently or for an undetermined period.
4. The prophylaxis of leprosy may be achieved by a system of medical, educative and
legislative measures. It should provide for the isolation and treatment of infectious lepers,
and particularly for the treatment of early cases in clinics and dispensaries: also for the
periodical examination of suspects. Special measures should be adopted for dealing with the
children of lepers and for patients who have recovered either after treatment or
spontaneously.
5. It is desirable that each country where leprosy exists to an important degree should have at
least one centre for the study of the disease, with research laboratories and special courses
for the medical profession and their assistants. Where this is not practicable, men should be
sent to some foreign centre for training.
6. Arrangements should be made to include instruction in leprosy in the curriculum of all
medical schools and colleges.
7. It is necessary to educate the public in regard to leprosy by modern methods of popular
teaching and propaganda.
8. Isolation of infectious lepers is a necessary measure in a comprehensive campaign against
leprosy, but it cannot be regarded per se as the sole means of prophylaxis. Its drawbacks can
 195

be mitigated by other measures applied concurrently. Isolation should be applied only to
cases that are considered infectious.
9. Any form of treatment in order to give satisfactory results requires to be combined with
suitable dietic and general hygienic conditions.
10. For special treatment, oils of the chaulmoogra group and their esters and soaps are
recommended.
11. The system of prophylaxis must be animated by the spirit of preventive medicine and social
hygiene.509




Conclusion


There never were any uniform preventive measures against leprosy, but some trends
dominated. Before the 1890s, debates on prevention were integral to debates between
competing disease models. The attendees at the first international leprosy conference
in Berlin in 1897 concluded that the disease was caused by a bacillus, that the disease
was therefore contagious, that every leper was a danger to his surroundings and that
the policies in Norway should be mimicked. After this, segregation through push-
strategies dominated. The goal was to force the lepers into isolation through
legislation and educating the population that lepers were dangerous. Less dominant,
but locally equally important, were pull-strategies aimed at making the lepers seek
voluntary confinement, as well as the practice of restricting the lepers from certain
vocations. The rise of contagionism also led to leprosy being included in quarantine
regulations constructed to deal with other diseases, but this proved difficult in
practice. Quarantine measures along the lines of what Reverend James C. Richmond
advocated in 1852 were never uniformly adapted.
The recommendations from the leprosy conferences were never compulsory,
but the reports in medical journals and at conferences indicate that having an
‘international consensus’ to refer to, as well as successes of leprosy campaigns in





509
The League of Nations Health Organisation. The Principles of the Prophylaxis of Leprosy. First General
Report of the Leprosy Commission. Geneva, April 1931: 9-10.
 196

other countries, were strong arguments in various settings. On the other hand, the
interpretation of the recommendations differed greatly. Even in medical textbooks,
Norway was withheld as advocating a ‘limited’ approach by one author; as an
argument for compulsory segregation by another.
In the early 1930s, the League of Nations’ Leprosy Commission agreed on a
new and universally applicable set of recommendations for prevention. This was a
compromise between segregation and voluntarism, and introduced dispensaries as
intermediates between institutions and the public. Their role was to provide both
treatments and permanent epidemiological control in order to detect new cases before
they reached an infective stage. As the discussions on standardization in terminology,
classifications and recordkeeping started to bear fruits, the League’s prime
recommendation when it came to prevention was to expand the repertoire of
preventive measures and tailor an approach suited to the local conditions.
The challenge to compulsory segregation originated in colonial India, where
segregation was never carried out and sanitary concerns remained part of the etiology
of the disease. Researchers organized in BELRA questioned both the premise that the
disease was highly contagious, that there were no cure, and that segregation was the
best means to remove contagion from society.
In the following chapter I will investigate hvow the theory of contagion was
introduced to the medical debates in between the 1860s and the 1890s, focusing on
Norway and India. Before this period, leprosy was understood to be due to a
combination of hereditary and sanitary conditions in both areas. I will open with a
visit to Bergen by the British physician Henry Vandyke Carter. The visit made him
convinced that the disease was contagious, and his report was the first to mention the
leprosy bacillus in print. Still, convincing others proved difficult: India and Norway
would represent two extremes in the debates on etiology, and how reports on leprosy
from other parts of the world were appropriated differed greatly.
The next chapter also marks a shift in the perspective. Instead of focusing on
the content of the debates and how this changed over time, in the following three
chapters my emphasis will be on science as communication; communication that
 197

needed to be organized. Each chapter will also be limited to shorter periods of time,
which will allow me to go more into detail.
 198

 199



5. Appropriating contagion


“Is Leprosy the same Disease in Western India and in Norway?”510 This was the first
question to be answered by surgeon-major Henry Vandyke Carter, who visited
Norway on behalf of the Secretary of State of India in the fall of 1873 “for the
purpose of studying the character, prevalence, and state-treatment of ‘Leprosy’.”511
Explicitly arguing that leprosy (Spedalskhed) in Norway was the same disease as True
or Black Leprosy (RăktăpƱti) in India was crucial to making Carter’s experiences
relevant back home.512
What Carter found in Norway was a system of leprosy institutions, including
three state asylums and a research hospital. He was also told about the network of
district physicians who since 1856 had been charged with annual registration of every
individual leper living in their area. Carter’s use of the term “the Enlightened
Kingdom” summarizes his impressions.513 During his visit, Carter also met with
Gerhard Armauer Hansen, at the time an assistant physician working at the
Lungegaarden research hospital. Hansen was increasingly convinced that the disease
was contagious. In addition to being introduced to Hansen’s line of reasoning, Carter
was the first foreign visitor to be shown the microscopy that could “point to the
parasitic origin of the disease.”514
In the early 1870s, the dominant understanding of the etiology of leprosy in
both India and Norway was that the disease was caused by a combination of
hereditary and external factors, such as climate and hygiene. The meeting with
Hansen made Carter change from seeing leprosy as an inherited ‘taint’ to seeing it as a
contagious disease. Hansen would remain Carter’s main contact in Norway for almost




510
Carter, Henry Vandyke. Report on Leprosy and Leper-Asylums in Norway; with references to India. 1874: 7
511
Letter from Carter to the Secretary of State for India, dated London November 24, 1873. In: Carter 1874:
A2.
512
Carter 1874: 6-7.
513
Carter’s report is used as the main contemporary source on Norwegian leprosy control in Zachary Gussow’s
influential book Leprosy, Racism and Public Health (1989), and Gussow borrowed the term “The Enlightened
Kingdom” for the title of the chapter on Norway. Later studies in Norway have shown the picture to be a lot
more nuanced, see: Andresen 2004, Vollset 2005, Hammerborg 2009.
 200


two decades, and in several publications Carter argued that India should take its cue
from the Norwegians. But how was the notion of leprosy being contagious
appropriated in these two vastly different contexts? How did the lessons from Bergen
influence discussions in Bombay and vice versa? And what was the role of the leprosy
bacillus in these discussions?
This chapter is about appropriation. Despite leprosy being put on the agenda in
numerous locations around the world, and researchers mainly of Western origin
throughout the world communicated and exchanged knowledge, I will show how the
same events and reports could be interpreted very differently. Knowledge from other
places was read in light of local context and previous experience. This meant that the
importance and potential impact of knowledge produced elsewhere could differ
dramatically. Competing disease models had different standards for what was
considered relevant observations, and both conditions on the ground and political
circumstance influenced how knowledge produced elsewhere was adopted. Secondly,
I will show that the act of producing knowledge was also active and selective. Not
every local event was reported elsewhere.
The chapter will start with Carter’s visit to Norway. What did Carter report
home, and how did his arguments for contagion play out in the context of the British
colony? Then, I will investigate the discussions on etiology that took place in Norway
and in the British Empire, and show that while there were clear parallels between
them, the political configurations, context and outcomes of the debates differed
greatly. Next, I will investigate the event that came to have wide and global
consequences: The discovery of the leprosy bacillus. My emphasis will not be the
genesis of the bacillus, but rather how it came into play in the medical and political
debates. To some, the bacillus was seen as proof that leprosy was the same disease all
over the world, but this was but one of a wide range of responses. The importance of
the bacillus, I will argue, was that it became a common frame of reference for those
arguing for contagion, proof that the disease was the same regardless of location, an





514
Carter 1874: 27.
 201

impetus for collaboration and circulation of knowledge.





Before leaving India


Henry Vandyke Carter qualified in medicine at St. George’s Hospital in London in

1852, and received his doctoral degree from the University of London in 1856. He
worked as demonstrator in anatomy, and collaborated with Henry Grey on producing
drawings for the influential textbook Anatomy: Medical and Surgical (1858).515 The
year Grey’s Anatomy was first published, in the immediate aftermath of the Indian
uprising, Carter moved to India and joined the Indian Medical Service. He would be
working in India for the next three decades, the first five years as acting professor of
anatomy and physiology at Grant Medical College in Bombay, and later with positions
as a surgeon at several hospitals.516
In the British Empire leprosy was put on the political agenda in the early
1860s after alarming reports on the spread of the disease from the Governor of the
British Windward Islands based in Barbados. The Colonial Secretary responded by
asking the Royal College of Physicians to find out whether or not leprosy constituted
a threat to the Empire. Based on returns from a questionnaire that the Colonial Office
circulated around the Empire, the Report on Leprosy (1867) concluded that leprosy
was ‘essentially a constitutional disorder’ best tackled by improving the health, diet
and living conditions of the native populations. Similar improvements, the report
argued, were what had caused the decline of leprosy in medieval Europe. The report
maintained that the disease was mainly hereditary, always non-contagious, and most




515
The lasting success of the textbook can be illustrated by its numerous editions. In 1883, Grey’s Anatomy was
printed in its tenth edition; by 1901 five more editions had been made. The 40th edition was published as a
celebration of the book’s 150 year anniversary in 2008. For a study of the context in which the book was
created, the people involved and the reception, see: Richardson, Ruth. The Making of Mr. Gray’s Anatomy.
Bodies, Books, Fortune, Fame. 2008.
516
Roberts, Shirley. “Henry Gray and Henry Vandyke Carter: creators of a famous textbook”. Journal of
Medical Biography. Vol. 8. 2000: 206-212; “Henry Vandyke Carter (1831-1897)”. List of the Carter papers in
the Wellcome Institute Institute for the History of Medicine. Online: http:
//library.wellcome.ac.uk/assets/wtl040084.pdf . His obituary was printed in The British Medical Journal, May
15, 1897: 1256-1257.
 202

importantly – it posed no risk to European colonialism.517 This led the Colonial
Secretary to issue a decree that “any laws affecting the personal liberty of lepers ought
to be repealed, [and] any action of the Executive Authority not enjoined by the law,
ought to cease.”518
Behind the decree was an acknowledgement that there were local differences
in how leprosy was approached in the Empire. Obviously, the disease must in some
places already have been considered a legal matter, but top colonial management
desired common standards based on the best scientific knowledge available. Despite
reports from the colonies to the colonial administration in London pointing in the
direction of contagion being the cause of the disease, the College of Physicians would
consistently defend the 1867-report. An often repeated phrase was that other reports
lacked “sufficient precision to be regarded as furnishing evidence in proof, or in
disproof, of the contagiousness of leprosy”.519

The worrying reports also reached Bombay Presidency where Carter worked,
and in 1867 the presidency Sanitary Commission launched its own leprosy census.
But when the Royal College of Physician’s report arrived and called off the alarm,
writing a report was no longer considered a priority. The returns gathered dust for
about three years until Carter, not interested in private practice and with time on his
hands, offered to analyze them. The returns contained data on almost 8.000
individuals suffering from the disease, 5.309 of them named, registered in ten (of
sixteen) districts in Bombay Presidency. This was “a number equal to 1 affected in
600 of the population”.520 Carter’s 170-page publication was structured on the 1867

report from the Royal College of Physicians, and first published in Transactions of






517
Edmond 2006: 51-60.
518
Report on Leprosy of the Royal College of Physicians Prepared for Her Majesty’s Secretary of State for the
Colonies, London, Her Majesty’s Stationary Office, 1867: vi. Quoted in: Pandya 2001: 41-42.
519
“Recent Official Correspondence relating to Leprosy. Communicated to the Editor”. British and Foreign
Medico-Chirurgical Review. 1874: 204-212, quote on p. 205. The correspondence, it seems, was initiated by
the Secretary of State for the Colonies, the Earl of Kimberley, asking the College of Physicians for their
comments on reports from the colonies.
520
Carter, H. V. “The Pathology of Leprosy; with a Note on the Segregation of Lepers in India.” Medico-
Chirurgical Transactions. Vol. 56. 1873: 277. Before this, Carter had been among the physicians who had
answered the questioner by the Royal College of Physicians.
 203


the Medical and Physical Society of Bombay in 1871.521 In it Carter argued that
leprosy was caused by a hereditary ‘taint’, but rejected the competing sanitary notion
that leprosy in India was caused by filth and lack of hygiene.522
Two years later, Carter published a paper on the pathology leprosy, repeating
that “heredity is the common cause of the complaint”.523 More importantly, however,
he now argued that leprosy could (and should) be controlled through state
intervention: There was no evidence to support the claim that the disease was in a
natural decline, and therefore practical measures were needed. These should consist
of strict segregation of indigenous lepers, moving them “to a central, cool, and
healthy locality” and – should a treatment be found – the erection of special leprosy
hospitals. The argument was backed by referring to the decline of the disease in
medieval Europe, an ongoing debate where Carter sided with those who believed it
was segregation, and not changes in diet and living conditions, that had led to the
decline of the disease: “Nowhere in the East does there appear ever to have existed
such a machinery; and there the disease is probably as rife as ever, and certainly
rendered more inveterate by this tolerance for centuries.”524 Segregation would make
the healthy shun the lepers, prevent marriage, and thus keep the disease in check;
“relieving burdened poor, and removing from sight a wretched class of
mendicants”.525 This was in direct opposition to the official ‘hands off’-doctrine
spelled out in the 1867 report by the Royal College of Physicians.
These publications were the immediate precursors when Carter in July 1873

received permission from the Secretary of State for India in Council “to proceed, at








521
Edmond 2006: 58; Pandya 2001: Chapter 4; Pandya, Shubhada. “Nineteenth Century Indian Leper Censuses
and the Doctors”. International Journal of Leprosy. Vol. 72, No. 3. 2004: 306-316. Leprosy was also part of
the nation-wide censuses of 1871/72, 1881 and 1891. See also: Kakar 1996: 215-230; Robertson, Jo. “Leprosy
and the elusive M. leprae: colonial and imperial medical exchanges in the nineteenth century.” História,
Ciências, Saúde-Manguinhos. vol.10, suppl.1. 2003: 13-40.
522
Pandya 2004: 311.
523
Carter, H. V. “The Pathology of Leprosy; with a Note on the Segregation of Lepers in India.” Medico-
Chirurgical Transactions. Vol. 56. 1873: 276.
524
Carter 1873: 280.
525
Op. cit.
 204

the expense of Government, to Norway for the purpose of obtaining all available
information on the subject of the disease.”526





Reporting home; falling from grace


Carter spent two months in Norway in the fall of 1873. There he found five leper
asylums with almost 900 beds, two of them in Bergen alongside
Lungegaardshospitalet, a specialized research hospital dedicated to clinical studies
and finding a cure for the disease. As Carter enthusiastically summarized; “The
hospital is thoroughly provided with all the matériel necessary for every variety of
curative procedure, and for all kinds of scientific research. The supply of drugs is
unrestricted, and the library and laboratory are freely maintained by Government in an
efficient manner”.527 In an appendix Carter included translations of the decrees to
establish the state institutions, the official regulations, including instructions for the
various positions, information on diet, and images and floor plans of the Leper-
Asylum in Bergen, suggesting that this should be copied in India.

In addition to the institutions, the Norwegian leprosy campaign consisted of a
system of compulsory notification of every known leper in the country, dating back to
1856.528 Fascinated, Carter had the official circulars with instructions on establishing
the system translated, including the tables used for the registration. The lists asked for
full names, residence, birthplace, sex, profession (“Condition or Station in Life”), age,
marital position (including whether the spouse was a leper or non-leprous), family
relations with other lepers, number of children and their ages (leprous/not leprous),
the duration and form of the disease (tubercular/anesthetic/mixed), and a section for
“Remarks, chiefly with reference to possible Causative Influences, such as Mode of




526
Letter from M. E. Grant Duff to H. Vandyke Carter, dated India Office July 11, 1873. In: Carter 1874: A2.
527
Carter 1874: 13. Also quoted in: Gussow 1989: 72. The travel to Norway would also result in the publication
Reports on Leprosy, Second Series, Comprising Notices of the Disease as it Now Exists in North Italy, the
Greek Archipelago, Palestine and Parts of the Bombay Presidency of India. (1876).
528
For details on the different projects that together resulted in what historian Morten Hammerborg has aptly
termed ‘the Norwegian leprosy apparatus’, see: Hammerborg 2009: Chapter 2.
 205

Life, Locality or Residence &c; and as concerns the Married, the Duration of

Wedlock”. Again, the argument was that the same information should be gathered in

India.


Based on these individual registrations, the annually updated statistics

documented that in Norway the prevalence of the disease was in decline. With no cure
available, this meant only one thing: The reduction of new cases was caused by the
institutions. For Carter, the main lesson from Norway was confirming the necessity
for prolonged state intervention: Building institutions and educating the population
that this was where the ‘lepers’ belonged.


It may be sufficient to state, amongst other valid reasons for the interposition of
Government, that the malady under notice is an altogether peculiar one in severity and
extent, and claims special consideration; that British rule in India would benefit itself and
subjects by an intervention to be recommended on grounds of both policy and humanity;
that delay is to be deprecated, and that the present time is well suited for enlisting the co-
operation of the people, who are tolerant only from an ignorance which it is our duty to
dispel by open, deliberate and rationally-founded action.529

The appendix also included two translated reports by district physicians on the habits
and diet of Norwegian peasantry in leprous and non-leprous districts. This was proof,
Carter argued, that cultural or sanitary conditions had no impact on the disease, and a
confirmation of what he believed before going.530 Regarding the etiology of the
disease, however, Carter was no longer convinced that heredity alone was an adequate
explanation: “the more promising inquiry would be that of its origin from a
combination or succession of influences which separately could not produce the
affection.”531 While pointing out that the Norwegian institutions originally were
erected to segregate the sexes and avoid leprosy being passed on to the offspring, he




529
Carter 1874: 29-30
530
Historian Shubana Pandya has argued that also the nation-wide leper censuses in India in 1871/72, 1881 and
1891 were used to support whatever preexisting set of believes the investigators had regarding the disease: “The
efforts to clarify the etiology and estimate the virulence of the disease in India by means of statistics were
animated by the desire to justify and embellish preconceptions.” (Pandya 2004: 315.)
531
Carter 1874: 27.
 206

also argued “that even a suspicion of leprosy being contagious is an item in favour of
the segregation of lepers.”532
Connecting the Norwegian experiences to India, the report included a
translation from the Indian weekly newspaper Loka Mitra (published in Karanese in
south central India in July 1870) on leprosy research in Norway, which indicates that
Carter was not the first in India to look to Norway for advice on the disease. Finally,
Carter included excerpts from proceedings and official documents in Western India
regarding the disease – an implicit argument that state institutions would be a natural
continuation of the policies already in place.533

While Carter swung both ways on the question of contagion or heredity in his
report from Norway, historian Rod Edmond has argued that in Carter’s monograph
On Leprosy and Elephantiasis, which was published only a few months later, the
transition was clear:


The very layout of this work demonstrated the recent conversion to contagion that Carter
had undergone. Thus, while the text maintained that ‘heredity is the common cause of the
complaint’, a series of long footnotes add that his recent acquaintance with investigations in
Bergen has led him to believe that the contagion case is ‘tolerably definite’.534


After returning to India, Carter would continue his studies on leprosy, both through
statistics and post mortems. Within a few years he would argue that the disease was
decisively contagious.535
Carter’s reports were but some of many studies carried out in order to decide if


leprosy was a threat to the British Empire.536 Among the physicians who held Carter’s




532
Carter 1874: 26. Italics in the original.
533
Carter 1874: 31-68.
534
Edmond 2006: 68-69. See also: Pandya 2001: 64-66.
535
In 1875 alone Carter conducted fifteen post-mortem dissections of lepers in Bombay. Carter, H. V.
“Memorandum on leprous nerve disease”. Transactions of the Pathological Society of London. 1877: 1-4. For
the arguments for contagion, based mostly on aggregated data, see. Carter, H. V. Modern Indian leprosy.
Bombay. 1876; Carter, H. V. Reports on Leprosy, Second Series. London. 1876. As almost all the actors in this
thesis Carter also studied other diseases, but this is outside my scope.
536
For an overview of concurrent leprosy studies in the British Empire, see: Robertson, Jo. “In Search of M.
Leprae: Medicine, Public Debate, Politics and the Leprosy Commission to India.” In: Dale, Leigh and Helen
Gilbert (eds). Economics of Representation, 1790-2000: Colonialism and Commerce. 2007: 41-59, esp.: 46-47.
 207

works in high regards, was William Munro, late medical officer to St. Kitts in the
West Indies. In his experience, the disease was contagious, and human intercourse
was the only means of propagation. By ‘intercourse’ he meant living together, not that
leprosy was a venereal disease. He was also opposed to claims that the prevalence of
the disease had increased due to vaccination, which had become a hot topic for debate
in Britain after smallpox vaccination through arm-to-arm inoculation was made
compulsory in 1871.537 To explain why not even more people caught the disease,

Munro added that the “probable primary cause is a want of salt combined with a
deficient vegetable diet”.538 Apart from the emphasis on diet as a necessary
component, Munro was fully in line with Carter’s arguments, and typically described
him as “one of the best living authorities on leprosy”.539 He also expressed
“admiration” for Carter’s change of position regarding etiology, a not very subtle
critique of the Royal College of Physician’s unyielding defense of their 1867-
report.540
In Britain, seeing leprosy as contagious was controversial. The main objection
came from the principal author of the 1867-report, Gavin Milroy. One generation
older than Carter, Milroy had qualified as a physician in Edinburgh in 1828.
According to his obituary, he “never practiced medicine on his own account, but, from
his early manhood, made choice of its literary path.”541 Milroy was an active member
of the Hunterian Society in Edinburgh (a medical society named in honor of the






537
In a circular dated Downing Street, September 4, 1873, the Secretary of State for the Colonies, The Earl of
Kimberley rejected that vaccination could propagate the disease, but added that “as the success of a system of
vaccination must largely depend upon the views prevailing amongst the public on the subject, it will be always
as well to use lymph which is beyond suspicion in this respect.” (“Recent Official Correspondence relating to
Leprosy”. British and Foreign Medico-Chirurgical Review. 1874: 212.) Leprosy would be a focal point for the
anti-vaccination movement in Britain for several decades. See i.e. Tebb, William. The Recrudescence of
Leprosy and its Causation. A Popular Treatise. 1893, also printed with the title Leprosy and Vaccination. For
studies on the British anti-vaccination movement, see: Porter, Dorothy. Health, Civilization and the State. A
history of public health from ancient to modern times. 2005 [1999]: 128-130.
538
Munro, W. Leprosy. Manchester. 1879: Prefactory Note. The work was a reprint from a series of papers
printed in the Edinburg Medical Journal (September 1876 to November 1879).
539
Munro 1879: 16.
540
“I can pay Dr. Carter no higher compliment than to express my admiration for his readiness to give up any
received theory which he has given much labour to prove the correctness of, when formerly unknown
circumstances show that another theory explains the facts better.” (Munro 1879: 77)
541
“Gavin Milroy”. The British Medical Journal. February 27. 1886: 425-426.
 208

Scottish surgeon John Hunter), and then the Epidemiological Society of London
where he was President from 1864 to 1866. In 1849 he was appointed Superintendent
Medical Inspector of the General Board of Health in London, and a year later he was
sent to study an outbreak of cholera on Jamaica, followed by assignments as a sanitary
commissioner for the War Office in the Crimea in 1855. In 1871 Milroy was sent to
the West Indies to investigate an alleged cure for leprosy developed by the French
doctor Louis Daniel Beauperthy working at Cumana in Venezuela.542

Milroy had marked himself as a public opponent of the quarantine system
already in the 1840s, and in 1858 he was appointed Honorary Secretary to a
committee set up by the National Association for the Promotion of Social Science to
report on the practices and results of quarantine worldwide. His modus operandi was
the same then as when later making the report on leprosy: Write a series of queries,
have them forwarded to the Foreign and Colonial Secretaries of State for circulation
among the Consuls and Colonial authorities, and then analyze the returns. His
conclusion was that all suggestions of leprosy being contagious were based on
superstition and ignorance – a position he would retain until his death in 1886.
Throughout the 1870s, Milroy would be London’s authoritative voice on
leprosy in the Empire. In addition to corresponding with the Colonial Secretary, from
1874 to 1880 he published a series of nine papers in the London-based Medical Times
and Gazette under the title “Is Leprosy Contagious?” insisting that calls from the
colonies for compulsory detention were uncalled for. When the Colonial Office
informed Milroy that Carter’s report from Norway was to be circulated to ‘the
Colonies in which leprosy prevails’, he requested that also his own latest paper
arguing that the disease was hereditary and that institutions were unnecessary, was
included as an addendum.543 This would be the pattern also for later research from the

colonies: The Colonial Office would circulate the reports, but always accompanied by
a corrective from the College of Physicians (meaning Milroy).
Carter’s specific recommendations after the journey to Norway were that India




542
Beauperthy died shortly after Milroy arrived. More on this in Chapter 3.
 209

should start constructing leper asylums for care and containment of possible disease
carriers, a leprosy hospital for further research, and learn more about the Indian leper
through collecting statistics and conducting special investigations in the ‘worst
districts’. Carter’s report described the Norwegian system as being run by a “Leper
Department”. Accordingly, the leprosy work in India should be organized
independently of the Sanitary Commissions, Agricultural Department, the Cholera
Commission, and the military Indian Medical Service where he began his career, “for
they concern a special subject, needing special knowledge, close attention, and
continuous observation for its elucidation.”544
Perhaps not surprisingly, this was not well received by India’s growing sanitary
department, which saw leprosy as clearly within their domain. In India Carter’s
immediate opponent was not Milroy, but James McNabb Cuningham. Like Milroy,
Cuningham had his medical doctorate from Edinburgh. This he received in 1851.
Cuningham then entered the Bengal Medical Service, and in 1868 he was made
sanitary commissioner to the Government of India, a primary advisor to the
government.545 As historian Jane Buckingham put it:



Much as the Royal College of Physicians in Britain had used the investigation of leprosy to
help develop its professional profile in the 1860s, the sanitary department employed control
over leprosy research in its effort to extend, as far as possible, its authority over public
health in India.546

Cuningham saw the calls for institution building and segregation of leprosy sufferers
as an impossible and futile undertaking. The vast number of lepers meant that
building institutions would be a huge burden on the government purse. Based on the
conclusions of the 1867-report, it was also completely unnecessary. Going through
Carter’s report from Norway, Cuningham pointed out that segregation in Norway was
only very partial. While 764 persons with leprosy were institutionalized in Norway by




543
Edmond 2006: 68.
544
Carter 1874: 30.
545
Buckingham 2002: 149.
 210

the end of 1870, there were 1.286 registered lepers who lived outside the institutions.
The partial institutionalization could not explain the decline in prevalence, and it
could not be considered evidence to suggest the disease to be contagious. As I will
show later in this chapter, similar lines of reasoning were repeated in the Report of the
Leprosy Commission in India (1893).547 The only recommendation Cuningham
endorsed was the call for more knowledge on leprosy in India – a task he successfully
argued belonged to his own sanitary department.
In March 1875, based on a resolution drafted by Cuningham, the Indian
Government decided that the next enquiry into leprosy should be a sanitary enquiry,
conducted by the sanitary department. Cuningham also persuaded the Governor-
General-in-Council that “it would not be advisable for the Government to publish and
circulate Dr. Carter’s paper, and thereby give it an authoritative character, as though
the question of the specific origin of leprosy has been decided, which is far from
being the case.”548 The mandate to the sanitary investigators was written by no other
than Gavin Milroy himself.549 This led The Lancet, which already in 1867 had argued
that Milroy’s report had underestimated the importance of contagion,550 to argue that
Carter had been ‘elbowed out’ of a field on which he had ‘thrown light by honest and
admirable work’. For Carter, departing from the official dogma would ruin his
prospects of promotion.551





546
Buckingham 2002: 148.
547
Leprosy in India. Report of the Leprosy Commission in India, 1890-91. Calcutta. 1893. See also: Pandya
2001: 67-69.
548
Maharashtra State Archives, General Department, Vol. 50, 1876: 20, quoted in Pandya 2001: 68.
549
Pandya 2001: 70.
550
The review was printed in three parts, where the two latter were dedicated to “the important question of the
contagiousness of Leprosy”. They especially highlighted N. C. Macnamara from the Indian Medical Service
whose independent analysis of the 107 reports from India concluded that the disease was probably contagious.
The Lancet review argued that “the facts which have been presented to the Committee in the various ‘replies’
received in answer to the ‘interrogatories’ are not sufficient upon which to form a just conclusion.”. (“The
Leprosy Report of The College of Physicians” Pt. I-III, The Lancet. 1867: 63-65, 189-190, 253-254, quotes on
p. 189.)
551
“Probably, as Dr. Carter’s views in reference to the general treatment of lepers turn out to be not in accord
with those of the Government, it may be convenient to deny Dr. Carter any facilities for prosecuting his
inquiries any further.” (Editorial. “Leprosy in India”. The Lancet. 1875: 458-459. Quoted in: Pandya 2001: 69;
Buckingham 2002: 150). As Buckingham points out, this was not an isolated event. In 1884, Carter was
unprecedentedly passed over for the position of provincial sanitary commissioner in Bombay. (Buckingham
2002: 151.)
 211

The sanitary report found ‘little or no evidence’ to support ‘the recent revival
of contagion theory’. Instead, its conclusions reaffirmed and strengthened the
conclusions from Milroy’s 1867-report.552 There was no reason for further state
involvement, other than to continue the sanitary approach that would improve colonial
health in general. That many in the general public, including local physicians,
withheld that the disease was contagious was seen as a proof that they lacked the
necessary unprejudiced view that proper science could offer. Finally, the lepers tended
to develop sterility, and the mortality rate of their children was ‘abnormally high’: “It
is therefore evident that unless there be influences other than heredity at work in the
locality, tending towards the production of the leprous condition, no serious increment
need be apprehended.”553
On the other hand, Henry Vandyke Carter did have supporters in the Bombay
Presidency. In 1875 he was asked to study leprosy in the villages of the Kathiawar
peninsula (now Gujarat), a district outside British colonial control.554 He was made
president of the Medical and Physical Society of Bombay and Dean of the Medical
Faculty of the University of Bombay.555 In June 1879, based on Carter’s
recommendations, the Government of Bombay decided that the Sassoon Infirm
Asylum in Poona should accept and maintain leprosy sufferers.556 Shortly thereafter
Carter again visited Europe, but this time due to illness and not primarily as a study
tour. After returning, Carter would continue to argue that India should learn from
Norway.










552
Lewis, T. R. and D. D. Cunningham. Leprosy in India: A Report. 1877: 56-58, as quoted in Edmond 2006:
80. See also: Pandya 2001: 71; Buckingham 2002: 147-152. Parts of the sanitary report was also printed in the
report Leprosy in Foreign Countries, published by the Department of Foreign Affairs on Hawaii in 1886. (Lewis,
T. R. and D. D. Cunningham. “Extracts from a report”. In: Leprosy in Foreign Countries. 1886: 78-81.)
553
Lewis and Cunningham 1886: 80.
554
Carter, Henry Vandyke. Report of a Tour in Káthiáwár. 1876. Bombay. 1877.
555
Pandya 2001: 57.
556
General Department, Bombay. Resolution No. 4900. “Establishment of Leper Asylums”. Dated Bombay
Castle, December 7, 1882: 1. Addendum to Carter, Henry Vandyke. Memorandum on the Prevention of
Leprosy by Segregation of the affected. 1884.
 212

Meanwhile, in Norway


The leprosy system Carter met in Norway was the outcome of both a disease model
which saw leprosy as hereditary and a model of the disease as caused by filth, lack of
hygiene and a low stage of civilization.557 Before returning to India, I will in the
following show how the Norwegian ‘leprosy apparatus’, as coined by historian
Morten Hammerborg, was established. Then, I will investigate how Milroy’s report
and Carter’s visit were appropriated in the Norwegian debates.558 Finally, what
happened when, around the time of Carter’s visit, contagion was introduced as a
justification for continued state involvement in leprosy?
As I showed in Chapter 2, Boeck and Danielssen had in the 1840s described
leprosy as having two distinct clinical forms, the anesthetic and the tubercular.559 In a
literary review tracing the disease back to the ancient Greeks, Boeck distinguished
between inner and outer causes which worked in combination. Heredity, an inner
cause, could explain almost all cases, while in some the disease developed
spontaneously. Boeck saw no shred of evidence for the theory of contagion put
forward in the Mosaic laws, a theory both he and Danielssen warned had led to
inhumane prosecution of the sufferers in medieval Europe.560 Other possible inner
causes were age (leprosy as part of puberty) and sex (making eunuchs immune to the
disease), but neither of these were seen as important. Of the external causes, climate
and telluric (soil) influences and foodstuffs (especially fish, but also the combination
of malnutrition, poor living conditions and filth) could all have some impact, while
mental affections, acts of violence, and divine intervention were presented as unlikely
explanations.561




557
Höegh, Ove Guldberg. Tabeller over de spedalske i Norge i aaret 1860 samt aarsberetning for samme aar.
1860: 16, as quoted in Vollset 2006: 49.
558
Hammerborg, Morten. Spedalskhet, galeanstalter og laboratoriemedisin – endringsprosesser i medisinen på
1800-tallet i Bergen. PhD-thesis. University of Bergen. 2009.
559
Danielssen and Boeck 1847.
560
The non-contagious nature of the disease was further confirmed through experiments with inoculations.
Notably, none of the inoculations were mentioned in Danielssen and Boeck’s monograph. For an overview of
these early experiments, see: Hansen, G. Armauer. “Uebertragung der Lepra von Mensch zu Mensch”.
Mittheilungen 1897. Bd. 2. 1897: 1-5.
561
Danielssen and Boeck 1847: 66-80, 90-113.
 213

According to Danielssen, who was responsible for the clinical work, leprosy
was caused by an imbalance in the blood, a dyscrasia. This meant that the disease was
not particular to the individual leprous lesion: Leprosy was not a skin disease but
affected the whole body. The argument was backed by post mortem examinations
which showed that also internal organs developed signs of the disease. Furthermore,
chemical analysis of the blood, a technique which was much discussed in European
medical journals in the 1840s, showed that ‘leper blood’ differed from healthy
blood.562

Through examining the pedigrees of those affected, Danielssen concluded that
the imbalance was mainly hereditary: “These tables show that of 213 individuals
attacked by leprosy, it is inherited in 189, and only in 24 has it developed
spontaneously”.563 The leprous dyscrasia could lie dormant in one generation, and
return with a vengeance in the next. Of the 213 cases Danielssen investigated, 155
had skipped one generation or more. The disease could also jump ‘sideways’ through
marriage. 120 of the 189 cases of inheritance were in the sidelines.564
As historian Michael Worboys has pointed out, to have several explanations
for the same disease was not usual in medicine in the mid-19th century.565 For
Danielssen and Boeck, to recognize the disease and to work to find a treatment was
more important than reducing it to a single cause. The argument that leprosy was
caused by a ‘hereditary taint’, as in Carter’s 1871 report, can be traced via the Royal
College of Physician’s 1867-report, to a translation of Danielssen and Boeck’s
monograph made available to the English-speaking medical community through a






562
The first review of Danielssen and Boecks research based on publications in Norsk Magazin for
Lægevidenskaben (1842), Ugeskrift for Medicin for Pharmacie (1843) and papers presented at the meeting of
naturalists in Grätz in Preussia (1844) and at the fourth Scandinavian meeting for naturalists in Christiania
(1844), explicitly asked for chemical or microscopical investigations. See: Editorial. “Boeck and Danielsen on
the Spedalskhed or Norwegian leprosy”. British and Foreign Medical Review. 1844: 346-353.
563
“Af disse Tabeller sees, at af 213 Individer angrebne af Spedalskhed er denne nedarvet hos 189, og at den
kun hos 24 har udviklet sig spontant.” (Danielssen and Boeck 1847: 263.)
564
Heredity in the sidelines was contested from the outset. In an otherwise positive first review of the
monograph, physician Jens Johan Hjort argued that only direct lineage qualified as heredity, and that the
argument that leprosy was a ‘family disease’ had probably been overstated. See: Hjort, Dr. “Om Spedalskhed
ved D. C. Danielssen”. Norsk Magazin for Lægevidenskaben. 1848: 169.
565
Worboys 2000.
 214

series of eight articles in The Lancet in 1856.566 Carter’s report from Norway
contained long excerpts from the 1847-monograph, showing that he too was aware of
this legacy.
Unlike in India, there were already institutions for leprosy in Norway in the
1840s. Danielssen’s clinical work was based on seven years of observations and post
mortems in St. Jørgens Hospital in Bergen, a patient-run independent institution
which had operated continuously for more than 400 years.567 Further north along the
coast, Reknes Hospital outside Molde was established in 1716, and Reitgjerdet
Hospital in Trondheim had since 1612 had a division for lepers. Based mainly on the
argument that the disease was an increasing threat to the nation, that further research
was necessary and that science could find a cure, the Norwegian Parliament funded
the research hospital ‘Lungegaardshospitalet’ which opened in Bergen in 1849 with
Danielssen as head physician. The research hospital burned to the ground on
Christmas Eve 1853, killing six patients and a night nurse, but it was reopened in

1859. Danielssen would keep the position as head of the research hospital until his
death in 1894.568
By the 1870s, the research hospital was well known outside the national
borders. This is evident both from Danielssen’s correspondence, publications, visits to
Bergen, and numerous honors from medical and scientific societies throughout
Europe.569 When Danielssen in June 1871 was contacted by Dr. Bakewell who
wanted to come to Bergen to demonstrate Beauperthy’s alleged cure for the disease




566
Buckingham 2002: 120; Edmond 2006: 46. The translation was published under the title “On the Nature and
Treatment of Leprosy” by Erasmus Wilson. It appeared a year after the French edition (Traité de al
Spedalskhed ou Eléphantiasis des Grecs, 1848) won the Prix Monthyon from the Academy of Sciences in Paris
in 1855. Danielssen visited London in 1853, but going through his private correspondence from this time
(which was discovered in his desk drawers in Bergen the summer of 2010 and is currently held by Bergen
Museum), I have found no indication that Danielssen corresponded with either Carter or Wilson.
567
St. Jørgens was first mentioned in a testament from 1411. For a history of the institution, see: Knudsen S. Å.,
et al. “De fattige Christi Lemmer”... Stiftelsen St. Jørgens historie. 1991.
568
Vollset 2005. In 1895 the patients and research activities were moved to the neighbouring ‘Pleiestiftelsen’,
and two years later the building was bought by the municipality who used it first as an isolation hospital and
from 1912 as a sanatorium for tuberculosis. The building was torn down in 1957.
569
For a list of references to the publications on the activities of the research hospital (“Lungegaardshospitalets
Virksomhed”) as well as an extensive bibliography of Danielssen’s published research, see:
http://www.whonamedit.com/person_bibliography/2321/. See also: Brunchorst, J. Bergen Museums Aarbog
1893. D. C. Danielssen. A biographical sketch. 1894.
 215

(see Chapter 3), part of the justification for not offering Bakewell any payment was
that the results of Milroy’s investigations in the Caribbean showed the cure to be
ineffective.570 Danielssen reported this before Milroy had published his report,
indicating that he was up to date also on leprosy-related research conducted
elsewhere.
As Hammerborg has emphasized, Danielssen and Boeck’s framing of leprosy
as a hereditary dyscrasia had direct political implications.571 Between 1850 and 1857,
the advisory Medical Committee to Parliament was especially successful in involving
the state in leprosy work. All three members of the committee used the theory of
heredity as the basis for their arguments, and in 1850 they suggested a law which
would make it illegal for people from ‘leprous families’ to enter into marriage. After
some debate, the suggestion was rejected. Inheritance in the sidelines meant the
precautions would apply to too many people, and there were worries that a marriage
ban would not result in fewer offspring but immoral and ‘unnatural sexual
behavior’.572 The committee’s other suggestion was to establish state institutions. The
argument balanced between compassion and control. That those suffering from the
disease needed care was beyond dispute, but those affected were a heavy financial
burden on the local communities. The main rationale for the state intervention was to
share this economic burden. This was coupled with the threat that without an
intervention the disease prevalence would only increase and finally get out of hand.573
In 1857 the leprosy asylums Pleiestiftelsen No. 1 opened next to Lungegaards-
hospitalet in Bergen with 280 beds.574 In 1861, both Reknes and Reitgjerdet were
expanded to 160 and 180 beds respectively.575 When Carter visited Bergen in 1873,
he was full of praise for the institutions, highlighting the segregation of the sexes “the




570
Danielssen, D. “Lungegaardshospitalets Virksomhed i Treaaret 1871-73”. Norsk Magazin for
Lægevidenskaben. 1874: 319-321. See also: Edmond 2006: 61-62.
571
Hammerborg 2009: Chapter 2.
572
“Betænkning afgiven til Departementet for det Indre fra dettes raadgivende Medicinal-Comitee, angaaendde
Foranstaltninger mod den spedalske Sygdom. Christiania den 30te December 1850.” Available online: http:
//digitalarkivet.uib.no/cgi-win/webmeny.exe?slag=visside&kat=lepra-eng&n1=4&n2=2&dok=rapport.htm. See
also: Vollset 2005: 44-47; Hammerborg 2009: 79-86.
573
Op. cit. See also: Vollset 2005: 44-47; Hammerborg 2009: 74-78.
574
Andresen 2004: 93-116.
 216

idea being that they [young and active lepers] should not be allowed to propagate their
disease to offspring, and this idea was the dominant one leading to the establishment
of asylums.”576
Historian Astri Andresen has in her study of Pleiestiftelsen No. 1 shown that
around the time of Carters visit, the initial optimism among the inmates flocking to
the institutions hoping to be cured was diminishing. Increasingly, the institution was
perceived more like a prison than a hospital. Consequently, those who were
sufficiently healthy (and had a place to run to) left the hospital without permission.577
While Carter in 1873 painted a rosier picture than Andresen, he too noticed that “The

helpless and infirm leper must obviously be cared for, and most asylum inmates are of
this class.”578
In addition to the institutions, the Norwegian leprosy apparatus consisted of a
network of district physicians who annually registered each individual leprosy
sufferer in their district. The genesis of the system was in 1854, when the Medical
Committee received permission from the state to appoint two physicians charged with
coordinating the national leprosy campaign, who were to report directly to the
Ministry of Domestic Affairs (‘Departementet for det Indre’). Through popular
lectures in the most affected areas they were to ensure that the institutions were used,
and that interest in the disease did not diminish.579 Presenting the apparatus as the
outcome of three parallel and competing medico-political projects, Hammerborg has
shown how establishing permanent leprosy commissions in all municipalities with
lepers was the brainchild of the head physician for leprosy (‘Overlege for den
spedalske sykdom’) in the Northern part of the country, Ove Guldberg Høegh. The
commissions, established in 1856, were headed by the district physicians, and
included the heads of the local governments. Four years after their inception, in 1860,





575
Vollset 2005: 58. For Carter’s description of these asylums, see: Carter 1874: 13-15.
576
Carter 1874: 15.
577
Andresen 2004: 93-116.
578
Carter 1874: 15.
579
In 1863, the head physician for leprosy reported that leprosy had been the main topic of 256 public lectures
around Norway. (Løberg, T. J. Tabeller over de spedalske i Norge i aaret 1864 samt aarsberetning for samme
aar. 1864:13, in: Vollset: 2005: 51-52.)
 217

the leprosy commissions were used as a model for local Health Commissions
(‘Sunnhetskommisjoner’) in all municipalities, the backbone of the Norwegian health
system for decades to come.580 Unlike in British India, there were no preexisting
sanitary commissions in Norway. Rather, the leprosy campaign was integral in
establishing the public health system.
The district physicians were also charged with keeping an updated registry of
every sufferer, to be submitted to Høegh annually for compilation and analysis.
According to Hammerborg, the questionnaires (which Carter translated and printed in
hope they could be used in India581) were designed to challenge Danielssen and
Boeck’s hereditary disease model in favor of a sanitary model.582 Still, it was more a
question of emphasis than a direct challenge. Danielssen and Boeck too had argued
that the disease could have multiple causes, and Høegh did not deny a hereditary
component. Høegh’s principal position, however, was that leprosy was a sanitary
concern caused by poor living conditions. In addition to keeping track of every
individual leper, the main task of the commissions was to educate the population and
work against “bad housing, poor clothing, deficient food and filth”.583
Høegh died in 1863, and Timandus Jonas Løberg in Bergen remained the sole

national Head Physician for Leprosy, alongside a position as physician at
Danielssen’s research hospital. Løberg saw the disease as caused by ‘the low stage of
civilization’ of the population, connecting it as did Høegh to climate, housing
conditions, hygiene and poor clothing.584 Again, this did not exclude a hereditary
component.
There were also other differences between Norway and the British Empire. In
Norway leprosy was a domestic disease, not something mainly found in overseas
colonies. Hence, declaring the disease not to be a threat to the colonizers, as Milroy




580
Schiøtz, Aina. Folkets helse, landets styrke 1850-2003. Det offentlige helsevesen i Norge 1603-2003, bind 2.
2003: 26.
581
Carter 1874: 43 (Appendix 6).
582
Hammerborg 2009: 86-92.
583
Höegh, Ove Guldberg. Tabeller over de spedalske i Norge i aaret 1860 samt aarsberetning for samme aar.
1860: 14, quoted in Hammerborg 2009: 88; Vollset 2005: 50-51.
 218

did in 1867, was never an option. The Norwegian physicians’ warning that the disease
would come out of hand without state intervention was also credible. The first census
of leprosy sufferers in Norway, conducted by the parish ministers concluded in 1836,
concluded that there were 659 ‘lepers’ in the country. Twenty years later, when the
national patient registry wae stablished, the number had reached almost three
thousand.585 On the other hand, with less than 3000 lepers registered at any one time,
the size of the problem was also more manageable than for instance in the Bombay
Presidency with almost 8000 known cases. In colonial India as a whole, 100.000
cases were considered a low estimate. Additionally, in India other diseases (especially
cholera) were a larger and more imminent threat to health. While the leprosy census
Carter analyzed showed that one of 600 persons in his presidency had leprosy, the
proportion was slightly lower than the average death toll to cholera in India every year
(1 out of 570). In 1877, which was one of the worst years, 357.430 cholera deaths
were recorded in Madras Presidency alone.586
A final vital difference was that in Norway the state employed physicians

working with leprosy were part of the elite class of public servants (‘embetsmenn’)
which dominated national politics.587 Unlike in London or colonial India, the
Norwegian leprosy physicians were not just advisors, but many were elected
representatives to Parliament. Boeck was elected to Parliament in 1845; his younger
colleague Danielssen was five times elected to represent Bergen in Parliament (1859-
60, 1862-64, 1871-1876); Løberg served three parliamentary terms (1865-67, 1871-
76). Danielssen and Løberg were also active in local politics. This means that they
had intimate knowledge of how the political system worked and were in a position to
influence policies from ‘within’.




584
Løberg, T. J. Tabeller over de spedalske i Norge i aaret 1862 samt aarsberetning for samme aar. 1862: 12,
as quoted in Vollset 2005: 49.
585
Vollset 2005.
586
Arnold, David. “Cholera and Colonialism in British India”. Past and Present, No. 113. 1986: 118-151,
numbers on p. 122.
587
In the Norwegian historiography, the term “embetsmannsstaten” (‘the civil servant state’) is the dominant
interpretation of the political system between the country getting its own constitution in 1814 and the
introduction of parliamentary rule in 1884. Seip, Jens Arup. Fra Embedsmansstat til ettpartistat og andre
essays. 1963.
 219

When Carter visited in 1873, Løberg was still administering the leprosy
apparatus and Danielssen was still in charge of the research hospital. In Christiania
(now Oslo), Carter met both the head of the Ministry of Health
(‘Medicinaldepartementet’) and Carl Wilhelm Boeck. Boeck was at that time the head
of the Division of Dermatology at the National Hospital (Rigshospitalet), and had just
returned from North America where he had examined leprosy among Norwegian
emigrants. His findings, he argued, confirmed his theory that the disease was
hereditary.588

In the early 1870s, the debates on the nature and causes of the disease had
reignited, with contagion as the relative newcomer. The debate was sparked not by
domestic concerns, but by reports from abroad. In 1871, the Report of the Royal
College of Physicians (1867) was introduced to a Norwegian audience by medical
professor Ferdinand Lochmann at the University of Christiania.589 To Lochmann, the
report was not a confirmation of heredity or that the disease was a sanitary concern,
but a major argument for the contagiousness of the disease. This he supported by
quoting the 24 statements (of a total 250 replies) from the report that all supported
this view.
Retired physician Johan Jørgen Hjort, who since the 1830s had argued that the
disease was connected to hygiene and that the importance of heredity had been
overestimated, soon rebutted that Milroy who had compiled and analyzed the replies
had reached the exact opposite conclusion:








588
Boeck, W. “Spedalskheden i de forenede Stater i Nordamerika”. Nordiskt Medicinskt Arkiv. Bd. 3, No. 1.
1871. This was the second of three such investigations. In 1863 Jens Andreas Holmboe, argued that his
investigation of Norwegian ‘lepers’ in North America confirmed his theory that the lepers’ health would
improve with changes in climate and lifestyle. In 1889 Gerhard Armauer Hansen would argue that his
investigation confirmed that the disease was contagious and that improved hygiene had stopped its spread. See:
Lie, H. P. “Norwegian Lepers in the United States: The investigations of Holmboe, Boeck and Hansen”.
International Journal of Leprosy. No. 3. 1938: 351-356; Gussow 1989: 81-82; Davidsen, Bjørn.
“"Forskerstafett" til Amerika 1863-1888.” Bergensposten. No. 4. 2001: 29-39. Available online: http:
//digitalarkivet.uib.no/sab/bp2001/side29.htm.
589
Lochmann, F. Om Spedalskheden. 1871. Incidentally, Lochmann was the model for Dr. Thomas Stockmann
in Henrik Ibsen’s play En Folkefiende (An Enemy of the People) from 1882, especially for Lochmann’s use of
the popular press to spread his messages.
 220

The all but unanimous conviction of the most experienced observers in different parts of the
world is quite opposed to the belief that leprosy is contagious or communicable by
proximity or contact with the diseased. The few instances that have been reported in a
contrary sense either rest on imperfect observation, or they are recorded with too little
attention to the necessary details as not to affect the above conclusion.590

While the report in colonial India gave Gavin Milroy the authority to define the
mandate for investigating leprosy as a sanitary concern, in Norway this was but one of
several reports from abroad. Gerhard Armauer Hansen, who since 1869 had worked
as assistant physician at the Lungegaarden research hospital, also pointed out that
Lochmann’s interpretation was “odd”. A better argument, Hansen argued, was found
in the works by the Dutch physician Charles Louis Drognat Landré. In 1867, based on
case histories of 12 children of European settlers in Surinam contracting leprosy,
Drognat Landré had argued that leprosy was an infectious disease propagated solely
by contagion.591 When Carter visited Norway, the debate on the nature and causes of
leprosy was on top of the agenda: “Respecting the causes of leprosy – a subject not
unconnected with the topic under notice – I have not during my tour in Norway found
less debate there than elsewhere.”592







590
“Report on Leprosy by the Royal College of Physicians prepared for Her Majestys Secretary of State for the
Colonies”, as quoted in Hjort, J. J. “Om Aarsagerne til den spedalske Sygdom.” Norsk Magazin for
Lægevidenskaben. 1872: 125, English in the original.
591
Hansen presented nine of the twelve case histories, and highlighted Drognat Landré’s publication as what
‘attracted my attention to contagion not being adequately investigated here.’ (Hansen, G. Armauer. “Om vort
Kjendskab til Spedalskhedens Aarsager og om vore Forholdsregler mod Sygdommen”. Norsk Magazin for
Lægevidenskaben. 1872: 21). Hansen would later praise Drognat Landré’s monograph as “the most valuable of
research about this [the contagiousness of leprosy]” (Hansen 1874: 80). The library catalogue from the research
hospital in Bergen contains both Landré’s Dutch original (De besmettelijkheid der lepra arabum. Utrecht.
1867) and the French translation of the treatise (De la contagion de la lèpre. Paris. 1867). See: Dethloff, H. G.
Katalog over Lungegaardshospitalets Bibliothek ved udgangen af aaret 1904. Bergen, 1905: 144. For more on
Drognat Landré, see: Menke, Henk E, William R. Faber, and Toine Pieters. “Charles Louis Drognat Landré and
Gerhard Henrik Armauer Hansen; contribution from a Dutch colony to the discovery of the leprosy bacterium”.
Leprosy Review. Vol. 81. 2010: 82-86. In comparison, the Royal College of Physicians dismissed Landré’s
work out of hand, arguing that “from the meagre and unauthenticated details of the nine cases cited in support of
the contagion of leprosy, the College feels that the evidence on which these inferences rest is quite insufficient
for the solution of any scientific question.” (Letter from George Burrows to The Earl of Kimberley,
dated December 1872. “Recent Official Correspondence relating to Leprosy”, The British and Foreign Medico-
Chirurgical Review. 1874: 207.)
592
Carter 1874: 26.
 221

The most sophisticated argument for contagion was presented in Hansen’s
report to the Medical Society in Christiania in 1874, which he later would refer to as
his main scientific contribution. The aim of the report was to find the laws that
governed why leprosy appeared.593 The report was written after he was granted a
scholarship from the Medical Society in 1870, which Hansen spent traveling to
Germany, Vienna and Venice to learn the latest research techniques.594 His literary
review stressed the numerous positions on etiology that existed among the Norwegian
physicians, ranging from inheritance, via degeneration caused by cultural stagnation,
to spontaneous appearances, miasma and contagion, as well as combinations of
causes. For Hansen, however, the disease was specific, contagious and decidedly not
hereditary.
Hansen’s conclusions were based on case histories from 69 families, statistics,
dissections, animal experiments and microscopy. The main argument hinged on
comparing Norwegian districts based both on his own travels, reports from physicians
and statistics from the patient registry that Høegh had established eighteen years
earlier. Hansen did, however, make a vital alteration to the original statistics: Instead
of reflecting the time each individual was diagnosed, he backdated the cases so that
the registry instead reflected when the disease first had made its presence known.595
When comparing different districts using these new figures, it was clear that the
disease appeared independent of filth and malnutrition, and regardless of climatic
factors such as weather or humidity. Yet, there was a strong correlation between
isolation and the number of new cases. In districts where those suffering from the
disease had been institutionalized, the number of new cases had declined rapidly,
while in districts where no ‘evacuation’ had taken place, there was a steady supply of
new cases. Furthermore, on the whole the decline had taken place faster than could be




593
Hansen 1874: 1-88. See also: Irgens 1984: 337-343.
594
In his autobiography, Hansen highlights studying microscopy with Max Schultze in Bonn. Caught in the
Franco-Prussian War, Hansen left for Vienna where he picked up Ernest Haeckel’s Natürliche
Schöpfungsgeschichte (1868). Alongside Darwin’s On the Origin of the Species (1859), this was at the
foundation for his worldview. (Hansen 1910: Chapter 4.) Hansen would soon present Darwin to a wider
audience through a series of articles in the local newspaper Bergensposten, and in the popular science magazine
Naturen which from 1887 also had its base in Bergen.
 222

explained had the disease been hereditary. The only explanation, Hansen concluded,
was contagion. ‘Evacuating’ lepers to the institutions had had the desired effect.


Only after leprosy has become endemic do the causes which point towards heritance appear.
If the disease was contagious, this could be explained quite naturally in that the first case
caught the contagion elsewhere and later it spread to the closes acquaintances – members of
the same family or lineage.596

Initially the report was intended to be printed as an independent publication, since the
columns in the Medical Association’s journal Norsk Magazin for Lægevidenskaben,
the only Norwegian medical journal at the time, were limited. Referring to Carter’s
interest and intent to produce a monograph based on his Norwegian experience,
Hansen insisted that the report instead was to be printed as an appendix to the journal.
This would ensure legitimacy, a larger distribution and hasten the publication without
disrupting other journal content.597 The chairman of the Association, Christian
Thorvald Kierulf, was also contacted by Carter directly.598 The ‘international’ interest
was the main argument in the decision to cover the expenses of printing the report as
an addendum to the journal, illustrating how knowledge exchanges were not mono-
directional. It was also on Carter’s suggestion that Hansen the following year
published a slightly shortened translation in The British and Foreign Medico-
Chirurgical Review.599
The only immediate response to the publication was a critique by Thorvald
Buchholz, district physician from Hadeland and a prolific writer. Buchholz argued
that Hansen had gone looking for proof for his theory of contagion, and bent the





595
Hansen 1874: 62-63.
596
“Först efterat spedalskheden er blevet endemisk opträde de tilfälde, der kunde tyde på arv. Var nu
sygdommen smitsom, kunde dette have en ganske naturlig forklaring, idet de förste tilfälde, erhvervede ved
smitte andetsteds, senere hyppigt smittede sin närmeste omgang, medlemmer af samme familje eller slägt.”
Hansen 1874: 36.
597
“Møte den 20de Mai 1874”. Forhandlinger i det Norske medicinske selskab i 1874. 1875: 140-143.
598
Op. cit. Kierulf had international contacts of his own: In the early 1850s, he befriended Rudolf Wirchow
while studying in Würtzburg, and was instrumental in inviting him to study leprosy in Norway in 1859. (Jæger,
Henrik. Videnskabernes Literatur i Det Nittende Aarhundrede. 1896: 232-233.)
599
Hansen 1875: 459-489.
 223

findings to fit this conclusion:



If the isolated researcher, as Hansen and many with him, start with preconceived ideas and
theories in which the entire research should be squeezed and the results bent to fit, it leads
to a misleading confusion – and Hansen’s report shows exactly such a highly one-sided
tendency that it must be an obligation to refute it.600


According to Buchholz, the association had made a mistake in printing Hansen’s

‘speculations’. In his view, the disease was not contagious but the result of an
inherited functional deficit brought forward by cultural and intellectual stagnation.
Any decline in prevalence was caused by cultural enlightenment. If the state
continued to pour money into costly state institutions instead of spending it on
educating the population, he predicted the decline in new cases would be only
temporary.601
Despite disagreements, suggesting that the disease was contagious did not lead

to Hansen being ‘elbowed out’ of further leprosy work, rather the opposite. When
Løberg in 1875 was made director of the National Hospital and Birth Clinic in
Christiania, Hansen was temporarily appointed the new ‘head physician for leprosy’
(‘overlege for den spedalske sygdom’), a position he would keep until his death in
1912. That Hansen in 1873 married the daughter of his immediate superior Daniel
Danielssen was probably of minor significance.602 More importantly, he was recruited
from the same position at the Lungegaarden research hospital that Løberg had had
before he was appointed in 1857. Before Hansen inherited the position, this was seen
as an administrative chore. With Hansen at the helm, this would quickly change.









600
“Gaar saaledes den isolerede Forsker, som Hansen og Mange med ham have gjort, du fra forudfattede Ideer
og Teoremer, indenfor hvilke altsaa den hele Forskning skal indklemmes og Resultaterne derefter bøies, saa
fremkommer herved en misvisende Uklarhed – og netop Hansens Indberetning viser en saadan høist ensidig
Tendents, som det maa være Pligt at tilbakevise. Kritikk var og er altsaa her paa rette Sted.” Buchholz, Thv.
“Mer om Spedalskhedens Væsen”. Norsk Magazin for Lægevidenskaben. 1875: 2.
601
Buchholz 1875: 42-43.
602
Stephanie Marie Danielssen died later the same year due to tuberculosis.
 224

Contagion and the law


As head of the Norwegian leprosy apparatus, Hansen reinterpreted the rationale
behind the state intervention. The institutions were no longer described as ‘good
homes’ to provide care, but as institutions for the isolation of a contagious disease.603
This went hand in hand with new legislation. In 1876, Hansen proposed an Act which
would make it illegal to accept leprosy sufferers in need of care in the ‘legd system’ –
the traditional system of accommodating poor people at local farms for a period
before they were sent to the next farm. For a contagionist like Hansen, this system
ensured that the disease would spread. Instead, poor leprosy sufferers should as a rule
be admitted to the public leprosy institutions.604 In addition, the legislation demanded
that the clothes and linens of deceased ‘lepers’ should be disinfected.
Underlying these measures was also a concern that the leprosy institutions had
almost 300 unoccupied beds while a majority of Norway’s registered ‘lepers’
remained outside the institutions. This was increasingly pointed out by physicians and
members of Parliament who argued that the costly and increasingly unpopular
institutions should be shut down completely. In Parliament, however, the supporters
of the law argued that it would “bring people’s attention to the disease, and this alone
will make the Act useful.”605 Voices of opposition were also heard, pointing out that

they were not convinced of the premise that leprosy was contagious. Bishop Jacob Liv

Rosted Sverdrup, for instance, argued:


As long as the population suffers from bad housing and malnutrition, a disease like this will
remain; as soon as the living conditions are improved, the disease will diminish. This is the
main cause for the reduction of the disease; the institutions have never performed miracles,
and they never will.606





603
Odelstingsproposisjon 24/1877; Vollset 2005: 72-74.
604
“Lov om Forsørgelsen af fattige Spedalske m. V.”, passed May 26, 1877: §2.
605
“(…) denne Lov vil virke til at vække en større Opmerksomhed hos Alle for Sygdommen, og allerede herved
vil Loven gjøre Nytte.” Ellingsen, Lasse. “Ang. Lov om Forsørgelse af fattige Spedalske.” Stortingstidende
1877, Forhandlinger i Odelsthinget. 1877: 198; Vollset 2005: 72.
606
“Saalænge Befolkningen lever slet, har daarlige Huse, slider meget ondt paa daarlig Kost, vil en Sygdom
som denne vedblive; saasnart Folkets Kaar bedres, vil Sygdomen mere og mere forsvinde. Det er Hovedsagen
 225

Despite opposition, the law was passed without much debate. The winning argument
was statements from the local Health Commissions which showed that the law would
confirm an already existing practice. From 1877 those affected by the disease were in
Norway sources of contagion in the eyes of the law, and were to be treated as such.
Leprosy in Norway was becoming a legal matter.
In 1885 a new and stricter leprosy Act was passed.607 The new legislation gave

the local Health Commissions power to request the police to forcibly move the
sufferers into the institutions if they failed to live up to the district physician’s
demands for isolation at home. At the same time, the district physicians would for the
first time be reimbursed for their traveling expenses visiting the lepers living in home
isolation. Again, all the preliminary work was done by Hansen, who from 1883
discussed the proposed legislation in all the Municipal Boards (‘Herredsstyrer’) in
Western Norway. He also sent the proposal to the 176 Health Commissions in
municipalities with leprosy patients: 148 supported the act, 10 were negative, while
18 sent their own suggestions, ranging from reviving the call for a marriage ban to
reorganizing the institutions to make them more attractive for the sufferers.608
In parliament, the proposed legislation was interpreted as a technical question
which demanded medical expertise. Since the suggestion came directly from ‘the men
of medical science’ several politicians argued that it was their duty to endorse it. As
the county governor Carl Lauritz Mechelborg Oppen in Northern Bergenhus county,
who supported the Act, put it:

The question at hand, namely if the danger of spreading the disease through contagion is in
reasonable proportion to the restrictions on personal freedoms that the suggestion intends,
and if the restrictions are a reasonable measure to eradicate the disease, can hardly be
judged by other than the men of medical science.609




til at Sygdommen fjernes; man har aldrig gjort Underværker ved Pleiestiftelserne og vil aldrig gjøre det.” Smitt,
Jacob Sverdrup. “Ang. Lov om Forsørgelse af fattige Spedalske.” Stortingstidende 1877, Forhandlinger i
Odelsthinget. 1877: 198, also quoted in Vollset 2005: 73.
607
“Lov angaaende Spedalskes Afsondring og Indlæggelse i offentlig Pleie- eller Helbredelsesanstalt m.V”,
passed June 6, 1885.
608
Vollset 2005: 80.
609
“Det, hvorpaa det her kommer an – nemlig, om Faren for den spedalske Sygdoms Udbredelse ved Smitte
 226

Again the argument was that the proposed act would remind the population that the
disease was contagious and thus encourage them to take proper precautions. Minister
of Justice Aimar Sørensen, however, warned that it was exactly this idea that had led
to inhumane prosecution of leprosy sufferers in antiquity and Medieval Europe:


This lesson was surely known in antiquity, it led to lepers being chased like wild animals
into the forests. I believe that the Act can be dangerous if it is used as such a lesson. People
are easily educated into seeing these people as outcasts of humanity that no longer possess
any human rights.610


The Act came into force on June 6, 1885. But Oppen’s assertion that the legislation
was the collective judgment of ‘the men of medical science’ soon proved to be
wrong. Only Health Commissions in districts with lepers, in other words those who
would get increased powers as a result of the Act, were asked for input. After the
legislation was enacted, this led to heated debates both in the Medical Society of
Christiania, and in two of the national medical journals.
The editor of the Journal for Practical Medicine (‘Tidsskrift for Praktisk
Medicin’, established in 1882), Nils Wulfsberg, argued that all health legislations
should be discussed in the medical societies and printed in medical journals before
being sent to the politicians. The new law would, he argued, result in persecution and
conflicts within families, and inevitably be abused. “From now on, leprosy is not a
disease that evokes involvement and aid, but a crime to punish.”611 Wulfsberg was
not opposed to the theory of contagion, but pointed out that nothing was known about
the precise mechanisms involved. For him, Hansen’s argument that the institutions




staar i rimeligt Forhold til den Indskrænkning i den personlige Frihed, som Forslaget tilsigter, og hvorvidt saadan
Indskrænkning vil blive et væsentligt Middel til den spedalske Sygdoms Udryddelse, – kan vel for Tiden
vanskelig bedømmes af andre end lægevidenskabeligt uddannede Mænd.” Odelstingsproposisjon 12/1885: 9.
610
“Den Opdragelse hadde visselig Folk allerede i Oldtiden; thi da jagede man saadanne Spedalske ligesom
vilde Dyr til de fjerne Skove osv. Jeg tror, at Bestemmelsen netop kan blive lidt farlig, hvis den skal tjene til at
opdrage i den Retning; Folk er meget tilbøielig til at lade sig opdrage paa den Maade, at de betragter disse
Mennesker som et Slags Udskud af Menneskeheden, der ingen Menneskerettigheder længere har.”
Storthingstidende. 1885: 193.
611
“Spedalskhed er fra nu af ikke en Sygdom, der vækker Deltakelse og berettiger til Hjælp, men en
Forbrydelse, hvorefter man hjemfalder til Straf.” (Wulfsberg, N. “Tvangslov og Stiftelser mod Spedalskhed”.
Tidsskrift for Praktisk Medicin. No, 15. 1885: 295.)
 227

were successful because the number of lepers declined, and the declining number of
lepers proved that the institutions were successful, was not enough to justify the new
law.612


Hansen chose to rebut the charges in his own medical journal, Medical Review
(‘Medicinsk Revue’, established in 1884 with Hansen as one of three editors). To
him, the law was ‘humane’.


My position in this regard, is that the most humane act is to protect the healthy from
catching the disease, and that those who have the disease have not only rights, but also
duties – the most important being to not spread the disease to their fellow man.613


According to Hansen, when faced with a disease for which there was no cure, a
humane approach meant prevention. “We are faced with a disease that everyone
acknowledges to be the most horrid and loathsome we know, and the goal is to
prevent its dissemination so that as few as possible will suffer from it.”614 Obviously
investigations into finding a treatment should continue, but until then “It is simply a
question of power and rights, the individual or the society (…) either the healthy must
run away, or the sick person must be put outside society, must be isolated.”615
Wulfsberg also pointed out that almost a third of the beds in the state

institutions were empty. Hansen agreed that the number of patients in the institutions




612
For Wulfsberg a more likely explanation for the decline of leprosy was that the Norwegian lepers had
immigrated to the United States. Hansen rebutted that only 52 known lepers had emigrated from Norway to the
US, while at the same time 3.901 have been admitted to the institutions. (Hansen, Gerhard Armauer. “Den nye
lov om Spedalskheden.” Medicinsk Revue. 1885: 362). Wulfsberg, in turn, pointed to the long incubation period
of the disease and that that many had probably left at the early onset of the disease to avoid detection.
(Wulfsberg, N. “Replik”. Tidsskrift for Praktisk Medicin. 1885: 407.) This debate was the direct precursor to
Hansen’s journey to the United States to investigate leprosy among Norwegian emigrants in 1888-1889.
613
“Min Opfatning i denne Henseende er den, at det er det mest humane at beskytte de friske Mennesker mod at
faa Sygdommen, og at de, der har Sygdommen, ikke alene har Rettigheder som Mennesker, men ogsaa
Forpligtelser, og blant disse som den vigtigste den at ikke paaføre sine Medmennesker Sydommen.” (Hansen,
Gerhard Armauer. “Tvangslov og Stiftelser mod Spedalskhed”. Medicinsk Revue. 1885: 285-286. The reply
was also printed in Tidsskrift for Praktisk Medicin. No. 19. 1885: 391-397.)
614
“Vi staar overfor en Sygdom, som af alle erkjendes at være en af de uhyggeligste og tækkeligste, man
kjender, og det gjælder om saavidt mulig at forebygge Sygdommens Udbredelse, for at saa faa som muligt skal
komme til at lide under den.” (Hansen, Gerhard Armauer. “Den nye lov om Spedalskheden.” Medicinsk Revue.
1885: 352.)
 228

did not fully explain the decline of new cases; rather, the fear of the leper was itself
the best deterrent. “I also believe that in certain districts there must be other factors at
play. These consist of progress of civilization which leads people no longer to
associate with lepers as freely as before.”616
Numerous physicians joined the debate. District physician Thorvald Buchholz,

who ten years earlier had argued it was a mistake to publish Hansen’s arguments for
contagion, repeated that leprosy was a constitutional disorder brought forward by
cultural stagnation and that the legislation was thus based on false premises.617 His
son, district physician Jerome Buchholz pointed out that if the disease was
contagious, it would already be covered by the National Health Act of 1860.
Referring to Milroy’s report from 1867, he concluded that since the disease was not
contagious, there was no justification for the legislation.618
Head physician Edvard Kaurin at Reknes supported the legislation with
reference to isolation or hospitalization being the accepted response to sufferers of
other contagious diseases, such as syphilis, typhus and cholera. What made him
uncomfortable was not that these were diseases that compared to leprosy usually were
resolved in a relatively short time, but the lack of definitive proof for contagion: “Was
the contagion in leprosy an undisputed fact, there could be no doubts about the full
justification of the law.”619 District physician in Lyster, H. R. Smith, saw the law as

nothing more than a natural extension of the relatively uncontroversial 1877 Act:







615
“(…) det er simpelthen et Magtspørgsmaal, hvem der har Ret, det enkelte Individ eller Samfundet (…) enten
maa de friske Mennesker rømme eller den syge Person må sættes udenfor Samfundet, maa isoleres.” (Op.cit:
354.)
616
“(…) jeg tror ogsaa, at der i visse Distrikter maa være endu andre Faktorer, der gjør sig gjældende, og jeg
tror, at disse bestaar i en fremadskridende Civilisation, der lidt efter lidt medfører, at man ikke omgaaes de
Spedalske saa ugenert som tidligere.” (Hansen, Gerhard Armauer. “Tvangslov og Stiftelser mod Spedalskhed”.
Medicinsk Revue. 1885: 289.)
617
Buchholz, Thv. “Om Tvangslov og Stiftelser mod Spedalskhed”. Tidsskrift for Praktisk Medicin. 1885: 383.
618
Buchholz, Jerome. “Den spedalske Tvangssmittelov”. Tidsskrift for Praktisk Medicin. 1885: 476-481.
619
“Var Kontagiositeten et ubestridelig Faktum, kunde der jo ikke reises Tvil om Lovens fulde Berettigelse. Den
fordrer jo kun det samme som ved enhver smitsom sygdom: Isolation eller Indlæggelde paa et Sygehus, og jeg
har aldrig hørt, at vore Bestemmelser om Syfilis, Kolera, Tyfis etc. er inhumane. De kan være høist ubehagelige
og brydsomme for dem, hvem disse Sygdomme rammer, men de er en bestemt Nødvendighed ligeoverfor det
hele Samfund.” (Kaurin, Edv. “Om den nye Lov angaaende Spedalskhed”. Medicinsk Revue.
1885: 349.)
 229

What is then new in the law of June 6, 1885? It gives district physicians’ compensation for
travels and diet for journeys to control the hygienic circumstances, and gives the Health
Commissions a tool to implement their decisions.620



Despite taking place after the law was in effect, and failing to achieve a legislative
rematch, the debate did have an impact. In a circular to the Health Commissions dated
September 15, 1885, Hansen clarified what was meant by the “adequate seclusion”
demanded in the legislation: The lepers must have their own bedroom, at least a bed
not used by others. They might eat with others but must use their own cutlery. The
district physician should “through the Health Commissions attempt to educate people
not to see intermingling with lepers as harmless.”621

While the debate probably made the implementation of the law less severe, it
did lead to forced hospitalizations. From 1891-1895, Reitgjerdet alone reported that
13 of their new patients had been admitted against their will.622
Outside the national context, however, this controversy was never mentioned.
When Henry Vandyke Carter in 1887 referred to the Norwegian legislation in a report
to the Bombay Government, again arguing that they were applicable to India, he made
no references to the dispute. Instead, Carter would echo Hansen’s claim that the
reason why the “sagacious and patriotic legislation” was not implemented earlier
simply showed “how difficult [it has] proved to overcome prejudice or to interfere
with the liberty of the subject.”623 Likewise, when Hansen in Berlin in 1897 proudly




620
“Hva Forandring bringer nu Loven af 6te Juni 1885? Den giver Distriktslægen offentlig Skyds- og
Diætgodtgjørelse til Reiser for at kontrollere de Spedalskes hygieniske Forhold og giver
Sundhedskommissionen et Middel til at faa sine Forskrifter iagttagne.” (Smith, H. R. “Loven om spedalskes
Afsondring m.v.” Medicinsk Revue. 1885: 365.) This opinion was echoed by district physician Lund, who saw it
as a threat which could be invoked against those who refused to comply with the instructions, but that would
never be used in practice. (Lund, Dr. “Den nye Lov om Spedalskes Afsondring og Indlæggelse i offentlig Pleie-
eller Helbredelsesanstalt m. v.” Tidsskrift for Praktisk Medicin. 1885: 397-407.)
621
“Som De vil se, er dette ikke mer end at forsøge paa gjennem Sundhedskommissionen at opdrage Folket til
ikke at betragte Omgangen med Spedalske som en ufarlig Sag.” (Hansen, Gerhard Armauer. “Den nye lov om
Spedalskheden.” Medicinsk Revue. 1885: 356.)
622
Norges Officielle Statistik, Tredie Række no. 287. Beretning om de spedalske i Norge i Femaaret 1891-
1895. 1896: 89.
623
Carter, H. V. Observations on the Prevention of Leprosy by Segregation. 1887: 2. The following year the
City of Bombay did pass a Municipal Health Act aimed at preventing the spread of dangerous diseases such as
cholera, but it turned out not to be of much help dealing with a chronic disease such as leprosy as there were no
facilities for lifelong segregation. (Pandya 2001: 144-153.)
 230

presented the Norwegian leprosy campaign as a system of segregation to be copied by
others, neither the debate nor any of the counter-arguments were mentioned. What
made the legislation successful, Hansen argued, was that it gave the local community
the tools they needed to get rid of the disease. Then it was up to them to decide if this
was something they wanted to achieve.


I find it more humane to protect people against leprosy than to give the lepers the rights and
opportunity to cause other people to catch the disease, and I have no doubt that that we are
doing humanity a big favor in being liberated from leprosy, and [through these measures] it
is indeed possible.624


While Hansen agreed that the disease was not highly contagious, the selective
presentation of the legislation probably influenced the appropriations elsewhere.
Coupled with Hansen’s definition of what a ‘humane approach’ entailed, namely
protection of the healthy majority through removing those suffering from the disease,
this is part of the explanation for the huge disparities in the later interpretations of the
‘lessons from Bergen’.
There was, however, one more difference between the two legislative debates
in Norway: References to the leprosy bacillus. This was not an argument for the 1877-
Act in Norway, nor was it part of the debates in either Norway or India in the 1870s.
In 1885, however, Wulfsberg emphasized that it was the presence of the bacillus that
convinced him that the disease was indeed contagious. The problem, as he saw it, was
that the presence of the bacillus did not indicate what kind of contact was necessary
for the disease to spread, whether the bacillus could live outside the body for instance
as a spore, or whether the disease thus could be spread indirectly. In short, the bacillus
did not say anything about how communicable the disease really was, and could




624
“Ich finde es dagen viel humaner, die Menschen gegen Lepra zu schützen, als den Leprösen das Recht und
die Gelegenheit zu geben, auch andere leprös zu machen, und ich zweilfe nicht, dass wir der Menschheit einen
grossen Dienst leisten würden, wenn wir dieselbe von Lepra befreien könnten; das aber ist unzweilhaft möglich.”
(Hansen, Armauer. “Erste Sitzung, Einleitung.” Mittheilungen 1897. Bd. II. 1897: 17.) The argument was
backed up by references to isolation of other contagious diseases, the reduction in new cases, and that isolation
gave a socio-economic return on investment. (Hansen, Armauer. “Die Isolirung der Aussätzingen und die dazu
erfordelichen Massregeln.” Mittheilungen 1897. Bd. II. 1897: 162-166.)
 231

therefore not decide what measures were necessary or effective. “The claim that since
bacilli are found, the causation is also found is very bold, as no other proof has been
presented other than their presence.”625 The bacillus could equally well be an outcome
of the disease rather than its cause.
In an independent publication, physician and medical biographer Frantz Casper
Kiær supported the legislation with no mention of the bacillus at all. Instead he based
his argument on the historical record: Where the lepers had been isolated, the disease
has diminished or disappeared – where no isolation had taken place, the disease had
been stable or increased.626 This was a repetition of Munro’s argument from 1879.
Hansen, finally, agreed that the presence of the bacillus alone did not prove

contagion, but withheld that this was irrelevant: “I have, as mentioned above, not used
the contagiousness of the disease as an argument in recommending the legislation, but
instead the results of the precautions already taken”.627 Precautions meant isolation.
Like in his 1874 report, the bulk of Hansen’s argument hinged on statistics comparing
new cases, institutionalization and mortality rates in different districts. But this time
Hansen also made frequent analogies with bacterial research on tuberculosis, which
he stressed had striking similarities with leprosy. Furthermore, the argument that the
bacilli were more abundant in the tubercular cases, and that these cases according to
the statistics were the most dangerous regarding possible disease transmission, shows
how in 1885 the presence of a bacillus was increasingly being activated both as an
argument for contagion and isolation, and for deciding whom among the leprosy
sufferers constituted the greatest danger to their surroundings.628
Before returning to India and the British Empire, it is necessary to examine

how the leprosy bacillus was introduced to the debates.




625
“Paastanden, at fordi Baciller er fundne, er ogsaa Aarsagen funden, er derfor i høi Grad dristig, fordi intet
andet Bevis foreligger end, at de er der.” (Wulfsberg, N. “Tvangslov og Stiftelser mod Spedalskhed”. Tidsskrift
for Praktisk Medicin. No, 15. 1885: 382-391, quote on p. 383.)
626
Kiær, F. C. Diskussion i det med. Selskab om Loven angaaende Spedalskes Afsondring m. v. af 1885. 1885:
7.
627
“Da nu Sagen staar saaledes med Hensyn til det strengt videnskabelige Bevis for Spedalskhedens
Smitsomhed, saa har jeg, som ovenfor nævnt, ikke benyttet Sygdommens Smitsomhed som Argument ved min
Anbefaling af Lovforslaget, med derimod Resultaterne af vore hidtidige Foranstaltninger mod Sygdommen”.
Hansen, G. Armauer. “Den nye Lov om Spedalskhed”. Medicinsk Revue. 1885: 358.
 232

Enter the bacillus


Already in a paper published in Norwegian in 1872, Hansen had suggested that
leprosy might be caused by “a virus or perhaps a fungus”, which he argued would
contradict the dominating theory that the disease was hereditary.629 At the end of his
1874 report, published in English the following year, he mentioned the results from
microscopy which he demonstrated for Carter during his visit:


“Examining he samples without any additives, one can here and there discover small rods-
haped elements either stationary or in a weakly oscillating movement; (…) If one adds a
drop of water, the rods move more lively and little by little more and more rods appear; the
older the lesion, the more rods. (…) The size is very different, varying from 0,006–0,0015
mm”.630


While this could be interpreted as a specific cause – strengthening the claim that the
leprosy was a specific (and therefore contagious) disease, Hansen underscored that
the results were uncertain: “a lot is still missing from the direct demonstration of the
specificity of leprosy, but I believe that this report on my research should also inform
about the steps I have taken in this direction.”631
As I have shown, the leprosy bacillus was not an argument for the 1877-Act in
Norway, nor was it part of the debate. In fact, when Hansen was made Head Physician
for leprosy in 1875 it seems he stopped using the microscope for research for several
years. It was not until the fall of 1879 that the bacillus was again presented as a fact,
directly relevant to questions of contagion, legislation and treatment. Despite





628
Op. Cit. 361.
629
Hansen, G. Armauer. “Om vort Kjendskab til Spedalskhedens Aarsager og om vore Forholdsregler mod
Sygdommen”. Norsk Magazin for Lægevidenskaben. 1872: 19-20.
630
“Undersöger man präparaterne uden nogen tilsätning, kan man his tog her opdage stavformige legemer enten
I ro eller I svag oscilllerende bevägelse; når cellerne ere bevarede hele, er deres antal ringe. Sätter man nu en
dråbe vand til präparatet, kommer stavene i livligere bevägelse og lidt efter lidt träde flere og flere stave frem,
jo äldre knuden er, desto flere. (…) störrelsen er meget forsjellig, varierer fra 0,006–0,0015 mm.” Hansen
1874: 77.
631
“det mangler endnu meget til den direkte påvisning af spedalskhedens specificitet, men jeg troede I denne
indberetning om mine undersögelser også at berette om, hvad jeg have foretaget i den retning.” Hansen 1874:
79.
 233

frequently being backdated to 1873, it was three events in the late 1870s that sparked
the lasting interest in the bacillus: Two visits to Norway, new research techniques
developed on the Continent, and bacilli being identified and demonstrated as the
cause of other diseases.
In the summer of 1878 the Swedish physician Fredrik Eklund traveled to
Norway to study leprosy patients, and the same fall he published his findings in a
book in Swedish. In the book, based on 36 Norwegian case histories, Eklund casually
mentioned having observed numerous bacteria in the ulcers, blood, tears and nose
tissues of most of the patients he had examined.632
In July 1879 the German physician Albert Neisser visited Norway and met
with Hansen who provided him with unstained slide preparations and other tissue
samples. Neisser had received his medical degree in Breslau two years prior. Several
of his teachers and colleagues were among the pioneers in microbiology, such as the
pathologists Julius Friedrich Cohnheim and Karl Weigert who researched staining
techniques, and biologist Ferdinand Cohn who had collaborated with Robert Koch in
developing smear tests for the identification of bacteria. Only weeks after he had
returned to Breslau, Neisser succeeded in staining the samples from Norway with
gentian violet and methylene blue, and in October 1879 he demonstrated the bacilli at
a meeting of the Silesian Society for National Culture and published the results.633

The attention led Hansen to publish a paper in Norwegian, German, French and


English titled “Bacillus Leprae” where he claimed precedence for the discovery.634

The goal of the paper was:






632
Eklund 1879. Probably due to language, there were few further references to Eklunds work by other than
Scandinavian speaking physicians. For more on Eklund’s arguments, see Chapter 4.
633
Neisser, A. “Über die Aetiologie des Aussatzes”. Jahresbericht der Schlesischen Gesellschaft für
vaterländische Kultur. 1879: 497–500. Neisser obtained his medical degree from the University of Breslau in
1877, and probably learned the histological staining technique from Julius Cohnheim and Karl Weigert before
they left Breslau for Leipzig in 1877 and 1878 respectively. From 1880 to 1882 Neisser had a junior faculty
position at the University of Leipzig, before returning to the University of Breslau.
634
Hansen, G. A. “Bacillus Leprae”. Nordiskt medicinsk Arkiv. 1880: 1-10; Hansen, G. A. “Bacillus Leprae”.
Virchow’s Archiv. 1880: 32-42; Hansen, G. A. “Bacillus Leprae, études sur la bactérie de la lèpre”. Archive de
Biologie. 1880: 1-16; Hansen, G. A. “The bacillus of leprosy”. Quarterly Journal of Microscopic Sciences.
 234

…to inform about my findings so far in search of the infectious agent, in part to claim
priority on the finding, and in part to present the details in the study that I due to the still
unsecure results did not present in my report to the Medical Association in Kristiania in
1874 regarding my research into the etiology of the disease.635



The main content of the paper was previously unpublished laboratory notes with
details on the examination of samples taken from eleven patients at Pleiestiftelsen in
Bergen, dating the first observation of the bacillus to February 28, 1873. While
Hansen in 1874 had stressed that he was not sure whether what he found were true
bacteria or not, now the reason for doubt was presented as practical difficulties in
producing convincing samples. The method Hansen had used in 1874, namely adding
distilled water and a 1% solution of osmium acid, produced specimens that it took a
trained eye and a sympathetic attitude to recognize.636
Throughout the 1880s, Hansen and Neisser would continue to publish updates
on the bacillus. The later interpretations differ when it comes to how much conflict
the question of precedence really created, and to what extent Neisser was really trying
to claim the discovery for himself.637 Although Neisser quickly stressed that “I have
never demanded priority for the discovery”,638 the question of precedence was not
finally decided until the meeting in Berlin in 1897. There Hansen was declared the
discoverer with Neisser as the one confirming the findings. In the intervening years
even some researchers visiting Norway referred to Neisser as the authority on the
bacillus without mentioning Hansen with a single word, such as the British physician




New Series. 1880: 92-102. According to his autobiography, it was Daniel Danielssen who convinced Hansen to
publish. (Hansen 1910: Chapter 4).
635
Op. Cit, first page. Quote taken from the English version of Hansen’s paper.
636
Hansen 1874: 77-78.
637
Czaplewski, E. “Albert Neisser und die Entdeckung des Leprabazillus”. Archiv für Dermatologie und
Syphilis. 1917: 513–530; Flite, G. L. and H. W. Wade. “The Contribution of Neisser to the Establishment of the
Hansen Bacillus as the Etiologic Agent of Leprosy and the So-called Hansen-Neisser Controversy”.
International Journal of Leprosy. 1955: 418-427; Vogelsang, T. M. “The Hansen-Neisser Controversy, 1879–
1880”. International Journal of Leprosy. 1963: 74–80 and 1964: 330–331; Irgens 1984: 337-343. For a
discussion on priority disputes, see: Merton, Robert K. “Priorities in scientific discovery: A chapter in the
sociology of science.” American Sociological Review. Vol. 22, No. 6. 1957: 635-659.
638
“(...) erkläre ich hiermit, dass ich nie die Priorität für mich in Angespruch genommen habe, bei Lepra zum
ersten Male Bakterien gesehen und auf sie hingedeutet zu haben”. Neisser, Albert. “Weitere Beiträge zur
Aetiologie der Lepra”. Archiv für pathologische Anatomie und Physiologie und für klinische Medizin. 1881:
514-542, quote on p. 515.
 235


Robson Roose.639 The immediate importance of the ‘controversy’ was, however, that
it changed the nature of the debate. While Hansen’s cautious statements in 1874 and
1875 provoked little response, the question was now not whether the bacillus was a
fact or not, but who should receive the honor for its discovery.
Two more events were central to making the perfect conditions for introducing
the leprosy bacillus to the medical community: New staining techniques developed
especially in the German-speaking world, and the identification of other bacillus
causing contagious diseases. German researchers such as Karl Weigert, Paul Ehrlich
and Robert Koch were pioneers in using various dyes for treating and staining
samples, making bacteria visible when observed through the microscope. In his 1880
paper Hansen especially highlighted Koch’s exemplary study of the etiology of
wound infections and his presentation of the anthrax bacillus as the inspiration for
resuming his laboratory studies.640 The plethora of papers and presentations of

bacteria in the early 1880s undoubtedly made the leprosy bacillus easier to accept than
ten years earlier, when arguing that diseases could have a singular cause was
controversial in itself. This illustrates how discussions on leprosy was integrated with
and influenced by circulation of medical knowledge in general.
In many of the papers on bacteriology, the steps taken were explained so that
others could reproduce them and ideally achieve similar results. When Robert Koch
identified the tuberculosis bacillus in 1882, only weeks passed before Paul Ehrlich
demonstrated a new staining method for coloring the bacteria to the Association of
Internal Medicine in Berlin. Koch’s method for staining the preparations was to use
an alkaline solution of methylene blue, the same technique Neisser had used in his




639
This was probably more an indication of available literature than a conscious choice in an ongoing debate.
Otherwise, Roose concluded that “The leprosy question in India will have to be grappled with some day, and it
will become more and more difficult as time goes on. Our knowledge of the disease is doubtless imperfect, but
we are fully cognizant of its horrible character, and of the means by which alone its spread can be arrested.
Compulsory isolation in suitable buildings and under proper care is urgently demanded in the interests not only
of the general community, but of the sufferers themselves.” (Roose, Robson. Leprosy and its Prevention as
Illustrated by Norwegian Experience. 1890: 96).
640
Koch, Robert. Untersuchungen über die Ätiologie der Wundinfektionskrankheiten. 1878. Two years later,
the study was translated to English by W. Watson Cheyne and published by the New Sydenham Society: Koch,
Robert. Investigations into the Etiology of Traumatic Infective Diseases. London. 1880. See also: Gradman
2009.
 236

demonstration of the leprosy bacillus. This rendered the preparations brown with the
bacillus remaining intensely blue. By substituting the methylene with aniline oil, the
preparation was rendered white with the bacteria colored red. The new method, which
was presented with enough detail for reproduction, also cut the time of producing a
sample from 24 hours to less than an hour.641 This probably made it more attractive
for others to put tissue samples under the microscope. The technique was printed in
other journals and given the name ‘Ehrlichs method’. Reports on observations of the
leprosy bacillus kept accumulating, and in 1882, the The British Medical Journal
published an editorial stating that the evidence for the bacillus was becoming stronger
every day.642
When Carter in 1884 for the first time presented the leprosy bacillus to an
Indian audience, he stressed that he had used Ehrlichs method to produce the
preparations.643 Hailing Hansen as the ‘discoverer’, Carter stressed that “In its fresh
state I once saw this organism at Bergen (1873), and soon after at Bombay”.644 A
footnote on page 27 of Carter’s report from Norway published in 1874 was indeed the
first time the bacillus was mentioned in any publication. Then, after referring to the
“minute organisms (a species of Bacterium) which are present in living leprous matter
taken from the interior of a ‘tubercle’”, Carter had quickly underlined that the
inquiries had not terminated in a proper demonstration.645 Also for Carter, it was only
in the 1880s with improved staining methods and bacteria being linked to several
diseases, that the observation could safely be backdated to this first time observation.
But how could observations in the microscope be connected to a specific
disease? As epidemiologist Lorenz Irgens has pointed out, the gold standard for




641
Ehrlich, Paul. “Aus dem Verein für innere Medicin zu Berlin. Sitzung vom 1. Mai 1882.” Deutsche
medizinische Wochenschrift. Vol. 8. 1882: 269-270. Ehrlich was a classmate of Neisser from Breslau and
cousin of Karl Weigert. In 1908 received the Nobel Price in Medicine for his work on immunity. For a list of
Paul Ehrlich’s publications, see: http: //www.pei.de/DE/institut/paul-ehrlich/publikationen/paul-ehrlich-
publikationen.html
642
Editorial. “The Bacillus of Leprosy”. The British Medical Journal. July 29, 1882: 174-175.
643
Carter, Henry Vandyke. Memorandum on the Prevention of Leprosy by Segregation of the affected. Bombay
Castle, March 5, 1884: 7. The paper was also referred to in The British Medical Journal, see: Edmond 2006:
82.
644
Carter 1884: 7.
645
Carter 1874: 27.
 237

proving a bacillus as the cause for a disease was set by Jacob Henle: 1) The bacillus
must be present in all patients with the disease, 2) it must be possible to cultivate
outside the organism, and 3) it must induce a similar disease upon inoculation into an
animal.646 Henle’s postulates would indicate the direction of further laboratory
research. For leprosy, as well as other diseases, the 1880s saw a range of laboratory
studies both regarding staining, inoculations and attempts at cultivating bacteria.647
Hansen’s presentation of his work at the Eight International Medical Congress
in Copenhagen in 1884 (where he backdated the discovery to 1871 or 1872) shows
the importance of Heinle’s postulates. In the presentation, Hansen argued that he had
found the bacillus in all tubercular cases he had examined. While he had observed no
bacilli in anaesthetic cases, some of these patients developed into mixed cases with
bacteria-rich tubercles. Thus, the explanation for the lacking bacilli was reduced to
deficits in the staining technique.648 In the discussion that followed, Neisser added

that the presence of the bacillus in the nerve trunks of anaesthetic cases had now
conclusively been established.649 Thus, Heinle’s first criterion was met.
Both Hansen and Neisser withheld that they had succeeded in cultivating the
bacillus using the same substance that Koch had used for cultivating tuberculosis.
Hansen acknowledged that cultivation was extremely difficult, but withheld that his
observations that the cultured bacilli had produced spores, probably directly inspired
by Koch’s similar observations of the anthrax bacillus, proved the cultivation was
successful.650 Neissers’ observations differed only slightly: “Regarding the spores, my




646
Irgens 1984: 341. The conditions were over time replaced by his student Robert Koch’s famous postulates,
first presented in 1882, and again at the International Medical Congress in Berlin in 1890.
647
For an early study linking the inoculation experiments on animals to previous leprosy research, see: Köbner,
Heinrich. “Ubertraugungsversuche von Lepra auf Thiere”. Archiv für pathologische Anatomie und Physiologie
und für klinische Medicin. 1882: 282-306. For an extensive review of the later experiments, see: Sugai, T and
D. Irisawa. “Gelungene Übertragungsversuche mit Lepra bei Säugetieren”. Lepra Bibliotheca Internationalis.
1908: 145-160.
648
Hansen, G. Armauer. “Die Aetiologie und Pathologie der Lepra”. Congrès Périodique International des
Sciences Médicales. 8me Session – Copenhague 1884. Comptre-rendu. Tomb III, Section de Dermatologie et
de Syphilidologie. 1886: 27-44.
649
Hansen 1886: 43.
650
Robert Koch’s demonstration of stained preparations of the anthrax bacillus, and Louis Pasteur’s presentation
of the famous anthrax immunization experiment at Pouilly-le-Fort were highlights at the previous International
Medical Congress held in London in 1881. Both presentations were reprinted in numerous medical journals.
 238

opinions differ from Hansen, but this is irrelevant. The most important is
acknowledging the Bacillus Leprae as the cause of the disease.”651
According to Hansen’s presentation in Copenhagen, only the third step,
producing the disease upon inoculation in an animal, remained. Despite repeated
experiments on cats, dogs, rabbits, fish and apes, all attempts at inoculation were
unsuccessful (with a possible exception of a dog inoculated by Neisser that had
developed a local lesion but then died before it had developed further). This was
probably because these animals were immune to the disease, Hansen argued. Thus,
the animal experiments “do not prove that the disease spreads from man to man, but
we can unfortunately not experiment on humans, at least not here in Europe.”652

To contagionists such as Hansen, Neisser and Carter, the bacillus proved that
the disease was the same all over the world. In the paper in Copenhagen in 1884
Hansen presented preparations provided by Carter in Bombay, as well as samples
from Granada produced by Neisser.653 When Neisser later that year for the first time
presented the bacillus in a general textbook, he added that he had observed the
bacillus in samples from Brazil, Romania, Palestine, Hundostan [India], Dutch
Guyana and Batavia. In addition he referred to descriptions by Cornil (Spain), Hillaret
and John Hillis (British Guyana), B. Hernando (Spain), Köbner (Brazil), Atkinson
(North America), Majocchi and Pellizzari (Italy).654 This indicates both the speedy
circulation of the new methods, and that the preparations themselves were easy to
transport. Reports that the bacillus was detected in leprosy sufferers also in other parts
of the world undoubtedly strengthened their argument for the bacillus.




651
“Bezüglich der Sporenbildung differire er mit Hansen, doch seien dies unwesentliche Punkte. Das
Wesentlischste sei die Anerkennung des Bacilus leprae als Ursache der Krankheit.” Hansen 1886: 44.
652
“Wenn alle diese Versuche überhapt etwas beweisen, dann ist es jedensfalls nicht mehr als dass wir bisher
kein Thier kennen, das leprös werden kann; sie beweisen aber nicht, dass die Uebertragung auf Menschen nich
gellingen würde; mit Menschen können wir aber leider nicht experimentiren, jedenfalls nicht hier in Europa.”
Hansen 1886: 32.
653
One year after going to Bergen, Albert Neisser visited a leprosarium in Granada, Spain, and continued his
bacteriological investigations. In addition, physician E. Wagner sent a specimen from Dutch Guyana. Thus, in
1881 his argument that the bacillus was universal to leprosy was supported by samples from four Norwegian
cases, three Spaniards and one patient from Dutch Guiana. The details on attempts at staining, cultivation and
animal experiments were all aimed at explaining the process so that the results could be reproduced elsewhere.
(Neisser 1881).
 239

At the same time, the discussion of the bacillus made up less than three of the
seventeen pages of Hansen’s paper in Copenhagen. The bacillus was an addition to
the case for contagiousness, not a decisive argument in itself. Like when making the
case for stricter legislations in Norway, the bulk of Hansen’s evidence consisted of
individual and family cases, local hygienic and cultural conditions, analogies with
other diseases, and that the build-up of a national leprosy apparatus coincided with a
documented reduction in new cases. Based on the assumption that 100 lepers
produced 10 new cases every 5 years, he showed mathematically that even partial
isolation would lead to a reduction in the number of new cases. The model was then
compared with the actual statistics from Norway, concluding that “the numbers show
a quite constant reduction in new cases in the following five year period, about 9% to
8%”.655 Since the disease (increasingly meaning the pathogen, the bacillus) was

universal, so was the mathematical model.
Not everyone was convinced. In the discussion that followed the presentation
physician Démétrius Alexandre Zambaco Pacha, educated in Paris and working in
Constantinople, argued that “the Mediterranean leprosy is not in absolute parallel to
the one in the North (…) it might have more in common with the leprosy of the
Orient”.656 He made no reference to the bacillus, but focused on the clinical diagnosis.
Around the Mediterranean the proportion of anesthetic cases was larger and the
disease produced changes in skin pigmentation. This fit better with clinical
observations from India than the observations from Scandinavia. Seeing leprosy in







654
Neisser, A.“Chronic Infectious Diseases oft he Skin”. In: Ziemssen, Hugo Wilhelm von. (ed.) Handbook of
Diseases of the Skin. 1885 [1884]: 318.
655
“Es zeigen diese Zahlen ein ziemlich constantes Procentverhältniss der neuen Fälle in einem Quinquennium
zur Zahl der Leprösen im vorigen, ungefähr 9% oder 8%”. (Hansen 1886: 39.) When Robert Koch received the
Nobel Prize in Medicine for his investigations and discoveries in relation to tuberculosis in 1905, he highlighted
“the exceptionally instructive example of the fight against leprosy in Norway” to justify the value of partial
isolation, and argued that the same lesson was applicable also to campaigns against tuberculosis. See:
http://www.nobelprize.org/nobel_prizes/medicine/laureates/1905/koch-lecture.html.
656
“La lèpre du midi n’est pas absolument pareille à celle du nord (…) un seul de ces sujets à quelque
ressemblance avec la lèpre d’Orient”. (Zambaco Pacha in: Hansen 1886: 40.) Interestingly, Zambaco Pacha’s
objections were not mentioned in the otherwise thorough review in The British Medical Journal, possibly
because the reviewer did not understand French. See: “International Medical Congress … Proceedings of
Sections”. The British Medical Journal. August 30, 1884: 426.
 240

different parts of the world as slightly different diseases did not initially lead him to
question Hansen’s findings – he merely declared them locally irrelevant.
Not only did the diagnosis differ, so did the etiology of the Mediterranean
leprosy. Zambaco Pacha’s argument was, typically, based on his own local experience
telling him that leprosy appeared mainly in families. “I have never observed a single
case of contagion.”657 When also his attempts at inoculation all failed, experience led
him to conclude that in addition to heredity most cases developed spontaneously,
possibly influenced by diet, climate and uncleanliness.
In the following decades Zambaco Pacha would continue to argue for this
disease model. In his 385 page monograph La contagion de la lèpre en l’état de la
science (1907), Zambaco Pacha argued that bacteriology, although an attractive
theory, could explain neither how contagion happened, nor why numerous examples
of people living “even in complete promiscuity” with lepers did not catch the disease.
In his opinion, time was overdue for the bacteriologists to apologize for their
speculative assertions.658 While the monograph received a devastating review by the
Tunis-based French physician G. Eichmüller in Lepra Bibliotheca Internationalis,
Zambaco Pacha’s publication is one of several examples of how different disease
models continued to compete for hegemony well into the 20th century.659 The review




657
“Je n’ai pas vu un seul fait de contagion de la lèpre.”( Zambaco Pacha in: Hansen 1886: 43.)
658
Eichmüller, G. “Zambaco Pacha: La contagion de la lèpre en l’état de la science”. Lepra Bibliotheca
Internationalis. 1907: 128. The book was followed by L’Hérédité de la Lèpre (1908), which argued for
establishing leprosy colonies to separate the sexes and thus prevent the heredity which he held to be the the
single undeniable cause of the disease. This conclusion was reached after decades of research. In the early
1890s, Zambaco Pacha had presented first a study of leprosy in Egypt, Palestine, Greek islands, Cyprus and
Crete (Zambaco Pacha, Dr. Voyages Chez les Lépreux. 1891), and then the the French Mediterranean in a
lecture for the Academy of Medicine in Paris. (Zambaco Pacha, Dr. D. A. La Lepre dans le Midi de la France
en 1893. Communication faite à l’Académie de Medecine le 9 mai 1893. 1893). Among numerous honors, he
received the Prix Monthyon from the Academy for his work. In addition to the International Medical
Congresses Copenhagen in 1884 he presented leprosy in international conferences (general and dermatological)
in London, Vienna, Rome, Paris, Moscow, Madrid, and Lisbon (Zambaco Pacha, Démétrius Al. Anthologie. La
Lèpre a travers les siècles et les contrées. 1914: V-VI). At the International Leprosy Conference in Berlin in
1897 he argued that Morvan’s disease and several other constitutional disorders were in fact variants of leprosy.
(Zambaco Pacha. “Des rapports qui existent entre la maladie de Morvan, la Syringomyélie, la Sclérodermie, la
Sclérodatylie, la Maladie de Reynaud, La Morphée des Contemporains, l’Aïnhum, l’Atripie musculaire
progressive Aran-Ducheune, et la Léprose.” Mittheilungen 1897. Bd. 2. 1897: 20-80).
659
Competing disease models could exist within the same Empire. In the Dutch colonies, for instance, leprosy
was in the middle of the 1880s considered non-contagious in the East Indies and a decidedly contagious disease
in the West Indies. (Van Eyk, Sprenger. “The Netherland’s Colonies”. In: Leprosy in foreign countries. 1886:
188-190.)
 241

also illustrates how contagion was the hegemonic position in the columns of this
international journal. Without exception, all studies not arguing for the
contagiousness of leprosy received negative reviews.
Those who recognized the bacillus as the core of the disease probably saw
reports from afar as more relevant compared to those who saw the disease as locally
or regionally distinct. But concurring that a bacillus was present did not necessarily
entail complete agreement. Instead, the demonstration of its presence spawned
numerous new disputes. Whether the bacillus was found inside or between the cells
was the focal point of a debate between Hansen and physician Paul Gerson Unna
from Hamburg that would last for a quarter of a century.660 In 1886, two years after

visiting Bergen, the French dermatologist Henri Leloir suggested that the bacillus
could be spread via mosquito-bites or other insects, a theory that also would lead to
both controversy and research efforts.661 The same happened with experiments on
animals, where apparently successful inoculations turned out to be difficult, if not
impossible, to reproduce.662
Around the turn of the century Moscow-based physician W. J. Kedrowski
would take Hansen’s theory of the bacilli producing spores as the starting point for
renewed cultivation attempts, and argue that the acid-fast bacillus observed through




660
Unna founded the semi-monthly Monatshefte für Praktische Dermatologie in 1882, and in 1884 he visited
Bergen. Back in Hamburg he had his own private skin clinic where he also taught international students the
latest clinical and laboratory techniques, as well as experiment with therapies. Unna’s position was that the
bacillus was mainly found in the lymph between the cells. This meant that the bacillus craved oxygen and could
be treated by removing the oxygen through drugs or applying pressure. To Hansen and Neisser, who claimed
that the bacillus was only found inside the cells, this strategy for treatment was meaningless.
661
Donald H. Currie’s dissections of 493 mosquitoes that under controlled conditions had fed on eleven leprosy
sufferers at the Public Health and Marine Hospital Service on Hawaii in September 1910 was probably the
largest such experiment. For an overview, see: Lebæuf. “Recherches expérimentales sur la valeur du rôle que
peuvent jouer certains insectes hématophages days la transmission de la lèpre.” Lepra Bibliotheca
Internationalis. 1914 : Fasc. 1, originally published in Bulletin de la Société de pathologie exotique. 1912. See
also: Benchimol, Jaime L. and Magali Romero Sá. “Adolpho Lutz and controversies over the transmission of
leprosy by mosquitoes”. História, Ciências, Saúde - Manguinhos, vol. 10 (supplement 1). 2003: 49-93.
662
For an extensive review of animal experiments on mammals such as rabbits, dogs, apes, guinea pigs, rats,
mice, cats and birds, see: Sugai, T. and D. Irisawa. “Gelungene Übertragungsversuche mit Lepra bei
Säugetieren”. Lepra Bibliotheca Internationalis. 1908: Fasc. 3. The largest experiment took place in San
Francisco, California, between 1908 and 1911, and consisted of examining 200.000 rats for the naturally
occurring ‘rat leprosy’’, a possible analog to human leprosy. The leprosy-like disease was found in lesions from
186 of the rats, giving a prevalence of one out of 1075. (McCoy, George Walter. “Observations on naturally
acquired rat leprosy”. Lepra Bibliotheca Internationalis. 1914: Fasc. 2, originally published in Public Health
Bulletin. Washington, July. 1913).
 242

the microscope was but one of several stages in the life cycle of the pathogen.663 In
general, however, the bacillus was not so much a topic in itself, but it was quickly
entangled in other debates regarding the nature of the disease, with direct
consequence first on legislation and therapies, and later also on diagnosis.
The bacillus was also made part of an already existing narrative based on
historical records. In Britain the argument that the global distribution of the disease
could be traced throughout history was introduced by William Munro, late Medical
Officer to St. Kitts in the West Indies and member of the Pathological Society of
London.664 In his book Leprosy (1879), Munro traced the first written sources on the
disease to Antiquity (whether it first occurred in Egypt, Africa, India or China
remained an open question), and its subsequent introduction to Western Europe from
Greece and the Middle East in early Medieval times. Its disappearance from Europe,
he argued, was a direct consequence of ‘lepers’ were being kept strictly apart from the
healthy. The disease was then introduced to the New World by the trans-Atlantic slave
trade. In the late 1840s, leprosy was transported over the Pacific as a stowaway with
the import of Chinese labor. This was also the case for Australia where the disease
too, according to Munro, was introduced by the Chinese.665 A central premise for the
argument was that leprosy was the same disease throughout history and throughout
the world. Munro frequently referred to reports on prevalence from physicians around
the world. Again, relating to the results of researchers in other parts of the world was
more relevant for the contagionists, than for those who, like Zambaco Pacha, saw the
disease as locally distinct. Munro made no mention of the bacillus, but the bacillus
would fit hand-in-glove with the narrative of a disease that throughout history had




663
See i. e. Kedrowski, W. J. “Über die Kultur des Leprabacillus”. Lepra Bibliotheca Internationalis. 1901:
Fasc. 4, originally published in Zeitschrift für Hygiene und Infektionskrankheiten. No. 1. 1901. Kedrowski’s
bacteriological model had some supporters, see i.e.: Bayon, H. “The Present Position of Leprosy Research
(Paper read before the Meeting of the British Medical Association at Cape Town 24. October 1912)”. Lepra
Biblioetica Internationalis 1914: 54. For an extensive (but by no means exhaustive) overview of cultivation
experiments, see: Thompson, J. Ashburton. “Experimental Leprosy: A perspective”. Lepra Bibliotheca
Internationalis. 1914, Fasc. 1.
664
Munro 1879.
665
For an account of leprosy as a foreign threat (a ‘yellow peril’) in colonial Queensland, and links between
leprosy and xenophobia, see: Robertson 1999. For a similar argument based on comparing the US leprosy
policies on Hawaii and the mainland, see: Moran 2007.
 243

spread around the globe. The bacillus did not create the argument, but certainly served
to strengthen it.
On the other hand, contagion was not the only disease model that took as its
starting point that the disease was the same all over the world. The prominent British
physician Jonathan Hutchinson argued that those having extensive local experience
“encounter some real disadvantage, in the risk that their attention may be
unconsciously drawn too closely to circumstances which are, after all, only local.”666
Since his own experiences with the disease was limited to the few leprosy sufferers

that ended up in London hospitals, as well as a visit to Norway in 1867, he argued that
he was in a better position to produce an unbiased account of the ‘whole picture’
compared to those who had worked with the disease their whole life. Given that the
disease was the same throughout the world and throughout history; his conclusion
was, as I showed in Chapters 3 and 4, that the disease was not caused by contagion
but eating badly cured fish.


“I believe that the advance of Christianity, with its salt-fish feasts, and not the Crusades,
was mainly conducive to the general prevalence of the disease in Europe during the Middle
Ages; that its spread is always due to food and never to contagion, and its disappearance to
an improved dietary, and not in the least to enforced isolation.”667

According to this theory, the appearance of lepers in the same family or geographical
area was explained by them having eaten the same poisonous food. It also explained
the global prevalence: “Wherever a community is to be found which subsists chiefly
on fish, there leprosy is present.”668





666
Hutchinson, Jonathan. “Memoranda for Future Investigations as to the Cause of Leprosy”. Journal of the
Leprosy Investigation Committee. Vol. 1, 1890: 67-89, quote on p. 67. Throughout his career Hutchinson
published about 1200 medical papers, and produced the quarterly Archives of Surgery (1890-1900). His list of
presidencies in medical societies include the Hunterian Society (1869-1870), the Pathological Society (1879–
80), the Ophthalmological Society (1883), the Neurological Society (1887), the Royal College of Surgeons
(1889), the Medical Society (1890), and the Royal Medical and Chirurgical Society (1894-1896). He was also
the Royal College of Surgeon’s representative to the Leprosy Investigation Committee (1889-1896) For a brief
biography, see: http: //www.whonamedit.com/doctor.cfm/887.html
667
Op. Cit. 68.
668
Op. Cit. 78.
 244

Hutchinson first presented the ‘Fish Hypothesis’ in 1858, and would support it
until his death in 1913.669 By the Tenth International Medical Congress in Berlin in
1890, he had incorporated the bacillus in the theory as the identification of the poison
that was found in the contaminated foodstuffs.670 Further research, Hutchinson
argued, should be to put fish under the microscope to search for the bacillus there.
After his theory was blatantly ignored at the First International Leprosy Conference in
Berlin in 1897, Hutchinson traveled to South Africa and India to interview lepers in
search of proof for the theory. The results of the journey were then presented at the
71st annual meeting of the British Medical Association in Swansea in 1903, where he
received a mixed response. Sir Patrick Manson, medical advisor to the Colonial
Office was not convinced: “If fish was the medium by which the bacillus entered the
body, how did it get into the stinking fish?”671 George Pernet, who by then had taken
over as the London-based editor of Lepra Bibliotheca Internationalis, was even less
diplomatic: “According to Mr. Hutchinson apparently, lepers who deny ever having
eaten fish are not to be believed, but their statement as to never having seen a leper
must be taken as an incontrovertible fact.”672 Hutchinson did have some supporters,
but in Lepra Bibliotheca Internationalis, where Hutchinson was listed as one of the
founding editors at the front page of every issue, reports would accumulate from
around the world showing no connection between leprosy and the eating of fish. Over
time the theory would be increasingly ridiculed to the effect that Hutchinson instead
chose to publish his theories elsewhere.673




669
For a typical defense of the fish-eating hypothesis, see: Hutchinson, Jonathan. “On Leprosy and its
connection with the use of uncooked fish”. Mittheilungen 1897. Bd. 2. 1897: 20-23.
670
Hutchinson, Jonathan. “The causes and origin of leprosy”. Verhandlungen des Internationalen
Medicinischen Congresses Berlin, 4.-9. August 1890. Bd. 4, part 13. 1892: 43-49.
671
Hutchinson, Jonathan. “Discussion in leprosy: Its etiology, histology and treatment”. Lepra Bibliotheca
Internationalis 1905: 202, originally published in The British Medical Journal, September 26, 1903.
672
Op. cit.: 203.
673
After George Pernet’s devastating review of Hutchinson’s 420 page monograph On Leprosy and Fish-
Eating. A statement of Facts and Explanations in 1906, Hutchinson’s publications were not referenced in Lepra
Bibliotheca Internationalis. “All modern evidence points to this, that leprosy is the result of the invasion of the
human organism by a micro-organism the bacillus of Hansen, from outside, and thus the disease is conveyed
from man to man. Medicine has left behind it, for good be it hoped, the dialectical methods of medieval times
and the old scholastic disputations of the Sorbonne, so humorously satirized by Rabelais. The publishers are to
be congratulated on the get-up of the book.” (Pernet, George. “Jonathan Hutchinson, London: On Leprosy and
Fish-Eating. A statement of Facts and Explanations (Constable, London, 1906, pp. 420)”. Lepra Bibliotheca
 245

Proof and human experiments


Even for those convinced that the disease was contagious and caused by the bacillus,
the lack of convincing and undispoted proof was problematic. To produce proof for
the theory of contagion was the direct motivation for experiments on humans. Some
of the experiments, such as the British-born German physician Eduard Arning’s
inoculation of a man sentenced to death for killing his lover’s husband on Hawaii in
1886, were made public and widely discussed.674 On the one hand the man did

develop leprosy after the inoculation, on the other it turned out he had family
members with leprosy, ate the same food as other ‘lepers’ and lived under the same
conditions. Hansen’s own human experiment in Bergen, though, did not receive
attention although it had direct consequences for his ability to do research.
After corresponding with Robert Koch in the fall of 1879 regarding his failed
attempts at producing leprosy in rabbits and cats, Koch suggested that these animals
were immune to the disease. Hansen then inoculated a female patient at Pleiestiftelsen
in Bergen suffering from anaesthetic leprosy. The experiment consisted of injecting
her in the eye with a sample from a patient with the tubercular variant. The goal was
to produce proof of contagion by using a person that beyond doubt was susceptible to
the disease. As Hansen later explained in his police statement; “even though the test
subject should suffer some, I chose a patient that had been a leper for several years
and therefore would not cause a new disease. I especially considered both the great
scientific and national importance of the question at hand.”675




Internationalis. 1907, Fasc 2.) In 1909, Hutchinson presented his fish-eating theory at the second international
leprosy conference in Bergen. From the published proceedings it appears it was simply ignored by the other
attendees.
674
Arning, E, “Eine Lepraimpfung beim Menschen und Demonstration einer Sammlung von Lepraabgüssen.”
Verhandlungen der Deutschen Dermatologischen Gesellschaft, I, Congress gehalten zu Prag, 10-12/6, 1889.
Wien, 1889. See also: Tebb 1893: Chapter 3; Edmond 2006: 90-92; Bushnell, O. A. “Dr. Edward Arning. The
First Microbiologist in Hawaii.” History of Science in Hawaii. No. 3. 1967: 1-30.
675
“Selv om vedkommende forsøgsobjekt skulde lide noget derved, når jeg til sådant valgte en patient, der
allerede i flere år havde vært spedalsk og hvem jeg derfor med mit forsøg ikke kunde påføre nogen ny sygdom,
og det, især som når jeg betenkte den store både videnskabelige og nationale betydning, afgjørelsen af det
forutliggende spørgsmål vilde have.” BSA. I.C.c.133. Byfogd og byskriver i Bergen, case number 99/1880.
“Forklaring fra G. A. Hansen til Overrettssagfører Mowinckel”, dated April 23, 1880. For details and
assessments of trial, see: Vogelsang, Th. M. “Gerhard Henrik Armauer Hansen 1831-1912: The Discoverer of
the Leprosy Bacillus: His Life and Work.” International Journal of Leprosy. 1978: 257-332; Robertson, Jo.
 246

After repeated complaints, the hospital minister August Grønvold took Hansen
to court, referring to “the fear and bitterness that the medical experiment has produced
in all the patients, an exasperation that can lead to unpredictable consequences”.676 In
a Royal Decree dated April 17, 1880, Hansen’s positions as physician and head of the
national leprosy apparatus were separated, and six weeks later Hansen was sentenced
in the Bergen Municipal Court to lose his licence to practice at the institution and pay
for the costs of the trial. The verdict was in line with the recommendation from the
Medical department. Hansen did, however, remain head physician for leprosy.677
After the verdict, Hansen’s office was moved to Bergen Museum, and his

production of new knowledge about leprosy could no longer be based on working
directly with patients. In other words: The sentence limited his ways of working, and
thereby the way of knowing the disease. The verdict made headlines in Norwegian
newspapers.678 But abroad, the sentence was not brought up in the later public debates
regarding the Norwegian leprosy legislations, nor in at any of the conference
proceedings or publications until rediscovered by Vogelsang in 1963.679
Although legislative texts were part of the knowledge that was circulated, as I
mentioned in the previous chapter, the exact details on what went on behind the
scenes were seldom mentioned. The physicians were selective in choosing what
stories to share with colleagues. Knowledge circulation was thus only the tip of the




“The Leprosy-Affected Body as a Commodity: Autonomy and Compensation”. In: Ferber, Sarah and Sally
Wilde. The Body Divided: Human Beings and Human ‘Material’ in Modern Medical History. 2011: 131-165;
Vollset 2005: 74-79.
676
“(…) den Frygt og Forbittrelse som samme medecinske Forsøg har fremkaldte hos dens samtlige Lemmer,
en
Forbittrelse, der kan medføre uberegnelige Følger.” Bergen State Archives: Kopibok for Pleiestiftelsen. Letter
to the supervisory committee, dated November 21, 1879. In: Vollset 2005: 75.
677
BSA: Byrettssak 99/1880: 5.
678
The case was referred to on the front pages of Bergensposten (June 3, 1880), Bergen Aftenblad (June 5,
1880), as well as the Christiania-based newspapers Dagbladet and Aftenposten. Vollset 2005: 79.
679
Vogelsang, T. M. “A serious sentence passed against the discoverer of the leprosy bacillus (Gerhard
Armauer Hansen), in 1880.” Medical History. 1963: 182-186. When Hansen in Berlin in 1897 presented an
overview of inocculation experiments on humans, he did not include his own experiments. (Hansen, G.
Armauer. “Uebertragung der Lepra von Mensch zu Mensch”. Mittheilungen 1897. Bd. 1, II. Abtheilung. 1897:
1-5.) Hansen did not mention the case in his autobiography. (Hansen 1910). In 1973, Justice Knut Blom of the
Norwegian Supreme Court concluded that the sentence was in accord with contemporary law and that the case
marked the genesis of the principle of informed consent in Norwegian medical research. (Blom, K. “Armauer
Hansen and human leprosy transmission. Medical ethics and legal rights.” International Journal of Leprosy.
1973: 199-207. See also: Vollset 2005: 74-79).
 247

iceberg, and underlines the need for local studies, as well as studies of transfers of
knowledge that can investigate each connection more closely. Although it is safe to
assume that not everything was written down, correspondence is a source that might
give further details than this study has allowed.




Rematch in the British Empire


Back in Britain, Gavin Milroy ended the public defense of his 1867-report around
1880 due to ill health. In his absence reports from the colonies arguing that the
disease was contagious, as well as explicit critiques of the 1867-report, were now
printed without immediately being rebutted by the College of Physicians. Both
Carter’s 1884-paper, where he presented his own bacteriological findings to audiences
in India, and his 1887-paper, where he again argued for Norwegian-style segregation,
was referred to in the British Medical Journal and The Lancet.680 The 1880s also saw
several publications arguing for segregation aimed at a general public.681 Still, it was
events in Hawaii, especially reports that the Belgian Catholic priest Jozef de Veuster
(better known as Father Damien) had caught the disease, which eventually would
force a rematch in the British Empire.682
As I mentioned in the previous chapter, the first report a of dramatic increase
of leprosy on Hawaii came in the mid 1860s when the German physician William
Hillebrand sent a letter to physician Ch. Macnamara in Calcutta where he argued that
the disease was in rapid increase on the islands. Macnamara in turn printed the letter




680
Edmond 2006: 82; Carter, Henry Vandyke. Memorandum on the Prevention of Leprosy by Segregation of
the affected. Bombay Castle, March 5, 1884; Carter, H. V. Observations on the Prevention of Leprosy by
Segregation. 1887. Both are available online from the National Library of Scotland: http:
//digital.nls.uk/indiapapers/browse/pageturner.cfm?id=74561442; http:
//digital.nls.uk/indiapapers/browse/pageturner.cfm?id=74559842.
681
I. e. Lambert, Agnes. Leprosy: Present and Past. The Nineteenth Century. 1884; Wright, Henry Press.
Leprosy and Segregation. 1885; Wright, Henry Press. Leprosy: An Imperial Danger. 1889. See: Edmond 2006:
84-85.
682
Carter was among those who highlighted Damien as a clear example of direct contagion: “[W]ith respect to
the seemingly direct communication of diseased to healthy persons living in intimate and prolonged contact
with the affected, several such affirmative instances are known; one of the latest, and perhaps clearest, is being
that of Father Damien at the Sandwich Islands.” Carter 1887: 3.
 248

as an appendix to his report Leprosy (1865). In it, Hillebrand claimed that the islands
had 230 ‘lepers’ among a native population of 67,000. More importantly, these were
all new cases: The disease “cannot be traced farther back than the year 1852, or at
most, 1848”.683 It had since spread rapidly, the first six cases in the immediate
neighborhood of the first. This showed that the disease could not be hereditary but
spread through contact. Again, contagionism did not depend on bacteriology or
Hansen’s discovery.
On Hawaii, Hillebrand’s reports led to the passing of an Act to prevent the
spread of leprosy in 1865. As historian Michelle Moran and others have shown, from
1866 more than a hundred leprosy sufferers and sent to the isolated ‘leper settlement’


of Kalawao on the island of Molokai very year.684 Between 1881 and 1908, 3,940


‘lepers’ were apprehended.685


When the Royal College of Physicians in 1874 was asked by the Colonial
Secretary to comment, they dismissed the observations as “lacking in precision, as
well as deficient in details,” pointing out that Hillebrand himself had arrived only in
1851.686 The claim that the disease was introduced by Chinese only three years earlier

was therefore considered hearsay evidence:


The apparent rapid increase of leprosy began to be noticed, too, coincidentally in point of
time with the establishment of the Queen’s Hospital and Dispensary, the number of lepers
who applied for relief at the hospital augmenting year by year. The truth may be that the
presence of the leprous amongst the population at large was only more clearly perceived on
account of their seeking relief in greater number at the hospital as this became better
known.687






683
Macnamara, Ch. Leprosy. Calcutta, February 3. 1865: 53.
684
Moran 2007.
685
Brinckerhoff, Walter R. and A. C. Reinecke. “A statistical study of an endemic focus of leprosy”. Public
Health Bulletin. No. 33. 1910: 3.
686
“Recent Official Correspondence relating to Leprosy”. British and Foreign Medico-Chirurgical Review.
1874: 206-207.
687
Op. Cit. In the late 1880s, Eduard Arning, the German physician who inoculated the Hawaiian murderer,
examined a large number of skeletons found in burial caves “without ever finding the characteristic lesions of
leprosy.” (“Debate on Leprosy at the International Medical Congress, Berlin, 1890.” Journal of the Leprosy
Investigation Committee. No 2. 1890: 233-234.; British Journal of Dermatology. September 1890;
 249

This did not put a stop to explanations based on contagion. In 1879 the reports from
Hawaii was a case in point for William Munro, who withheld that what was unfolding
on the islands in the Pacific was a repetition of what had happened in medieval
Europe: “The spread of the disease has been like that of all epidemics at their
commencement – fearfully rapid – and reminds us of its behaviour in Europe after the
Crusades, when everything was in its favour. There were last year no less than 700
lepers in the Leper Settlement which has been established by the Government 20
miles from Honolulu”.688

Already the year after Milroy died, in 1888, reports from the colonies as well
as continued bacteriological findings led the Colonial Secretary to ask the College of
Physicians if they still maintained that the disease was hereditary. In the reply the
College acknowledged that this opinion had never been accepted by the general
public of the colonies where leprosy was endemic, and set down a new Leprosy
Committee to again investigate the pathology of the disease.
A month later, on April 15, 1889, Father Damien died of leprosy on
Molokai.689 The news soon reached other parts of the world through the popular
press. In Norway, this was seen as a confirmation that Hansen had been right all
along, and that the measures taken had avoided a disaster. In Britain it caused a public
outcry. For some, it was proof that the disease indeed did pose a danger to Europeans;
for some it was an argument for further support to missionaries and their selfless
sacrifices. For yet others, it merely showed that the ‘Biblical’ disease still existed, and
that the sufferers deserved better care.690





Verhandlungen des Internationalen Medicinischen Congresses Berlin, 4.-9. August 1890. Bd. IV, part 13.
1892: 45.)
688
Munro 1879: 38.
689
The Belgian Roman Catholic missionary Damien de Veuster (Father Damien) had worked among the eight
hundred lepers in the secluded settlement Kalaupapa since 1873, and in 1884 he was diagnosed with leprosy.
To missionaries, his death from the disease later became a powerful symbol of martyrdom, and religious self-
sacrifice. See: Edmond 2006: 90-102; Moran 2007: 21ff; Gould 2005: 59-102.
690
In the Prince of Wales’ dinner speech at a fundraising for The National Leprosy Fund in London on January
13, 1890, he took the latter view. The death of Damien was a reminder that it was “imperative that something
should be done, not only for the sake of the unhappy lepers themselves, but for t he benefit of the whole
community.” The pinnacle of the talk was a letter presented by a leper to Lord Lawrence (later Viceroy of
India), probably from the mid-1850s, which underscored the desperation on behalf of those affected by the
disease: “Hail, cherisher of the afflicted. Be it known to your enlightened mind that your devoted servant has
 250

The most important outcome was the establishment of The Father Damien
Memorial Committee with the Prince of Wales as its president.691 As subscriptions
and donations were raised, the Committee was soon renamed The National Leprosy
Fund.692 In addition to erecting a memorial to Father Damien, the formation of a fund
for indigent British ‘lepers’ in the United Kingdom, and sponsoring two ‘Leprosy
Studentships’, reassessing ‘the leprosy problem’ in India was established as one of the
top priorities. Both the College of Physicians and the Royal College of Surgeons were
invited to nominate members to a special Leprosy Commission to India, which made
the College of Physician’s Leprosy Committee obsolete.693 Sparked to a large extent
by events in Hawaii, the National Leprosy Fund would in the early 1890s be the
driving force for a rematch over the question of etiology in the British Empire.694 As I
showed in the previous chapter, their conclusions in 1893 would be that although the
disease could technically be classified as a contagious disease due to the presence of
the leprosy bacillus, claims that the decline of the disease could be attributed to
compulsory isolation was “entirely erroneous”. Instead, the report repeated that the
disease was in practice best addressed through sanitary improvements.

Though in a scientific classification of diseases leprosy must be regarded as contagious and
also inoculable, yet the extent to which it is propagated by these means is exceedingly small.




been a leper for many years. My limbs have fallen off piece by piece; my whole body has become a mass of
corruption; I am weary of life; I wish to die. My life is a plague and disgust to the whole village, and my death
is earnestly longed for. It is well-known to all that for a leper to consent to die, to permit himself to be buried
alive, is approved of by the gods, who will never afflict another individual of the village with a similar malady. I
therefore solicit your permission to be buried alive. The whole village wishes it, and I am happy and content to
die. You are the ruler of the land, and without your leave it would be criminal. Hoping that I may obtain my
prayer, I pray that the sun of prosperity may ever shine on you.” (“Account of the Dinner in aid of ‘The
National Leprosy Fund.’” Journal of the Leprosy Investigation Committee. No. 1, 1890: 14-20, quotes from
pages 17-18.)
691
The Prince of Wales traced his interest in leprosy to 1885, when he visited a leprosy asylum in Norway.
(Abraham, Phineas S. “Introduction: Account of the Origin of the National Leprosy Fund”. Journal of the
Leprosy Investigation Committee. No. 1. 1890: 5-20. See also: Edmond 2006: 90-107.)
692
For details, see: Edmond 2006: 92-99.
693
The Commission had six members. The National Leprosy Fund nominated George N. Curzon, Under
Secretary for India (chairman) and Edward Clifford; the Royal College of Physicians nominated Dyce
Duckworth and G. A. Heron; the Royal College of Surgeons nominated Jonathan Hutchinson and N. C.
Macnamara. In addition, an Executive Committee had the following members: Ferdinand Rotschild (chairman),
F. Londin, Andrew Clark, James Paget, J. Fayrer, W. Guyer Hunter, Jonathan Hutchinson, E. Clifford,
Algernon Borthwick, Edward Lawson and J. R. Somers Vine.
694
Edmond 2006: 107-108.
 251

(…) Leprosy is indirectly influenced by insanitary surroundings, such as poverty, bad food,
or deficient drainage or ventilation, for these by causing a predisposition, increase the
susceptibility of the individual to the disease.
Leprosy in the great majority of cases originates de novo, that is, from a sequence of
concurrence of causes and conditions, dealt with in the report, and which are related to each
other in ways at the present imperfectly known.695


In Bombay the question of etiology was up for a rematch even before the National
Leprosy Fund got involved. After returning to Bombay around 1883, Carter continued
to stay in touch with Hansen who forwarded him the latest official statistics from
Norway. These provided the basis for reports Carter published in 1884 and 1887,
where he again argued that the decline of leprosy in Norway was unexplainable
“except upon the hypothesis of contagion, no other explanation of events seems
possible”.696 All efforts to suppress the disease, Carter argued, should be based on this
premise. According to Pandya, newspaper editorials in Bombay subscribed fully to
the model of leprosy as contagious, and argued for legislations aimed at removing
especially poor and vagrant leprosy sufferers from the streets.697 Most of the local
physicians, however, referred to Milroy and saw no scientific basis for contagion and
segregation.698 Leprosy in the vast Indian countryside was not an issue.
Towards the end of the 1880s, after pressure from the local elites who feared

that the disease was dangerous, the Bombay government felt forced into action. In

1888 the City of Bombay passed a Municipal Act for preventing the spread of


“dangerous diseases, such as cholera”,699 but attempts at applying the legislations to









695
Leprosy in India. Report of the Leprosy Commission in India, 1890-91. Calcutta. 1893: 4. This was a
compromise which not everyone agreed to. In a special foreword, five out of ten members of the British
Commissioner’s Executive Committee categorically denied that leprosy was contagious altogether: “We dissent
from the opinion expressed in the body of the Report of the Special Committee on the subject of the Contagion
of Leprosy, and from the recommendations founded on that opinion.” (op. Cit: 11, Signed: Andrew Clark,
James Paget, J. Fayrer, W. Guyer Hunter and Jonathan Hutchinson).
696
Carter 1884: 6.
697
Pandya 2001: 181.
698
Pandya 2001: 189.
699
Pandya 2001: 146.
 252

leprosy proved of no avail. There were simply no facilities for what given the chronic
nature of the disease in fact would mean life-long quarantine.700
The following year, in 1889, a ‘Draft Leper Bill to make Provision for the
Isolation of Lepers and the Amelioration of their condition’ was suggested by the
central government in Calcutta. The bill was aimed at isolating beggars and vagrant
lepers in ‘retreats’, to be funded by the local authorities. It also opened for voluntary
isolation as extensive as local circumstances allowed. Those who escaped were
subject to re-arrest, regardless of whether the admission was voluntary or not.701 After
pressure from London the legislation was postponed pending the report of the
Commission.702 The immediate effect of the Leprosy Commission to India was thus to
delay action on the ground.
The underlying problem in India was not just opposition from London, but lack
of funds. This was made clear in Bombay already when the Sassoon Infirm Asylum in
Poona at the beginning of the 1880s asked the government to cover the increased
expenses connected to accepting ‘lepers’.703 While on one hand referring extensively
to Carter’s arguments for segregation, the local government in Bombay declined the
request for funds, explaining that this would lead to “a very great cost – so great that
however much His Excellency the Governor in Council may wish to alleviate the
sufferings of lepers, he cannot undertake to meet the whole of the expenditure with
due regard to other claims on the public revenues.”704 Instead, Carter’s reports were
again circulated “with the hope that they will attract the attention of wealthy
philanthropists both in this Presidency and elsewhere.”705
Despite new legislations drafted in 1895 and enacted in 1898 banning lepers

from certain trades, the hands-off approach would be the dominant method dealing






700
Pandya 2001: 148.
701
Pandya 2001: 150-1, Appendix 5.2.
702
Pandya 2001: 144-153, Appendix 5.3
703
General Department, Bombay. Resolution No. 4900. “Establishment of Leper Asylums.” Dated Bombay
Castle, December 7, 1882: 1. Addendum to Carter, Henry Vandyke. Memorandum on the Prevention of
Leprosy by Segregation of the affected. 1884.
704
Op. Cit.: 5.
705
Op. Cit.: 5.
 253


with leprosy in India.706 According to the national leprosy censuses, more than
100.000 individuals were affected, and even on a provincial level the problem was
simply too large to handle. The Indian government perceived other diseases
(especially cholera), as well as famine, as larger and more imminent threats. As I have
shown earlier in this chapter, cholera alone claimed more lives every single year than
the total number of individuals affected by leprosy. Sanitary measures and calls for
philanthropy became the ‘one size fits all’-proscription which also fit the economic
capacities of the colonial rule. In Bombay a donation from Sir Dinshaw Petit and
support by Municipal Commissioner H. A. Acworth, led to a leper asylum with
capacity for 200 patients being opened in 1890 (within a few years expanded to 300
beds), the Homeless Leper Asylum.707 Similarly, the vast majority of the leprosy
institutions established in India were financed mainly through private donations,
either local philanthropists or more commonly by foreign missionaries. These
measures reached but a fraction of those affected by the disease. By 1920, when the
census showed 109.094 known lepers in India, the Mission to Lepers cared for 4.707

‘leper inmates’; 2.068 leprosy sufferers were admitted to Government or Municipal


Asylums, while 1.021 persons were in Native State Asylums.708

Taking the question of etiology up for a rematch, and thereby postponing
action on the ground, was not the only impact of the National Leprosy Fund. As part
of his duties as secretary of the Fund, Phineas S. Abraham established a medical
journal, Journal of the Leprosy Investigation Committee (1890-1891). In addition to a
thorough presentation of the background for the National Leprosy Fund, Hutchinson’s
fish theory made up the main paper in the first issue in 1890. Editor Phineas S.




706
For the full text of “An Act to Provide for the Segregation and Medical Treatment of Pauper Lepers and the
Control of Lepers Following Certain Callings”, see: Pandya 2001: Appendix 5.4.
707
Abraham, Phineas S. “Remarks on Leprosy in the British Empire”. The British Medical Journal. November
13. 1897: 1411. The name was changed to Acworth Medical Asylum in 1904; in 1955 to Acworth Leprosy
Hospital. It is currently a municipal hospital that provides outpatient leprosy diagnostics and therapeutics, in
addition to training of physicians. It also has a medical museum. See http://www.theacworthleprosymuseum.org.
The genesis and early administration of the asylum is detailed in Pandya 2001: Chapter 9.
708
The Mission to Lepers. Report of a Conference of Leper Asylum Superintendents and Others on the Leper
Problem in India. Cuttack, Orissa Mission Press. 1920: Appendix IV and V. The number of patients includes
Ceylon and Burma, who were not enumerated by the leprosy census for India. Thanks to Kathleen Vongsathorn
for sending me digital copies of this report.
 254

Abraham sent copies of the journal to numerous researchers in the world. The replies,
which in turn were printed in later editions, included letters from Norway (G. A.
Hansen), Hawaii (A. Lütz), Hong Kong (Patrick Manson), South Russia (Münch),
Madeira (Jno Keene; J. Goldschmidt), New Brunswick (J. C. Taché), New Orleans
(Ohmann-Dumesnil), Finland (L. W. Fagerlund), Iceland (W. T. McCormick), New
Zealand (R. H. Bakewell) and British Guiana (Dr. Castor). In addition to providing
local information on prevalence as well as how ‘the leprosy problem’ was handled in
different locations, the columns had discussions on etiology and vaccination, as well
as abstracts of publications and debates first published elsewhere. While the journal
was a short-lived affair, it can be seen as the first attempt at organizing leprosy as a
global concern through the means of a medical journal. Many of those who
contributed were invited to attend the Berlin conference in 1897.
As I showed in the previous chapter, the Berlin conference concluded by
passing resolutions acknowledging the bacillus as the cause of the disease, and that
the measures taken in Norway should be the model for other countries to mimic. On
behalf of the British delegation, Phineas S. Abraham presented no less than sixteen
Acts passed around the empire, proof that the Empire was not completely passive. On
the other hand, in accepting the resolution he emphasized that the measures taken
should be “applicable to the special social conditions of the districts” and that “the
isolation which be propose[d] is really only partial”.


Accepting as we do that the cause of leprosy in Hansen’s bacillus [sic], that leprosy must
therefore be regarded as an infective disease, and that the human tissues – so far as we know
at present – are the only soil in which these bacilli can develop, – it seems only logical that
the isolation of diseased persons is the proper scientific method to prevent the dissemination
of leprosy. But from other practical consideration, it appears to me that attempts at the
absolute isolation of lepers must be in many places quite futile. Where the lepers are few
and public opinion unanimous as to the necessity for their exclusion, such measures might
be possible, but where the cases are numerous and not desirous of being separated from
them, harsh measures of isolation and segregation become impossible – their chief result
being the concealment of cases.
 255

(…) There are still many medical authorities of eminence who strongly disapprove
of stringent legislation; and until medical opinion is unanimous and our knowledge of the
pathology and etiology more complete, it will be futile to expect all governments to adopt
strong measures. The question of legislation, indeed, must be left to the individual
governments. This is especially so for the British Empire – where the social and political
conditions in her different colonies and dependencies vary so very much.709


In Norway, being presented as a model for others to copy was taken a sign of honor.
In Britain, it led the Colonial Secretary Joseph Chamberlain to ask the Royal College
of Physicians again if they saw reason ‘to change their previously expressed opinion’
regarding segregating lepers in the Colonies. Despite contagionism still being the
challenger to the status quo among the British medical elite, a consensus from an
international congress was hard to ignore.
In 1898 The Royal College of Physicians concluded for the first time that

Milroy’s 1867-Report had been ill-founded:



That the communicability of Leprosy, by direct or indirect means, from Lepers to the
healthy, must now be accepted as an established fact, the evidence in support of this belief
being conclusive: and that there is no evidence of the disease arising or spreading in any
other way.710


As Pandya has pointed out, no physicians from India attended the international
leprosy conference in Berlin. Although the medical authorities in London stopped
insisting that the disease was not contagious, this had few consequences when it came
to actual policies. The prospect of segregating a hundred thousand individuals or
more was unrealistic. Leprosy was never very contagious, and compared to other
diseases the burden of leprosy was relatively mild. Over decades the health system
had been primed towards sanitary improvements, and leprosy was simply not






709
Mittheilungen 1897. II Abtheilung. Berlin. 1897: 196-197. See also reports on the Leprosy conference in
The British Medical Journal. 1897: 1196, 1409-1414; Rosenthal, O. V. Internationaler Dermatologen-
Kongress abgehalten in Berlin vom 12.-17. September 1904. 1. Band. 1904.
710
Leprosy Committe Report. December 6. 1898, in Edmond 2006: 108-109.
 256

considered a threat that needed to be singled out. The funding of leprosy institutions
continued to rely on philanthropy, especially missionaries.





Conclusion


The main difference between the debates in Norway and British India revolved
around whether leprosy demanded special intervention. In the 1850s, the Norwegian
state built institutions and started registering people affected by the disease. The
disease was considered to be hereditary, and state involvement was primarily aimed at
distributing the economic burden caused by the disease. Hansen’s initiative for new
leprosy acts was based on the premise that the disease was contagious, but was seen
as continuation of existing practices that did not demand new investments.
In the British Empire, however, the Royal College of Physician’s report from

1867 established a ‘hands off’ policy which would remain the official doctrine of the
Empire until the end of the century. From the mid-1870s Carter argued that the
Norwegian system had led to a reduction in new cases, but his efforts to introduce
similar measures in British India were met with a cold shoulder. The colonial
government did not have the capacity to invest in leprosy prevention, and compared to
the burden caused by other diseases leprosy was a minor problem.
The bacillus was introduced to the debates in the 1880s. New bacteriological
methods for staining tissue samples, and bacillus being identified as the cause of other
diseases were vital to making the bacillus relevant, but neither in Norway nor in India
was the bacillus itself at the center of the argument. Apart from its mere presence, too
much was unknown about its role in the pathology of the disease.
The circulation of knowledge did not trump local experience, rather the actual
exchanges show that circulation was an active and selective process both in deciding
what local knowledge should be disseminated to a wider scientific community and in
deciding what experiences from other places was considered locally relevant. When
appropriating knowledge from elsewhere, it seems the researchers put most emphasis
on their own experiences. They were more welcoming to reports that reinforced the
 257

views they already held than reports which pointed to other conclusions. The more an
actor had invested in publicly defending a particular disease model, the less likely he
was to change his mind in light of new evidence. This explains why several radically
different disease models, all claiming to be universally applicable, continued to exist
side by side.
Impacts on local or national practices depended on the relative position of the
one presenting the arguments. In Norway, calls for segregation came from the
administrative head of the national leprosy campaign. From this position, Hansen
managed to bypass the medical elite in the capital of Christiana and convince
Parliament to pass the leprosy acts of 1877 and 1885. In India, the argument was
presented by a provincial physician as a challenge both to the increasingly powerful
sanitary department and the authority of the medical elite in London. There are strong
indications that this impeded Carter’s chances of promotion. Not all actors shared the
same relations to funding bodies like the state, and the social and political
circumstances differed from place to place. These mechanisms were not limited to
Norway and British India, or the specific period between the 1870s and the 1890s.
The appropriation of knowledge from afar was also shaped by the actual
situation on the ground. Despite more than 100.000 people being affected by the
disease, in India leprosy was a minuscule threat to public health compared to the
staggering death tolls claimed by especially famine and cholera.
Circulating knowledge can be seen as conscious efforts to overcome these
local differences. All the actors I have focused on in this chapter actively published,
which indicates that they saw their own experiences and conclusions as relevant to
others. They also referred to works produced by other actors, and although the
interpretations differed, they clearly saw research conducted elsewhere as relevant.
Placing local experiences in context with findings from elsewhere was increasingly
important in justifying the credibility of a report.
The resolutions from the first international leprosy conference in Berlin in

1897 concluded that leprosy was contagious. The appropriation of these conclusions
differed. In Norway, this was but a confirmation that the already established system
 258

was well founded, in London it led to yet another rematch on the contagiousness of
the disease. When a number of international experts had reached a consensus, their
arguments were hard to ignore. The topic for the following chapter will be the
attempts to organize the circulation of knowledge on an international scale.
 259



6. Connecting the world of leprosy


In the fall of 1896, the American physician Albert S. Ashmead announced in several
medical journals that he had corresponded with Gerhard Armauer Hansen, and that
the government of Norway would soon issue official invitations to an international
congress of leprologists to be held in Bergen the following year.711 Ashmead’s goal
for the congress was to form a permanent international committee to dictate leprosy
policies and channel funds to leprosy institutions in the ‘civilized world’. However,
his announcement was premature: Hansen was unsure of the merit of the scheme, and
when he instead was approached by a competing group of European physicians
working for a different vision of international leprosy collaboration, he withdrew his
support. What were these visions, how were the conferences planned, and how did
they find their form? How were the conferences received?

This chapter will investigate the interlinked roles of meetings, correspondence
and medical journals in the circulation of knowledge about leprosy between the mid-
1890s and the Great War. How did knowledge move from place to place? What
efforts were made to organize the circulation of knowledge in this period? What were
the impacts of these efforts?
The first part of the chapter will outline the general background for the
international conferences, and then investigate how the leprosy conferences came
about. Next, I will investigate the tradition of medical journals, particularly the
quarterly Lepra Bibliotheca Internationalis (1900-1914). What practices could the
founders of this specialized publication draw upon when it came to medical journals?
What was the content of the journal, and what was its role in the circulation of
knowledge regarding leprosy?
Finally, I will discuss how the various arenas for circulation of knowledge
were connected by examining a particular research project that argued for a link
 260

between leprosy and cancer. The case shows how knowledge made available through
circulation itself could give rise to new research topics. It also demonstrates how
discussions on new knowledge took place not only in the columns of Lepra
Bibliotheca Internationalis, but how this journal can be seen as the tip of the iceberg
for research being published and discussed in a range of medical journals, as well as
in meetings in medical societies and official reports. Finally, the case shows how
different actors could have fundamentally different understandings of the status not
just of reports published in other parts of the world, but of publications published in
the past.





The rise of international congresses


In the historiography, the need for international cooperation and coordination in

matters of health has been linked both with industrialization, urbanization, increased
international travel and commerce, and the successive waves of cholera epidemics
that hit Europe from the 1820s and 1830s.712 From 1851, International Sanitary
Conferences aimed at standardizing quarantine regulations to stop the spread of
cholera, plague, and yellow fever were arranged more or less every fifth year.713 As
David Fidler has put it: “The nature of the problem – diseases spreading across
borders through international trade and travel – demanded international
714
cooperation.”





711
Ashmead, Albert S. “Congress of Leprologists: Letter to the Editor.” Dated New York, August 4, 1896. The
Journal of the American Medical Association. August 15, 1896: 387. A similar invitation was published in The
British Medical Journal on October 3, 1896: 974, titled “Proposed International Congress of Leprologists”.
712
See i.e. Bynum, W. F. “The rise of science in medicine, 1860-1913”. In: Bynum, W. F., Anne Hardy,
Stephen Jacyna, Christopher Lawrence and E. M. Tansey. The Western Medical Tradition, 1800 to 2000. 2006:
221-228.
713
Howard-Jones, Norman. The scientific background of the International Sanitary Conferences 1851-1938.
World Health Organization. 1975. The following International Sanitary Conferences were held in Paris (1859),
Istanbul (1866), Vienna (1874), Washington (1881), Rome (1885), Venice (1892), Dresden (1893), Paris
(1894), Venice (1897), Paris (1903, 1912, 1926 and 1938). For a list of diseases discussed at each conference,
see: Bynum 2006: 223.
714
Fidler, David P. “From International Sanitary Conventions to Global Health Security: The New International
Health Regulations.” Chinese Journal of International Law. Vol. 4, No. 2. 2005: 329.
 261

In addition to the sanitary conferences, which aimed at giving policy advice,
there were conferences aimed at discussing the latest medical research. The largest
were the series of international medical congresses that started in Paris in 1867 and
lasted until 1938.715 The medical conferences had a clear leadership who were
responsible both for the practical arrangements and publishing proceedings of the
papers and the oral discussions. On the one hand, the international conferences grew
out of local or national meetings mainly in Europe; on the other hand they provided
exemplary models for further local or national meetings. The number of attendees
grew steadily, and had by the 10th meeting in Berlin in 1890 reached almost 6000. The
conferences were increasingly criticized for being a victim of their own success; they
had grown too large to be of any use.716 As more people got organizational experience
and found others with similar interests, as well as from plain necessity,717 the

conferences were divided into more manageable and specialized sections. From the

1880s different specializations started arranging their own international congresses,
such as the First International Congress of Dermatology and Syphiligraphy arranged
in Paris in 1889 where leprosy was among the topics discussed.718
International conferences were not limited to medicine. In 1907, Union of
International Associations (UIA) was established with its seat in Belgium by
internationalists Henri La Fontaine and Paul Otlet to enhance collaboration between







715
The following conferences were held in Florence (1869), Vienna (1873), Brussels (1875), Geneva (1877),
Amsterdam (1879), London (1881), Copenhagen (1884), Washington (1887), Berlin (1890), Rome (1894),
Moscow (1897), Paris (1900), Madrid (1903), Lisbon (1906), Budapest (1909) and London (1913).
716
5,737 physicians attended the congress in Berlin. For a typical critique arguing that the number of
participants made it hard to facilitate discussions or establishing new contacts, see: Hanssen, Klaus. “X.
internationale medicinske kongres i Berlin”. Medicinsk Revue. Vol. 7, No. 9. 1890: 273-276. “In conclusion one
can hardly judge the success of the congresses base don the number of attendees; one is perhaps closer to the
truth by describing the benefit as inversely proportional to the number of participants (…). The scientific
reunions have undoubtedly had a prominent importance for international scientific work, and the desire to meet
with scientists from other nations will undoubtedly continue in the future ensuring there will be more such
meetings; it only boils down to finding the arrangement which will make them the most fruitful.” (Hanssen
1890: 276).
717
Weisz, George. Divide and conquer: a comparative history of medical specialization. 2006: 229.
718
The Congresses of Dermatology and Syphiligraphy continued with meetings in Wien (1892) and London
(1896). In Paris (1900), the conference was part of the 13th International Medical Congress, before again going
‘independent’ in Berlin (1904), New York (1907), and Rome (1912). After the disruption caused by The Great
War, the Eight International Dermatology Congress was arranged in Copenhagen in 1930.
 262

international associations and to serve as a center for documentation.719 Although
their lists were not complete, UIA document the overwhelming increase in the annual
numbers of international congresses in the second half of the 19th century (Figure 2,
below).720


































FIGURE 2. Union of International Associations. Les congrès internationaux de 1681 à 1899. Liste complète.
1960; Union of International Associations. Les congrès internationaux de 1900 à 1919. Liste
complète. 1964.



When the schemes for arranging an international leprosy congress were hatched, it
was both a continuation of a long tradition of international medical conferences and in
line with concurrent trends of increasing specialization.









719
For more on the Union of International Association, see: http: //www.uia.be/
720
The table in Figure 2 was compiled by Stijn Van de Perre for the Third International Research Conference of
the Voluntary Action History Society arranged at the University of Liverpool in 2008, and is used with
permission.
 263

The congress that never was


As historian Shubana Pandya has shown, the first international leprosy conference
was the outcome of two competing schemes.721 Gerhard Armauer Hansen, who after
the death of Danielssen in 1894 became the primary reference point for most
foreigners interested in leprosy in Norway, was invited to join both schemes. In the
following I will investigate the opposing proposals for a leprosy conference. What
were the visions for organizing leprosy internationally? How were the conferences
planned, and why did only one of them succeed?
The first scheme for an international conference emerged in correspondence
between the physicians Albert Sidney Ashmead and Jules Goldschmidt in December
1895.722 Ashmead was from Philadelphia and since 1882 he had a private practice in

New York. Goldschmidt was from Mainz in Germany, and had since 1869 worked as
superintendent for the lepers at the Lazaretto Hospital in Funchal at the Portuguese
Island of Madeira.
In 1890 Ashmead began to publish on leprosy in Japan, where he from 1873 to
1876 had been Foreign Medical Director and lecturer at the Imperial Japanese
Hospital in Tokyo.723 In the spring of 1895 he received national attention in the
United States after reporting in the columns of The Journal of the American Medical
Association on an anonymous New York resident with leprosy, publicly refusing to








721
Pandya 2003: 161-177.
722
Letter from Goldschmidt to Ashmead, dated Paris 26.12.1895 (CPP: MSS 2/0029, Box 2: Ser. 2.1:
Goldschmidt, Jules). Exerpts were printed in: Ashmead, Albert S. “Proposed International Congress for the
suppression of leprosy”. Journal of Cutaneous and genito-urinary diseases. July. 1896: 280-282. See also:
Ashmead, Albert S. “What a leprosy congress should be”, The Lancet, August 14, 1897: 414; Ashmead, Albert
S. “Proposed International Congress of Leprologists”, The British Medical Journal, October 3, 1896; Ashmead,
Albert S. “The Leprosy Congresses”. Medical Record. January 9, 1897: 53; Pandya 2003: 161-177.
723
Ashmead got the position in Japan after attending to Prince Adzuma, brother of the emperor of Japan, who in
1873 was a student at the United States Naval Academy at Annapolis, Maryland. “Ashmead, Albert S.”
National cyclopedia of American Biography, New York, 1905. (CPP: MSS 2/0029, Box 1: Ser. 1); Ashmead,
Albert S. “Tuberculosis and leprosy in Japan. A study in ethological pathology”. The Journal of the American
Medical Association. August 15, 1891: 254-262; Ashmead, Albert S. “Leprosy in Japan - Intermediary Host
Function in its propagation”. Journal of Cutaneous and genito-urinary diseases. June. 1890: 220-227;
Ashmead, Albert S. “Syphilis and leprosy in Japan”. Journal of Cutaneous and genito-urinary diseases. June.
1890: 233.
 264

notify the Board of Health.724 This was published in a context where the question of
what to do with the ‘lepers’ who had been isolated on North Brother Island outside
New York since 1891 was still an open question.725 Ashmead’s case was discussed in
the chairman’s address at the 46th Annual Meeting of the American Medical
Association at Baltimore in May 1895, as part of the argument that the federal
government should establish a leprosy colony on the US mainland.726 In the following
years Ashmead published numerous papers on the history of leprosy in the Americas;
how the disease was introduced, how it was spread, and what had been done to
combat it. His main argument was that left to itself, the disease would inevitably
proliferate and get out control.
Goldschmidt’s research was mainly based on his own experiences at Madeira,
and focused on treatment and prevention.727 In 1891, Goldschmidt had been among
those taking part in the tuberculin trials (see Chapter 3). Three years later he
published a survey of leprosy globally, which argued that leprosy was a threat
originating in ‘uncivilized countries’, especially India and China. The disease needed
to be stopped through segregation of cases, a stern denial of entry to all diseased
subjects, and surveillance of all suspected individuals.728








724
Ashmead, Albert S. “A puncture with a bone of a living fish in the West Indies, followed by leprosy in a
Caucasian subject”. The Journal of the American Medical Association. March 16. 1895: 396-397; Ashmead,
Albert S. “Leprosy Case – Where it should be reported”. The Journal of the American Medical Association.
April 13. 1895: 563.
725
For more on the Board of Health in New York’s controversial decision to isolate suspected lepers on North
Brother Island, see i.e.: “The Chinese Lepers Secluded”. The New York Times. August 16. 1891; “The Lepers at
Bellevue”. New York Times. October 19. 1897.
726
Montgomery, Liston Homer. “Chairman’s Address”. The Journal of the American Medical Association.
August 31. 1895: 346-347. It would be more than two decades before a federal institution was established on
the US mainland. See: Moran 2007: Chapters 3 and 4.
727
Mittelmaier, Carl and Julius Goldschmidt. Madeira und seine Bedeutung als Heilungsort: Nach vieljährigen
Beobachtungen geschildert. 1885; Goldschmidt, Julius. Die Lepra auf Madeira, 1891. Goldschmidt sent a copy
of the book to Ashmead in 1895.
728
Goldschmidt, Julius. “Zur Aetiologie und Prophylaxis der Lepra”. Berliner klinische Wochenschrift. No. 7.
1894. It was in this paper, which Goldschmidt also sent to Ashmead in December 1895, that the idea of an
international congress was first voiced. See also, Goldschmidt, Julius. “Vorschläge zur Verhütung und
Unterdrückung der Lepra”. Mittheilungen. Bd. 2. 1897: 16; Pandya, Shubhada. “The first international leprosy
conference, Berlin, 1897: the politics of segregation”. História, Ciências, Saúde – Manguinhos. Vol. 10
(supplement 1). 2003: 164-165. Goldschmidt also took part in the first tuberculin trials on leprosy, see Chapter
5.
 265

The two found each other after Ashmead sent a letter to Goldschmidt
containing two studies he wanted feedback on. One argued that leprosy, goitre and
dwarfism were signs of degeneration and “evidences of the dying out of a race”, the
other argued that leprosy was introduced to the Americas after Columbus. The papers
were mainly based on information and images gathered through correspondence with
physicians and anthropologists around the world. Goldschmidt’s reply, with copies of
his own publications attached, was printed in The American Anthropologist and The
Journal of the American Medical Association.729 This was Ashmead’s modus

operandi, his approach to science. He corresponded with experts and published
updates in medical journals, before finally compiling the research into independent
publications.730
When promoting the idea of an international congress, Ashmead would use the
same approach: Write letters to physicians, diplomats and heads of states – and
publish the replies as letters to the editor of various medical journals.731 While he
repeatedly stressed that the scheme was Goldschmidt’s idea, and the two coordinated









729
Ashmead’s two papers were: “Racial Degeneracy in America: Goitre and Dwarfing”, published in the
University Medical Magazine January, 1896, and “Pre-Columbian leprosy” printed as a 6-part series in The
Journal of the American Medical Association, April-June 1895, and as special reprint later that year.
Goldschmidt’s reply (CPP: MSS 2/0029, Box 2: Ser. 2.1: Goldschmidt, Jules) was printed in The American
Anthropologist, Vol. IX. June 1896: 219 and The Journal of the American Medical Association. 1896: 993. As
Michel Moran has shown, the connection between leprosy and race would remain central to US discussions on
leprosy for decades. Moran 2007.
730
This way of producing knowledge was not new. In 1860-1862, for instance, after returning from studying
leprosy in Norway, the German physician Rudolf Virchow published five papers on the history of leprosy in
Archiv für pathologische Anatomie und Physiologie und für klinische Medizin (“Virchow’s Archive”) under the
heading “Zur Gesichte des Aussatzes und Spitäler, besonders in Deutschland” (1860: 138-162, 273-329; 1861:
43-93, 1862: 166-198, 459-512). The first paper consisted of an overview of available literature, along with a list
of questions on present and past leprosy and leprosaria, with a request for other physicians to contribute. This
request was also printed other medical journals, such as Deutsche Klinik, April 25, 1860: 159-160, The Medical
Times and Gazette, July 28, 1860: 93-94, and The Lancet, July 23, 1860. The four follow-up papers were based
on the replies. See: Rather, I. J. A commentary on the medical writings of Rudolf Virchow: based on Schwalbe’s
Virchow-Bibliographie, 1843-1901. 1990: 116-121.
731
In addition to The Journal of the American Medical Association, Ashmead published ‘letters to the editor’ in
American Antropologist, Journal of Cutaneous and genito-urinary diseases, Medical Record (New York), The
Magazine of Medicine (Atlanta), The British Medical Journal and The Lancet. The practice of publishing the
same paper in different journals to ensure a larger audience, contrary to the editors’ claims to exclusivity, was
controversial. See: Ashmead, Albert S. “The Editor and the Contributor”. The Journal of the American Medical
Association. December 4, 1897: 1177.
 266

extensively behind the scenes, the American soon took over as the driving force in
recruiting potential participants.732
From the outset, Ashmead and Goldschmidt’s brainchild had global and
political ambitions. The two physicians shared the view that leprosy was caused by a
bacillus, spread by contact from man to man, that there was no efficient cure, and that
the only way to stop the threat was through compulsory segregation. The argument
was backed up by references to experiences from around the world. In Russia, “during
the period in which it was generally believed that the disease was not contagious, the
leper hospitals were closed; leprosy increased apace.” In the Sandwich Islands
(Hawaii) the lack of efficient segregation had caused the disease to “spread in an
unheard of manner. In 1865, there were 230 lepers in a population of 45,000. In 1881
and 1882, there were 4,000 lepers. (…) In Colombia, while there was no isolation,
leprosy increased in forty years from 400 to 27,000 cases.”733

The solution, the two agreed, was strict segregation in order to stamp out
leprosy already existing, and international regulations to avoid the introduction of new
sources of contagion through migration. Probably inspired by the international
sanitary conferences, the means to achieve this “philanthropic undertaking” was to
arrange a congress for expert delegates representing governments. The task of the
congress would be to establish a permanent committee to channel funds, support
institutions and dictate policies.


The delegates of the different governments will form an international committee, to be

permanently active. Funds will be raised by that committee in all civilized countries, and
applied to the support of leper asylums in those countries where either the willingness or the
capacity to help those institutions is wanting or insufficient. All problems concerning
leprosy will be submitted to that international committee.








732
In the two years leading up to the Berlin conference in 1897, Ashmead received 28 letters from Goldschmidt,
most of them regarding the planned congress. (CPP: MSS 2/0029, Box 2: Ser. 2.1: Goldschmidt, Jules (i-iii)).
733
Ashmead, A. S. “Antileprous Serum”. The Journal of the American Medical Association. January 27, 1897:
181.
 267

It is hoped that by this common and universal effort against the dreadful scourge it
may, in a comparatively short time, be wiped off from the surface of the world.734


One of the first to be invited to join the scheme was the Norwegian physician Gerhard
Armauer Hansen, whom Ashmead and Goldschmidt both admired as the discoverer of
the leprosy bacillus, “the greatest of leprologists”.735 In a letter quoted by Pandya,
Ashmead stated that “A Leprosy Congress without Hansen would be a play of Hamlet
with the Prince of Denmark left out”.736 That Hansen by the mid 1890s had a unique
status was reflected also elsewhere, such as in the review of Hansen and Carl Looft’s
textbook Leprosy: in its Clinical and Pathological Aspects (1895) in The America
Journal of the Medical Sciences. The review opened as follows:


The name of one of the authors of this book, Armauer Hansen, the discoverer of the bacillus
of lepra, is in itself sufficient guarantee that something more than a compilation may be
expected, and in this respect we have not been disappointed. Dr. Hansen has for more than
twenty years been engaged in studying leprosy in Norway and elsewhere, and the good work
that he has accomplished entitles him to be listened to with respect. His words are
authoritative.737

Hansen had worked as a physician at the Pleiestiftelsen leprosy hospital in Bergen
since 1868, and in 1875 he was appointed chief physician for leprosy. As I showed in
the previous chapter, Hansen was the architect behind the increasingly stern national
leprosy legislations passed in 1877 and 1885, which combined surveillance and
segregation either at home or in one of four state institutions.738 According to
Ashmead and Goldschmidt, Norway was the only country which took the threat of
leprosy seriously, and they held the segregation policy responsible for the dramatic




734
Ashmead, Albert S. “Congress of Leprologists: Letter to the Editor.” Dated New York, August 4, 1896. The
American Medical Journal. 1896: 387. The same argument was also presented in Ashmead, A. S. “What a
leprosy congress should be”. The Lancet. August 14. 1897: 414.
735
Ashmead, Albert S. “The Object of the Berlin Leprosy Conference”. The Journal of the American Medical
Association. February 27. 1897: 425.
736
Ashmead to Falcao, 6.9.1896 in: Pandya 2003: 166.
737
“Review: Leprosy: in its Clinical and Pathological Aspects.” American Journal of Medical Sciences.
November 1895: 586.
 268

reduction in the number of lepers. The Norwegian experience was a success other
countries should mimic.
Ashmead had first contacted Hansen in 1894 as part of researching pre-
Columbian leprosy.739 In July 1896 Ashmead invited Hansen to be part of a
‘provisional committee’ consisting of Hansen, Goldschmidt and himself. After briefly
discussing the matter with the director of the national medical service, Michael
Holmboe, Hansen replied that it would be a good idea to arrange a meeting in Bergen,
“the head-quarters of the story of leprosy”.740 According to Hansen, the purpose of the
congress should be for foreign scholars to learn from the Norwegian experience: “we
hardly had anything to learn from foreigners while we are capable of giving good
information. (…) I beg you kindly to give me your opinion on this point so that the
matter as soon as possible can be laid before the Norwegian government.”741
Ashmead interpreted the reply as though only minor practical arrangements were

standing in the way before formal invitations could be issued. Immediately after
receiving the response, he started spreading the news of the upcoming congress to be
held in Bergen in 1897, both in letters to journal editors, physicians, politicians and
diplomats.742


It has seemed desirable to publish all over the world the fact that the government of Norway
will next year probably convoke a congress of leprologists, and delegates from all civilized





738
Vollset 2005: Chapter 5.
739
Did leprosy exist in the Americas before Columbus (‘in pre-Colombian times’)? Based on the skeletal
remains found in burial sites, Ashmead argued that there was no indication that leprosy existed in the ‘New
World’ before being introduced by Europeans and their slave trade. Hansen replied with sending Ashmead
photographs from Dr. Kaurin’s collection of leprous preparations at Reknes Hospital in Trondheim, Norway, for
comparison with bones of the Peruvian mummies. (Hansen to Ashmead, dated Bergen 2.2.1895, CPP: MSS
2/0029, Box 2: Ser. 2.1: Hansen, G. Armauer). One of the photographs, an image showing the disease’s effects
on the bone structure of a hand, was printed in The Journal of the American Medical Association. April 27,
1895: 632.
740
Hansen to Ashmead, dated Bergen 9.7.1896 (CPP: MSS 2/0029, Box 2: Ser. 2.1: Hansen, G. Armauer). See
also Pandya 2003: 167.
741
Op. cit.
742
Among the politicians Ashmead contacted were President Grover Cleveland of the United States, Governor
General Lord Aberdeen of Canada, Emperor Wilhelm II of Germany and President José Diaz of Mexico. In
addition he appealed to the governments of Great Britain, France, Italy, Spain, Mexico, the republics of South
America, South Africa, Japan and China. (Ashmead, Albert S. À Berlin! Open letter to all leprologists. Dated
New York, January 22, 1897 CPP: MSS 2/0029, Box 2: Ser. 5 (iv) “Leprosy”)
 269

countries, especially from those which, by the suffering of their own people, are especially
interested in the question of leprosy. Hansen, the discoverer of the bacillus, suggested that
this congress should be held at Bergen, Norway (...) Norway and Hawaii have already
expressed their willingness to send their delegates.743


In the following months, Hansen sent a series of letters expressing worry that
Ashmead had misunderstood: No final commitments had been made and he was in no
position to make pledges on behalf of his government. Norway was a poor country
and Hansen was skeptical of Ashmead’s goal of a permanent committee of
officials.744 In September he withdrew from any active part in the planning.745
Ashmead then contacted the Norwegian government directly and demanded a final

decision, and they in turn turned to Hansen. In November 1896 Hansen pulled the
plug, stating that “the government did not find it convenient to convoke the said
congress.”746
According to Pandya, Ashmead’s presumptuous announcement that the
Congress would be funded by the Norwegian government was part of the reason why
Hansen in the fall of 1896 opted out of the scheme. In addition, Ashmead’s repeated
emphasis that Norwegian lepers were responsible for one of the three foci of the
disease which together made leprosy a public health problem for the US probably did
not make collaboration very inviting.747
By Hansen’s final withdrawal, Ashmead had received support for the scheme

from seventeen leprologists from Berlin (Germany), Bogota (Columbia), Breslau





743
Ashmead, Albert S. “Congress of Leprologists: Letter to the Editor.” Dated New York, August 4, 1896. The
Journal of the American Medical Association. August 15, 1896: 387. A similar invitation was published in The
British Medical Journal on October 3, 1896: 974, titled “Proposed International Congress of Leprologists”.
744
CPP: MSS 2/0029, Box 2: Ser. 2.1: Hansen, G. Armauer; Pandya 2003: 169.
745
“I should best like if you and Dr. Goldschmidt alone took the task of convoking the Congress on your
shoulders; but should you think it very desirable to have my name, you may use it, but on the condition that the
Congress is only regarded as arranged by us. If the Congress then will meet in Bergen, I hope still that the
Norwegian government will pay the business matters; the best would be if the participating governments each
paid their tribute.” Hansen to Ashmead, dated Bergen 4.9.1896 (CPP: MSS 2/0029, Box 2: Ser. 2.1: Hansen, G.
Armauer). The letter was published in The Journal of the American Medical Association. February 27, 1897:
426.
746
Letter from Hansen to Ashmead, dated Bergen 1.11.1896 (CPP: MSS 2/0029, Box 2: Ser. 2.1: Hansen, G.
Armauer).
747
Pandya 2003: 169.
 270

(Germany), Canton (China), Cape Town (South Africa), Hawaii, Jamaica, Lisbon
(Portugal), London (United Kingdom), New York (United States), Paris (France), Rio
de Janeiro (Brazil), St. Petersburg (Russia), Tokyo (Japan), Tracadie (Canada), as
well as officials from United States, Canada and Mexico. In addition, invitations had
been sent to the governments of China, France, Germany, Great Britain, Italy, Japan,
Russia, South Africa, the republics of South America, Spain and United States.748
Hansen’s retraction was thus initially not perceived as a fatal blow, but with Bergen

off the table, the question of location was brought to the top of the agenda. In a
context where a growing number of physicians had experience arranging international
medical conferences, two options were seen as especially viable: London or Moscow.
London had numerous successful medical conferences to look back on,
including the Third International Congress of Dermatology in early August 1896.749
There Goldschmidt had promoted the plans for an international meeting for the
prevention of leprosy, and several of the expected participants had attended. Ashmead
corresponded with the president of the conference, Jonathan Hutchinson, and through
the US ambassador in London he secured an endorsement by Queen Victoria.750
The other option was Moscow, which was scheduled to host the Twelfth

International Medical Congress in August 1897. Many of the leprologists were
expected to attend. As the planning proceeded, continuous updates were printed in
various medical journals.

It was at first proposed to hold this congress at Bergen, Norway, out of compliment to
Hansen. As the latter has renounced his claim, and left that question to be decided by those
who will work for the scheme, and as there is among the present workers a division of
opinion as to the comparative merits of London and Moscow, nothing can be said for the





748
Ashmead, Albert S. À Berlin! Open letter to all leprologists. Dated New York, January 22. 1897. (CPP:
MSS 2/0029, Box 2: Ser. 5 (iv) “Leprosy”.)
749
The First and Second International Congress of Dermatology were held in Paris (1889) and Vienna (1892).
These grew out of the 7th International Medical Congress, hosted in London in 1881, which was the first in the
series to have its own section on dermatology. After a successful repetition in Copenhagen in 1884, dermatology
became a permanent feature of the international medical conferences.
750
Letter to John Ridleley Carter, Secretary to the US Ambassador, from Arthur Bigge, Private Secretary to the
Queen, dated London Sept. 21, 1896. The Journal of American Medical Association. October 24, 1896: 922.
 271

present, as to the place where the congress will meet. Invitations will be issued, we hope, by
one government to the other governments, to send each an official delegate. These delegates
will form a permanent international committee, whose business it will be to formulate laws
suitable for each country.751





All talk and no action?


Ashmead contacted more physicians than the seventeen who endorsed the scheme.
Especially the goal of involving politicians and establishing a permanent committee
was controversial.752 One of those opposed was the Danish physician Edward Ehlers,
who parallel to Ashmead and Goldschmidt worked on a rival plan for an international
meeting of leprosy experts.753 While Ehlers too believed that leprosy needed to be
defeated through globally coordinated efforts, he had a different vision of how a
world without leprosy should be achieved.
Ehlers had qualified in medicine in 1887, and in the following years he studied
dermatology in Berlin, Breslau, Vienna and Paris. In 1891, he received a doctorate
degree for a study on syphilis, and started working as a specialist of skin- and
venereal diseases in Copenhagen.754 Four years later his study of leprosy in Iceland
won a prize in an international essay competition arranged by the British National







751
Ashmead, Albert S. “Congress of Leprologists”. The Journal of the American Medical Association. October
24, 1896: 922. See also: Ashmead, Albert S. “Proposed International Congress of Leprologists”. The British
Medical Journal. October 3, 1896: 973-974.
752
In his letters, Hansen repeatedly pointed out that “As to your proposal of a permanent international committee,
I do not clearly see what good such a committee should do.” (Letter from Hansen to Ashmead, dated Bergen
September 28, 1896. CPP: MSS 2/0029, Box 2: Ser. 2.1: Hansen, G. Armauer). Likewise, director Wm.
Havelburg at the Bacteriological Laboratory at the Hospital Dos Lazaros in Rio de Janeiro, Brazil (who traveled
to Europe in the fall of 1896), argued that: “Particular progress in our knowledge of leprosy and its treatment has,
in the last years, not been made. Therefore, what are we going to do with a special congress? He who in
this matter wants to talk about it, finds ample opportunity in the general congresses (Interior Medical
Dermatologic Hygiene, or the International Congresses).” The Journal of the American Medical Association.
July 25, 1896: 219-220.
753
Letter from Ehlers to Ashmead, dated Copenhagen, September 18, 1896. The Journal of the American
Medical Association. October 31, 1896: 968.
754
Rosekamp, Erik. Kraks Blaa Bog. 1929: 238; Limon, C. “Edvard Ehlers”. Annales de Dermatologie et de
Syphiligraphie, Ser. 8, 1937: 358-461; Dansk Biografisk Leksikon: Edvard Ehlers.
(http://www.denstoredanske.dk/Dansk_Biografisk_Leksikon/Sundhed/L%C3%A6ge/Edvard_Ehlers)
 272

Leprosy Fund.755 There he argued that the prevalence of leprosy in Iceland had
declined due to “popular dread of contagion”, but that the disease had increased after
the Government in 1848 had decided to close down the four leprosy hospitals as the
population falsely believed the disease was no longer a threat:


Surely the hospitals played but a slight part in the combat against the disease, but it must not
be left out of consideration that their existence indicated that the disease was still to be
feared. On the contrary, the abolishing of the hospitals and the administration's throwing up
the game could not help giving the population the idea, which Iceland's superior physicians
persistently maintained, that the disease was on the point of becoming extinct
spontaneously, and that it did no longer deserve any interest.756

Ehlers agreed with Ashmead and Goldschmidt that the disease was contagious, that
isolation of dangerous cases was necessary to protect the healthy, and that Norway
provided the gold standard for official leprosy control.757 He also agreed that the fight
against the disease called for international cooperation. But Ehlers’ goal was not a
congress to produce a permanent supranational committee or international laws. If the
politicians were interested they could attend, but for science the chief imperative was
to gather knowledge. In line with this, Ehlers’ vision was a conference to work out a
scientific consensus among experts in the field. As he wrote in a letter to Ashmead:
“We do not want to make a congress of leprology, it is a conference which takes place
between renowned leprologists. The governments are invited to send delegates, but








755
Ehlers, Edward. “Conditions under which Leprosy has declined in Iceland”. In: Newman, Ehlers, Impey.
Prize Essays on Leprosy. The New Sydenham Society, London. 1895: 151-189. Ehlers was also involved in
organizing the leprosy asylum Laugarnes on Iceland opening on October, 1897, and an asylum at St. Croix at
the Danish West Indies in 1903. Both were financed by the Danish Odd Fellows society.
756
Ehlers 1895: 187.
757
For Ehlers it was important that the approach was ‘humane’, echoing an argument first made by Danielssen
and Boeck some 50 years prior: “I am for isolation according to the Norwegian system, that is, the isolation of
the diseased, who are incapable of taking care of themselves, and whose presence among other persons
constitutes a real danger for the well. But I am not an admirer of the barbarians of the Middle Ages, who burned
and imprisoned with horrible ceremonies the poor lepers, segregating them from their families and their
friends.” Ehlers, Edvard. “The Leprosy Questions”. The Journal of the American Medical Association.
December 18, 1897: 1282, translated from French in the journal Janus, July/August 1897.
 273


these delegates are not to have in the conference a special position.”758


Based on taking part in discussions among leprologists in Europe, both through
studying, reading publications and regularly attending medical conferences, Ehlers
knew that there were competing models among the medical authorities on the nature
of the disease. As I showed in the previous chapter, the findings of the British Leprosy
Commission in India from 1893 concluded that though the disease was technically
contagious, it must be addressed through improvements in the sanitary surroundings.
Ehlers’ co-winner in the British National Leprosy Fund essay competition in 1895, the
British physician George Newman, argued against contagion based on a comparative
study of the history of the disease.759 At the Third International Congress of
Dermatology in London in August 1896, where Ehlers also attended, The British
Medical Journal reported that the discussion which followed the session on leprosy
“was very animated, and turned on the contagious and non-contagious character of the
disease.”760
While Ashmead corresponded and saw the letters he received as inherently
public and therefore worth publishing, Ehlers recruited support mainly by meeting
colleagues face to face. To Ehlers, letters were private. Medical journals should
disseminate results of research, they were not part of the decision making process.





758
Letter from Ehlers to Goldschmidt dated November 16, 1896, then forwarded to Ashmead. (CPP: MSS
2/0029, Box 1: Ser. 2.1: Ehlers, Edvard). See also: Ashmead, Albert S. “The Object of the Berlin Leprosy
Conference”. The Journal of the American Medical Association. February 27, 1897: 425.
759
“The whole weight of historic evidence is opposed to the supposition that contagion was the cause of the
spread of the disease, and that segregation was therefore the cause of its decline.” (Newman, George. “On the
History of the Decline and Final Extinction of Leprosy as an Endemic Disease in the British Islands”. In:
Newman, Ehlers and Impey. Prize Essays on Leprosy. The New Sydenham Society, London. 1895: 1-150,
quote on p. 91.) Newman’s method was to compare the diet and sanitary conditions in medieval Britain and
contemporary China, India and Iceland – places where the disease still existed. His conclusion was that “the
disease being diffused neither by contagion nor heredity, has under favourable hygienic circumstances a
tendency to die out. Hence, the decline and final extinction of endemic leprosy was due, not to segregation, but
to this general tendency under favouring circumstances, viz. to a general and extensive social improvement in
the life of the people, to a complete change in the poor and insufficient diet (...) and to agricultural
advancement, improved sanitation and land drainage.” (Newman 1895: 109, italics in the original.)
760
“Third International Congress of Dermatology”. The British Medical Journal, August 15, 1896: 410-411.
Although the ‘contagionists’ were gaining terrain, prominent physicians such as the president of the congress,
Jonathan Hutchinson, withheld that the only model which could explain the global distribution of the disease
was consumption of badly cured fish. Hutchinson was also founder and honorary secretary to The New
Sydenham Society, which published Ehlers prize essay on leprosy in 1895. (Hutchinson, Sir Jonathan. The New
Sydenham Society: Retrospective Memoranda. 1911.)
 274

Two months after the congress in London, in the beginning of October 1896, he
traveled to Berlin to discuss the idea of arranging an international leprosy conference
with colleagues there.
In Berlin, leprosy was already on the agenda after worrying reports of an

‘outbreak’ of leprosy in Memel. Among politicians, the fear of leprosy as a threat
from the east was growing. When Ehlers arrived, Robert Koch, respected
bacteriologist and director of the Royal Prussian Institute for Infectious Diseases, had
just returned from undertaking a survey of the reported leprosy epidemic on behalf of
the Prussian government.761 He quickly agreed to join Ehler’s scheme for an
international conference. In addition to his bacteriological research, Koch had
extensive experience from attending and organizing conferences, and was well known
among European physicians.
Ehlers also recruited Oscar Lassar, who was equally well known among the
European leprologists. Lassar had his own private clinic for skin diseases in Berlin
and was one of the founders of both Monatshefte für praktische Dermatologie (1882)
and the Berlin Dermatological Association (1886). In 1890 he had been the general
secretary at the International Medical Congress in Berlin (where Koch had presented
Tuberculin, see Chapter 3). Three years later Lassar left the Monatshefte and founded
the competing Dermatologische Zeitschrift. In 1894, Lassar took the initiative for an
international fundraising to set up a memorial in honor of the recently deceased
Norwegian physician Daniel Danielssen, resulting in donations from 175 individuals
and associations in Europe, Russia and the United States.762 Like Ehlers and

Goldschmidt, Lassar had also taken part in the heated discussions on the
contagiousness of leprosy in London in August, 1896.763
Agreeing that the disease was contagious, caused by a bacillus and sharing




761
Koch, Robert. Die Lepra-Erkrankungen im Kreise Memel. Jena, 1897. First published in Klinisher
Jahrbuch. Vol. 6. 1897: 239-253.
762
The money was used for a commemorative plaque which over the over the entrance to the leprosy hospital
Pleiestiftelsen No. 1 in Bergen, which Lassar unveiled. Fourteen of the thirty physicians present at the funeral
would later attend the Berlin conference. (Lassar, Oscar. “Zur Erinnerung an Daniel Danielssen”.
Dermatologische Zeitschrift. Vol 2, No. 5. 1894: 534-544.). The plaque is still on display over the entrance of
the building in Bergen, now named “Norsk Medisinsk Fødselsregister”.
 275

Norway as a central point of reference, they then approached Hansen who agreed to
form a second ‘preliminary committee’. That the invitation came from three
physicians Hansen had met face to face on earlier occasions probably made it more
attractive to join this scheme than to cooperate with Ashmead, a physician he had
never met, and with a plan he did not fully approve of.
Together, Ehlers, Lassar, Koch and Hansen quickly secured endorsement from
the German Emperor for an international congress. Initially the conference was
planned to take place in March 1897 under the presidency of Robert Koch, but after
Koch was sent to South Africa to investigate cattle plague in December 1896, it was
re-scheduled for October 1897.764 When it became clear that Koch’s African
engagement would take longer than anticipated (he would stay abroad for 18 months),
he was replaced by the renowned German physician Rudolf Virchow. Virchow was
widely known for his innovative work on cellular pathology, comparative pathology
and social medicine. Like Lassar, Virchow was also a well-known editor. Since co-
funding the medical journal Archiv für pathologische Anatomie und Physiologie und
für klinische Medizin in 1846, he had developed a wide network and was one of the
first to review new ideas as they were submitted for publication.765 In 1859 Virchow
had visited Danielssen in Bergen after an invitation by the Norwegian government.
The ‘father of cell pathology’ was also president at the International Medical
Congress in Berlin in 1890, and honorary president of the Berlin Medical Association.
The members of the preliminary committee all shared the belief that leprosy
was contagious and caused by a bacillus, but agreed that in order to bring the
scientific society together, they had to find an angle which did not exclude their
European colleagues who strongly opposed contagionism. In February 1897, Ehlers
sent the first round of invitations to a conference on “the distribution and geographic
extension of leprosy”, in German, French and English. The conference was to be held
in Berlin in October 1897 with support and assistance from the German




763
“Third International Congress of Dermatology”. The British Medical Journal. August 8, 1896: 355.
764
“The leprosy congress”. The British Medical Journal. November 21, 1896: 1528.
 276

government.766 By June 1897, a detailed program was ready for a week-long
conference with more than fifty confirmed speakers.767 In addition to sending the
invitations directly to physicians, it was disseminated by Prince Hohenlohe,
Chancellor of the German Empire, in official diplomatic dispatches to “all civilized
states”. The invitations were in turn forwarded to the national medical associations,
before finally being printed in full or in abstracts in the medical journals.768
The final program was based on the returns to the call. The largest section was
on the distribution of leprosy in a total of 35 countries. There were also more than
twenty lectures on themes ranging from therapeutics to how best to run a leprosy
institution; from pathological anatomy to culturing the leprosy bacillus; from
competing etiological explanations to the history of the disease. A few of the papers
addressed migration of ‘lepers’ and to what extent the rise of leprosy in the colonies
constituted a danger to the colonizers at home and abroad. Hansen himself raised the
question: Should segregation be voluntary or compulsory? Lastly, there were
invitations to present objects for an exhibition with anatomical specimens,
microscopy, photographs, maps and publications.
Upon learning that Ehlers had recruited Hansen, Koch and Lassar, as well as
secured government sponsorship, Ashmead officially renounced his scheme in
January 1897.769 Still, as he learned more of the plans of his European colleagues, he
was increasingly critical. First, he saw no reason to extend invitations also to
physicians who publicly opposed the doctrine of contagion and isolation, positions






765
After the death of the co-founder Benno Reinhard in 1852, the journal was mainly referred to as Virchow’s
Archives.
766
For the original invitation (in French), dated February 23, 1897, see: CPP: MSS 2/0029, Box 1: Ser. 2.1:
“Ehlers, Edvard”. Ashmead published the invitation, along with his reply, under the heading “The Leprosy
Conference” in The Journal of the American Medical Association. March 27, 1897: 613.
767
Ehlers, E., Hansen, G. Armauer, Koch, R. and Lassar, O. Einladung und Programm zur Lepra-conferenz.
Berlin. October 1897. 1897. http: //da2.uib.no/cgi-win/WebBok.exe?slag=lesbok&bokid=lepra. From the outset
the Europeans dominated. 36 of the 52 speakers were from European countries, four from Latin America, three
from North America and the Middle East, and two from Asia, Russia and Africa respectively.
768
See i.e. “Program of the Berlin Lepra Congress”, The Journal for the American Medical Journal, July 10,
1897: 82; “A Leprosy Conference in Berlin”. The British Medical Journal. July 24, 1897: 247. “The Leprosy
Congress in Berlin”. The British Medical Journal. August 21, 1897: 482.
769
Ashmead, Albert S. À Berlin! Open letter to all leprologists, dated New York, January 22, 1897. (CPP: MSS
2/0029, Box 2: Ser. 5 (iv) “Leprosy”).
 277


Ashmead considered “un-scientific”.770 Second, the conference lacked plans for

tangible outcomes. The problem, as Ashmead saw it, was not a lack of knowledge, but
lack of action.771 To discuss prevalence was a waste of time.


I do not see that there is any use of further talk about the distribution and geographic
extension of leprosy. All these things are on record, and nothing is easier for any person
anxious to obtain some light on any subject connected with this question than to consult
what all good libraries offer.772


That “all these things are on record” was simply false. In addition to occasionally
being quite inaccurate when summarizing the views of others and being virtually
unknown among the European leprologists, this and similar statements made it easy
for the Europeans to dismiss Ashmead as unqualified. In the summer of 1897, Ehlers
confronted Ashmead in the columns of the Dutch journal Janus, which in turn was
translated and published in The Journal of the American Medical Association:

“I see today with a certain displeasure that three of the publications, as numerous as they are
little important, of Dr. Albert S. Ashmead have been inserted in the sixth issue of your paper
(May and June). One of the publications, that entitled “Leprosy Overcome by Isolation in
the Middle Ages,” is absolutely useless. The author is pleased in this to attribute to me an
opinion which I have never professed, eide, that the isolation of the lepers would be useless.
One will never find that opinion expressed in my work. (…) Will you “kindly” ask Mr.
Ashmead to quote in future the passages from my writings to which he refers, in order to
avoid writing perfectly useless notes and attributing to me opinions which I do not have.”773




770
“Our idea was, and has always been, that the only way to combat and eventually destroy the dreadful scourge
was the isolation of lepers, enforced by law. In one generation, leprosy not being hereditary, the victory would be
complete. (…) We declare at once that we are that we are contagionists, and that we do not believe that anything
but absolute isolation can destroy a disease which afflicts nearly a million of human beings. (…) In
this respect, we are intolerant.” (Ashmead, Albert S. “The Object of the Berlin Leprosy Conference”. The
Journal of the American Medical Association. February 27, 1897: 425.
771
“We want to do something; they come together to talk. (…) It is a conference to amuse us fellows, us
leprologists, not at all to destroy the most horrible punishment that ever nature has put upon mankind.”
Ashmead, Albert S. “The Object of the Berlin Leprosy Conference”. The Journal of the American Medical
Association, February 27, 1897: 425-426, italics in the original.
772
Ashmead, Albert. “Leprosy Conference” (reply), The Journal of the American Medical Association. March
27, 1897: 613.
773
Ehlers, E. “The Leprosy Question”. The Journal of the American Medical Association. December 18, 1897:
1283 (translated from Janus July/August, 1897).
 278

That Ehlers’ initial invitation was addressed at “colleagues whose works are well
known” only made matters worse. Ehlers intention was probably to include the
European colleagues who attended the scientific conferences, while excluding the
numerous authors who in the early 1890s, especially in Britain, had published books
on leprosy. Unaware of this context, Ashmead interpreted the phrase as an attempt by
Ehlers to exclude him as an unqualified amateur. The public conflict that ensued was
vicious, and peaked with Ashmead printing a 12-page pamphlet entitled “Ehleriana”
where he questioned Ehlers’ competence, experience and charged him with “stealing
the idea” for the congress after the London meeting in 1896.774 In the end, Ashmead

refused to attend the meeting in Berlin, but the American did send several papers to
be read along with proposals for resolutions. They were unanimously voted down.775





Interpreting the leprosy conferences


In total 151 persons signed up for the conference in Berlin 11-16. October, 1897. The
list of participants included 44 delegates representing 22 governments. According to
the published list of participants and staff, 122 attended in person.776 The members of
the ‘preliminary committee’ constituted the leadership. After a suggestion by Oscar
Lassar, Virchow was elected President of the conference, with Hansen and Lassar as
Vice-Presidents and Ehlers as Secretary in Chief. Adding prestige, the conference was
opened by the Secretary of State representing the Government of the German Empire,
Count von Posadowsky. The Imperial Chancellor, Prince von Hohenlohe, later gave a
reception in honor of the members of the conference.777 Within months, the papers







774
“At that time our work was in full blast, known all over the world, and could not well be unknown to Dr.
Ehlers, who knows how to read, and, I suppose, corresponds with some civilized persons. Any unprejudiced
person will come to the conclusion that it was our work that stirred him into action.” Ashmead, Albert S.
Ehleriana. 1897: 10. (CPP: MSS 2/0029, Box 1: Ser. 2.1: “Ehlers, Edvard”).
775
Mittheilungen 1897. II Abtheilung. Berlin. 1897: 194.
776
“Liste der Theilnehmer und Mitarbeiter”. Mittheilungen 1897. I. Abtheilung. Berlin. 1897: V-IX. The list
included postal addresses to make it easier for the attendants to keep in touch also after the conference.
777
Special Correspondence. “The Leprosy Conference”. The British Medical Journal. October 17, 1897: 1122.
 279


and discussions at the conferences were published in two comprehensive volumes.778


For those not attending in person, the immediate outcome depended on where
they received their information. The British Medical Journal published updates as
special correspondence throughout the conference.779 In an editorial the following
week, they congratulated both the organizers and the German government on the
achievement and predicted that the official transactions would become “one of the
most important contributions yet made in the literature of the subject.” For their
readers, the main result was the adoption of a ‘middle course’ regarding leper
segregation:


While acknowledging leprosy to be a bacillary disorder, and in the category of the infective
diseases, it recommends only such legal measures as have proved serviceable in Norway –
such as the notification of cases, detention of vagrant lepers, and the isolation as far as
possible, in their own homes, of such lepers as can be maintained with proper sanitary
precautions by their own families.780

Ashmead’s home journal, The Journal of the American Medical Association,
concluded that the conference did not “appear to have developed anything specially
sensational, either in its discussions or its findings or resolutions, as perhaps might
have been expected to be the case.” The main impression was that the general tone of
the convention “was opposed to the excitement of any general alarm on part of the
public as to the possible dangers from this disease, at least as far as the principal
civilized countries are concerned”. Stressing that many important questions were still





778
Mittheilungen 1897. Berlin. 1897.
779
Editorial. “The International leprosy conference, Berlin”. The British Medical Journal, 1897: 1122; 1197.
780
Editorial. “The International leprosy conference, Berlin”. The British Medical Journal. October 23, 1897:
1196-1197. Three weeks later, the recommendations weres reprinted in an issue dominated by the survey of
leprosy in sixteen countries in the British Empire that Phinneas S. Abraham had presented at the conference.
His argument was that any intervention must depend on local circumstances, that the Empire was not passive,
and that the question of contagion was still not settled: “The social and political conditions in the different
countries are so varied, that it is manifestly out of the question that any uniform or universal system for the
management of lepers will be possible. (…) We must not forget that our knowledge of the etiology of leprosy is
still far from complete; and although we may form theories and impressions from the imperfect data which are
before us, we are not justified in dogmatically insisting upon conclusions which are practically only based upon
such mere theories.” (Abraham, Phineas S. “Remarks on Leprosy in the British Empire”. The British Medical
Journal. November 13, 1897: 1409-1414.)
 280

unsettled, the conclusions boiled down to common-sense compromises: “The
Congress probably acted judiciously in not endorsing any alarmist opinions, while yet
advising reasonable precautions against possible contagion and spread of this
loathsome disorder.”781
To the readers of the Norwegian monthly Medicinsk Revue, the main outlet of

the medical community in Bergen, Hansen reported that the conference had raised
two new and interesting questions: Could leprosy be detected earlier by looking for
bacilli in the nasal membranes, and why did some lepers become anesthetic and other
tubercular? “It seems fortunate if we in this country could be able to answer these two
intricate questions, it would increase our nation’s honor.”782 Monatshefte für
praktische Dermatologie chose to print extensive and non-commented abstracts from
the daily discussions.783
That the interpretations could differ was well known. On the last day of the
conference, the secretaries therefore wrote a condensed report in German, English and
French, which they argued “will be especially desirable for those members who are
delegated by their respective Governments, and who will have to make reports on the
subject”. The report concluded that “Every leper is a danger to his surroundings”, but
that the risk to family and fellow workers varied with the sanitary conditions. The
bacillus was “accepted as the virus of the disease”, while the theory of heredity “has
lost ground in comparison with the now generally-accepted opinion of its
contagiousness.” As for treatment, it was concluded this had only palliative results.
Therefore, emphasis must be put on prevention.784




781
Editorial. “The late leprosy congress”. The Journal of the American Medical Association. November 13,
1897: 1021-1022. Two weeks later, Ashmead commented that: “I have no doubt, when the complete report of
the transactions is published, you will find that the majority of the conference has not at all so sanguine and
non-alarming opinion as you seem to imply. (Ashmead, Albert S. “The Late Leprosy Congress”. The Journal of
the American Medical Association. November 27, 1897: 1125-1126.)
782
Hansen, G. Armauer. “Nogle leprasprgsmaal”. Medicinsk Revue. 1897: 324-325. The questions were
followed by an official resumé of the general conclusions in German. (”Resultatet af leprakonferensen i Berlin”.
Medicinsk Revue. 1897: 326-327.) In his memoirs, Hansen would later highlight the Berlin conference as the
place where he understood that the discovery of the leprosy bacillus had made him famous. (Hansen 1910:
Chapter 5).
783
Jessner, Dr. “Internationale wissenschaftliche Leprakonferenz. Bericht.” Monatshefte für praktische
Dermatologie. 1897: 446-457, 500-508; 550-561.
784
Mittheilungen 1897. II Abtheilung. Berlin. 1897: 190-194. For the full report, see: Appendix 2.
 281

The report was printed in various medical journals, often with editorial notes.
Even after reaching an agreement on resolutions and an official report, the
interpretations would continue to differ.
Despite not attending, Ashmeads initiative did impact the agenda. Several of
the physicians Ashmead had recruited ended up going, and the results of trials with
Carrasquilla’s serum therapy developed in Columbia and distributed by Ashmead
before the conflict with Ehlers arose were discussed (see Chapter 3). And although
Ashmead’s own suggestions for resolutions were voted down by unanimous decision,
they were the direct inspiration for resolutions being passed at all.785 Ashmead’s
contributions were, however, not mentioned in any of the reports, and at the
conference Ehlers was celebrated as its sole initiator.786
While the Fifth International Dermatological Congress in Berlin in 1904 was

aimed at presenting the actions taken after the first conference (see Chapter 4), the
second international leprosy conference in Bergen in 1909 would take its cues from
1897-conference. Headed by Hansen, a committee was established to make the
preparations. The official invitations were sent by the government and spread through
diplomatic dispatches, in letters to the attendants at the first conference, and printed in
medical journals. At the conference the sessions would be organized in the same
manner as in Berlin, with papers read and resolutions passed repeating the
recommendations from Berlin (see Apendix 2).787 Many of the papers were dedicated
to establishing the prevalence of the disease in different states; the official opening




785
Hansen, G. Armauer. “Die Isolierung der Aussätzigen und die dazu erforderlichen Massregeln”,
Mittheilungen 1897. II Abtheilung. Berlin. 1897: 162-166.
786
Mittheilungen 1897. II Abtheilung. Berlin. 1897: 200.
787
At a special meeting on August 20, 1909, after the conference was officially over, the British and Colonial
delegates endorsed the resolutions and passed nine additional points renouncing the anti-contagious sentiments
presented by their countrymen in Berlin 1897. The resolutions argued for compulsory notification and to
“separate the leprous from the non-leprous by segregation in settlements or asylums” under strong regulations
would provide “the most efficient means of mitigating the sufferings of the leper and of assisting his recovery,
and at the same time [it] will produce a reduction and ultimate extinction of the disease”. The resolutions were
signed by delegates from Great Britain, Australia, Cape Colony, Natal, Transvaal, Orange River Colony,
Rhodesia, British Guiana, Bahamas and Fiji. Bayon, H. “On the necessity or advisability of segregation in
relation to the conditions and spread of Leprosy in South Africa at the present time; the measures to be provided
for the prevention and cure of Leprosy: and the suitability of Robben Island as a place of detention for Lepers.
Report by the Gouvernment Research Bacteriologist to the Department of the Interior.” Lepra Bibliotheca
Internationalis. 1914: 131-138.
 282

was headed by King Haakon VII who, like the Imperial Chancellor Prince von
Hohenlohe, attended a dinner for the conference members. While the first conference
in Berlin involved 151 members and 44 delegates representing 22 governments, the
second conference in Bergen attracted 168 attendees from 27 countries.788 After the
conference, the transactions were published in two volumes.789
Still, some things had changed in the period between Berlin and Bergen. Both
an open invitation asking for input in the planning phase, and call for papers and the
final program were published in the medical journal Lepra Bibliotheca
Internationalis.790 Afterwards, 52 of the papers read were printed in the journal. What
was this journal, where did it originate and what was its relation to the conference?





Lepra Bibliotheca Internationalis


While the suggestion of establishing a specialist journal was discussed at the first
international leprosy conference, no decision was made. In the following, I will
investigate how the journal came about and what the ambitions were. I will then show
that similar to international medical meetings, the number of international medical
journals also exploded in the second half of the 19th century.
Behind the proposal for “an Archive of Leprosy for scientific and statistical
reference” in 1897 were Edvard Ehlers, Gerhard Armauer Hansen, Ernest Besnier and
Albert Neisser.791 All but Ehlers had previous experience in establishing medical
journals. Besnier, from 1873 director at the Hôpital Saint-Louis in Paris, was a co-
founder of Annales de dermatologie et de syphiligraphie (1869). Neisser, from 1882




788
The conference does merit closer study than what I have found time to. A good starting point for such an
investigation would be the digital copy of the archival material from the organization committee available
online: http: //da2.uib.no/cgi-win/WebBok.exe?slag=lesbok&bokid=leprakonferanse
789
Lie, H. P. II Internationale Wissenschaftliche Lepra-Konferenz: Abgehalten vom 16 bis 19. august 1909 in
Bergen (Norwegen). Mitteulungen und Verhandlungen. Band I, Band II. London, Paris, Leipzig. 1909.
790
The open invitation was printed in Lepra Bibliotheca Internationalis 1908: 75, and was signed Armauer
Hansen and H. P. Lie. The program, “Programme provisoire de la Deuxième Conférence Internationale
Scientifique contre la Lèpre devant avoir lieu du 16 au 19 Août 1909 à Bergen, Norvège”, was published in
Lepra Bibliotheca Internationalis. 1909: 125ff.
791
Mittheilungen 1897. II Abtheilung. Berlin. 1897: 160-161.
 283

professor of skin- and venereal diseases and director at the University hospital in
Breslau, was co-founder of the German Dermatological Association (1888), and co-
editor of Archiv für Dermatologie und Syphilis and Bibliotheca Medica. Hansen from
Bergen was a co-founder of the Norwegian Medicinsk Revue (1884). All regularly
attended the international medical congresses. Besnier, Ehlers and Neisser had all
attended the discussion at the international congress in London in 1896.
The proposed journal was part a proposal to appoint a 20-man international
leprosy commission to be charged with arranging further conferences. The four
researchers also suggested that the commission should prepare a general reference
work on leprosy. However, after critical remarks by Rudolf Virchow who did not see
the need for a specialized journal, only the point about establishing a committee to
pave the way for a leprosy society received support from the attendees.792
The lack of an official mandate did not stop thirteen of the twenty members of

the committee to move forward with the planned journal at their own initiative. Again,
the proposal came from Ehlers, who for the lifetime of the journal would remain the
main editor and personal owner of the rights to the journal. Co-editors were Ernest
Besnier (Paris), Karl Dehio (Dorpat), Gerhard Armauer Hansen (Bergen), James
Nevins Hyde (Chicago), Jonathan Hutchinson (London) and Albert Neisser (Breslau).
On the front page of all issues were also the names of the 80 physicians who
sponsored the publication. With but a few exceptions, all had attended the Berlin
conference.
The main objective of Lepra Bibliotheca Internationalis was to keep up to date
on what was published about leprosy elsewhere. This included papers in medical
journals, as well as reports and legislations. As Ehlers put it in the introduction to the
first issue:


We understand that we need more emphasis on how the realization of the studies will be




792
Mittheilungen 1897. II Abtheilung. Berlin. 1897: 160-161. The elected members were: Rudolf Virchow (Berlin, honorary
president); Besnier (Paris), Hansen (Bergen), Neisser (Breslau), Ehlers (Copenhagen), v. Düring (Constantinople), v. Petersen (St. Petersburg), Campana (Naples),
Kalindero (Bucharest), Lassar (Berlin), Mr. Jonathan Hutchinson (London), Dr. Phineas Abraham (London), Dr. Glück (Sarajevo), Dyer (New Orleans), Engel Bey (Cairo),
Falco (Lisbon), Alvarez (Noholulu) and Köhler (Berlin)
.
 284

facilitated by considerable centralization of all efforts in a same international body, put
together not only scientific papers, but also projects of administrative and legislative order,
and inserting in document original work, counts, reports and analysis of all publications
related to leprosy.793


The papers in the smaller section of original works, Originalia, varied greatly both in
scope and topics. The larger section, Relata, was divided into seven fixed subsections.
Annuaria leproseriarum featured annual reports from leprosy hospitals around the
world, and served a dual purpose: First, it provided insights into the running of
institutions. Second, it provided templates on how the annual reports could be written
and what kind of information they could contain. Historia was a section for
discussions on leprosy in the past, with a particular focus on Medieval Europe. How
was leprosy introduced to an area, why did it spread, how did it decline? Geographia
consisted mainly of case-studies from different locations. In addition to discussions of
prevalence of the disease (some highlighting culture or diet, others race), this section
also featured updates and controversies surrounding erection of new leprosy
institutions. Anatomia pathologica referred mainly to diagnosis of individuals and
discussions following the display of patients at meetings of medical associations.
Somewhat overlapping, Pathologia focused on disease models, attempts at cultivation
and laboratory experiments with animal models. Therapia concerned treatment;
production, administration and effects of drugs, the effects of exercise, climate and
diet, as well as tests on animals. The last category, Prophylaxis, Legislatio etc.
provided updates and discussions on proposed and passed legislations around the
world, often including the legal texts.
The boundaries between the different categories were blurred. Individual cases
were often discussed in relation to treatment; country-studies in Geographia often
included reports both on legislations and history. From 1906, professor Otto Hamann
at the Royal Library of Berlin published annual lists of recent literature on leprosy,
something which until then had been left to general publications such as Paul




793
Ehlers, Edvard. “Préface”. Lepra Bibliotheca Internationalis. 1900: 2.
 285

Clemens von Baumgarten’s Jahresberichte über die Fortschritte in der Lehre von den
pathogenen Organismen (1885-1917). In addition, there were also several book
reviews.
The structure of the journal, especially its emphasis on relata, was a
consequence of what the editors assessed to be most useful for its readers. The
decades surrounding the turn of the 20th century saw a host of medical journals which
had leprosy as part of their area of interest.794 The challenge for the leprologists was
not to find a journal to publish in, but to keep up to date on colleagues elsewhere.
Over its fifteen years of existence, Lepra Bibliotheca Internationalis published
papers from more than 220 different sources, including 145 medical journals, 54
different meetings and conferences, and 20 official reports. Some physicians seem to
have been responsible for translating from other languages, like A. Grünfeld from
Odessa who translated numerous Russian studies into German. Publishing abstracts
was the main strategy from the editors to ensure that the journal should be considered
the primary resource for leprosy-related research.
From 1900 to 1914, when war made continued publication impossible, Lepra
Bibliotheca Internationalis was published quarterly in London, Leipzig and Paris
(from 1909 also New York). The content was written in German, French and English.
After the first few issues where some of the original papers had abstracts in the two
other languages, there were no parallel translations. While the abstracts often were in
a different language than the original papers, to take full advantage the reader had to
master all three languages.
It is not clear what circulation Lepra Bibliotheca Internationalis had, or how
widely read it was. A consequence of giving references to publications in other
journals priority over original content was that the journal itself was seldom referred
to. The number of authors indicates the size of the research community: Throughout
its lifetime, papers by 523 different authors were printed in full or in abstracts. Only




794
For instance: Archiv für Dermatologie und Syphilis (Wien, 1880), Journal of Cutaneous and genito-urinary
diseases (New York, 1882), Monatshefte für praktische Dermatologie (Hamburg, 1882), The Journal of the
 286

three authors published more than ten papers.795 The ten most published researchers
produced a total of 108 papers,796 the top twenty 166 papers in total. Despite many
physicians producing knowledge about leprosy occasionally, the number of actors
studying leprosy consistently over time was limited: 328 researchers were only
referenced once.

While unpretentious, the abstracts formed a genre in itself and can be seen as
incidental steps towards standardization. In addition to usually (but not always)
including references to the original reports, emphasis was on outcomes that could be
generalized. In some cases this meant focusing on the methods used, in others the
results achieved. Increasingly, what could be quantified was underscored at the
expense of the particulars. As I discussed in Chapter 3 on treatment, this meant a shift
from focusing on individual sufferers to studies conducted on larger groups of
patients, usually in institutional settings. Only when the results seemed at odds with
the observations of others, local context was highlighted as a potential explanation.
More and more the abstracts were void of traces of the local context in which the
observations or interventions had taken place. These characteristics of the genre of
abstracts were not limited to Lepra Bibliotheca Internationalis. Rather, the
phenomenon seems to be found in medical journals in general. I have not found a
single medical journal from this period which did not publish abstracts of other
publications in one form or another.
The ten most quoted journals in Lepra Bibliotheca Internationalis were:
















American Medical Association (Chicago, 1883); Medicinsk Revue (Bergen, 1884), Dermatologische Studien
(Hamburg/Leipzig, 1886), Centralblatt für Bakteriologie (Jena, 1887).
795
J. Ashburn Thompson, Sidney (20), Edouard Jeanselme, Paris (15) and George Pernet, London (13).
796
Edvard Ehlers (9), Gerhard Armauer Hansen (9), Isadore Dyer (9), MM. Kermogrant (9), Jonathan
Hutchinson (8), Lebæuf (8), H. P. Lie (8).
 287

TABLE 2: Top ten journals publishing original papers presented as abstracts
in Lepra Bibliotheca Internationalis (1900-1914).





As the list indicates, discussions on leprosy took place in several medical contexts.
Leprosy was a tropical disease, a colonial disease, an exotic disease, a skin disease
(dermatological), a matter of public health and a part of medicine in general. Lepra
Bibliotheca Internationalis did not alter the practice of leprosy discussions taking
place in other medical journals. What changed was that the subscriber got a way to
keep reasonably updated on leprosy as a defined by ‘the international scientific
community’. It was not education or a specific organization that held the community
together, but the journal itself.
The journals that were referenced all had their different histories and local
contexts. Often they were backed by local or national societies, often they were
established as a reaction to a perceived deficiency in the already existing journals.
Hand in hand with the international conferences being more and more specialized, the
new journals too specialized. The Norwegian monthly Medicinsk Revue (‘Medical
Review’), founded by the Bergen research community in 1884, is a prime example.
Medicinsk Revue was the third medical journal published in Norwegian. The
oldest still in existence was Norsk Magazin for Lægevidenskaben (‘Norwegian
 288

Journal for Medical Science’), established in 1840.797 By the late 1870s the journal
was increasingly perceived to be elitist, exclusive and more interested in theory than
actual medical practice. In 1881, it was supplemented by Tidsskrift for Praktisk
Medicin (‘Journal for Practical Medicine’) aimed at bringing practical and useful
information to the country’s increasing number of medical practitioners.798 For the
research community in Bergen, the two medical journals based in the capital of
Christiania were perceived to be provincial.799 According to the medical community
in Bergen, the two other Norwegian journals missed out on the groundbreaking
research taking place elsewhere, mainly in Germany. This was the niche the three
physicians Eduard Bøckmann, Gerhard Armauer Hansen and his brother Klaus
Hanssen wanted to fill by Medicinsk Revue, subtitled Minutes and translations from
the Lungegaardshospitalet library.800 The editors had the Lungegaarden research
hospital as their base, and the catalogue from 1904 shows that library subscribed to
148 different international medical journals.801

From the outset, the mission statement for Medicinsk Revue was to bring
foreign medical knowledge ‘home’ to colleagues nationally; “through summaries
make our medical profession aware of the most significant foreign medical
literature”.802 Just as the later Lepra Bibliotheca Internationalis, the journal also had a
section for original work, as well as summaries of the discussions taking place in their
meetings.
The ambition of bringing foreign knowledge to a domestic audience was not a

Norwegian invention. Already in 1836, John Conolly and John Forbes had established




797
The first Norwegian language medical journal was Eyr – et medicinsk tidsskrift (1826-1837). Eyr was
published by a reading group of physicians in Christiania, which in 1833 evolved into the Medical Association
of Christiania (‘Lægeforeningen i Christiania’) that founded Norsk Magazin for Lægevidenskaben. In 1847 the
association was renamed The Norwegian Medical Society (‘Det norske medicinske Selskab’) which still exists.
See: Larsen, Øivind. “Det norske medicinske Selskab som kunnskapsformidler.” Michael. 2008: 96-101.
798
Schiøtz, Aina. “Vårt fag – likeså meget en kunst som en vitenskap – Tidsskriftet 1881-1906”. Tidsskrift for
Den norske lægeforening. 2006: 9-13.
799
For more on this community, see: Hammerborg 2009: 172-178.
800
86 out of the journals in the library catalogue were German, followed by the category “French, Italian and
other” (23 titles), “Scandinavian, Danish and Finish” (22), and “English and American” (17).
801
Dethloff, H. G. Katalog over Lungegaardshospitalets bibliothek ved udgangen af aaret 1904. Bergen. 1905.
 289

British and Foreign Medical-Review or Quarterly Journal of Practical Medicine and
Surgery dedicated to a similar endeavor. By the 1890s, most medical journals had
sections dedicated to publishing abstracts and shortened translations of relevant
content published elsewhere. Outside the medical conferences, medical journals were
the main communication line for reaching colleagues domestically as well as abroad.
First, it reached the immediate subscribers. Second, the results of the studies were
printed as abstracts in other journals.





Leprosy and cancer


In addition to continuing the tradition of bringing updates from other journals,
providing a common frame of reference, and help streamline the interpretation of the
conferences and other events, how did Lepra Bibliotheca Internationalis impact the
circulation of knowledge regarding leprosy? In the following I will investigate a
particular research project linking leprosy and cancer. The case will show how
different elements in the circulation of knowledge could work in concert, how
knowledge production about leprosy often was motivated by research in other parts of
medicine, which role Lepra Bibliotheca Internationalis and other medical journals
had in circulating knowledge, and how the circulation made it possible to research
leprosy without meeting anyone suffering from the disease. It also shows how
fundamental debates on epistemology and the status of previous publications could be
played out.
In 1911 and 1912, three papers on a possible connection between leprosy and
cancer were published in Lepra Bibliotheca Internationalis. The researcher was
physician Peter Munch Søegaard from Nordheimsund, a rural community by the








802
“…et Tidsskrift, beregnet paa gjennem Referater at gjøre vor Lægestand bekjendt med det væsentligste af
Udlandets medicinske Literatur.” Bøckmann, Eduard, Hansen, G. A. and Hanssen, Klaus. “Program”.
Medicinsk Revue. Vol. 1, No. 1, 1884: 1-2.
 290

Hardanger fjord in Norway.803 Søegaard was not affiliated with any research
institution or leprosaria, and his research relied solely on what was already available
in medical journals, reports and correspondence. His work, in turn, was discussed in
learned societies, reviewed and sparked new research. To relate to previous studies
and to publish overviews of current literature was not new, but the case shows how it
was possible to open new research topics by combining issues never discussed in the
original papers. Søegaard’s argument was that leprosy protected against cancer.
Like leprosy, cancer research was organized on an international scale in the
first decade of the 20th century. However, the models differed. In 1904 a monthly
international journal was established, Zeitschrift für Krebsforschung. Two years later
an international conference for cancer research was held in in Heidelberg and
Frankfurt, followed by the creation of Die internationale Vereinigung für
Krebsforschung (The International Association for Cancer Research) in 1908.804
Physicians in several countries, including Norway, established national cancer
research committees.805 One widely used research method was ‘clinical statistics’; to
organize large-scale projects with the goal of gathering as much standardized clinical
data as possible, and then analyze it statistically. It was in this context Søegaard in
1909 published his first two papers on cancer, based on statistical analysis of patient

records from the small county of Vikør (3.400 inhabitants). The results were




803
Søegaard, Munch. “Lepra und Carcinom”. Lepra Bibliotheca Internationalis. 1911: 92-97; “Die relative
Krebsimmunität der Leprakranken. (Die Sekundärinfektionen, Kachexie)”. Lepra Bibliotheca Internationalis.
1911: 172-180; “Weitere Untersuchungen über die Krebsstarblichkeit undet den Leprakranken”. Lepra
Bibliotheca Internationalis. 1912: 128-132. In the 1890s, Søegaard had been a physician in Wisconsin, USA
(1892-1894) and Matadi, Kongo (1894-1895) before returning to practice as a physician in different towns in
Norway.
804
The initiative for the journal, conference and association came from the German cancer research committee
established in 1900. The association promoted national memberships which committed the member countries to
begin practical work against cancer. Britain (1902), France (1906) and the USA (1907) soon established their
own national associations. By the outbreak of war, fifteen countries had joined the International Association for
Cancer Research: Argentina, Belgium, Chile, Denmark, Greece, Italy, Japan, Netherlands, Portugal, Russia,
Switzerland, Hungary and Austria. France left the association in 1913, United States in 1914.
805
The Norwegian national cancer research committee was established in 1907. Its first initiative was to
distribute ‘cancer forms’ to gather standardized clinical data on individual cancer cases, hoping to get 10,000
replies. By the end of 1911, only 36 percent for the physicians had replied to the call, returning in total 3.200
forms. “This is not in itself negligible, but far from the response we had hoped for.” (Unsigned. “Den norske
kræftforskning”. Medicinsk Revue. 1911: 669-670). By the outbreak of war, the question of whether or not the
Norwegian committee should join the international association was still up for debate. (Søegaard, Munch.
“Samfundet og de kræftsyke”. Supplement to Tidsskrift for den norske Lægeforening. No. 17. 1914: 80.)
 291

compared to published statistics from cancer research in Britain, Germany, Sweden
and Norway.806
Similar to leprosy, a major and contested question within cancer research was
whether a disposition to cancer could be inherited, if cancer was a sanitary concern, or
whether the disease was contagious. The results varied from 1,8 percent of cancer
patients coming from families with cancer in a German study, to 46,5 percent in a
British study. “But the strangest of it all, is that while dr. Juliusberger with his 1,8 and
3,0 percent, and dr. Williams with his 15 percent argue that their statistics support the
assumption of an inherited disposition – Dr. Bashford argues that his 46,5 percent
proves the opposite.”807 Søegaard’s preferred theory was that in insanitary conditions
cancer could be contagious (‘cancer à deux’). The experts disagreed, and so did their
methods. One strong argument against contagion came from the Imperial Cancer
Research laboratories in London, where experiments on mice had failed to produce a
single case of contagion through inoculation. According to Søegaard, this only
showed that laboratories did not reflect the actual conditions in rural insanitary
conditions, which was where ‘cancer à deux’ appeared.808








806
Søegaard, Munch. “Omkring kræftspørgsmaalet. Arvelighed. Cancer à deux.” Norsk Magazin for
Lægevidenskaben. 1910: 1045-1075. See also: Søegaard, Munch. “Et bidrag til norsk Kræftforskning”.
Medicinsk Revue. 1909: 305ff.
807
“Men det merkeligste af alt er, at medens dr. Juliusberger med sine 1.8 og 3.0 pct. og dr. Williams med sine
15 pct. mener at have leveret statistiske tal, der støtter antagelsen af en arvelig disposition, – saa mener dr.
Bashford, at hans 46.5 pct. afgiver et bevis for det stikk modsatte.” Søegaard 1910: 1050.
808
In all, Søegaard identified fifteen ‘cancer farms’ in Vikør; insanitary households where more than one person
was affected. The paper received a negative review in The British Medical Journal, attacking Søegaard’s
diagnosis, supporting the value of laboratory experiments: “Dr. Soegaard does not in any instance record a
histological confirmation of the diagnosis, and in determining the occurrence of cancer in the families he is
apparently quite satisfied with the statement of doctor or patient’s relatives that the mother or some other
relative died of cancer. The value of his deduction is therefore greatly impaired, because we cannot be quite
sure that the reported cases were in reality cases of cancer, and further that the negative cancer did not contain
some cases of carcinoma or sarcoma. (…). In attacking Dr. Bashford’s deductions that the absence of infection
in his mice speaks against any risk of infection, the author regards the conditions obtaining in his Norwegian
village as favourable to infection, and those obtaining in the Imperial Cancer Research laboratories as
unfavourable. To this proposition exception must be taken. In the former case innumerable factors may be
playing a part, and the results obtained are uncertain, since histological confirmation of the diagnosis is wanting;
while, in the latter, contact is present and other factors are to a great extent excluded, and scientific
investigation of each tumour enables the observer to be certain of every record.” (Unsigned. “Inheritance and
infection in cancer.” The British Medical Journal. 1910: 1987). However, it is not clear whether Søegaard ever
read this; at least he never rebutted the charges.
 292

Søegaard’s interest in leprosy was raised in 1910, by a single paragraph in the
American Annals of Surgery: “Not a single case of cancer was found among the
lepers, notwithstanding the special search instituted in the matter, but this may be due
to the fact that the lepers in the United States belong mostly to the non-Caucasian
races.”809 Ignoring the question of race, Søegaard hypothesized: “that the lepers in
USA should turn out to be immune to cancer has led me to investigate the situation in
Norway, where we in this regard have such a rich material that we should be able to
reach a final conclusion.”810
Going through official statistics of recorded deaths in the Norwegian leprosy

hospitals, the author found that of 2269 deaths, only 19 were diagnosed with cancer.
When ignoring those dying under the age of 40, where it could be objected that the
cancer had not had time to develop, the number rose to seventeen out of 1205 deaths.
Even these ‘least favorable numbers’ produced a death rate to cancer of only 1,4
percent. This was well below the general statistics, where the most recent data from
1906 concluded that 8,5 percent of the Norwegian population died from cancer. Could
it be that leprosy protected against cancer? If so, why?

How this should be interpreted, I will leave to the learned. The most reasonable explanation
is that the lepers have a strongly reduced susceptibility to cancer. (…) Should it, however,
turn out that cancer is an infectious disease it is most certainly significant that the lepers
either in institutions or in private isolation do not have freedom to mingle. They have no
intercourse with people with cancer, and are therefore not exposed to the same dangers as
the rest of us who are free to come and go as we please.811





809
Levin, Isaac. “The Study of the Etiology of Cancer based on Clinical Statistics”. Annals of Surgery. Vol. 51,
no. 6, June. 1910: 778. The paper was read before the American Surgical Association on May 4, 1910, and
presented the first 4000 cases collected by a project instituted by the George Crocker Special Research Fund.
The study consisted of sending a ‘cancer schedule’ with 22 questions regarding individual patients to major US
hospitals and then treating the responses statistically – the same method used in cancer research in Norway.
810
“(…) at de leprøse i U. S. A. skulde vise sig at være immune mot cancer, har foranlediget mig til at anstille
en undersøgelse av forholdet her i Norge, hvor vi i denne henseende har et saa rikt undersøkelsesfelt at vi måtte
kunne komme til et endegyldig resultat.” (Søegaard, Munch. “Lepra og cancer. Meddelelse til Bergens
lægeforening.” Medicinsk Revue. 1910: 635-640, quote on p. 636.) The ‘rich material’ referred to the national
leprosy registry established in 1856. From the 1860s, it also included ‘cause of death’.
811
“Hvorledes dette egentlig skal tydes, det vil jeg overlate til de lærde at avgjøre. Det rimeligste er, at vi
virkelig hos de leprøse staar overfor en sterkt nedsatt mottagelighet for cancer. (…) Skulde det virkelig vise sig
at kræft maa betragtes som en infektionssykdom, saa tør det ganske visst ha sin betydning at verken stiftelserne
 293

Before his first paper on leprosy and cancer was published in Berliner klinische
Wochenschrift, the manuscript was sent to the Medical Association in Bergen, and
discussed at their meeting on December 1, 1910. In accordance with the long
established custom both in Bergen and other medical societies, the paper and
following discussion was published in the society’s own outlet, Medicinsk Revue. In
the discussion, questions were raised to why the numbers differed in different leprosy
asylums, and whether there was any merit to Søegaard’s thesis that through being
segregated to protect the population the lepers were themselves protected from cancer
in the population. No conclusions were reached apart from encouragement that the
research should continue. The author himself had sent the report in a letter, and was
not present at the discussion.
Some months later, Medicinsk Revue published a short note with statistics from
the medical director at the Holdsveikraspitalinn leper asylum in Laugarnesi on
Iceland. Having read the presentation in the Norwegian journal, Sæmundur
Bjarnhjedinsson confirmed that he too had the impression that leprosy patients were
less prone to cancer.812
Encouraged, Søegaard wrote a follow-up paper, referring to more published
statistics, numbers from hospital reports, as well as papers in sixteen different medical
journals.813 This shows that even for a physician in a rural community it was possible
to get access to a wide range of published medical journals. By now, Søegaard had
concluded that his thesis that leprosy prevented cancer was proved: “We have in our
lepers found a group of people that show strikingly low cancer mortality.”814 Future
research, he argued, should focus on explaining this fact.





eller privatpleiens leprøse har et freies Leben und Treiben. De har ingen omgang med kræftsyke personer, de
utsetter sig ikke for de samme noxer som vi andre der kommer og gaar som vi selv lyster.” Op. cit: 640.
812
Bjarnhjedinsson, Sæm. “Lepra og Carcinom”. Medicinsk Revue. 1911: 336-338.
813
In Søegaard, Munch. “Den relative kræftimmunitet ved lepra.” Medicinsk Revue, 1911: 526-536. The
journals referred to were: Annals of Surgery, Archive für pathologische Anatomie, Medical Chronicle,
Deutsche medizinsche Wochenschrift, Berliner klinishe Wochenshrift, Beitrag zur klinischen Chirurgie, The
Medical Record, Wiener medizinsche Blat, München medizinsche Wochenschrift, Le Scalpel, Presse médicine
Belge, Deutsche Zeitschreift für Chirurgie, Archive für Chirurgie, Medizinsische Klinikk, St. Petersburger
medizinische Wochenschrift and The Edinburg Medical Journal.
814
“Vi har i vore leprøse fundet en gruppe medmennesker, der utviser en paafallende lav kræftdødelighet.”
Søegaard, Munch. “Den relative kræftimmunitet ved lepra.” Medicinsk Revue. 1911: 536.
 294

Also this second paper was published in Berliner Klinische Wochenschrift.
From there the papers were picked up and spread to new audiences through Lepra
Bibliotheca Internationalis, accompanied by an editorial remark by the main editor
Edvard Ehlers asking if others could confirm the findings.815
The third and final paper in the series was read and discussed at the meeting of


the Bergen Medical Society on April 12, 1912.816 Søegaard had strengthened the
argument that leprosy prevented cancer by comparing the leprosy numbers with
registered deaths in mental asylums. These inmates were also isolated under medical
surveillance, lived in similar housing, were served similar food and the inmates were
recruited from more or less the same strata of society.817 In the asylums, cancer
mortality rates were three times higher than those found in the leprosy asylums.
Søegaard also referred to statistics and letters of support from Sweden, Iceland,
London, Trinidad, Bombay, as well as from several physicians working with leprosy
in China, again showing that distance did not necessarily obstruct circulation. Still,
the most interesting was the discussion that followed in Bergen.
H. P. Lie was critical. In addition to being a member of the Bergen Medical
Association and co-editor of Medicinsk Revue, a member of the Norwegian cancer
research committee since 1907 and newly appointed national chief physician for
leprosy after the death of Gerhard Armauer Hansen in February 1912, Lie was the
director at Pleiestiftelsen No. 1 in Bergen. This institution was by Søegaard presented
as ‘the most cancer infected leprosy hospital in Norway’. Going through the hospital
records Lie found that cancer was first mentioned in 1882. He also found that
practices regarding diagnosis had changed over time, including the use of autopsies to
provide post mortem confirmations: “It is only after my accession in the 90s that
provisions have been made so that dissections cannot be refused when the physician







815
See: Berliner Klinische Wochenschrift. No. 51, 1910; No. 26 and No. 38, 1911. The discussion continued in
No. 22, 1912, and in Lepra Bibliotheca Internationalis. 1911: 92-97, 172-180 and 1912: 128-132.
816
Søegaard, Munch. “Videre undersøkelser vedrørende kræftdødeligheten blandt de leprøse.” Medicinsk
Revue. 1912: 276-289.
817
Søegaard 1912: 287.
 295


deems it necessary.”818 When limiting the statistics to the cases where the cause of
death was confirmed post mortem, eight out of 252 deaths were caused by cancer –the
same prevalence as those found in the mental asylums. This, Lie argued, meant that
Søegaard’s thesis was wrong. “A general statistical rule is that statistics which is
uncertain should not be used as proof for the rare, unusual or deviant from general
rules. Hence, I withhold that the material presented cannot be used to prove that
cancer is rare among lepers.”819 Although Lie doubted the validity of Søegaards
theory, he suggested that the argument should be presented for the International
Leprosy Commission that had been elected at the Second International Leprosy
Conference in Bergen in 1909, “requesting that it should be raised as a distinctive
case for leprosy research, and then future will tell if, after all, dr. Munch Søegaard’s
assumptions turns out to be correct.”820
Søegaard, who again did not attend the meeting in person, probably read the

reaction only after it was printed in Medicinsk Revue. He immediately wrote a furious
response:

For two generations our leprologists have published their five year reports with extracts,
tables and lists. None here at home have studied them, and thus we have not heard a word
about their reliability. But then a man arrives, suggesting that there might be golden nuggets
also for cancer research among these numbers. He uses the official death lists from the
leprosy statistics in the same way as other statisticians have used the lists and tables on
contagious disease from state- and district physicians. Only then is the warning call
sounded: You must not take our lists and tables seriously!821




818
“Det er først siden min tiltrædelse i 90-aarene at der er kommet bestemmelse om, at sektioner ikke kan
negtes, naar lægen anser det paakrevet.” Lie, H. P. “Diskussion”. Medicinsk Revue. 1912: 289-290.
819
“En almindelig statistisk regel er ogsaa den, at en statistikk, hvis sikkerhet er tvilsom, ikke bør anvendes som
bevis for det sjeldne, usedvanlige eller det fra den almindelige regel avvikende. Derfor kan de her omhandlede
opgaver efter min opfatning ikke anvendes til bevis for cancerens sjeldenhet hos leprøse.” Lie 1912: 290.
820
“Jeg skulde derfor ville foreslaa for dr. Munch Søegaard, at saken forelægges for den internationale
leprakommission, hvori er representanter fra en rekke land med meget lepra, med anmodning om, at dette
spørsmål optages som en særskilt sak i lepraforskningen, og da vil fremtiden kunne vise om det dog ikke er som
dr. Munch Søegaard antar.” (Lie 1912: 290.) Lie did not mention that he himself was a member of the
committee, nor does it seem he made any efforts to forward the suggestion himself.
821
“Her har nu i over to menneskealdrer vore leprologer utgit sine 5-aars beretninger med ekstrakter, tabeller og
lister. Ingen her hjemme har studert dem, og saa lenge har vi da heller ikke hørt noget om listernes paalitelighet.
Men saa kommer en dag en mand og mener: maaske findes her guldkorn ogsaa for kræftforskningen blant disse
tal. Han benytter leprahospitalenes officielt utgivne dødslister paa samme maate som andre statistikere har
 296

According to Søegaard, Lie not only criticized his work, but also all his predecessors
for having published ‘unusable statistics’. And, if Lie already knew the statistics were
unreliable, why was he not warned before making a fool of himself in front of an
international audience?
Shortly thereafter, Lie replied, also in the columns of Medicinsk Revue. Lie
praised the careful statements in the first paper, where Søegaard had suggested that
reduced susceptibility might be possible. The problem, as Lie saw it, was that
Søegaard too soon moved on to try and explain this connection.822 As Søegaard was
more and more convinced leprosy protected against cancer, Lie reached the opposite
conclusions. The statistics were flawed. His main argument was epistemological: The
statistics reflected the disease models concurrent to the time of production, and not
the currently held models.


The last half century has changed so much in perceptions of almost all diseases, leprosy in
particular, that this also was reflected in medical statistics. (…) If we return to the leading
scientists of that time [the 1860s], we will find that affections today not recognized as
aspects of leprosy, were perceived to be leprous affections. (…) I therefore withhold that the
older notions of what leprosy was must have influenced the physicians’ clinical gaze and
their perceptions of what other diseases might have been combined with leprosy.823

Still keeping the possibility open that there might be a connection, Lie repeated the
suggestion of bringing the question to the attention of the International Leprosy
Commission so that the question could be properly investigated.






benyttet stadsfysikatenes og distriktslægernes tabeller over smitsomme sykdommer. Først da gjøres der anskrik:
Du maa da ikke ta vore lister og tabeller for det ramme alvor!” Søegaard, Munch. “Kræftdødeligheten paa de
norske lepraasyler. Vor medicinalstatistiks paalitelighet. Tilsvar til overlege Lie’s kritikk av mine meddelelser til
Bergens medicinske selskap.” Medicinsk Revue. 1912: 453-457, quote on p. 453.
822
Lie, H. P. ”Kreftdødeligheten paa de norske lepraasyler.” Medicinsk Revue. 1912: 722-726.
823
“De siste halvt hundreda aar har forandret saa meget i opfatningen av nær sagt alle sykdommer, ikke minst
spedalskheten, at de heller ikke for statistikken har kunnet gaa sporløst hen. (…) gaar vi til datidens ledende
videnskapsmænd, vil vi finde, at ogsaa disse har regnet til spedalskheden affektioner, som nutiden ikke
anerkjender som leprøse. (…) Jeg mener saaledes i det anførte at ha vist, at den eldre tids opfatning av, hva der
har været spedalsket, har maattet ha indflydelse paa lægernes kliniske blikk for og opfatning av andre
sygdommer, som har kunnet være kombinert med lepraen.” Lie, H. P. “Kræftdødeligheten paa de norske
lepraasyler. Svar til dr. Munch Søegaard” Medicinsk Revue. 1912: 724-725.
 297

Søegaard got the final word: A six point list expressing ‘sadness’ that the
statistics were wrong, that they should never have been published, that Lie
undermined his predecessors abilities to make diagnosis (stressing that he himself was
not to blame, as he had no hand in diagnosing or producing the statistics), that this
was yet another proof that arrogant medical researchers frowned upon practicing
physicians trying to contribute with new knowledge; concluding that “I wish Armauer
Hansen was still alive.”824 After this he never again published anything on leprosy.825

It is unclear if Søegaard ever approached the international leprosy commission.
In Lepra Bibliotheca Internationalis a short follow-up was published by head
physician Dr. Biehler at the State Leprosarium in Riga in 1913. Between 1891 and
1913, 160 of 194 deaths had ended in autopsies, of these ten persons had cancerous
tumors. This was a higher proportion of cancer than in the general hospital and close
to the general prevalence in the population. He also revisited Søegaard’s statistics and
concluded that the Norwegian physician had consistently relied on the highest
possible numbers regarding prevalence of cancer in the general population. His
conclusion was that there was not the slightest indication of any connection between
leprosy and cancer immunity.826
The hypothesis that leprosy protected against cancer did, to my knowledge,
never reemerge. Still, the case shows that a physician in a rural community could have
access to a wide range of medical publications, including reports and medical journals
seemingly intended for domestic audiences elsewhere. It also shows how publications
in themselves could form the basis for the production of new knowledge, but that this
was far from unproblematic.




824
“ Gid Armauer Hansen nu hadde levd.” Søegaard, Munch. “Replikk til dr. H. P. Lie”. Medicinsk Revue.
1912: 727.
825
Peter Munch Søegaard did, however, continue his research on cancer. The summer of 1914, he traveled to
Germany, France, Britain, Denmark and Sweden financed by the Norwegian Roll’s scholarship to bring back
knowledge of ‘the socio-humanitarian aspect’ of cancer. This resulted in a booklet, Samfundet og de Kræftsyke
(1915), which also contained information on cancer work in Austria, Russia, Spain, Switzerland and USA. The
report was published with financial support from Norwegian life insurance companies, and distributed as a
supplement to Tidsskrift for den norske Lægeforening. No. 17. 1915. All surpluses from sales were channeled to
the Norwegian Cancer Committee.
826
Biehler, R. “Die Krebssterblichkeit unter den Leprakranken des Rigaschen städtischen Leprosariums”. Lepra
Blibliotheca Internationalis. 1913: 148.
 298

The debate between Søegaard and Lie clearly shows how views on medical
statistics and scientific truths could differ. For Lie, medical statistics were a reflection
of the best knowledge available at any given moment. Medical science was thus not
merely a matter of accumulation: New standards for diagnosis did not make previous
observations completely obsolete, but they could not be taken at face value. Looking
back in the records required special expertise. For Søegaard, however, the
observations were either true – or should not have been published in the first place.
Finally, the case shows circulation in practice. First, Søegaards study was
based both on previously published research and correspondence with experts
elsewhere. Second, the papers he wrote were discussed in local medical meetings and
consequently published in the local medical association’s medical journal, comments
included. The publication in turn sparked responses from readers elsewhere, in this
case Bjarnhjedinsson on Iceland, and later Biehler in Latvia. This was common for
the medical journals and an integral part in the dynamics of circulation. Third, papers
published one place could be reviewed elsewhere, sometimes without the authors’
knowledge. Although Søegaard’s first paper was published in a Norwegian and
German journal, the only direct response I have found was a negative review in The
British Medical Journal which it seems unlikely that Søegaard ever read. Circulation
of knowledge did not mean everyone had access to everything that was published, not
even everything that was directly relevant for their ongoing research projects. Fourth
and finally, although it is not clear if this was Søegaard’s intention, his publications in
Berliner klinische Wochenschrift were put under scrutiny in Lepra Bibliotheca
Internationalis. This was in line with the editors’ strategy to ensure the journal’s
status as the primary resource for leprosy-related research around the world. Without
the journal, it is unlikely that Søegaard’s hypothesis would have received as much
attention, nor that it relatively quickly could be put to rest after having been tested
elsewhere.
 299

Conclusion


Prior to the First International Leprosy Conference in Berlin (1897), circulation of
new medical knowledge regarding leprosy was integrated in circulation of medical
knowledge in general. Observations, and conclusions based on these, were
disseminated through travels, personal meetings, books, journals, reports and
correspondence. The widespread practice of publishing abstracts from other medical
journals formed a genre in itself, and can be seen as a step towards international
standardization. Over time, local particularities were downplayed also in the original
research papers.
Not every study circulated. For the leprologists, the lack of a unifying

‘international body’ made it hard, if not impossible, for researchers to keep up to date
on relevant studies produced elsewhere. There was not one center and one periphery,
but different centers and different peripheries. Some centered on institutions, others
around medical journals. Different disease models (accompanied by different ways of
producing knowledge) were living side by side.
The initiative to organize leprosy workers were inspired by shared local
circumstances, namely the perception by Western physicians and governments that
leprosy was on the rise and that it had to be stopped before overwhelming the world.
Norway became a focal point, and was frequently highlighted as the only civilized
country that through consolidated efforts successfully had turned the trend and was
about to get the leprosy problem under control. But when the American physician
Ashmead argued that time had come for action, his European counterparts argued that
gathering more knowledge and reaching a consensus among the experts had priority.
Both schemes had their supporters, but the latter argument won out. The Europeans
were the first to secure government support. It seems that having met face to face at
prior medical conferences made collaboration easier than corresponding with
unknown colleagues. The result was the first international leprosy conference held in
Berlin in 1897, and soon thereafter the journal Lepra Bibliotheca Internationalis.
The journal and international meetings passing resolutions and
recommendations did not mean that appropriation, as discussed in the previous
 300

chapter, suddenly stopped being important. This is reflected for instance in the
various reviews of the Berlin conference. In The British Medical Journal (London), it
was hailed as an important success – stressing that the recommendations were already
implemented in most of the British Empire. In Medicinsk Revue (Bergen), it was seen
as an opportunity for new research to bring glory to the nation. In the Journal of the
American Medical Association (Chicago), the conference did not live up to the hype.
Over time the leprosy conferences and the journal created a shared space which
facilitated dissemination, collaboration, standardization, and also new ways of
producing knowledge. The ambition of the journal was to present updated overviews
of ongoing leprosy related activities worldwide, especially (but not limited to)
medical research. Søegaard’s hypothesis that leprosy prevented cancer shows that
Lepra Bibliotheca Internationalis was not only an expert forum. A physician with no
institutional affiliation could have his results published and tested by leprosy
researchers around the world.
That leprosy was the same disease all over the world was an implicit
premise for the relevance of knowledge produced elsewhere, and only in exceptional
cases a topic for debate. Possibly this reflected the editors’ position: The initiatives
for both journal and international conferences came from researchers who were
convinced that the disease was caused by the leprosy bacillus, and that its presence
could be demonstrated everywhere. This was not the only disease model, but its
hegemonic position was illustrated for instance in reviews of research based on
alternative views.
The outbreak of World War I brought Lepra Bibliotheca Internationalis to an
abrupt stop after two issues in 1914. In the following chapter I will discuss the
competing and complimentary attempts at reestablishing the global leprosy research
community in the interwar period, focusing on the travels and meetings of the
relatively small group of individuals involved.
 301



7. Interwar globalization


On June 29, 1926, the Brazilian physician and leprologist Heráclides César de Souza-
Araújo arrived in Bergen. He had left his position as head of the rural sanitary service
(‘Serviço de Saneamento Rural’) of Pará district in northern Brazil two years earlier,
and a month before embarking on what was to become a three year journey, he had
opened Brazil’s first agricultural colony for lepers, Lazaropolis do Prata. Boarding a
ship in Rio de Janeiro in July 1924, the journey had taken him through North
America, across the Pacific to Hawaii, Japan, Hong Kong, the Philippines, Singapore
and India, through the Middle East and finally Europe.
The voyage was undertaken under the auspices of the International Health
Board of the Rockefeller Foundation and the Oswaldo Cruz Institute in Brazil. It was
made “in the hope of stimulating the beginning of a general campaign against this
terrible scourge. (…) exclusively to study the serious problem of leprosy, hoping to
use the knowledge thus achieved in the control of this disease in my own country.”827
What did de Souza-Araújo find around the world? And how did his mission to import

knowledge on leprosy from abroad to Brazil end up as an initiative to organize
leprosy work on a global scale?
As I showed in the first part of the thesis, in the interwar period the belief in
strict segregation that had dominated before the war was challenged by arguments for
voluntary treatment. In this chapter I will investigate the initiatives for consolidating
leprologists globally in the 1920s and early 1930s, focusing on the actors and
organizations involved behind the scenes, such as de Souza-Araújo, the Rockefeller
Foundation, the League of Nations, the Leonard Wood Memorial, Société de
Pathologie Exotique and BELRA. As I showed in the introduction to the thesis, the
outcome of these efforts was a global apparatus for leprosy that would last for 70
years. What did it take to achieve this? Who were involved and what were their
backgrounds? What happened behind the scenes?
 302

The outbreak of war in 1914 brought the journal Lepra Bibliotheca
Internationalis to a complete halt. Traveling was restricted and consequently no
conferences were arranged. Even correspondence was increasingly difficult. In
addition, more pressing issues surpassed leprosy both among physicians and on the
public agenda; leprosy would never get the same attention as before the war. While
The British Medical Journal published an annual average of 50.2 papers on leprosy
from the turn of the century to the outbreak of war, that average dropped to 14.6
during the war.828 In the 1920s and 1930s the attention given to leprosy, as measured

in number of published research reports in the journal, stabilized at around 35
publications per year.
In some ways, the events in the 1920s and 1930s were a repetition of the
endeavors discussed in the previous chapter, but with new actors and new
geographical centers of gravity. Most of the people involved in the interwar period
had not been involved in the events described in the last two chapters, but this past
provided inspiration of a past golden age of collaboration. This was a lesson that
through collaboration and sharing experiences they could build on each other’s results
and avoid repeating the mistakes made by others. The goal of ultimately eradicating
the disease remained, and establishing new infrastructure for circulating knowledge
was seen as a key step in fulfilling this aspirations.
Finally, the chapter will investigate the legacy of Bergen. The reason why de
Souza-Araújo went to Bergen was primarily because of its famous past, and not the
research going on at the time of the visit. How did the role of Bergen change? Was
Bergen still relevant?













827
De Souza-Araújo 1929: 3.
828
Before the war, the annual number of publications in The British Medical Journal peaked at 74 in 1903; the
lowest was 27 in 1908. During the war, there were 19 publications on in 1915 and 1916, while in 1918 only 8
stories on leprosy were published. Source: Free text-search on “leprosy” at http: //www.bmj.com/search.
 303

The world is not the same


During the journey, de Souza-Araújo experienced huge differences when it came to

how “the problem of leprosy” was coped with around the world. In India, where the
number of leprosy sufferers now was estimated to be between 200.000 and 700.000
individuals, less than nine thousand persons were institutionalized. The majority of
the establishments were run by missionary organizations, and more often than not the
inmates were free to come and go as they pleased. In Iraq with an estimated 300
lepers, they were treated as outcasts and de Souza-Araújo was told that many fled to
larger towns to hide in the crowds. Establishing a leper colony had been considered,
“but its cost is a drawback and the compulsory segregation of individuals of different
tribes, races and religions presents almost insurmountable difficulties.”829

At the other end of the spectrum was the Perpetual Asylum (‘Zensei Byo-in’)

37 kilometers west of Tokyo. This was one of five state run institutions; the backbone
in Japan’s expanding anti-leprosy campaign. De Souza-Araùjo was present when
three groups of sanitary experts from the Far East received parts of their 45 day
training course organized by the League of Nations:

We were accompanied on this visit by all the technical staff of the asylum, who wore aprons
and leather boots (top boots). To each visitor they furnished apron and cap. Two nurses
wearing gauze masks, carried trays with pieces of gauze and balls of cotton wool drenched in
disinfectants, and the usual objects for clinical and dermatological examination. Every time a
doctor touched a patient the nurse offered him the means to disinfect his fingers or hand. The
visit finished, which was long and very interesting, we retired to the medical post where our
aprons and caps were taken off. There, while we washed and disinfected our hands, we kept
our feet on mats drenched in a strong disinfectant solution, as is done in the leprosaria of
DUTCH GUIANA. Passing from this disinfectory to the building of the administration, we
were invited to gargle with a disinfectant solution and to wash our faces with gauze soaked in








829
De Souza-Araújo 1929: 264. De Souza-Araújo later served on the World Health Organization (WHO)
Expert Panel on Leprosy and on the council of the International Leprosy Association.
 304

alcohol. Later I observed that these hygienic precautions are customary in the
830
establishment.


At the remote island of Culion in the Philippines, where de Souza-Araújo had spent
Christmas in 1925, he found the leper colony organized to mimic society in general,
with its own police force, fire brigade, post office, shoemaker, and court system.
Seven hundred healthy persons were hired to provide care for more than 5.300 lepers,
making this the largest leprosy colony in the world:


The leprosarium is almost a town: it has 47 concrete buildings, 19 of strong heavy material
and 30 of light material. The lepers own 616 houses of their own, in the village and in the
farming district, most of them being built of light material. They have still 25 business houses,
of which there four societies [sic], being two funerary and two athletic, a band and an
orchestra.831

At the Molokai leper settlement in Hawaii, de Souza-Araújo found a similar parallel
society. On his first day there he observed the juridical system in action: “On
September 26th I was present, at the trial of a Corean leper, (A case of nodular
advanced leprosy) accused of having made and sold pineapple wine. The barrel,
containing half the liquid made, was brought to the Court by the Police Officer, who
accused the prisoner of having sold the drink, because it was impossible that he had
drunk in 2 days, nearly 20 quarts.”832 The judge was a 45 year old ‘neural-leper’ who
was interned in 1906. Unlike Zensei Byo-in and Culion, however, the number of
inmates at Molokai was in decline following new legislations encouraging voluntary
isolation – making forced segregation the exception. In 1925 Molokai had 533 lepers,
down from 1.213 in 1890.





830
De Souza-Araújo 1929: 109.
831
De Souza-Araújo 1929: 146. See also: Wade, H. W. and Jose Avellana Basa. ‘The Culion Leper Colony’.
American Journal of Tropical Medicine, Vol. 8, No. 5, 1923: 405-6; Robertson, Jo. “Culion, the ‘Island of the
Living Dead’: or Another Look at Leprosy and Citizenship”. In: Andresen, Astri, Kari Tove Elvakken and Tore
Gronlie (eds.) Politics of Prevention, Health Propaganda, and the Organisation of Hospitals 1800-2000.
Bergen. Rokkansenteret, Report 10. 2005: 81-92.
832
De Souza-Araújo 1929: 84.
 305

When de Souza-Araújo arrived in Bergen in the end of June, 1926, he expected
Bergen to be one of the highlights of the trip. In the research literature, Bergen was
presented as the birthplace for scientific investigations into the disease: This was the
place where Danielssen and Boeck in the 1840s had distinguished leprosy from other
affections of the skin, and thus established what the German pathologist Rudolf
Virchow after a visit in 1859 had termed “the foundation for modern leprology”.833
De Souza-Araúja was proud to own a copy of Johan Ludvig Losting’s colored atlas


that accompanied the work.834 However, with the passage of time this was no longer
considered a go-to textbook but a treasured relic of the past.
Bergen was also the site where the leprosy bacillus was first observed by
Hansen.835 By the end of the 1920s the bacillus was accepted by the medical research
collective as the cause of the disease, and it was at the center of a whole range of
practices around the world; from bacteriological detection in the laboratory being the
final proof in contested cases, to the rationale for various social policies aimed at
controlling those individuals who were infected. The bacillus was seen as proof that
leprosy was the same disease all over the world, and the bacillus was a cornerstone in
the argument that leprosy was a global disease, a disease which required global
coordination to control and ultimately eradicate.
In addition to Bergen being presented as the first global capital of leprosy
research, Norway was repeatedly highlighted as the first country in the world which
had raised a successful and modern campaign against the spread of leprosy. De
Souza-Araújo highlighted Norway as the example for other countries to follow.
According to the “highly expressive statistics”, the number of new leprosy cases in




833
Skinsnes, O. K. “Notes from the History of Leprosy”. International Journal of Leprosy. No. 41. 1973: 220-
237. De Souza-Araújo paraphrased Virchow with the following expressions: “The city of Bergen, Norway,
where Danielssen, Boeck and Hansen established the foundations of the modern leprology.” (De Souza-Araújo
1929: Fig 4, caption) and “BERGEN, the cradle of modern leprology” (de Souza-Araújo 1929: 15). The
secretary of the League of Nations Leprosy Commission used the following phrase: “The moderen era opened
with the clinical research work of Danielsen and de Boeck, the bacteriological phase with Hensen’s discovery.”
(Burnet, E. Provisional report presented to the Leprosy Commission at its meeting at Tokyo in April 1930”*.
Geneva, January 1930: 1. LNHO: CH/Leprosy/7.) *The meeting in Tokyo never took place, instead the report
was presented in Bangkok, December 8-12,1930. More on this later.
834
De Souza-Araújo 1929: 319.
 306

Norway had been reduced from around thousand new cases per five years in the


1850s and 1860s, to less than ten in the 1920s.836 Upon returning to Brazil, de Souza-
Araújo argued that the Norwegian experience showed that a successful campaign
against the disease went through three ‘logical’ stages: First, private initiative
characterized by material assistance and collaboration of doctors and benefactors;
second, official medical attention and establishment of a state leprosy apparatus; and
third, forced segregation: “finally, after there was a considerable number of beds for
the sick and the process of transmission was known, the government decreed and
executed its severe measure.”837 Brazil was still at the first stage, de Souza-Araújo
argued. His desire was that the Brazilian government should imitate the Norwegian
experience: “The result will be identical.”
In 1926, de Souza-Araújo stayed in Bergen only for a week. Unlike most other
places he visited he felt it was more to learn from the past than the present. He visited
Pleiestiftelsen and St. Jørgens hospital, the two remaining leprosy institutions, but
found them largely deserted. Pleiestiftelsen had 280 beds, but only 57 patients, “most
of whom very aged people”.838 At St. Jørgens hospital, which had almost 150 patients
when Danielssen did his first clinical, anatomical and chemical investigations in the
1840s, only seven remained.839
Accompanied by district physician Dr. Høygaard, his son and daughter, de
Souza-Araújo traveled to the nearby island of Herdla to experience the Norwegian
home seclusion in practice. This was one of the three main components of Norway’s
“mixed segregation system”, the others being state institutions and surveillance of
each individual leper. The first patient they visited was a 19 year old man, whose




835
The first images in de Souza-Araújo’s monograph were photographs of these three Norwegian physicians,
“In memorandum”.
836
De Souza-Araújo. 1929: 321.
837
De Souza-Araújo, H. C. “Desigualdade dos problemas da lepra nos países europeus ou A História da lepra
na Europa”. Boletim da Sociedade de Assistência aos Lázaros e Defensa Contra a Lepra. Vol. 2, no. 12, 1930:
11-14, referred to by Poorman, Elisabeth. “The legacy of Brazil’s leper colonies. O legado das colônias de lepra
no Brasil”. Cadernos saúde coletiva, Rio de Janeiro, Vol 16, no. 2. 2008: 313. As Poorman argues, this is a
typical example of how the Norwegian leprosy campaign was reframed and used in national debates: A specific
national model was given legitimacy by being presented as an imported success.
838
De Souza-Araújo. 1929: 324.
 307

father, uncle, sister, grandfather and grandmother had all had died from leprosy. The
man was, however, impossible to find.


He had fled away from home, and we had no chance to meet him.
He does the same, Dr. HOYGAARD told me, every time he foresees a visit, least
they may transfer him to the asylum, and conceals himself. We entered his house and room.
We asked his neighbours for information about his way of living. The reply was that he
frequented their houses and used to play and have intercourse with other young people in the
village.

This patient having once more infringed the law of prophylaxis, the district
physician decided to have him arrested and transferred to BERGEN.840


The next patient was a fisherman’s wife and mother of six.


“I examined her and her children. I did not notice any sign of active leprosy in her, nor any
symptom of the disease in her offspring. Be it as it is, they all live in a candid promiscuity.
Her husband appears at home only on Saturdays.”841



A second disappointment was that he did not get to meet the head of the Norwegian
leprosy campaign, H. P. Lie, who after the death of Hansen in 1912 had taken over
the position as chief physician for leprosy. When de Souza-Araújo arrived, Lie was
off on an inspection journey in Finmark in the far north of the country. Instead the
Brazilian met with another foreign visitor: The Soviet professor Alexis Wladimiroff,
director of the Institute of Experimental Medicine in Leningrad and president of the
Commission of Studies on Leprosy in Russia. After a meeting among Russian
leprologists in Leningrad, Wladimiroff had been commissioned on behalf of the
Soviet government to create an updated report on prophylaxis of leprosy and policy
advice on how to protect the wider society against the disease. He was therefore sent







839
From 1896, St. Jørgens was not allowed to accept new patients. For a discussion of the increasingly tense
relations between the private and the state institutions, see: Vollset 2006: 65-71.
840
De Souza-Araújo. 1929: 325.
841
De Souza-Araújo. 1929: 325.
 308

to Bergen.842 In Lie’s absence, de Souza-Araújo ended up giving Wladimiroff the
information he was asking for.843 Chance meetings and chance events were common
in the transnational history of leprosy.
The interwar period saw a soar of international journeys, although traveling as
such was not a novel activity among physicians working with leprosy. As mentioned
in Chapter 2, Danielssen and Boeck going on long travels abroad was a central part in
establishing Bergen as the world capital for leprosy research eight decades earlier. A
study by Hanne Winge Kvarenes shows that about fifty percent of the Norwegian
physicians working during the period 1840-1880 had been on study trips abroad.844 I
do not know how representative this was for physicians in other countries, but among
those involved in organizing medicine internationally, traveling was an activity they
shared. What changed in the interwar period was that the journeys were faster, longer
and less expensive than earlier. Both in terms of expenses and practicalities, the world
was shrinking.
The most common reason for physicians traveling was to receive training, and
de Souza-Araújo began his journey in North America with a stay at the newly
inaugurated School of leprology at the National Leprosarium at Carville, Louisiana.845
He also took special courses in Hygiene and Public Health at John Hopkins and


Columbia University in the USA.846 A second reason was to bring home experiences





842
Letter from H. C. de Souza-Araújo to Prof. Alexis Wladimiroff, dated July 3, 1926, written in Bergen.
(LNHO: 12B-R898/52570). See also De Souza-Araújo. 1929: 15.
843
De Souza-Araújo 1929: 15; Letter from de Souza-Araújo to Dr. L. Rajchman, medical director of the League
of Nations Health Committee, dated October 6, 1926, titled “Leprosy as a world’s sanitary problem’, written in
Siracousa, Sicily. (LNHO: 12B-R898/52570, p. 24)
844
Kvarenes, H. W. “Travel accounts in the Norsk Magazin for Lægevidenskaben, 1840-1880.” In: Ø. Larsen
(ed.). The Shaping of a Profession. Physicians in Norway, Past and Present. Science History
Publications/USA. 1996: 276. During the same four decades, 78 travel reports were published in Norsk
Magazin for Lægevidenskaben (Norwegian Magazine on Medical Science), including information on travel
grants and transcriptions of international meetings.
845
The year de Souza-Araújo visited Bergen, in 1926, 31 physicians, 56 nurses, 60 students of medicine and 75
dentists visited the hospital with the purpose of familiarizing themselves with leprosy. De Souza-Araújo 1929:
34.
846
De Souza-Araújo 1929: 8. For a study of how Japanese physicians traveling to Germany between 1868 and
1914, see: Chen, Hsiu-Jane. “Eine strenge Prüfung deutscher Art”. Der Alltag der japanischen
Medizinausbildung im Zeitalder der Reform von 1868 bis 1914. Abhandlungen zur Geschichte der Medizin und
der Naturwissenschaften, heft 109. 2010. For a study of the impact of the educational schemes of the League of
Nations and the International Health Board of the Rockefeller Foundation, with focus on a Spanish setting, see
 309

in order to inform new policies and practices, which was the explicit goal of de
Souza-Araújo’s travel. A third reason for traveling was to attend meetings and
conferences and meet colleagues there, which de Souza-Araújo also took part in. A
fourth, which de Souza-Araújo was not involved with, was to charter new territory:
To look for specific diseases such as leprosy. This was mainly done by Europeans in
colonial possessions.
The visits only provided information on the actual situation on the ground at
the given moment of the visit. Most of the information de Souza-Araújo collected was
based on a combination of interviews, reports, papers and other researcher’s
monographs. Each of the 40 chapters in the volume he published after the trip, one for
each country visited, included photographs of the premises, a presentation of the local
history focusing on how the disease (meaning the leprosy bacillus) originally was
introduced to the country, and details on the efforts taken to control the disease.847

Names and places were in capital letters both to credit those who had contributed with
information and to show the readers who they could get in touch with for more
details. In addition, he portrayed the local practices and approaches to epidemiology,
pathology, serology and therapeutics, legislation, and statistics on number of known
lepers in- and outside the institutions. Each chapter ended with a list of relevant
literature.
De Souza-Araújo’s main interest was in the institutions erected to combat the
disease, including architecture and experiences on organizing the daily lives of the
inmates down to details on diet and cost per day per inmate. The expressed intention
was to present both successes and failures, so that the readers could avoid making the
same mistakes as had been made elsewhere. However, in practice failure to de Souza-





Barona, Joseph L. “Public health experts and scientific authority”. In: Andresen, A, W. Hubbard and T. Ryymin
(eds). International and Local Approaches to Health and Health Care. 2010: 31-49.
847
The ‘fourty countries’ investigated by de Souza-Araújo were, in chronological order: United States of
America, Canada, Hawaii, Japan, Korea, China, Philippine Islands, Federated Malay States, Malacca Straits
Settlements, Dutch East Indies, India, Kingdom of Iraq, Syria, Palestine, Kingdom of Aegypt, Tripoli, Malta,
Tunisia, Algeria, Marocco, Greece, Turkey, Roumania, Bulgaria, Yougoslavia, Hungary, Austrian Republic,
Tscheco-Slovakia, Poland, Germany, Denmark, Iceland, Sweden, Norway, Great Britain, Holland, Belgium,
France, Switzerland, Italy, Spain and Portugal. The 400 page report Leprosy Survey made in Fourty Countries
was published as a book in both English and Portuguese (with the title Lepra em 40 Países) in 1929.
 310

Araújo meant not taking the problem of leprosy seriously, success meant detection,
erection of institutions and increasingly strict segregation of those affected. In the
1920s this was an increasingly disputed position.





A contested legacy


As I showed in Chapter 4, the question of forced segregation versus voluntary
treatment was the main scientific controversy regarding leprosy in the 1920s. Both
camps praised the Norwegian leprosy apparatus, but with different emphasis. While
de Souza-Araújo saw Norway as proving his theory that a successful campaign went
through three necessary steps leading to strict segregation, Sir Leonard Rogers and
Ernest Muir had firmly established an opposite camp. For Rogers and Muir, Norway’s
campaign was successful because of its persistence and humanitarianism, and the
measures were not universally applicable:


The success of the great Norwegian test of segregation has thus completely demonstrated
once for all the efficacy of that measure under conditions permitting of its thorough and
persistent application, and has furnished a model and humanitarian example for the
imitation by other countries, which can be relied on to be effective in exact proportion to the
efficiency with which it is put into operation.848

Based on Hansen’s presentation of the history of leprosy in Norway given at the first
International Leprosy Conference held in Berlin in 1897, Rogers and Muir too
highlighted the rapidly declining number of leprosy sufferers in Norway. In other
words, both camps agreed that Norway had led a successful campaign – but disagreed
on what had caused it. While de Souza-Araújo argued that the Norwegian experience
showed that ‘severe measures’ were necessary, Muir and Rogers saw it as proof that
eradicating leprosy could be achieved using a ‘humanitarian approach’.




848
Rogers and Muir. 1925: 110. Both had worked at the Calcutta School of Tropical Medicine, and were in
1924 founders of the British Empire Leprosy Relief Association, BELRA.
 311

Unlike de Souza-Araújo, Rogers and Muir repeatedly stressed that the
Norwegian success was due to ideal conditions which could not be expected in
colonial contexts. There the approach would have to be modified “to suit the
conditions pertaining to various countries presenting different degrees of advance in
hygiene, education, financial and political evolution, and with public opinion, which
all greatly influence the problem to be dealt with”.849 Thus, Muir and Rogers argued,
the Norwegian approach was applicable only to ‘civilized’ countries. This is
consistent with what Helen Joy Power argued in her PhD thesis on Sir Leonard
Rogers: As a committed imperialist, he saw the best way to manage imperial
possessions would be to westernize their inhabitants.850 According to Rogers, a
general and compulsory segregation would be impossible in “poor and backwards”
countries: Policies that were passed were seldom implemented, and strict segregation
only forced lepers to go into hiding – an argument that had been a minority view
among leprologists since before the turn of the century. Finally, even if these
obstacles could be overcome, it was not realistic that countries such as India could
build enough institutions, whether it was self-sustaining agricultural colonies,
hospitals, asylums or leprosaria, to accommodate the great number of people affected
by the disease.851 The latest decennial census from India (1921) showed that India had
102,513 lepers, “but there is no doubt that the returns are much below the truth,
especially when we take into account the large number of early cases not recognizable
except after careful examination by an experienced medical man”.852 A survey among







849
Rogers and Muir. 1925: 126.
850
Power, H. J. Sir Leonard Rogers Frs (1868-1962): Tropical medicine in the Indian medical service. Thesis
submitted to the University of London for the Degree of Doctor of Philosophy. 1993: 276. (Wellcome Trust
Library). See also: Boyd, John S. K. “Leonard Rogers. 1886-1962”. Biographical Memoirs of Fellows of the
Royal Society. Vol. 9, 1963: 261-285.
851
Rogers and Muir 1925: 105-106. For an in-depth classification of the different missionary leprosy asylums in
India between 1886 and 1947, see: Robertson, Jo. “The Leprosy Asylum in India: 1886-1947”. Journal of the
History of Medicine and Allied Sciences. Vol. 64, no. 4. 2009: 474-517. For an exemplary study of practices
and negotiations at a local level, see: Buckingham 2002.
852
Rogers and Muir 1925: 36-37. According to the secretary of the League of Nations Leprosy Commission,
Etienne Burnet, Muir estimated that the numbers were at least seven times as high. (Burnet, E. “League of
Nations Health Organisation. Report on the Study Tour of the Secretary of the Leprosy Commission in Europe,
South America and the Far East. January 1929 - June 1930.” (C. H. 887). Geneva, 1930: 15-16.)
 312

thirty of the patients under Muir’s care showed that only two had been entered in the
census as ‘lepers’.853
Rogers and Muir strongly argued that leprosy was more contagious in certain
stages than others, and that the chance of catching the disease declined with age. This
had decisive impact on the question of segregation: Children of lepers should be
segregated as early as possible (preferably at birth) to avoid contagion. At the same
time, only those with active ulcers were considered highly contagious and therefore a
possible threat to public health.
Compared to de Sousa-Araújo, Rogers and Muir presented a different way of
knowing leprosy. The ultimate goal of getting rid of leprosy was the same, but they
had a different stance regarding what observations were considered relevant
knowledge. While the Brazilian focused on leprosy as prevalence in populations, and
saw segregation as a means to bring down the number of new cases, Rogers and Muir
put emphasis on treatment of individual sufferers and alleviating their surroundings.
In their view, leprosy was curable as long as the treatment started early. The two were
pioneers in developing and testing treatment based on injections of chaulmoogra oil
(see Chapter 3). In their monograph Leprosy (1925), the Norwegian experience was
used to underline that segregation was futile: Even in Norway, five of six cases were
overlooked for three years or more after the onset of the disease, “clearly
demonstrating the impossibility of discovering the great majority of leprosy cases in
the early stages as long as their only prospect was isolation from their relatives with
no appreciable hope of recovery.”854
Compared to de Souza-Araújo’s report, however, Rogers and Muir’s
monograph would have the greatest impact, both immediately and over time. In the
summer of 1925, only months after Leprosy was first published, Evald Tomanek from
the League of Nations Health Section was sent to London to meet with Rogers.
Tomanek concluded that “the publication ‘Leprosy’ by Sir Leonard Rogers represents




853
Quoted in de Souza-Araújo 1929: 231.
 313

a monograph written by authority in our days on the subject”, and that “there was no
need for the League to publish another monograph.”855 New editions of Leprosy,
updated with the latest research into therapeutics, were published in 1940 and 1946.
Writing a book can be seen both as an outcome of the effort it took to produce
it, and a vessel to get the knowledge to those who could use it. The monographs by de
Souza-Araújo and Rogers and Muir represent two radically different perspectives,
both on how to go about gathering knowledge, what observations were considered
relevant, how to present the findings, and in advice on what practical measures should
be taken based on this. Both relied on the writings of others, but supported their
conclusions through conscious choices of what they considered relevant in the vast
body of medical literature and empirical observations. The authors were all
considered prestigious medical scientists, they met and discussed, and when de
Souza-Araújo published four years after Rogers and Muir, he appropriated the content
by referring mainly to the sections in Leprosy which he agreed.
Rogers and Muir’s take on leprosy was also spread through courses held at the
Calcutta School of Tropical Medicine and Hygiene, and several key actors involved in
making leprosy a global issue received their training in Calcutta. The school officially
opened in 1920 after Rogers as professor of pathology at the Calcutta Medical
College had promoted it for a decade. The same year Rogers returned to London and
Muir, a former medical missionary in Bengal, was recruited as head researcher of the
new school. The Calcutta School soon became a renowned center for training of
physicians for out-patient clinics, as well as a center for further research into
treatment. The school was not a closed leprosy asylum, but relied on people choosing
to be diagnosed and receive treatment for three hours every day voluntarily. When de
Souza-Araújo spent the whole of February 1926 at the School of Tropical Medicine in






854
Rogers and Muir, 1925: 110. The monograph was organized in six sections: History and distribution,
epidemiology and communicability, prophylaxis, etiology, clinical aspects and treatment. The first half was
based mainly on available literature, the second on observations from India.
855
Tomanek, Evald. Memorandum concerning the statistics of leprosy to the Medical Director, dated July 21,
1925. Medical Director of the League, Ludwig Rajchman, agreed. (LNHO: 12B-R898/42641/29272. The reply
from Rajchman is found in the same folder.)
 314

Calcutta, Muir was the director. The ‘Calcutta approach’ to leprosy was written on the
wall, quite literally:


In the waiting room of the dispensary, there exists exposed a graphic with lots of advices to
lepers. Among these, there are the “Golden Rules” reading as follows:
1. – Leprosy is acquired by contact with lepers. Children are especially liable to infection.
Infectious lepers should occupy a separate room, and should use separate clothes, bedding,
eating and drinking utensils and should not touch food, clothes, furniture, or other things
which are used by healthy people.
2. – Take plenty of exercise: walking, dumbbell, games, etc.

3. – Take nourishing food in abundance, but not excess, well-cooked, but not over-cooked.
Take plenty fresh fruits and vegetables. Avoid the following: a) stale food; b) partly
decomposed food; c) food preserved by salting; d) highly spiced food; e) highly milled
grains; f) narcotics as alcohol, opium, ganja, tobacco; g) an excess of meat or fish.
4. – Keep the bowels open, by diet if possible, otherwise by means of laxatives.

5. – Keep the skin clean. Bathe at least once daily and apply friction to the skin, rubbing on
chaulmoogra oil.
6. – Keep the mind active and cheerful.


7. – Keep the body strong and try to avoid other diseases.856




To de Souza-Araújo, this was humbug. In a lecture at the Faculty of Medicine in
Madrid on November 29, 1926, de Souza-Araújo expressed his misgivings for the
“exaggerated optimism in the modern treatments and the influence of the so-called
‘Indian System’ of prophylaxis”. In his view, the treatments did not work, and
propagating false hope would eventually backfire. Referring to the more liberal
policies recently implemented at Hawaii, he argued that the public administration
“must re-start the systematic seclusion of all its lepers, otherwise incurs the risk of a
disaster, which would have effect in discrediting the modern prophylaxis, producing a
bad influence, of pessimism, in the public opinion.”857






856
De Souza-Araújo 1929: 244ff. The referred to poster is also found in E. Muir. Leprosy. Diagnosis,
Treatment and Prevention. Cuttack: Orissa Mission Press. 1924: 23.
857
De Souza-Araújo 1929: 97-98.
 315

Publishing monographs were but some of several strategies the two parties had
in common. They also created organizations organized teaching.





Organizing and educating


In 1924, four years after returning from India and being appointed lecturer at the
London School of Tropical Medicine, Rogers established the organization British
Empire Leprosy Relief Association (BELRA). January 27 the following year, an
Indian Council of BELRA with headquarters at the Calcutta School of Tropical
Medicine and Hygiene’s Department of Leprosy was established by Muir. The same
year, a second Indian headquarters opened at the Red Cross Society Office in New
Delhi. The organization had prominent leadership, with the Prince of Wales as patron,
and Secretary of State for Foreign Affairs, The Secretary of State for the colonies,
Secretary of State for India, The Viceroy of India and the Governor-Generals of
Canada, South Africa and New Zealand as vice-presidents. This shows both Sir
Leonard Rogers status among the political elite in the British Empire, but also that
leprosy research still was considered an important issue among its top officials.
BELRA had three main objectives: To collect and disseminate knowledge
related to diagnosis and treatment of leprosy, including training courses in treatment;
to encourage and carry out research; and finally to carry out propaganda with the
overriding principle that the stigma attached to the disease should disappear.
Between establishing BELRA and de Souza-Araújo’s visit in July 1926,
Rogers had spent time raising funds for the association, formulating its policy and
establishing contact with people working with leprosy within the British Empire (and
occasionally outside its borders). In 1924, Rogers sent a questionnaire to all British
possessions through the British Foreign, Colonial and India offices asking for
information regarding leprosy. This provided the basis for a report that was sent to
both policy makers and the League of Nations, stressing that leprosy was not a highly
 316

contagious disease and that segregation in most cases was futile.858 In addition to
giving courses in Calcutta, Muir prepared a booklet (“Diagnosis, treatment and
prevention”) and two pamphlets (“Truths about leprosy” and “What the people should
know about leprosy”) which were distributed to all who contacted the organization.
He also gave public lectures.859 The main message in these early BELRA-publications
was that the solution to the problem of leprosy was to educate the public so that they
could recognize the signs of the disease and avoid the carriers:


The ideal method of prevention would be the hindering of all contact. This was attempted
on an extensive and expensive scale in the Philippine Islands and proved a failure as means
of stamping out the disease. What stamped leprosy out of England was to a large extent the
effort of individuals and bodies of people to keep lepers from mixing with healthy people. It
was through an enlightened public opinion which was aware of the contagiousness of the
disease. Other conditions, such as improved diet and improved sanitation, were also helpful,
but these are useless apart from enlightened public opinion and public spirit.860

Through the publications and training, BELRA was put in touch with active leprosy
workers who in turn could supply information, case-histories, statistics and reports, as
well as do clinical trials.861 From 1928, BELRA published a quarterly journal which
distilled both findings and literature, Leprosy Notes. In 1930, under the editorship of
Dr. Robert Cochrane, it was renamed Leprosy Review and shaped into a medical
journal.862 The ambition was that the journal should serve as a common ground, an





858
In the report Rogers stressed that “the guiding principle should be that in the long run any advantages gained
by rigid segregation of advanced cases may be dearly bought at the expense of driving the early ones to hide
themselves until no longer amenable to the now available improved methods of treatment.” Rogers, Sir
Leonard. “Memorandum on the prevalence of and prophylaxis against leprosy in the British Empire, based on
replies to the questionnaire of the British Empire Leprosy Relief Association; with suggestions for dealing with
the problem.” 1925: 29, italics in the original. Addendum to letter from Rogers to Ludvig Rajchman, head of the
League of Nations Health Organization, dated London October 27, 1925. (LNHO: 12B- R898/42641/29272).
859
See i.e.: Muir, Ernest. Popular lecture on leprosy, illustrated with lantern slides. Lahore. 1925.
860
Muir, E. Leprosy. Diagnosis, Treatment and Prevention. Cuttack: Orissa Mission Press. 1924: 28.
861
Power 1993: 222. Among the leprosy workers who contacted BELRA were physicians working for
American Near East Relief at the leper colony Spinaloga near Crete, made famous in Victoria Hislop’s novel
The Island (2005).
862
Editorial. “Leprosy Review: Origin, policy, content, circulation, finances and the future.” Leprosy Review.
Vol. 70, No. 2. 1999: 126. Available online: http: //www.leprahealthinaction.org/lr/June99/editorial.html. When
 317

arena for leprosy workers to update and keep updated on research that went on
elsewhere.863
During his journey, de Souza-Araújo too established an international
organization for leprosy researchers, La Société Internationale de Leprologie. This
was officially founded in Professor Edouard Jeanselme’s home in Paris on the last day
of 1926, and the total (but meager) income from de Souza-Araújo’s monograph was
set aside for the organization.864 Unlike BELRA, which saw its geographical area
primarily as the British Empire, and secondarily English speaking leprosy workers
elsewhere, de Souza-Araújo had global aspirations. In addition to facilitate
cooperation between leprologists all over the world through an international medical
journal on leprosy, de Souza-Araújo wanted the collaboration to result in an updated
prophylaxis for leprosy control, international centers for research and training, and
that the organization should work out technical advice to stimulate government
involvement in leprosy work.
In his monograph, de Souza-Araújo argued that the idea for the organization
came during his travels, and was a topic for discussions from his first stop at the
Carville in 1924. After experiencing the efficient collaboration between leprologists






the quarterly International Journal of Leprosy began publishing in 1933, BELRA’s abstracts from Tropical
Diseases Bulletin were highlighted as “most valuable, but they have hardly lessened the need of a regular full-
scope journal of leprosy”. (H. W. Wade. “The International Journal of Leprosy. An editorial Statement.”
International Journal of Leprosy. Vol 1. no. 1. 1933: 2.)
863
While the scope was similar to that of Lepra Bibliotheca Internationalis, BELRA’s main reference was
Mission to Lepers in India and the Far East. Mission to Lepers had been established in 1874, and from 1897 they
published the quarterly journal Without the Camp. Rogers, himself a devote Christian, believed the missionaries
put too much emphasis on the gospel and not enough on research. Several of the active members of BELRA in
the 1920s were recruited from Mission to Lepers, such as the organization’s first secretary, Reverend Frank
Oldrieve who had been the Secretary for India for the Mission to Lepers, and his successor Dr. Robert Cochrane
and Muir, who both had backgrounds as medical missionaries in Bengal. For discussions on the activities of
Mission to Lepers in India, see i.e. Joseph, D. George. “‘Essentially Christian, eminently philantropic’: The
Mission to Lepers in British India.” História, Ciências, Saúde-Manguinhos, vol. 10, suppl. 1,
2003: 247-275; Robertson, Jo. “The Leprosy Asylum in India: 1886-1947.” Journal of the History of Medicine
and Allied Sciences. Vol. 64, no. 4. 2009: 474-517. See also: Bailey, W. Fifty Years’ Work for Lepers 1874-
1924. London. 1924; Miller, A. Donald. An Inn Called Welcome. 1965; Davey, Cyril J. Caring Comes First:
Story of the Leprosy Mission. 1987.
864
Edmundo Jeanselme was the president of The Third International Leprosy Conference in Strasbourg in 1923,
and had been attending the conferences in Berlin in 1897 and Bergen in 1909. The last section of de Souza-
Araújo’s monograph includes summaries and abstracts of more than forty letters and statements made by
researchers all over the world, summarizing the efforts to organize the society. De Souza-Araújo 1929: 18-19,
366-388.
 318

from Zensei-Byoin in Tokyo and the world’s largest leper colony at Culion in the
Philippines in December 1925, the main obstacle was identified by chief pathologist
Herbert Windsor Wade: “But how could we think of organizing a Society of
Leprology since we ignore who are the Leprologists? We have first of all to discover
them.”865 Establishing contact with possible collaborators thus became another
rationale for the journey around the world.
De Souza-Araújo’s vision was to restart Lepra Bibliotheca Internationalis, and
let this be the spearhead for a global leprosy organization. A week before arriving in
Bergen, he visited Edvard Ehlers in Copenhagen and was formally given the
ownership of the journal. The accompanying organization should have 120 expert
members elected by leprologists in countries with the disease, 120 representatives of
the sanitary services, research institutions and leprosy associations (such as BELRA
and missionary organizations), as well as ten honorary presidents. It is clear that the
Brazilian expected that many of the people he had discussed the scheme with during
his travels would fill key positions. The organization was to be split in an Eastern and
a Western branch. After a suggestion by Ehlers, he pointed out H. P. Lie in Bergen to
be the general secretary of the European, African and Latin-American branch of the
association, as well as the regional editor for the planned journal. After being
contacted by mail, Lie prepared a front page for Lepra Bibliotheca Internationalis,
starting with volume XVI.866 But moving the organization and the journal from the

drawing board into the real world proved difficult.
First, not all leprologists were interested in the society. When the scheme was
presented at the Third Congress of Dermatology for French speaking doctors in
Brussels in 1926, “the matter proved to be of little interest to French
dermatologists.”867 In France, leprosy was already one of several diseases covered by
Société de Pathologie Exotique. Next, BELRA had already plans for expanding their




865
De Souza-Araújo 1929: 366. The researchers at Culion also collaborated with colleagues at Hawaii and
several of the physicians had received training from Muir in Calcutta. It seems Wade also kept in touch with his
predecessor, Dr. Oswald E. Denney, who in 1921 was recruited from Carville to be the director at newly
nationalized US National Leprosaria at Carville, Louisiana.
866
De Souza-Araújo 1929: 373.
 319

activities, or alternatively establish an English-speaking organization in collaboration
with Wade and others.868 Third, the League of Nations was already in the process of
establishing its own leprosy commission. Finally, unlike BELRA, de Souza-Araújo’s
organization lacked friends in high places to give legitimacy and the necessary
financial support to get it off the ground. But the initiative was not in vain. When
leading leprologists met in Manila in 1931 and established the International Leprosy
Association and the International Journal of Leprosy they took de Souza-Araújo’s
framework as the starting point for the discussions. With the exception of Jeanselme,
the leadership of the new organization was identical to the one de Souza-Araújo had
proposed.869 The Brazilian was to hold the position as vice-president for the Western
Branch of the International Leprosy Association from 1932 to 1956.
After spending the rest of the year in Western Europe and North Africa visiting
laboratories, hospitals, and attending several conferences (including meeting Sir
Leonard Rogers in London and Ludwik Rajchman of the League of Nations in
Geneva), de Souza-Araújo embarked on S. S. Cap Polanio in Lisbon January 15,
1927. After eleven days he was back in Rio, and was appointed head of leprosy
research at the Oswaldo Cruz Institute, a position he would keep until 1956.870 The
task of spreading the lessons he had learned on his three year journey started
immediately. In February 1927, he gave a 40 hour course on leprology to 23 pupils;
21 physicians and two pharmacists who were students at the Oswaldo Cruz
Institute.871 When de Souza-Araújo in October 1931 enrolled 31 students it was the
third such course. By then, the program had expanded to twenty days with five hours




867
De Souza-Araújo 1929: 366.
868
Immediately after de Souza-Araújo’s visit to Culion, Wade sent questionnaires to his contacts around the
world and invited them to help ‘find out who the leprologists are’. Rogers and Muir initially refused to support
de Souza-Araújo’s organization with reference to their own initiative, but after discussing it with Wade, they
both agreed to give it a chance – provided the terms of membership and policies was still open for debate:
“Failing that we shall probably probably proceed with our original scheme, I trust in friendly co-operation with
your own association.” (Letter from Rogers to de Souza-Araújo, dated July 21st, 1929, in Souza-Araújo 1929:
375).
869
For de Souza-Araújo’s full list of members of Societe Internationalis de Leprologie, dated Paris December
15, 1926, see: LNHO: 12B-R898/29272/52570.
870
Poorman 2008: 312.
871
Letter to Dr. L. Rajchman from H. C. de Souza-Araújo, Rio de Janeiro, April 26, 1928. (LNHO: 8A-
R5872/2634)
 320

of lectures each day. Topics dealt with were history, geographic distribution,
epidemiology, etiology, pathology, clinical features, treatment and prophylaxis. The
course also included visits to various anti-leprosy organizations in Rio and Sao
Paulo.872
The knowledge was spread not just to other Brazilians. Before leaving Europe,

in January 1927, de Souza-Araújo was involved in organizing a Regional Technical
Committee for leprosy in Portugal. Later the same year he did the same in Brazil,
Argentina and Uruguay, as well as setting up a provisory committee for Paraguay.873
In 1939 he was invited by the Colombian government to assess the country’s control
program against leprosy, and gave a course on the disease which was attended by 32
physicians, 24 of whom were members of the leprosy staff of the Colombian Ministry
of Hygiene.874 In Colombia he promoted the establishment of a leprosy society with
forty members, ten of whom were later elected members of the International Leprosy
Association set up in Manila in 1931.
De Souza-Araújo also kept his interest in spreading knowledge through
medical journals. Upon returning to Brazil, he took over as editor in the journal
Memórias do Institudo Oswaldo Cruz. In Colombia, he promoted the establishment of
a quarterly leprosy journal, Revisita Colombiana de Leprología.
Setting up scientific societies and giving specialist training were both a goal in
itself and means to spread knowledge. In these areas de Souza-Arújo succeeded. In
the short run, however, his plans for an international organization failed due to a
mismatch between funding and ambitions. Several of the people he met on his journey
were interested in collaboration but de Souza-Araújo failed to keep them updated
about his work.875 Yet, in the long run de Souza-Araújo’s organization set the





872
Rev Med.-Cir. Brazil. Vol. 40 (1932), referred to in International Journal of Leprosy, No. 1, vol. 1. 1933:
110.
873
De Souza-Araújo 1929: 386-387. The committees were tasked with studying the problem of leprosy in the
country; focusing on statistics and epidemiology, etiology and prophylaxis, clinical studies and therapeutics,
and to work to create ‘centers for studies’.
874
Obregón, D. “The anti-leprosy campaign in Colombia: the rhetoric of hygiene and science, 1920-1940.”
História, Ciências, Saúde - Manguinhos. Vol. 10 (supplement 1). 2003: 200-201.
875
One of those who raised this concern was H. P. Lie of Norway. See: Letter from Lie to Madsen, dated
Bergen August 25, 1930. (LNHO: 8A-R5894/27029/6714)
 321

premises for how the later International Leprosy Association and International
Journal of Leprosy should be organized. In comparison, BELRA was a success due to
influential members and secure funding within the British Empire. Although the two
organizations shared the goal of eradicating the disease, they promoted opposite and
competing approaches on how to reach the goal.
However, these were only two of several interrelated initiatives aimed at
eradicating leprosy on a global scale. The League of Nations was also involved with
leprosy. The credit for leprosy ending up on League’s agenda was much due to
another successful medical association, Société de Pathologie Exotique.





The League gets involved


Since the early 1920s leprologists had expressed the hope that an alliance with the
League of Nations would put pressure on member states to raise campaigns to
eradicate leprosy. As de Souza-Araújo wrote in a letter to Ludwik Rajchman, the
director of the League’s Health Organization after being asked to summarize the
results of his travels: “The coordination of efforts of all nations and the international
cooperation (…) are imperative for a general campaign against leprosy, and the
Health Section [of the League of Nations] has prestige and power to obtain it.”876 De
Souza-Araújo met Rajchman in the Far Eastern Bureau of the League in Singapore in
1925, and when the two met again in Geneva in September 1926 the Brazilian urged
the League to get involved. By then the League was already pursuing several
strategies for engaging in leprosy work on a global scale.
The initiative for an alliance between the leprologists and the League had come
from the Third International Leprosy Conference held in Strasbourg, July 28-31,
1923. In one sense the conference was a continuation of the leprosy researchers’





876
Handwritten addendum to letter from Souza-Araújo to Dr. L. Rajchman, medical director of the League of
Nations Health Committee, dated October 6, 1926, written in Siracousa, Sicily. (LNHO: 12B-R898/52570).
Italics underlined in the original.
 322

previous initiatives to achieve global consensus on the disease, and the preceding
conferences held in Berlin 1897 and Bergen in 1909 were frequently referred to. Like
its predecessors, it was a conference for physicians working with leprosy in various
places. In total, 34 different countries were represented. Several of the participants
had taken part in all the previous conferences, such as professor Jeanselme from the
Faculty of Medicine in Paris, who was the President at the Strasbourg conference. On
the agenda were sessions on statistical data, etiology, pathology, treatment,
prophylaxis and legislation. It resulted in a set of resolutions and recommendations as
well as the publication of the proceedings (See appendix 2). Just as Prussia had sent
the invitation to the first conference, and the Norwegian government invited to the
second, the official invitations in 1923 were sent from the French Foreign Ministry.877
The initiative behind the Strasbourg conference came from a group of mainly
French physicians who was interested in leprosy as one of several ‘exotic diseases’.
The leading organizers of the Strasbourg-conference were deeply involved in Société
de Pathologie Exotique, established in 1907. Emile Marchoux, General Secretary at
the conference, was one of the Société’s founding members. Both Marchoux and
Jeanselme had attended the Second International Conference in Bergen in 1909 as the
society’s official representatives.878 Ten more of the thirty members of the organizing
committee were active members of the association.879
Although the organizers presented the conference as a continuity of the Berlin-
and Bergen conferences, the conference marked a break with pre-war leprosy work
with regards to participation. Of the fifteen persons who at the second international
leprosy conference in Bergen in 1909 had been elected and charged with organizing a
third conference, only three attended the Strasbourg meeting.880






877
Copy of the official invitations, as well as program and the list of members of the organizing committee, are
found in LNHO: 12B-R898/29272.
878
Anmeldte deltagere i Leprakonferencen i Bergen, 15.-19. aug. 1909. Regional State Archives of Bergen.
(http: //da2.uib.no/cgi-win/WebBok.exe?slag=lesside&bokid=leprakonferanse&sideid=4)
879
Membres de la Société de Pathologie Exotique. Archives de l’Institut Pasteur. (Available online: http:
//www.pasteur.fr/infosci/archives/f_spe2.html);
880
In Bergen in 1909, the initial 20-man Leprosy Commission from Berlin was reduced to fifteen members.
“Wahl neuer Mitglieder der Internationalen Leprakommission.” Lepra Bibliotheca Internationalis. 1910: 375.
 323

It could be argued that the Société de Pathologie Exotique provided an
inspirational model for both BELRA and de Souza-Araújo’s aspirations to create an
international leprosy organization. The mainly French society did not merely provide
legitimacy when dealing with policy makers, but also proved that a national
organization could provide the necessary resources to organize journals and
international meetings. In 1908 it began publishing the periodical Bulletin de la
société de pathologie exotique, which soon became one of the most frequently
referred journals in Lepra Biblioetica Internationalis, with 22 abstracts of original
papers on leprosy in the six years the two journals coexisted.
The leaders of the organization made important policy decisions, such as
setting the agenda for international meetings, choosing the venue, and deciding whom
to invite. The Third International Leprosy Conference was organized in the French
city of Strasbourg mainly because it coincided with the celebration of the Pasteur
centenary. Many of the founding members of Société de Pathologie Exotique
considered themselves ‘Pasteurians’, and to be part of anniversary appears to have
been a goal in itself.881
In addition to inviting physicians who had published on leprosy, a personal
invitation was sent to Ludwik Rajchman, from 1921 to 1939 director of the League of
Nations Health Organization. Rajchman did not find time to attend, but after
consulting with the president of the Health Committee, the Dane Thorvald Madsen,
he decided to send staff-member Dr. Hector Rulot.882 The official invitation which
arrived in early June was signed by the Foreign Office of a member state, the Health









That the Strasbourg conference could be interpreted as a ‘coup’ was pointed out in a letter from H. P. Lie to Dr.
Wade, January 31st, 1931: 4. (LNHO: 8A-R5894/27029)
881
The centenary was celebrated with international meetings as well as an international scientific exhibition
(L’Exposition Internationale du Centenaire de Pasteur) which was opened on June 1, 1923, in the presence of
the President of the French Republic, members of the French government, and scientific delegates from all over
the world. However, when the Third International Leprosy Conference took place on July 28 – 31, most of the
prominent guests had already returned home.
882
Letter from Dr. Rajchman to Prof. Madsen, dated 28. juni 1923; letter from Professor Madsen to Dr.
Rajchman, dated 3rd July, 1923. (LNHO: 12B/26213X/11346)
 324

Committee was still expanding its scope of operations, and Rajchman was definitively
open for suggestions.883
According to Rulot’s report to Rajchman after the conference, it was “not very
interesting or fruitful, and that it appeared from a practical point of view, that the 3rd
Conference will not produce much effect on the various Governments concerned.”884
In his opinion, the only glimmers of hope were Dr. Lie’s presentation of the anti-
leprosy campaign in Norway, and Dr. Rabello’s presentation of the laws and sanitary
regulations in Brazil. Those were the only papers that gave insights other states could
learn from.
As Rulot saw it, the main problem was that the conference had not been able to
establish the geographic distribution and prevalence of leprosy throughout the world.
This would be “essential” in order to:


a) discover if leprosy is a real danger to the world, and how contagious it is;

b) establish the necessity or otherwise of taking specific steps, either national or
international.
The appeal to the League of Nations shows that the Conference felt its helplessness, and gives
the League an opportunity of stepping onto the breach and demonstrating the value of its
existence.885

That the conference did not live up to the expectations seems to have been the
consensus also among those who attended. After a discussion where two of the
delegates promoted an alliance with the Office International d'Hygiène Publique
(founded in 1907 as a continuation of the International Sanitary Conferences with





883
For a thorough study of the League of Nations Health Organisation, see: Borowy, Iris. Coming to Terms with
World Health. The League of Nations Health Organisation, 1921-1946. 2009. See also: Borowy, Iris.
“International Social Medicine between the Wars: Positioning a Volatile Concept”. Hygiea Internationalis. Vol.
6, No. 2. 2007: 13-35.
884 rd
“Note by Dr. Rulot on the 3 International Leprosy Conference.” (LNHO: 12B-R898/29272)
885
Op. cit. Shortly after this, Dr. Rulot moved on to a scheme on interchange of specialist medical officers
working with tuberculosis, which began early in 1924. Delegates from thirteen countries, accompanied by Dr.
Rulot of the headquarters staff of the Health Section of the League, visited eight countries, and studied the
organization of the anti-tuberculosis campaign in each, illustrating how circulation of knowledge and
international aspirations were not specific to leprosy. (“Medical News”. The British Medical Journal. August
22. 1925: 364)
 325

headquarters in Paris), the majority of delegates voted to seek an alliance with the
League of Nations. The last three of the six recommendations were a plea for help
addressed directly to the League:


4) The League of Nations should resume publication of the periodical “Lepra-Archives

Internationales de la Lèpre”.

5) The League of Nations should establish an international information office on Leprosy.

6) The League of Nations should make endeavors to secure statistics on cases of leprosy
throughout the world.886


According to Rulot, such collaboration would be mutually beneficial. On the one
hand, the leprologists were in desperate need of help and legitimacy from the League
for its international aspirations to succeed. On the other hand, this would give the
League’s Health Committee a chance to prove its raison d’être. In June 1919 the
Treaty of Versailles had directed the League to take steps in matters of international
concern for the prevention and control of disease,887 but until 1924 the Health
Organization existed only as a provisional committee.
Rulot’s suggested strategy from October 1923 was to start with the countries
that already counted leprosy among notifiable diseases, and adopt their standards of
diagnosis and surveillance. The League should contact these countries and prepare a
preliminary report based on their experiences.888 However, no initiatives could be
made before the issue had been formally discussed in the Health Committee. The
question of leprosy was consequently added as issue number 67 for the second session
of the Health Committee, held May 7 the following year.





886
Resolutions and recommendations from the Third International Conference on Leprosy, Strasbourg 1923.
(LNHO: 12B-R898/29272). For the full report, see Appendix 2.
887
Article 23 (f) in Covenant of the League of Nations, adopted in Paris on April 29, 1919, states that the
Member of the League “will endeavour to take steps in matters of international concern for the prevention and
control of disease.” (http: //cil.nus.edu.sg/rp/il/pdf/1919 Covenant o 20the League of Nations-pdf.pdf) See also:
Weindling, Paul. “Introduction: constructing internationa health between wars”. In: Wendling, Paul (ed).
International health organisations and movements, 1918-1939. 1995: 7-8.
888
Unsigned. “‘Statistics on Cases of Leprosy’. Scheme for a preliminary enquiry on the notification of Leprosy
in the various countries and on the available statistics of cases in response to the 6th recommendation of the
International Conference on Leprosy, 28th-31st July, at Strasbourg.” Dated 13.10.23. (LNHO: 12B-
R898/29272/29272)
 326

To present “the problem of leprosy” for the Health Committee, Rajchman
invited Emile Marchoux, general secretary at the meeting in Strasbourg. Marchoux
painted a picture of leprosy as a scourge which affected millions all over the world,
that devoted scientists since 1897 had done all in their limited powers to stop the
disease, and that the League needed to step in to foster global cooperation. He
presented the recommendations passed at the Strasbourg meeting and urged the
League to take action.
After a short discussion the League agreed to follow up on the last of the
Strasbourg resolutions, namely establishing the global prevalence of the disease. “On
the proposal of Sir George Buchanan, the Committee decided that the Medical
Director should publish statistical information concerning leprosy and that the
publication of a monograph written by a duly qualified person should be taken into
consideration later.”889 As historian Iris Borowy has shown, this was in line with the
League’s involvement in other diseases.890 The plea that the League would take upon

itself to publish a scientific journal, which was what the leprologists gathered in
Strasbourg had considered the most important undertaking, was declined. Again, the
British representative Sir George Buchanan voiced the decisive argument: “It would
be impossible to undertake the publication of the paper referred to above because it
would create a precedent.”891 Buchannan, skeptical of the League infringing on the
sovereignty of independent states, saw no need for the League to expand their
activities and act as editors for a niche medical journal.
In order to publish statistical information concerning leprosy, the League
needed to gather the necessary expertise. Despite the limited mandate, Ludwig
Rajchman started several parallel investigations. In June 1925, he sent staff member
Evald Tomanek to London to meet with BELRA. One year earlier, its secretary
Reverend Frank Oldrieve had published a paper in the journal International Review of





889
Extract from P. V. of the First Meeting of the 2nd Session of the Health Committee. 7. May, 1924: 2. “67.
The question of Leprosy.” (LNHO: 12B-R898/29272)
890
Borowy 2009.
891
Extract from P. V. of the First Meeting of the 2nd Session of the Health Committee. 7. May, 1924: 2. “67.
The question of Leprosy.” (LNHO: 12B-R898/29272)
 327

Mission where he had estimated the number of lepers in the world to be about 3.6
million. Oldrieve argued that due to improvements in treatment, the goal of ridding
the world of leprosy was within reach:


Ten years ago it would not have been possible to speak of ridding the world of leprosy as
being a practical proposition. Now, however, the conditions have so greatly altered that I
believe we ought to look forward to getting rid absolutely of this terrible disease which has
afflicted mankind for so many thousand years; we ought not to be willing merely to
contemplate this as a desirable aim, but to set to work immediately to accomplish it.892


Rajchman saw BELRA as a potential partner. BELRA’s initiative of sending
questionnaires on leprosy to all British possessions through the Foreign-, Colonial-
and India- offices in 1924 went hand in glove with fulfilling the League’s mandate of
providing statistical information on the disease. Oldrieve himself spent the last six
months of 1924 traveling in India and the East on behalf of BELRA to get first-hand
knowledge about the situation on the ground.
Rajchman did not rely on BELRAs report alone. A second initiative involved
Emile Marchoux. Inspired by BELRAs initiative, Marchoux was commissioned to
prepare a questionnaire on leprosy which the League then sent to the ministers of
health of all countries in the world, both members and non-members of the League.
The questions asked were almost a direct copy of the program at the Strasbourg
conference where Marchoux had been the General Secretary: Prevalence, diagnosis,
sex and age upon discovery, localization of lesions, treatment, prevention, institutions
and legislation. The questionnaire underscores the commission’s continuation of the
leprosy conferences.893






892
Oldrieve, Frank. “Ridding the World of Leprosy”. International Review of Mission. Volume 13, Issue 4.
1924: 595. Exactly what these ‘altered conditions’ entailed was not spelled out, but it seems likely that Oldrieve
referred both to improved means of communication and the promise of chaulmoogra based treatments.
893
Marchoux. Proposed questionaire on leprosy. Dated November 10, 1926. (LNHO: C.H./Leprosy/1). The
initiative was also a recognition that the Health Section’s request for “a brief statement about the number of
leprosy observed the last ten years, as well as any observations on this disease in your country”, sent out in
November 1925 failed to produce useful feedback. The 1925-request was an addendum to a request from the
Italian delegation concerning the study of prevalence and prevention of Trachoma. (LNHO: 12B-R898: various
 328

The League in Latin America


The League of Nation’s third and most consequential initiative involved the Brazilian
Carlos Chagas. Since 1917 he had been the director of the medical research institution
“Instituto Oswaldo Cruz” (formerly “The Federal Serum Therapy Institute”) in Rio de
Janeiro, and from 1920 director of Brazil’s Department of Public Health. His views
on leprosy were radically opposite to Rogers’ insistence on voluntary treatment.
Chagas was the architect behind Brazil’s newly implemented anti-leprosy campaign,
which consisted of compulsory notification and obligatory isolation in agricultural
colonies for those who were able to work, asylums for invalid lepers, and sanatoria
for rich lepers. The legislation opened for police assistance in examination and
isolation of suspected lepers.894
In 1922 Chagas was appointed as a member of the League’s Health
Commission. On what seems to have been his first visit to Geneva for the Fifth
Session of the Health Committee in October 1925, he gave a presentation that stressed
the importance of raising a coordinated international campaign against leprosy. After
convincing the committee that “the problem of leprosy” needed more attention, he
was charged with preparing a report “on the prevalence of leprosy and the measures
applied to prevent its spread in Latin America.”895
At this time political relations between the League and Latin America,
especially Brazil, were strained. When it was clear that Germany in 1926 would be
offered a permanent seat on the Council of the League of Nations, Brazil (followed by
Spain) felt bypassed and decided to withdraw from the League. Some weeks before
Brazil pulled out, Time Magazine reflected a common view when it an editorial




folders). The limited replies showed that more specific instruction and increased standardization was needed in
order to produce comparable responses.
894
De Souza-Araújo, H. C. “The Leprosy Problem in Brazil”. The American Journal of Tropical Medicine.
Vol. 5, No. 3. 1925: 222ff. The first agricultural colony was opened by de Souza-Araújo in Para a month before
he departed on his travel around the world. To finance the anti-leprosy campaign, ‘Law No. 4440, December
31, 1921’, established a special fund for the prevention of leprosy in Brazil. The fund constituted 30 percent of
Federal taxes from the sale of alcoholic beverages. However, the annual income of about $3.000.000 was soon
used for other purposes.
895
Report on the Work of the Fifth Session of the Health Committee, Geneva, October 8-14, 1925. (LNHO:
12B/47209/31035).
 329

argued that “It suggests that League states may avoid unwelcome responsibilities by
dropping out of the League, and yet expect to continue to reap many of the advantages
of League membership by ‘collaborating’ in the manner of the US.”896
In the shadow of this political conflict, Carlos Chagas was the architect behind
a scheme to establish an international center for leprosy research in a partnership
between Brazil and the League. In 1928 he invited Rajchman and Madsen to visit
public health administrations and research institutes in Argentina, Brazil and
Uruguay. As Iris Borowy has argued, the tour was made to promote the little-known
League of Nations and avoid more South American countries from withdrawing. The
leprosy research center was its most successful outcome.897

The ambition was that the leprosy center should deal with prophylactic and
therapeutic aspects of leprosy, and be placed at Chagas’ Oswaldo Cruz Institute in
Rio de Janeiro.898 The expenses were to be split between the Brazilian government,
the League of Nations and the Brazilian philanthropist Guilherme Guinle.899 The
League’s contribution would be reserved for covering the costs for international
specialists visiting the research center.
Political instability, uncertainty regarding Brazil’s relations with the League,
along with the League wanting a second opinion on Chagas’ scheme, meant that the
plans were postponed until after Getúlio Vargas military coup in 1930. When the
situation had stabilized, the Brazilian government offered to set up the center and put







896
Editorial. “The League of Nations: Brazil Out”. Time Magazine. Monday, May 21, 1928. The United States
was never a member of the league, but collaborated closely and had members on several of its committees.
897
Borowy 2009: 214ff.
898
In promoting the plans, it seems Chagas worked both sides of the table. On the one hand he used his position
in the League of Nations to advocate the scheme towards Brazilian politicians. On the other hand, he used the
politicians support to promote the center in the League. See for instance the letter from Premier and Foreign
Minister of Brazil, Octavio Mangabeira from 1929, which welcomed Chagas’ scheme with open arms: “…the
Brazilian Government attaches the greatest importance to this scheme of international co-operation, which would
include the conversion of the present classes in public health at the School of Medicine (Facultade de Medicina)
at Rio de Janeiro into an international school of public health, for the technical education of medical officers in
Brazil and other countries of Latin America, and the creation in Brazil of an international centre for the study of
leprosy.” (Letter from Mangabeira to the Secretary General Eric Drummond of the League of Nations, dated
March 17, 1928. (LNHO: 8A-R5872/2634/2634; C. H. 710.))
899
Guinle was the owner of the port of Santos, and had previously sponsored a central hospital, a research
hospital and a network of dispensaries for Rio de Janeiro. (Borowy 2009: 217, note 132).
 330

it at the League’s disposal. Its main objective was outlined in a letter dated April 15,

1931:



To undertake any work which may contribute towards the prevention of leprosy by means of
epidemiological, clinical and biological research, with special reference to treatment; and by
means of a specialized course of instruction open to scientists, doctors and hygienists of the
countries which may desire to take advantage of this course, to promote universal co-
operation in the campaign against leprosy.900


The center opened in April 1934 and was active until the philanthropist Guinle
(appointed first Chairman of the Committee of Management) in 1939 announced that
he would not renew his grant, reducing its funding by almost 50 percent. Facing this,
the Brazilian government decided to pull the plug. The numerous reports in the
League following up on the center contain several complaints from foreign visitors
that the working language was Portuguese, that the skills in other languages were
poor, and that this made it hard to fulfill the ambitions as an international reference
point for leprosy research. The death of Chagas in November 1934, only six months
after the center opened, also came as a blow. The activities of the center, however,
merits further investigations.
An unforeseen consequence of the international research center in Rio was
increased international attention to the library service of the Leprosy Prevention
Department (Departemento de Profilaxia de la Lepre) in the Brazilian capital of São
Paulo. Opened at around the same time as the center in Rio de Janeiro, the department
worked to compile a complete catalogue of references to leprosy in research papers.
By 1944 their library contained more than 100.000 references, and answered an
annual average of 185.000 consultations by correspondence from all over the world.
To lift the burden of replying to the individual requests, a 1.935 page bibliographic








900
International Centre for Research on Leprosy at Rio de Janeiro. (LNHO: CH/Leprosy/9). The center was
built on the same model as the International Institute of Intellectual Cooperation in Paris, inaugurated January
16, 1926, and the International Institute for the Unification of Private Law in Rome, inaugurated May 30, 1928.
 331

index of leprosy was published in three volumes in English and Portuguese,
containing about 30.000 references to literature available at their library.901





The League’s Leprosy Commission


Although the research center in Rio was his main interest, Carlos Chagas’
Preliminary Report on the Problem of Leprosy (1926) was also the genesis of the
League of Nations’ Leprosy Commission. Instead of merely focusing on Latin
America, Chagas saw leprosy as an issue for all countries in the world. Based mainly
on reports written by the same physicians who at the leprosy conference in Strasbourg
in 1923 had argued for the League to involve itself with leprosy in the first place, as
well as selected government statistics, Chagas argued that “Leprosy is a medico-social
subject which demands the attention of the Health committee of the League of
Nations in order that the co-operation of all civilized countries may be obtained in
combating this terrible scourge.”902
Leprosy was presented as a disease which made special appeal to both human
pity and fear, and was a problem found in every part of the world. While some
countries made great efforts to combat the problem, others lacked technical resources
for effective prophylaxis. Especially the ‘highly civilized countries’ needed to step in,
regardless of whether they had the disease or not. They had the necessary knowledge
when it came to organizing a civil defense, and it was in their interest to stop the
disease before it was introduced from abroad. The underlying threat was that if no
action was taken it was just a matter of time before the problem of leprosy got out of
hand. This bears striking similarities with the arguments used on a national level, for
instance in Norway in the 1840s and on Hawaii two decades later.








901
Keffer, Luiza. Índice Bibliográfico de lepra. 1500-1943. Departemento de Profilaxia de la Lepre de São
Paolo. Brasil. Vol 1-3. 1944-1947.
902
Chagas, Carlos. Preliminary Report on the Problem of Leprosy. 1926: 1. (LNHO: 12B-R898/50806/29272)
 332

The conclusion of Chagas’ preliminary report was that the League should set
up a special commission to study the problem of leprosy in all its aspect:


I. To spread in the main centers of leprosy modern knowledge regarding the disease, in order
that measures may be taken which will effectively restrict infection.
II. To promote and assist investigation into the treatment of leprosy.

III. To endeavor, with the aid of specialists, to elucidate the mechanism of infection, an exact
knowledge of which is indispensible as the rational basis for prophylaxis.
IV. To arrange for the exchange of specialists between countries in which leprosy exists, and
organize special leprosy research centers.
V. To promote and assist the publication of an international review, the special purpose of
which would be to spread knowledge concerning leprosy.
VI. To promote international legislation with the object of preventing the transmission of
leprosy from one country to others.903


The report was discussed at the sixth session of the Health Committee held at Geneva
from April 26th to May 1st, 1926, and in a situation where the League felt it was about
to lose its foothold in Latin America, Health Committee gave full support to Chagas’
plans. This meant a wide expansion of the League’s ambitions related to leprosy.
Even the question of establishing an international medical journal, which two years
prior had been flatly declined, was now back on the agenda.
The first step in fulfilling the new mandate was to find collaborators. Chagas
was charged with finding international experts to a special Leprosy Commission to
tackle leprosy on a global scale. He went to medical experts who were already
collaborating with the League. Five of the six members of the Leprosy Commission
were already on the permanent Health Committee: Carlos Chagas (Brazil, Chairman
of the Leprosy Commission), Surgeon General Hugh Smith Cumming (USA),
Colonel J. D. Graham (India), Doctor Thorvald Madsen (Denmark, also President of
the Health Commission) and Doctor Ludwig Rajchman (Poland, also Medical director
of the League). The last member of the Leprosy Commission, Professor Maturo





903
Op. cit.: 9.
 333

Nagayo (Japan), did not have a prior position with the Health Organization but was
already involved in the League’s exchange program for foreign medical researchers
through courses at his Government Institute for Infectious Diseases at Tokyo.904 All
the members were medically trained, all had high-ranking positions in their national
health systems, and all had prior experience with leprosy work.
The first official meeting of the Leprosy Commission was held in Paris, on
May 14, 1928. Until then the League had been operating more or less as an extension
of the International Leprosy Conference. Now, the League itself would be the driving
force behind international collaboration regarding leprosy.
However, already the first preliminary exchange of views showed that
collaboration would prove difficult. Chagas, Cumming, Nagayo and Madsen argued
that the League should promote state segregation. Rajchman was undecided, while the
Public Health Commissioner with the Government of India, Colonel J. D. Graham,
insisted that the situation on the ground was too differentiated for a ‘one size fits all’-
approach. Instead, Graham argued, leprosy work must be country-specific and any
expenditure on public health measures should correspond to the relative importance
of the disease. Based on his experience in India, leprosy could not be considered a
major threat to public health, and segregation was both impractical and counter-
productive.
To sidestep the potential conflict, the commission initially decided that the
main focus should be on collecting knowledge, not on how it should be applied. This
was based on the same line of arguments that resulted in the international leprosy
conferences. Still, the means differed: The League’s joint program focused on
facilitating research and training in early diagnosis, methods of communication and
treatment.905 This should be done through international research centers, the already
mentioned center in Latin America and one more to be situated in the Far East.





904
League of Nations Health Committee: Minutes of the Ninth Session. LNHO: C. 107. M. 38. 127. III (C.
H./9th Session/P.V), 1927: 49.
905
“Communication from the Commission for the Study of Leprosy to the League of Nations Health
Organization”. Dated Geneva, May 24, 1928. (LNHO: C.H./Leprosy/3, found in LNHO: 8A-
R5887/4621/4621).
 334

Most importantly, the committee agreed to hire a secretary. They chose the
French physician and bacteriologist Dr. Etienne Burnet, who earlier had collaborated
with the League on scientific cooperation regarding health in post-war Poland and
Russia. He had also worked as deputy director at the Pasteur Institute in Tunis but left
the position after a conflict with its main director Charles Nicolle. Since 1926, Burnet
had been a member of the Société de Pathologie Exotique. From October 1, 1928,
Burnet was officially employed by the League of Nations staff.906 He was to be the

only one working full-time for the Leprosy Commission.
Burnet did not start from scratch. Since 1925, scattered statistics on leprosy
was reported from the Oriental Bureau of Epidemiology of the League of Nations
(more often referred to as the Far Eastern Bureau).907 De Souza-Araújo, who in the
beginning of September 1926 met Ludwig Raichman in Geneva, had prepared a 31-
page document detailing his findings from traveling around the world.908 There were
also piles of responses to Marchoux’ questionnaire, giving details both from states,
institutions and missionary organizations.909 Before Burnet arrived, it appears that
these reports had more or less been collecting dust. Burnet also soon realized that not
all states had bothered to answer the requests for information. Finally, although








906
Burnet would keep the position as secretary for the Leprosy Commission until August 31, 1936, when he
was appointed director at the Pasteur institute in Tunis following the death of Charles Nicolle.
907
The office was opened in 1925 to facilitate the exchange of epidemiological intelligence from 35 ports in
twelve countries. During the first years its network of epidemiological intelligence had expanded to 76 ports in
27 countries. It was soon authorized to act as a center to coordinate scientific research and instruction for
medical statistic, and to distribute information on international health work. (Borowy 2010: 15.)
908
De Souza-Araújo, H. C. Leprosy as a world’s sanitary problem. October 5, 1926. (LNHO: 12B-
R898/52570).
909
There were also letters to the League from individuals wanting to contribute. On December 26, 1923,
Cathrine Blomefield from Johannesburg, South Africa, contacted the League with a special print of her Thesis
on the Prevention of Leprosy (1923), an 11-page pamphlet which argued that leprosy “is produced by the lack
during a lifetime of a diet containing animal fats and fresh meat” (1923: 5). Blomefield, the daughter of the
English Major W. B. Arnison of Penrith, requested the Health Director of the League to promote her as a
candidate for the Nobel Prize in medicine for 1924. Rajchman acknowledged receiving the document, but took
no action. Over the following month, Blomefield wrote more letters, including a three-page “Part II” of the
thesis, and asking to be nominated as a member of the Health Commission. Frustrated by the lack of support,
the correspondence ended with Blomefield wanting the documents returned: “If the information in typed
manuscript is not to be used may I ask for its return, (properly stamped please) as the labour of copying is a
consideration, and the Leagues lack of interest in the prevention of leprosy is not so great as to cause me to
spend another £23 in printing.” (LNHO: 12B-R898//33565x/29272)
 335

Marchoux had given the recipients detailed instructions, the replies were not
comparable.
In order to learn about the leprosy situation around the world, it was not
enough to read documents. Almost the whole of 1929 he did as de Souza-Araújo had
done some years earlier: He went on the road. First, Burnet and Chagas visited
leprosy centers in Europe. Then Burnet left on a five-month journey to South America
to follow up on Rajchman and Madsen’s journey the year before. The goal of the
journey was both to promote the League and to gather knowledge about leprosy:
Incidence, legislations, provision of leprosaria and dispensaries, methods of treatment
and the latest research efforts. Burnet found that while the public health
administrators were positive and welcoming, they lacked trained personnel and a
system which could produce basic health statistics.910 In lectures on leprosy, Burnet

recommended isolation of contagious cases, rigorous separation of children from
leprous parents and the creation of leprosy societies to study the etiology, pathology
and bacteriology of the disease.911 He was also looking for potential sites and
collaborators for the planned international research center, and ended up agreeing
with Chagas that his set-up in Rio de Janeiro would be best suited for a center of
scientific, epidemiological, therapeutic and experimental studies into leprosy.





A matter for technical experts


With Burnet traveling, nothing much happened in the Leprosy Commission. This was
a source of frustration. At the first meeting in Paris, each member had been charged
with preparing reports on the research taking place in their home countries. Graham
commissioned Muir from BELRA and the School of Tropical Medicine and Hygiene








910
Borowy 2009: 218. For Burnet’s report of the travels in Europe, Latin America and the Far East, see LNHO:
C. H. 887.
911
Obrégon 2003: 185.
 336

in Calcutta to write a bibliography on leprosy research in India from 1900 to 1928, but
initially refused to share it with the League:


We also here have prepared a bibliography of leprosy research in India and I think it is a
very complete one. In view, however, of the fact that I have received no information of any
kind from Dr. Burnet, Secretary of the Leprosy Sub-commission, and I consider that some
information at least is due from the Secretary of the Commission to its members – I do not
propose to send anything meanwhile to the League until I hear more. The leprosy
discussions reported in the proceedings of the Health Committee are not very illuminating
and it is extremely difficult for me to form any idea of what is happening.912


Only after Ludwig Rajchman stepped in and pointed out that Graham himself had
been present at the thirteenth session of the Health Committee when Burnet’s journey
had been approved (in the letter he even attached the minutes of the meetings), did
Graham apologetically agree to forward the report containing 192 references to
leprosy research in India.913 While Chagas officially was the leader of the
commission, and Burnet its secretary, it appears that Rajchman was involved in most,
if not all, decisions. Burnet consistently asked for his consent before taking any
action. Apart from initial recruitment and promoting the research center in Brazil,
Chagas does not seem to have been deeply involved with the work of the commission.
In addition to lack of communication and disagreements on the merits of
segregation, the question of missionaries was to become another contested issue. The
replies to Marcheux’ questionnaire showed much of the leprosy work around the





912
Letter from Colonel J. D. Graham to Dr. Frank Boudreau, Chief of the League of Nations Epidemiological
Intelligence and Public Health Statistical Service, dated Simla, July 12, 1929. (LNHO: 8A-R5887/14019). The
report from Muir was dominated by the ‘Calcutta school’: About a quarter of the references, 52 papers, were
written by Muir; 21 by Rogers. (Muir, Ernest. Researches on Leprosy in India (1900-1928). (LNHO:
C.H./Lèpre/6)).
913
Letter to Graham from Rajchman, dated Geneva August 27, 1929. (LNHO: 8A-R5887/14019). Five days
earlier, acting director of the League’s Health Section Frank Boudreau had written a letter to Graham which
stressed that there had been no other meetings in the commission, and that since there was no news, there had
been no need for further communication. That Rajchman himself stepped in might suggest that he feared the
British would withdraw from the commission altogether. In his letter, Rajchman explained that Burnet would
use the information gathered to write a general report to the Leprosy Commission and the Health Committee,
that this would be an important report, and that he personally hoped that the Indian bibliography would be
included.
 337

world was not considered a state issue, but was instead left in the hands of religious
orders and missionary organizations. In 1924 the Mission to Lepers, in collaboration
with 33 missionary agencies, provided for the maintenance of 96 institutions for
lepers in twelve different countries.914 Many of the medical missionaries had decades
of experience in the field, and missionary organizations had their own networks for
circulating knowledge, including journals, newsletters and conferences for asylum
directors. According to BELRA’s first secretary Frank Oldrieve, himself a former
missionary:


Missionaries have always been in the forefront in carrying on leper work, and they will
probably still lead. (…) it is generally recognized that the best leper work in any country is
that which is done under missionary superintendence. It needs a man or woman who has been
touched by the hand of Christ to a deep sympathy with those who are in the greatest need
successfully to carry on work amongst these poor outcasts.915


Should missionaries be invited to the League of Nations Leprosy Committee?
The most vocal opposition came from the American Hugh Smith Cumming.
Since March 3, 1920, he had been Surgeon-General of the United States Public
Health Service, as well as director of the Pan-American Sanitary Bureau. In 1921 he
had been in charge of nationalizing the National Leprosy hospital in Carville, USA,
which until then had been administered by the missionary organization Daughters of
Charity for almost three decades under the name Louisiana Leper Home.916 In
Cumming’s experience, most missionaries lacked medical training and were therefore
unqualified to give advice: “My attitude has been that we should have on the Leprosy
Commission men whose views on the etiological and medical phases of the subject








914
Oldrieve 1924: 597. The remark was made addressing a missionary audience. In total the Mission to Lepers
ministered to some 18,000 lepers and un-tainted children. Most of their institutions were small: 31 of the 46
asylums were in India had fewer than 100 inmates, and the total of 5,428 lepers institutionalized in India was
about the same as Culion alone. (de Souza-Araújo 1929: 241)
915
Oldrieve 1924: 600-601.
916
Moran 2007: 123ff.
 338

are to be regarded as quite sound.”917 This meant ignoring both the European Mission
to Lepers and the American Mission to Lepers (whose general secretary Dr. W.
Danner was a “Doctor of Divinity”), despite their active involvement in various
leprosy institutions around the world. Leprosy was a public health issue, and
missionaries were with their religious perspectives considered unreliable.
Cumming also explicitly opposed involving Sir Leonard Rogers and the British
Empire Leprosy Relief Association. While BELRA presented itself as a voluntary
scientific organization, it collaborated closely with Mission to Lepers and several of
its leaders were former missionaries. In both meetings, letters and telegrams,
Cumming consistently referred to Rogers’ views concerning therapeutics as
“unsound”. The sources do not indicate why, but it could be argued that Rogers’
insistence that leprosy was curable and not highly contagious, and that the best way
forward was voluntary treatment in out-patient clinics, was a direct challenge to the
policies of segregation that Cumming had implemented in the United States and that
he also promoted through the Pan-American Sanitary Bureau. That Rogers from time
to time jazzed up his documents with peculiar proverbs made it easy to label him as
‘unscientific’. His Memorandum to Rajchman from 1925, for instance, concluded like
this:

In South Africa part of the money being saved by release of uninfective cases is to be devoted
to research, and when we remember how much advance has already been made within a single
decade, we should press on with this work in the assured faith that if you cast your bread upon
the waters you shall surely find it after many days.918










917
Letter to Dr. C. L. Park, Assistant Director, League of Nations Health Section, from Surgeon-General H. S.
Cumming, dated Washington, November 15, 1929. (LNHO: 8A/16440/4621) Cumming was also involved in
organizing de Souza-Araújo’s journey, and supplied him with a letter of introduction. (De Souza-Araújo 1929:
7)
918
Rogers, Sir Leonard. “Memorandum on the prevalence and prophylaxis against leprosy in the British Empire,
based on replies to the questionaire of the British Empire Leprosy Relief Association; with suggestions for
dealing with the problem.” 1925: 29. For more on BELRA and its collaboration with Christian missionaries, see:
Worboys 2000: 207-218.
 339

The rest of the commission agreed that leprosy was a ‘technical’ issue, and that this
excluded missionaries. Despite Cumming’s repeated protests, Rajchman did indeed
invite Rogers to be part of the Leprosy Commission. After all, he was considered
Britain’s leading expert on leprosy, Britain was an important member of the League
and a large proportion of the world’s lepers lived in the vast British Empire. Tuesday
October 15, 1929, Rajchman sent a telegram to all members proposing Rogers as a
new affiliate. When Cumming’s telegraphic reply (“Rogers views concerning
therapeutics leprosy considered unsound here suggest marchoux unna or mccoy =
cumming =”919) arrived in Geneva at 19.00 in the evening two days later, a personal

invitation to Rogers had been sent by telegram only a few hours earlier. Rogers,
however, declined the invitation due to lack of time.920 Unknown to Rogers, this way
the commission dodged a potential conflict.
In total the committee was expanded with four new members: Dr. G.
Alexander Mitchell (Chief Health Officer for the Union of South Africa, Pretoria),
Professor Ernest Muir (School of Tropical Medicine and Hygiene, Calcutta, India),
Dr. H. Windsor Wade (Chief Pathologist of the Public Health Service of the
Philippine Islands and Medical advisor to the Leonard Wood Memorial for the
Eradication of Leprosy, Manila), and Dr. N. E. Wayson (surgeon, Public Health
Service of the United States of America, Leprosy Investigation Station, Honolulu,
Hawaii).921 The new members had similar background as the existing six: All of them
were trained physicians, all of them had experience from leprosy work, all of them
were in leading positions in their home countries, and none of them were missionaries
or persons with other academic backgrounds.




919
Telegram from Cumming to Rajchman dated Washington, October 17, 1929. (LNHO:8A-
R5887/15292/4621)
920
This was not the first time Rajchman tried to recruit Rogers to collaborate with the League. Two years prior
to the official meeting in Paris, Rajchman had invited Rogers on behalf of BELRA to attend a preliminary
meeting with Marchoux and Chagas. Then, too, Rogers declined: “I should like to be able to comply with the
request, but I very much fear I should be of no use to the Committee, as unfortunately owning to a bad ear for
sounds I can neither speak or understand French or any other language than English, and when I attended the
Strasbourg Leprosy Conference I was quite unable to follow either the papers or the discussions, so unless
Professor Chagas has a good knowledge of English (which I learned at the leprosy conference Professor
Marchoux has not) it would be quite useless for to go over Paris confer with them.” (Letter from Rogers to
Rajchman, dated London, May 22, 1926. (LNHO: 12B-R898/51481).)
 340

Leprosy in the Far East


Burnet stayed in Geneva less than four months before he set off on another journey,
this time to the Far East. Leaving Geneva on December 20, 1929, Burnet’s itinerary
shows that on the way he visited Calcutta, Singapore, Saigon (now Ho Chi Minh City,
Vietnam), and the Philippines before arriving in Japan. From there he proceeded to
Hawaii, went on to San Francisco, crossed the United States by train and finally
returned to Europe departing from New York. The main goal was Osaka, where the
next meeting of the Leprosy Commission was planned to be held in conjunction with
the quadrennial Congress of the Association of Medical Science of Japan in April
1930. On top of his agenda was to assess the possibility of establishing a second
international research center in Japan. Burnet’s requirements were that it must be
placed in a country where leprosy was endemic and clinical material “as abundant as
possible”. Furthermore, a center had to build on an existing institution near a large
town with a university and scientific institutions; it should have access to laboratories
for therapy, bacteriological tests and pathological anatomy (including autopsies), and
be ready to accept an international staff on temporary basis and provide practical
training.922 Japan qualified on all accounts.
By the time Burnet set sail for the planned meeting in Osaka, leprosy had long
been on the public agenda in Japan. Three decades after Japan’s opening to the West
in 1854, Christian missionaries had started to erect ‘leper houses’.923 A national
survey in 1904 indicated that the number of lepers was increasing dramatically, and
that there were more than 30.000 lepers in the country. A Leprosy Prevention Law
was enacted in 1907, which divided the country into five health regions. In 1909 a
public sanatorium was established in each region to accommodate vagrant lepers.924




921
LNHO: C. H./Lèpre/8.
922
Burnet, Etienne. Report on the Programme of work of the Leprosy Commission. 1930: 9-10. (LNHO: 8A-
R5893/16680/6714; LNHO: C.H.887(a).)
923
Gould 2005: 133-141.
924
Ohtani, Fujio. The Walls Crumble. The Emancipation of Persons Affected by Hansen’s Disease in Japan.
1998: Chapter 2. The book is a translation from Japanese of “The History of the Repeal of the Leprosy
Prevention Law: Love Conquers, the Walls Crumble”, published in 1996 to celebrate the repeal of the “Leprosy
Prevention Law”.
 341

Like Brazil, Japan was on a path towards forced segregation. In 1931, the laws were
expanded to encompass all lepers: “Any and all patients who suffered from leprosy
would be institutionalized in a state or prefectural government administered
sanatorium, and the expenses involved in such institutionalization would be covered
by the central or prefectural governments.”925 The establishiment and expansion of
institutions went hand-in-hand with medical research. Before Burnet left from
Geneva, Maturo Nagayo provided his fellow members of the Leprosy Commission a
two-volume index of 348 commented research papers on leprosy produced in Japan
between 1890 and 1928.926
Burnet was thrilled by what he found in Japan. “The organisation of the

leprosaria (in Japan) is one of the best in existence, and each establishment has a
remarkably well-equipped laboratory attached to it. All the dermatological clinics of
the universities have consultation clinics for lepers.”927 However, unlike in Brazil,
discussions with the Japanese Government were still at a preliminary stage. The plan
was that the strategy should be discussed in conjuncture with the meeting in Osaka,
where the Leprosy Commission would be present in full. But despite the Commission
at this point only consisted of six members, coordination across the globe proved
complicated. Chagas, Cumming and Rajchman found it impossible to fit the meeting
in their schedules, and on February 24, the decision was made to postpone the
meeting since only Madsen, Graham and Nagayo would be able to attend.928 By then,
Burnet was well underway. Surprisingly, the highlight of the journey turned out not to
be Japan, but rather the Culion leper colony on Philippines.
Inaugurated in 1906 by Victor G. Heiser, then the Director of Health of the

Philippines, Culion had initially been a remote island where leprosy sufferers had








925
Ohtani 1998: 61.
926
Nagayo, Maturo. Recherches sur la lepre au Japon (1890-1928). (LNHO: C.H./Lépre/5).
927
Burnet, Etienne. Report on the Programme of work of the Leprosy Commission. 1930: 13f. (LNHO: 8A-
R5893/16680/6714; LNHO: C.H.887(a).)
928
Letter from the Deputy Secretary-General of the League of Nations to the Director of the Japanese Bureau to
the League of Nations, dated Geneva February 24, 1930. (LNHO: 8A-R5887/13191/4621)
 342

been dumped and left to die, out of sight – out of mind.929 During the first four years
of its existence, between 1906 and 1910, 5.403 lepers were sent to Culion: 3.154 died
and 114 ran away. The worst year was 1908 with more than three funerals per day.
1.603 new patients were admitted and 1.221 deaths were registered.930 By the mid-

1920s, it was also the largest leprosy research center in the world with almost six
thousand patients.
The architect behind the research facilities was Herbert Windsor Wade. In
1921 Wade had been recruited from the Philippine General Hospital and appointed
chief pathologist and acting chief physician at Culion by the newly appointed
Governor-General to the Philippines, Leonard Wood. Both Wood and Heiser, now
director of the International Health Division of the Rockefeller Foundation, strongly
promoted the use of Culion as a center for isolation and treatment of leprosy patients.
Wade was given liberal budgets.931 In the first year Wade hired eighteen physicians
and twenty-one trained nurses – in addition to the nuns who were already working
there. New buildings were erected, and experimental treatment tested on a grand
scale. By 1925, about one third of the Philippine health budgets were spent on leprosy
and it had spawned public criticism that expenses were out of proportion to the








929
Victor G. Heiser would later argue: “There were twelve hundred new cases developing every year and
practically nothing was done about them. (…) Segregation is always cruel. We did not want to separate husband
and wife or children and parents. But segregation is cruel to relatively few whereas non-segregation threatens an
entire people. I believed that isolation not only protected others from contracting leprosy but, furthermore, was
the most humane solution for the leper himself. Instead of being shunned and rebuffed by the world, he could
have an opportunity to associate with others of his kind in pleasant relationship.” (Heiser 1936: 227.)
930
De Souza-Araújo 1929: 154, Table No. 26.
931
Long, Esmond R. “Fourty Years of Leprosy Research. History of the Leonard Wood Memorial (Americal
Leprosy Foundation) 1928 to 1967.” International Journal of Leprosy. Vol. 35, No. 2. 1967: 239-253. Victor
George Heiser was himself a physician specializing in tropical medicine with a special interest for leprosy. As I
showed in Chapter 3, his encouraging results of treating some of the patients with the ‘Heiser-Mercado’-
mixture, a blend of chaulmoogra and camphor oils and resorcinol, was important in redefining leprosy from a
herbal palliative to a curative drug. (US Public Health Report, supplement no. 20, 1914.) Acting as Associate
Director of the International Health Division of the Rockefeller Foundation, Heiser was also the main sponsor of
de Souza-Araújo’s journey in 1924-1927. Heiser was also an avid traveler, who reportedly circled the world
17 times on his medical missions. His travels are recounted in his autobiography An American Doctor’s
Odyssey: Adventures in Forty-Five Countries (1936). This became the sixth best-selling non-fiction book in the
United States in 1936, with more that half a million copies sold. (Wall, Rosemary. “The International Health
Division’s Views on Nursing Practice, Policy and Education in British Malaya.” Rockefeller Archive Center
Research Reports Online. 2010: 2. (http: //www.rockarch.org/publications/resrep/wall.pdf)
 343


number of those affected.932 It was also increasingly clear that the military-inspired
strategy of eradicating leprosy from one island at the time through segregation (see
Chapter 4) had failed.
Inspired by Muir’s Calcutta school, a national “Dual Plan” was suggested by
the Culion Medical Board in September 1925, which was led by Wade. The plan
consisted of new cases being assigned to out-patient treatment stations in the principal
leprous regions, and only those whose treatment failed were to be transferred to the
leper colony of Culion. This would, over time, cut costs. However, lack of funds
made it impossible to establish the necessary number of out-patient treatment stations.
Besides, although Wade and Chief Physician Casimiro B. Lara at Culion were able to
present cures from 15% to 20% of advanced cases, the majority remained beyond
treatment.933
Instead of cutting the expenses, Wade’s solution was to look for alternative
funding. Dorothy Paul Wade (Wade’s wife) moved back to the United States in 1925
in order to organize a fundraising-campaign. The goal was to rise two million dollars
for research and treatment. She recruited Pierre Burgess from the New York fund
raising firm “Ward, Wills, Dreshan and Gates”, and together they set up the
“American Committee for the Eradication of Leprosy”. Like BELRA, it had a high
ranking executive committee.934 Until then, the model of private fundraising was used
primarily by missionary organizations. To avoid stepping on their toes the committee
agreed to confine their attention to medical research, leaving the welfare field open








932
Chapman, Ronald Fetts. Leonard Wood and Leprosy in the Philippines. The Culion Leper Colony, 1921-
1927. University Press of America. 1982: 91ff. In comparison, approximately 30,000 Filipinos died from
tuberculosis annually. (Chapman 1982: 105).
933
Obregón 2003: 188. They did however register ‘improvement’ in a majority of cases. More on treatments in
Chapter 3.
934
The executive committee included James G. Harbord (former Chief of Staff of the United States Army and
Chairman of the Board of the Radio Corporation of America), Hemry L. Stimson (Governor General of the
Philippines after Wood, and later US Secretary of State and Secretary of War), Charles Evans Hughes (former
Secretary of State and later Chief Justice of the Supreme Court), Owen D. Young (Chairman of the Board of the
General Electric Company and former Chairman of the Board the Radio Corporation). Also involved were
William Howard Taft (Chief Justice of the Supreme Court and former President of the United States), and
George Horace Lorimer (editor of the Saturday Evening Post).
 344

for voluntary organizations such as the American Mission to Lepers who by then had
expanded from Latin America to also engage with leprosy work in Asia.935
In the midst of the five year fundraising campaign, in 1927, General Wood
died during surgery in the United States.936 The complete organization was set up in
New York in his name as a nonprofit organization: “The Leonard Wood Memorial for
the Eradication of Leprosy”. Their mission statement was “to carry on, maintain and
support laboratory investigation, clinical observation and all manner of research with
respect to the disease leprosy; to disseminate information concerning the source,
diagnosis, treatment and prevention of leprosy”. Burgess was made its director in
1928 and became the first President in 1930; Mrs. Wade served as Permanent
Secretary of the Board, while Mr. Wade was officially hired as Medical Director in
January 1931.
When Burnet arrived in the Philippines and was welcomed by H. W. Wade, the
construction of laboratories at Culion and Cebu was well underway. More than four
thousand patients took part in clinical trials for new treatments. In 1930, the journal of
the Philippine Islands Medical Association reported that 1.600 patients were rendered
bacteriologically negative over a period of seven years, and were consequently
allowed to leave the leprosaria.937
In addition to research and the national leprosy campaign, Wade believed that
international collaboration and coordination of efforts were necessary to fulfill the
goal of eradicating the disease. With two million dollars pledged from over fifty
thousand subscribers in the United States, the Leonard Wood Memorial had the






935
Long 1967: 241-2. Several missions were also actively engaged at Culion, illustrating how religion and
science was in no way mutually exclusive when it came to practices towards leprosy sufferers.
936
According to de Souza-Araújo, the death of Wood was the main reason why his Société internationale de
Leprologie remained inactive: “this sad event having happened in the UNITED STATES in July 1927, caused
some trouble amongst the official elements of that remote country [The Philippines], and the collaboration
works between them, Europe and ourself to strengthening the basis of the International Society of Leprology
suffered an awfully long interruption, of now two years, without any improvement of the situation.” (Souza-
Araújo 1929: 388, dated September 1929.)
937
Between 1922 and 1930, 1.845 individuals were released on parole or discharged after consistently testing
negative for the presence of the leprosy bacillus for at least two years. During the fifteen years prior, mere 47
persons were discharged for similar reasons. (Report from Jacobo Fajardo, Director of Health of the Philippine
Health Service, to Burnet, dated March 4, 1932, p. 28. (LNHO: 8A-R5931/36851/29090))
 345


finances to move the scheme forward.938 When Burnet explained that the next
meeting of the League’s Leprosy Commission was intended to be held in the Far East,
Wade saw the opportunity of including the League’s members in his scheme. The
goal was the same as de Souza-Araújo’s: To facilitate international collaboration
through an international leprosy organization that could publish an international
medical journal. The way forward would be to invite the League’s Leprosy
Commission along with key researchers to a prolonged meeting in Manila, with all
expenses covered by the Leonard Wood Memorial.939
After Burnet’s visit, Wade started contacting people in his network, asking

them to suggest persons to invite to the planned Manila meeting. As he stated in the
official invitation: “The attendance will be limited to those having had a considerable
personal experience with leprosy and its problems.”940 Although officially the
initiative came from the Leonard Wood Memorial alone, the Manila meeting was
scheduled for early January 1931 so that the members of the League of Nations
Leprosy Commission in personal capacity could go there directly from their meeting,
which by then had been rescheduled for Bangkok in December 1930.
Each name on the list of attendees was discussed and approved by Wade on
behalf of the Leonard Wood Memorial, Victor Heiser on behalf of the Rockefeller
Foundation and Etienne Burnet (in collaboration with Ludwig Rajchman) on behalf of
the League of Nations. Again, the question of missionaries and the position of Sir
Leonard Rogers were controversial. After receiving a list of potential participants
from Ludwig Rajchman containing both the names of Muir and Rogers, Wade wrote
in reply to Burnet: “from his [Rogers] writings one can but gather that his mentality




938
F. P. G. “Special Correspondence: The Leonard Wood Memorial for the Eradication of Leprosy”. Science.
June 9, 1933:562-562.
939
This was not a new suggestion. Already in April 17, 1925, the secretary of BELRA, Frank Olderve had in a
letter to Dr. Tomanek of the League of Nations suggested pursuing a similar strategy: “I have for some time had
in mind that before very long an attempt ought to be made to get together half a dozen men, or perhaps a few
more than that, who are conversant with leper work in various countries where a good deal is being undertaken,
so that we might discuss the question of dealing with the whole problem on a world basis. As a matter of fact we
have had a little talk about it here, and we rather strongly feel that in the near future it would be a very good thing
if a small conference could be convened, perhaps here or in Geneva, to deal with this matter, and as far as we can
be of service we should be delighted to do everything that we can.” (LNHO: 12B-R898/42389/2942).
 346

has not improved of recent years (…) he seems to be little more than a propagandist
for Muir’s work. These two may be expected to argue and vote as one.” Wade also
blocked the attendance of missionaries: “they would, I fear, burden our conference
with non-contributors to technical discussions.”941





An unprecedented compromize


After the cancellation of the Osaka-meeting, the second meeting of the Leprosy
Commission was held in Bangkok during the Eight Congress of the Far-Eastern
Association of Tropical Medicine on December 8 to 12, 1930. To hold the meeting in
concert with a large medical conference was mainly a question of having experts
close at hand and being able to quickly disseminate the outcomes, but was also a way
to cut the costs. As Chagas himself was unable to attend, professor Bernhard Nocht,
Director of the Institute of Tropical Diseases in Hamburg, was invited to be the
president of the meeting.942 There, finally, Burnet reported on what he had learned
during his travels around the world.


…a whole complex of circumstances was hampering progress in the study and prevention of
leprosy, viz., insufficient organisation, unsystematic use of resources, uncertainty on points of
paramount importance for the establishment of the bases for prophylactic work, and a certain
lack of contact and agreement between medical men and research workers in different
countries.
(…)
Thus the question of segregation and prophylaxis still remains a subject of controversy
between advocates of freedom on the one hand, and of coercion on the other. The results of
the enquiry which included the consultation of a large number of leprologists, show that any




940
LNHO: 8A-R5914/20600/20600. Discussions on practicalities and whom to invite are also found in this
folder.
941
Letter from Wade to Burnet, dated Manilla September 2, 1930. (LNHO: 8A-R5914/20600/20600)
942
Nocht was for a time considered the post of director of the planned International Centre in Rio de Janeiro,
and six months after the Bangkok meeting he was sent there to inspect the organization of the center. (LNHO:
8A-R5872/19117/2634). The Brazilian government, however, insisted the post was to be given to the
philanthropist Guinle as a reward for donating half of its budgets.
 347

meeting of experts would be divided into two camps; those who may be described – by
analogy with another problem of social hygiene – as partisans of abolition and those who are
in favour of regulation. The concessions which those two schools are obliged to make in the
course of practical work prove that they have some common ground and justify the hope that
they would come to an agreement upon a programme of work.
We have given our reasons for thinking the present time is ripe for international co-
operation for the prophylaxis of leprosy. Leprologists of all countries have welcomed the
Health Committee’s action in regard to this matter and it is no exaggeration to say that they
hope and expect that the Leprosy Commission will promote the organization of concerted
action, even becoming to some extent a centre for this work.943


The first point on the agenda was establishing international research centers in Rio de
Janeiro and Japan. The plan was that the two centers should provide training for
leprologists from all over the world. The workers at the centers were in turn required
to spend time in the research centers in Calcutta, Culion and on Hawaii to build on
their experiences. In addition, the centers should address the contested question of
treatment. Access to a large number of patients would make it possible to follow up
on their work with comparative experiments with drugs such as the chaulmoogra
derivates. While the center in Brazil was in operation between 1934 and 1939, the
research center in Japan was never put under the auspices of the League. Planning had
not come to an end when Japan on March 27, 1933, in response to the international
condemnation of the occupation of Manchuria in September 1931, announced its
withdrawal from the League of Nations.
The next point on the agenda was Burnet’s draft report on prophylaxis. All
agreed to the need for closer collaboration around the world and more standardization
on methods and terminology. In an attempt to avoid historical connotations of
persecution, both camps agreed to instead of “segregation” use the term isolation, and
that further work was necessary in order to reach a global classification of especially
diagnosis and treatment. Beyond that, the commission was split. One group focused





943
Burnet, Etienne. Report on the Study Tour of the Secretary of the Leprosy Commission in Europe, South
America and the Far East. January 1929-June 1930. Geneva. 1930: 1-2. (LNHO: 8A/R-5893/16680/6714)
 348

on special treatment, the other on isolation, mirroring the debate between de Souza-
Araújo, Rogers and Muir discussed at the beginning of this chapter, as well as in the
end of Chapter 4.
The final report of the commission was a compromise. It recommended simple
and elastic laws focusing on notification and isolation of bacteriologically positive
cases in state facilities in accordance with the conditions in the particular country.
Based on the premise that most of those affected caught the disease as children, they
also recommended that children of lepers should be removed from their parents and
periodical examination at schools. These measures were to be supplemented by
education and propaganda aimed at the general public, both to recognize the disease
in its earlier stages and to prevent new cases.944 The widely distributed report on

prophylaxis was arguably the most important document the League’s Leprosy

Commission produced (see Appendix 4).

After presenting their conclusions in a plenary meeting of the congress of the
Far-Eastern Association of Tropical Medicine, the members of the commission (apart
from Mitchell who had to return to South Africa) traveled together to Manila to attend
the Wood Memorial conference from January 8 to 23, 1931. By attending in personal
capacity the Memorial could cover all expenses and the question of acquiring an
official invitation from the Philippines was bypassed.
The Manila conference took off where Bangkok ended, but now with 23


members.945 It was reported back to the League of Nations Health Commission in full




944
The outcome and summary of the discussion is found in LNHO: 8A-R5930/30632/29090.
945
The complete list of attendees was as follows: Dr. Etienne Burnet, Secretary of the Leprosy Commission of
the League of Nations Health Organisation (Geneva); Dr. Robert G. Cochrane, Secretary of the British Empire
Leprosy Relief Association (LNHO: don), Mr. H. I. Cole, Chief Chemist at Culion Leper Colony (Philippine
Islands); Dr. J. Fajardo, Director of Public Health at the Philippine Islands; Major-General J. D. Graham,
Commissioner for Public Health with the Government of India; Dr. G. Gushue-Taylor, Superintendent of the
Mackay Memorial Hospital (Formosa , later Taiwan); Dr. V. G. Heiser, Director for the Far East of the
Rockefeller Foundation (New York).; Dr. Lee S. Huyzenga, Superintendent of the Mission Hispital in Jukao,
Kwangsi (China); Dr. H. Joyeux, Director of the Public Health Bureau in Hanoi (Tonkin, later part of Vietnam);
Dr. A. N. Kingsbury, Director of the Research Institute in Kuala Lumpur (Federate Maly States, later
Malaysia); Dr. P. H. J. Lampe, Director of Public Health (Surinam); Dr. C. B. Lara, Principal Medical Officer
at Culion Leper Colony (Philippine Islands); Dr. A. C. Leroy des Barres, Inspector-General of the Public Health
Service (French Indo-China, later Vietnam); Dr. J. Lowe, Medical Inspector at Dichpali Leprosy Hospital
(India); Dr. J. L. Mazwell, Lister Institute of Medical Research in Shanghai (China); Professor Ernest Muir,
Leprosy Research Laboratory at Calcutta School of Tropical Medicine and Hygiene (India); Dr. E. E. Neff;
 349

as an extension of the Bangkok meeting. Instead of formal papers, the whole time was
devoted to discussions. The conference was split in eleven sub-commissions dealing
with definition and description of lesions, clinical questions, prophylaxis,
classification of leprosy, special treatment, program of research, and the foundation of
an International Leprosy Association and an international medical journal. The
committees prepared memoranda which in turn were discussed by the whole session
before being incorporated into the findings of the committee.946
Again, the two schools of thought were present, and again the conference made
unprecedented efforts at reaching compromises. Over two weeks, which included a
lengthy visit to the Philippine leprosy institutions of Cebu, Zamboanga, Iloili and
Culion, the members had time to get to know each other’s views and find a common
ground. There was unanimous agreement on the need for international interchanges
and study tours, standardization of methods and terms used in recording and reporting
leprosy work. The conference gave its full support to the Leprosy Commissions
Prophylaxis report and that the League’s Leprosy Commission should encourage and
coordinate research.947
Relating directly to La Société Internationale de Leprologie, the organization
that was set up by de Souza-Araújo in 1926 but never had started any practical work,
the conference decided to establish a new organization using La Société as a model.






Medical Inspector at Mogokai Central Leper Hospital (Fiji Islands); Dr. Bernhard Nocht, Geheimer
Medizinalrat, Director of the Institute of Tropical Diseases, Hamburg (Germany); Dr. M. Ota, Tohoku Imperial
University, Sendai (Japan); Dr. J. N. Rodriguez, Inspector of Treatment Stations for the Public Health Service
(Philippine Islands); Dr. J. C. Tull, Government Pathologist at the Singapore Straits Settlement (now Malaysia);
Dr. H. Windsor Wade, Chief Pathologist of the Public Health Service of the Philippine Islands and Medical
Director of the Leonard Wood Memorial for the Eradication of Leprosy (Philippine Islands/New York); Dr. N.
E. Wayson, Surgeon at the Leprosy Investigation Station on Honolulu for the Public Health Service (United
States).
946
Cochrane, Robert G. “The Campaign against Leprosy: International Conference in Manila.” The British
Medical Journal. April 18. 1931: 680-681. In June 1929, Robert Greenhil Cochrane replaced Frank Oldrieve as
Medical Secretary of BELRA. Prior to this he had been Medical Advisor to Mission to Lepers, practicing in the
leprosy Asylum at Purulia, Bengal. Cochrane’s extensive travels are reflected in his list of early publications:
Leprosy in India: A Survey (1927), Leprosy in Europe, The Middle and Near East and Africa (1928) and
Leprosy in the Far East (1929). All books were published on World Dominion Press that mainly specialized in
missionary literature from all over the world. In 1926 he published the booklet How to rid a country of leprosy.
His obituary was printed in The British Medical Journal. Vol. 291, August 31, 1985: 608.
947
Report from the Leprosy Commission to the Health Committee, 1931: 15-22. (LNHO: 8A-
R5930/30632/29090)
 350

The temporary officers charged with finalizing the rules and regulations of the
organization were all men with previous experience from international anti-leprosy
work: President Victor G. Heiser from the Rockefeller Foundation; Vice-President for
the Western Section, Professor Carlos Chagas of Rio de Janeiro; Vice-President for
the Eastern Section, Dr. Ernest Muir of Calcutta; General Secretary Dr. Robert G.
Cochrane of London; General Treasurer, Mr. William H. Brown, Ph.D., of Manila;
Sir Leonard Rogers of London, Dr. Etienne Burnet of the League of Nations
Secretariat and Professor de Langen of Batavia were elected general Councilors.
The most important task for the association was to establish an international
journal of leprosy, “to serve as the principal, and a truly international medium of
publication of worthwhile articles on leprosy, and as a collecting medium for all other
material of similar nature that is not published therein originally.”948 By the first issue
of the journal, the association had almost 340 members from all over the world.





The symbol of Bergen


By the early 1930s, to what extent was Bergen and the heritage of a successful
campaign that had brought the problem of leprosy under control still considered
relevant? When the history of leprosy in Norway was presented at the Third
International Leprosy Conference in Strasbourg in 1923 by head of the national
leprosy apparatus, H. P. Lie, the case was perceived to be one of the highlights. But,
as I have argued, the legacy of Bergen was contested. Researchers like de Souza-
Araújo argued the Norwegian experience showed that strict segregation was
necessary in a campaign to eradicate the disease, others, such as Muir and Rogers,








948
Wade, H. W. “The International Journal of Leprosy. An Editorial Statement.” International Journal of
Leprosy. Vol. 1, No. 1. 1933: 2. Regular membership with rights to vote was, however, “limited to persons with
recognized medical degree, and those with other scientific qualifications who are, or have been, actively
connected with leprosy work.” (Cochrane, Robert G. “Association News”. International Journal of Leprosy.
Vol. 1, No. 1. 1933: 94).
 351

argued that Norway was proof that the goal could be achieved using a humanitarian
approach.
In Etienne Burnet’s report on leprosy in Europe, South America and the Far
East (1930), Norway was the first country that was presented. This was the birthplace
of scientific investigations into leprosy, and according to Burnet, Norway was still
relevant: “A visit to the special hospital at Bergen and to Dr. Lie’s laboratory is
essential for all students of leprosy.”949 But the interpretation of the historical success
had changed. “Norway is the classic example of the progressive eradication of leprosy
through the systematic isolation of lepers – not, however, by forced internment in
leprosaria.”950 This was in stark contrast to Hansen’s explanation at the first leprosy
conference in Berlin some three decades earlier, where the success was explained by
succeeding in keeping the lepers away from the healthy. By the early 1930s, emphasis
was shifted in favor of the progress of hygiene and general welfare:


Segregation on liberal lines has therefore been sufficient to bring about a decline in leprosy
which promises to lead to the total eradication of the disease. Norway is a sparsely populated
country, where the standard of living is improving, education is widespread and social
hygiene is very well advanced.951

This interpretation was in line with Lie’s explanation for the cause of the decline of
the disease in Norway: Isolation did play a considerable role, but the decline of the
disease could not be explained without connecting it to sanitary and economic
improvements: “The great decrease in the prevalence of the disease since 1856 must
therefore be regarded in the light of the great progress the country has made during
that time in all respects, and not least in hygiene and sanitation.”952 As I discussed in
Chapter 2, leprosy was no longer simply a matter of the presence of a bacillus alone,




949
Burnet E. League of Nations Health Organisation. Report on the Study Tour of the Secretary of the Leprosy
Commission in Europe, South America and the Far East. January 1929 - June 1930. (C. H. 887). Geneva.
1930: 6.
950
Burnet 1930: 6.
951
Burnet 1930: 7.
952
Lie, H. P. “Why is leprosy decreasing in Norway?” Transactions of The Royal Society of Tropical Medicine
and Hygiene. No. 4, 1929: 357-366, quote on page 366.
 352

predisposing causes and sanitary conditions were also part of the explanation. It was
increasingly accepted that leprosy could be addressed by sanitary improvements, and
the explanation of the past changed accordingly.
Throughout the 1920s, Lie was the only Norwegian who was in touch with the
group of actors actively engaged in making leprosy an international concern. He still
believed there was much to be learned, and was a strong supporter of global
centralization of leprosy work.953 Lie was among those invited to the Manila meeting,
but declined the invitation. Instead he wrote a series of heated letters to Thorvald
Madsen, the newly elected head of the Health Commission, where he predicted that
the Manilla meeting would be a failure because it lacked sufficient international
representation. None of his contacts in South America had heard of the plans.
Besides, an international society already existed (La Société Internationale de
Leprologie) and Lie had already prepared a frontpage for its planned journal.



In my opinion, this Conference in the Philippines cannot adopt any resolution of an
obligatious character for a great number of States interested in the Leprosy question. Its
dealing with the question of the establishment of an International Leprosy Society and the
creation of an International Leprosy Periodical can only be of a quite temporary character.954


Lie’s predictions proved wrong. The International Leprosy Association (ILA) exists
to this day, and in September 2013 it arranges the 18th International Leprosy
Congress, this time in Belgium.
The meeting at Manila in 1931 established a division of labor between the ILA
and the League of Nations which was continued by the World Health Organization.
The International Journal of Leprosy was published for 73 years until 2005 when due







953
H. P. Lie’s detailed his call for centralization in this way: “a place, an institution or a journal where one could
find information from all areas and all countries regarding leprosy and its suppression – and where one could
seek advice and guidance in this question. To create such a center must therefore in my opinion be on top of the
agenda when now working to suppress leprosy, that all countries and all people belong together and need each
others help to a greater or lesser degree.” Letter from Lie to Madsen, dated Bergen August 8, 1930. (LNHO:
8A-R5894/27029)
954
Letter from Lie to Madsen, dated Bergen August 25, 1930. (LNHO: 8A-R5894/27029)
 353

to raising costs it became financially unviable. The Manila-meeting thus established a
lasting framework for leprosy as a global concern.
Despite not attending, Lie was at the meeting in Manila appointed secretary-
treasurer for the Western section, associate editor of the International Journal of
Leprosy and ex-officio member of the General Council. This was the same position
that de Souza-Araújo had envisioned for him in his planned organization. De Souza-
Araújo himself was appointed vice-chairman of the Western branch. Marchoux, who
after being general-secretary at Strasbourg was the first to present leprosy as an issue
for the League, was appointed chairman of the Western branch. In the Eastern section,
Ernest Muir from Calcutta was appointed chairman, Kensuke Mitsuda from
Nagashima vice-chairman, and James L. Mazwell associate editor with the same
status as Lie.
Lie was not the only high-ranking official appointed to the organization not
present in Manila. In February, 1932, a general council was held in London and
officers and councilors were officially nominated for five-year terms in office. H. P.
Lie accepted his position. He also exhibited the insignia that had been used for the
second International Leprosy Conference held in Bergen in 1909, which to this day is
the official seal of the International Leprosy Association:


This bears, in formal representation, Saint George, the ancient patron of European lepers,
overcoming a dragon; it has neither sectarian nor nationalistic significance. The suggestion
of struggle and idealism in this medallion appealed to the members of the General Council
present, and after discussion it was voted to adopt it, with certain modifications, as the
insignium of the Association.955


Despite being highlighted as an ‘essential’ place to visit by Burnet, by the early 1930s
Bergen had been reduced from a leading world capital of leprosy research to a
unifying symbol of a past success, a symbol open for interpretation. Everyone agreed
the Norwegian campaign had been a success, but the interpretations of why the




955
Cochrane, Robert G. “International Leprosy Association. Present status of the Organization of the
Association.” International Journal of Leprosy, Vol. 1, No. 1. 1933: 98.
 354

campaign had succeeded depended on what policies the one making the comparison
wanted to promote. The Norwegian physicians themselves ensured that Bergen
continued to stay relevant through reinterpreting the past through the lens of new
epidemiological models.





Conclusion


This chapter has shown that in the 1920s, several concurrent and parallel initiatives
were involved in making leprosy an international concern under global coordination.
Several actors were involved. They came from different locations and used different
strategies to reach their goal: Traveling around the world, establishing international
organizations, forming alliances with the League of Nations and Rockefeller
Foundation, setting up international research centers and publishing monographs. At
the same time, the number of actors involved was relatively limited. Several knew
each other personally and collaborated on various schemes. They all had medical
training, experience with leprosy work, and most came from high-ranking positions
within national health systems. Although the actors and their organizations were new,
travelling, establishing organizations and forming alliances were not particular to the
period between 1920 and 1933 but a central mechanism in organizing the circulation
of knowledge.
Despite a deep divide between the advocates of compulsory segregation and
advocates of voluntary treatment, the initiatives came together in an International
Leprosy Association with its own international journal. This was achieved by building
on the previous initiatives and gathering 23 individuals with direct experience in
leprosy work around the world for a two week meeting in Manila. The attendees were
hand-picked and approved by H. W. Wade, representing the private foundation
Leonard Wood Memorial which was the main funding body of the association,
Etienne Burnet, representing the League of Nations Leprosy Commission, and Victor
G. Heiser, representing the Rockefeller Foundation. Despite the fact that much
leprosy work on the ground was left in the hands of philanthropic organizations
 355

(mainly various Christian missions), missionaries were explicitly excluded. Regular
membership in the International Leprosy Association was “limited to persons with
recognized medical degrees, and those with other scientific qualifications who are, or
have been, actively connected with leprosy work.”956
The objective of the association was to encourage global collaboration and

coordination with the shared goal of eradicating leprosy.



The purposes of the International Leprosy Association are to encourage and facilitate
mutual acquaintance between persons of all nationalities who are concerned in leprosy work
and the co-ordination of their efforts; to facilitate the dissemination of knowledge of leprosy
and its control; to aid in any other practical matter the anti-leprosy campaign throughout the
world; and to this end to publish a scientific journal of leprosy.957


The division of labor between the physician’s International Leprosy Association, the
International Journal of Leprosy and the League of Nations Leprosy Commission
would be the main structure for coordinating leprosy work globally for the next seven
decades. After the Second World War, the activities of the League were taken over by
the World Health Organization. Missionaries and representatives from other
philanthropic organizations were excluded from positions of formal power, but were
allowed to be non-voting members and encouraged to make donations. Publishing in
the columns of the journal was, at least in theory, open for all with a special interest in
leprosy. This setup did not entail agreement, nor did it force a unification of practices.
What it did provide, was a shared context which brought almost all leprosy workers
together in a global collective, directly- or indirectly.
Leprosy had become a global disease. Leprosy was globalized.













956
Cochrane 1933: 95.
957
Cochrane 1933: 94.
 356

 357



8. Final remarks


How did the knowledge of the leprosy bacillus move from being an entity observed
by one person in a laboratory in Bergen to being accepted as the defining character of
the disease all over the world? In this thesis I have argued that this simple question
has a complex answer.
As I have written conclusions to each chapter of the thesis, the purpose of this
concluding chapter is to take a step back and give an overview of the thesis as a
whole. I will begin with arguing why using the moment of discovery as a starting
point would have been problematic. I will then recapitulate my strategy and findings
and point out what I believe to be the strengths and drawbacks of my approach.
Finally, I will return to the three debates I presented in the introduction and
summarize my contributions.





Rethinking a genesis


It would have been possible to create a linear narrative which started in the office of
Gerhard Armauer Hansen on February 28, 1873, and ended with the unveiling of the
bust in August 1901 celebrating Hansen as a discoverer. This story would have shown
how the bacillus was first mentioned as a footnote to Henry Vandyke Carter’s report
from his visit to Bergen in 1873, and then in two reports by Hansen in 1874 and 1875.
In this narrative, it is clear that the importance of the bacillus initially was overlooked.
In these publications from the 1870s the bacillus was not presented as a great
discovery but preliminary and uncertain results of ongoing research into the causes of
the disease. The reception was poor, and began to change only after Hansen’s claim to
priority in 1880, which is when the date of the discovery first was published.
Hansen’s claim was prompted by Albert Neisser’s successful staining of the
bacillus in preparations he had received during a visit to Bergen in the fall of 1879.
Hansen’s publications in French, German, English and Norwegian the following year
 358


were the first time the bacillus received any real attention. Increasingly, the question
was not whether the bacillus existed or not, but who should receive the honor of the
discovery. This was first settled at the first international leprosy conference in Berlin
in 1897, where Hansen was hailed as the discoverer and Neisser as the one who had
confirmed the findings. In the intervening period, some pointed to Neisser as the
authority on this new entity, but from the early 1890s Hansen was increasingly
highlighted as the discoverer.
The linear story would highlight how events outside the narrow field of leprosy
made the bacillus easier to accept in the early 1880s than seven years earlier. In 1873,
the claim that a disease had a singular cause was controversial in itself.
Demonstrations of germs as the cause of other contagious diseases made the bacillus
easier to accept. Improved staining techniques developed especially in the German-
speaking world, as well as demonstrations of the presence of the leprosy bacillus in
samples from other parts of the world using these techniques, helped make the
existence of the bacillus more secure. In 1884 the bacillus was for the first time
mentioned in a medical textbook. Still, it was first after the conference in Berlin that
the bacillus was generally included as part of the presentations of leprosy in medical
textbooks.
Apart from its mere presence, demonstrating a direct causal relationship
between leprosy and the bacillus proved difficult. Instead the argument for the entity
as a cause rather than an effect rested on two analogies. The first was the resemblance
with the bacillus causing tuberculosis. This entity was of the same size, behaved in
similar ways and could be stained using the same methods. The second rested on
epidemiological and historical evidence which showed that when the disease was
introduced into a new area it spread rapidly, and that this could be reversed when
people affected by the disease were isolated.
At the conference in 1897, Hansen was able to document that the number of
new cases had gone down. This success, Hansen argued, was explained by the
Norwegian leprosy campaign. While Hansen had relied on epidemiological findings
when architecting and arguing for the increasingly strict leprosy Norwegian
 359

legislations in 1877 and 1885, in 1897 the bacillus was used as an argument also in
debates on the prevention of the disease. From the first decade of the 20th century a
widespread line of reasoning began with the bacillus as proof that the disease was
contagious, and ended in segregating the sick from the healthy as the logical
conclusion. In 1901 a bust of Hansen was unveiled in Bergen, funded by ‘colleagues
and friends from all countries’.
As a postscript to this linear story, I could have argued that the final
recognition came only after the second international leprosy conference in Bergen
1909. Here the bacillus was presented as the common denominator: Proof that leprosy
was the same disease all over the world. The bacillus explicitly made knowledge
produced elsewhere locally relevant. After the conference was officially over, also the
delegates from the British Empire endorsed the bacillus as cause of the disease, that
the disease was contagious and that it should be met with segregation.
All these elements are found in this thesis. However, early in the research I
realized that the linear narrative of a bacillus conquering the world was problematic.
First, its importance was not to be found at the moment of discovery. Rather,
recognizing the discovery as relevant and significant was a process that took several
years. Exactly what impact the bacillus had differed from place to place, and so did
the time and way it was introduced to the debates. It was not until others were
convinced of the existence and relevance of the bacillus that agreeing on its origins
(the discovery) became important. Agreement on a story of the genesis of the bacillus
was reached only in the first decade of the 20th century. The genesis must therefore be

seen as outcome of a process – not its start. Using the genesis as the starting point
would mean accepting this backdating and turning a blind eye to the different
meanings the bacillus had in different places and at different points in time.
Second, a narrow focus on the bacillus as a genesis would have meant giving it
a privileged position that is not supported by the sources. Not everyone knew about
the bacillus, not everyone saw it as relevant, and not everyone agreed that the bacillus
could explain every significant aspect of the disease. The bacillus was but one of
several coexisting and competing ways of knowing leprosy.
 360

Third, even when accepting the existence of the bacillus, its implications
differed from place to place and changed over time. As the bacillus increasingly was
introduced to already existing debates, the outcomes differed. The most obvious
example is in prevention: Systems of segregation were not implemented everywhere,
or in the same way. But also when it came to diagnosis, even in the interwar period
when the leprosy bacillus was generally accepted as the cause of the disease, its role
differed from place to place.
In order to answer the main research question I therefore had to develop a
different narrative. The main novelty in this thesis has been to separate the content of
the debates from how the circulation of knowledge was organized.





Diagnosis, treatments and prevention


In the first three content chapters I focused on the arguments that were presented in
debates on diagnosis, treatments and prevention between the 1850s and 1930s. All
these themes existed prior to the bacillus. I have shown how the bacillus was made
relevant in different locations, in different debates and at different points in time. De-
centering the bacillus made it possible to show both the breadth of the debate, how the
dominant positions changed over time, as well as give symmetrical attention also to
the arguments that in hindsight turned out to be wrong. The approach let me
investigate the impacts of the bacillus without giving it an a priori privileged position.
Before the advent of bacteriology, deciding if a person was ‘a leper’ depended
on clinical diagnosis: If you looked like a ‘leper’, you had leprosy. At the Berlin
conference in 1897 Hansen insisted that detecting the leprosy bacillus was required to
establish a diagnosis, but this was never unanimously accepted. Observing the
bacillus in the laboratory was a welcome confirmation in uncertain cases, but not
finding it was seldom enough to reverse a verdict based on clinical signs and
symptoms. The new way of knowing (bacteriology) was an addition, not a
replacement for the old. Still, it drew attention to the drawbacks of clinical diagnosis,
especially the need for specialist training and the fact that different physicians could
 361

reach different conclusions. Attempts at making a mechanically objective test which
could bypass the need for clinical judgment failed. In the 1920s, there were still local
differences, and in borderline cases the verdict could depend on where the diagnosis
was made. Yet, from around 1910 the bacillus did have an important impact: It made
leprosy a disease you could get well from. If a bacillus had been detected, its
disappearance meant that the disease had disappeared. Terms like ‘arrested’,
‘bacteria-free’ or later ‘burned out case’ would have been meaningless without
accepting that the disease was caused by the leprosy bacillus. This practice was first
adapted in South Africa and then spread. Still, that people affected by leprosy could
be paroled was never universally accepted. In Japan, for instance, the official doctrine
remained ‘once a leper, always a leper’.
When it came to treatments, the leprosy bacillus became part of the rationale
for testing new drugs from the early 1890s. After the failure of Carrasquilla’s serum
therapy at the end of the decade, explaining how a drug would interact with the
bacillus became a requirement for new drugs. Testing drugs was an impetus for
collaboration between physicians working in different locations: Each individual case
was unique, and therefore the efficacy of a drug could only be determined in larger
trials. However, the observation in the microscope did not disentangle the disease
from the person affected by the disease, and testing new drugs had to be conducted on
those suffering from the disease directly. From the first decade of the 20th century,

collaboration with professional manufacturers made the new substances more
accessible, but this did not solve the main problem: While some of the numerous
drugs tested against leprosy reportedly did some good for some of those affected by
the disease, at least initially, the goal of producing consistent cures failed.
Measures for prevention were closely intertwined with etiology. Contagion
was linked to isolation or segregation, heredity to marriage prohibition, the fish eating
hypothesis to diet, and where insanitary surroundings were seen as a cause, sanitary
measures were presented as the best means of prevention. There were also hybrid
etiologies with hybrid solutions. The argument for state institutions in Norway,
erected in the middle of the 19th century, was primarily to alleviate the economic
 362

burden of the disease. This seems to have been an exception: As long as the leprosy
was believed to be hereditary, the disease was generally perceived to be a problem for
the individual and their families. From the 1880s and 1890s, the bacillus became
entangled with the argument that leprosy was contagious and that segregation was the
best means to prevent others from falling victim to the disease. Contagion made
leprosy a problem for the healthy. Contagion existed before the bacillus based on
epidemiological data and historical evidence, such as in the case of Hawaii and in
Munro’s narrative of leprosy as a disease that throughout time had reached a global
distribution, but the bacillus served to strengthen the argument.
The belief in contagion and segregation was at its strongest between the 1890s
and the 1920s. The recommendations from the international leprosy conferences
concluded that since leprosy was caused by a bacillus every leper was a danger to his
or her surroundings, and the best means of prevention was segregation. The
Norwegian system was highlighted as a golden standard in finding a balance between
the freedoms of the individual and society’s need for protection. The exact nature of
the lessons from Norway was contested: For some, this was an argument for strict
segregation, for others it was proof that a relatively mild approach was sufficient. In
any case, the recommendations gave supporters of contagion an international
consensus to refer to. Proponents of other explanations had no such agreement to put
forward in local debates.
The bacillus alone did not decide what policies should be pursued, but three
strategies stood out in the debates that followed: Segregation Acts and educating the
healthy that ‘lepers’ were dangerous so that they would be forced into institutions
(push), presenting the institutions as attractive refuges providing proper medical care
(pull) and placing restrictions on the activities of those suffering from the disease,
such as banning them from certain trades. The researchers seldom saw proscribing
policies as conflicting with the goal of producing knowledge. Rather, more often than
not, the initiatives for doing something about ‘the leper problem’ came from the
physicians themselves.
 363

Discussing diagnosis, treatments and prevention in separate chapters has had
some drawbacks. Often these topics were interlinked, such as in the controversy
surrounding chaulmoogra in the interwar period. Chaulmoogra was a treatment that
by the time it was introduced to Western medicine already had been in use as a natural
remedy in parts of Asia for several centuries. After being regarded mainly as
palliative, from the turn of the 20th century collaboration with chemists searching for
its active components led to derivatives that some claimed to be a potential cure.
From the 1920s, BELRA was the primary proponents of chaulmoogra as a cure,
provided the treatment started early enough and was combined with diet, exercise and
cleanliness. Proponents of chaulmoogra argued that since a cure now existed,
identifying the ill and potentially ill in local communities through dispensaries and
offering voluntary treatment should replace segregationist institutions. In other words:
Treatments meant that strategies for prevention should change. Opponents pointed at
the bacillus: Since the derivatives did not interact with Bacillus tuberculosis, there
was no reason why chaulmoogra should have any effect against Bacillus leprae.
Another line of criticism was that the efficacy of chaulmoogra had never been
demonstrated in comparative trials. Indirectly this linked chaulmoogra to diagnosis, as
it brought attention to the fact that diagnosis differed from place to place, and that
there were no international standards for classifying cases.
While the bacillus did become an argument in already ongoing debates, it also
gave rise to new and lasting controversies, such as whether it was found inside or
between the cells, whether it could spread via insects, or whether or not the entity had
a life-cycle of its own with the acid-fast bacillus as but a stage in a complex
morphology. In my narrative, this aspect has been pushed into the background.
Furthermore, the bacillus was enlisted as an argument in more disputes than those I
have investigated. Although the narrative of a disease that throughout history had
spread around the globe already existed, accepting the existence of the bacillus had a
huge impact on the question of the natural history of the disease. In the thesis I have
tried to reflect the debates also when they went beyond my predefined categories, but
 364

in hindsight I am not sure whether this aspect of my argument has been sufficiently
clear.





Making knowledge move


In the last three content chapters I investigated how medical knowledge about leprosy
was made to move, how the circulation of knowledge was organized and the
mechanisms involved. Each chapter was limited to shorter periods of time, focused
specific aspects, and the relatively few actors involved. My emphasis was on
appropriation (Chapter 5), journals and conferences (Chapter 6) and travels, meetings
and organizations (Chapter 7), but I also touched upon textbooks, correspondence and
education. Again I tried to give attention also to the initiatives that ended up as blind
alleys.

I found appropriation to be a key concept for explaining how the same
observations could be given different meanings in different places. Circulation of
knowledge was an active and selective process both in what knowledge should be
shared, how it was made available to others, to what extent actors in other locations
considered it relevant, how the knowledge was interpreted, and to what extent the
knowledge was accepted by others. For instance, I have shown how the same report
could be given radically different meanings when introduced as arguments to debates
in other contexts. A report that in the British Empire would establish that the official
doctrine should be a hands-off approach to leprosy was in Norway introduced as an
argument for contagion. A thesis from Surinam that in Norway inspired new research
into contagion was in Britain dismissed as ‘lacking in necessary precision’. The
outcomes of conferences were reported differently from journal to journal, and it
would take more than eight decades before the human experiment that led Hansen to
lose his right to practice as a physician at the leprosy institutions in Bergen was made
known to the rest of the world. I have also shown that the relative position within
local hierarchies of the one introducing new knowledge could be decisive. Besides,
 365

the relative importance of leprosy compared to other diseases differed from place to
place. Local context did matter. Not everything circulated.
In general, the actors I have investigated seem to have put more emphasis on
their own experiences than reports produced elsewhere. The more an actor had
invested in defending a particular disease model, the less likely it was that he would
change his mind in light of new observations or arguments. In effect, several radically
different disease models existed simultaneously. While there still were local
differences in the 1930s, however, the scope of explanations was much narrower than
eighty years earlier. The explanation, I have argued, is to be found in how the
circulation of knowledge was organized.
In the 1850s, discussions on leprosy were part of medicine in general. As
Western medicine became increasingly specialized in the latter part of the century,
leprosy was discussed as part of dermatology, bacteriology, and as a tropical or
colonial disease. Leprosy became a specialty of its own right around the turn of the
20th century through the birth of a transnational research community with

international conferences and a shared medical journal as their main unifying features.
The leprosy conferences set out to establish the prevalence of the disease in various
parts of the world and were an important arena for debate and exchanging experiences
on how to treat and prevent the disease. The scheme aimed at creating a global
organization of experts that could dictate measures for leprosy prevention failed. But
also the international conferences were aimed at political changes, as evident by the
topic for the follow-up conference in Berlin in 1904, which asked what actions had
been taken in light of the conclusions reached at the first conference.
I have shown that relatively few actors were involved in organizing the
conferences, and that for them, the bacillus was an impetus for collaboration.
Securing the support of Hansen was seen as vital. Hansen was not only hailed as the
discoverer of a bacillus, he was also head of the Norwegian leprosy system. By 1897,
Norway was the only country in the world which could document a success in
reducing the number of new cases. In a context where leprosy was seen as a possible
 366

threat, and the health of the population increasingly important for Western states, this
was something to be mimicked.
In addition to establishing the prevalence of the disease in 22 countries, the
bacillus was the main topic for debate. Based on its presence and Hansen’s argument
that the successful campaign in Norway was due to segregation, most of the attendees
agreed that every leper was a danger to his or her surroundings and had to be isolated
for the benefit of the healthy. At the next international leprosy conference in Bergen
in 1909, where experts from 27 countries took part, the bacillus was presented as the
common feature of the disease. Regardless of local conditions, the bacillus was the
same. The bacillus proved that knowledge produced elsewhere was locally relevant.
In addition to the international leprosy conferences, the medical journal Lepra
Bibliotheca Internationalis (1900-1914) was instrumental in making leprosy a
specialty. The journal did not stop leprosy for being relevant for medicine in general
or a range of other specialties, but was aimed at presenting an overview of studies and
reports published elsewhere. This increased the circulation of knowledge, and
contributed to an increased streamlining of how to produce knowledge about leprosy.
Based on the reviews of publications arguing for disease-models which did not center
on the bacillus, it is clear that accepting the bacillus as a scientific fact was necessary
to avoid ridicule.
While disagreements continued to exist, and local practices remained unique,
the publications gave easy access to observations, arguments, legislations, and
experiences from other places. This, in turn, was used as arguments in local debates
and added to the prestige and expertise of the actors involved.
In the interwar period, the French association Société de Pathologie Exotique
took the initiative to a third international conference in Strasbourg in 1923. The main
outcome was that the organizers succeeded in making leprosy a concern for the
League of Nations. In addition to establishing an international leprosy center in
Brazil, issuing policy advice and encouraging states to organize production of
knowledge about the disease, The League of Nations Leprosy Commission was one of
several actors involved in organizing leprosy workers globally. The main fruit of this
 367

labor was the International Leprosy Association (ILA), established in Manila 1931,
with its own medical journal, International Journal of Leprosy (1931-2005). Other
key actors in the interwar period were The Leonard Wood Memorial, Victor G.
Heisser from the Rockefeller Foundation, and Heráclides César de Souza-Araújo
who, after a three year worldwide journey financed by the Rockefeller Foundation,
established the organization La Société Internationale de Leprologie. While the
society never had a single meeting, it provided the organizational model for the ILA.
Despite trying to emphasize also the ‘failed’ attempts at organizing the
circulation of knowledge, one unintended consequence of my approach of
investigating medical debates has been that the medical actors have ended up as the
ones with the most agency. This was partly true, in that most of the actors I have
investgated had authoritative positions towards those affected by the disease and often
were actively engaged both in producing knowledge and in advocating leprosy
policies. But although I have tried to look for the voices of those affected by the
disease, for the researchers I have investigated the subjective experiences of being
affected by the disease were increasingly seen as less important than their own expert
observations. The leprosy bacillus only increased this tendency. Furthermore, as
previous localized studies have shown, the physicians were not the only actors
involved in the decision making processes, nor was Western medicine the only system
for producing medical knowledge. Additionally, in parallel to the physicians,
missionaries also developed their own transnational networks for the circulation of
knowledge which should be investigated further.





Wider contributions


In the introduction I presented three debates which this thesis relates to and seeks to
add to: To what extent bacteriology constituted a radical break with previous
understandings of disease; debates within the history of science regarding
transnationalism, localism and the places of knowledge; and the growing body of
research on the history of leprosy. In the following I will summarize my contributions.
 368

In regards to the debate on whether bacteriology constituted a revolution
in medical thinking about disease, I put Michael Worboys and Andrew Cunningham
forward as representative of opposing positions. Worboys has argued that ‘there was
no bacteriological revolution’, while Cunningham has withheld that the introduction
of single causes of disease constituted a shift so radical that the identities of disease
before and after bacteriology became ‘incommensurable’. Worboys is right in that
most physicians were not involved in bacteriological research and that to them,
bacteriology had no immediate practical implications. Cunningham is equally correct
in that bacteriology over time led to a radical epistemic shift in the understanding of
the causes of disease. The difference between the two conclusions is not just choice of
period (1870-1910 or 1895-1930) or actors (general practitioners or vanguard actors),
but how they relate to the practice of ‘backdating’, which none of them reflect upon.
The physicians who accepted bacilli as the cause of disease only later dated the
knowledge back to when it was first observed. Despite the bust of Hansen being
erected in 1901, for instance, the justification was the discovery that happened three
decades earlier. While further research is necessary to establish whether my findings
on leprosy are generalizable to other fields of knowledge, it does seem evident that
agreeing on a moment of a significant discovery could only be established in
hindsight. This agreement had several implications. First, establishing a universal
genesis of new knowledge hid the fact that it took time before this knowledge was
made relevant elsewhere and that this played out at different times and at distinct
ways. It also backdated arguments and clarifications that were made during this
period of negotiation. In addition to bacteria being observed using the same methods
in different locations, shared narratives of their origins and their discoveries added to
the universal character of bacteriological knowledge. While bacteriology must be
considered an addition and not a replacement for other ways of knowing disease, and
the immediate impacts of bacteriology were probably too small to justify the term
‘revolution’, the term is meaningful to describe the way actors in the 1920s and 1930s
gave meaning to the epistemological changes that had happened over the past half
century.
 369

Regarding the debates on transnationalism, localism and the places of
knowledge, I have tried to follow James Secord’s suggestion of seeing science as
communication. For more than three decades historians have successfully brought
science down to earth by showing how the production of knowledge is a practice that
takes place in specific locations. It seems increasingly clear that something falls
between the ‘gaps’ when investigating science in single locations at a time. Local
production of knowledge does not happen in a vacuum. In this thesis I have argued
that studying the circulation of knowledge as a practice in its own right might be a
way to bridge these gaps. An important motivation for scientific publications was that
the knowledge should benefit and be recognized by colleagues in other locations, and
relating to knowledge produced by others has been at the core of any scientific
community. My contribution to this debate has been to provide an in-depth example
of how such a study can be conducted, namely through investigating both the content
of the transnational debates and how the circulation of knowledge was organized.
In the period from the 1850s to the 1930s, leprosy moved from being primarily
a local/national concern to an issue which facilitated global cooperation and
coordination. I believe this mirrors changes that also occurred in other parts of
society, and not necessarily limited to the sciences. Although the history of leprosy is
unique, with internationalization and tension between unification, standardization and
claims of universality on the one hand, and local specificity on the other, this seems
relevant beyond the history of leprosy. I have tried to read the sources not in search of
timeless truths but as arguments in ongoing debates. This has made it possible to
show how different and competing truths about leprosy coexisted. There were
different opinions regarding what constituted the cutting edge of research, which
actors could provide the best expertise, and what places should be considered centers
and peripheries. This approach has allowed me to show how interpretations changed
over time, including interpretations of the past, and might be a useful insight also for
other transnational studies.
My main contribution to the growing body of literature of the history of leprosy
has been to provide a detailed overview of how the transnational circulation of
 370

knowledge was organized, the ongoing debates regarding diagnosis, treatments and
prevention, and how dominant positions changed over time. Although I have not
investigated every transnational relation, I believe this study provides a summary of
the international ‘outside’ that will benefit future localized studies. In addition to
focusing on what went on in a specific place, these studies might also investigate how
the local actors related to knowledge produced elsewhere and how this knowledge
was appropriated. However, this is not to say that historians should all become
transnationalists. Although the circulation of knowledge was important in providing
access to arguments and experiences elswehere, localized studies are necessary in
order to further nuance how these played out in local debates. As this study has built
extensively on previous and mainly localized studies, I will be the first to argue that a
transnational perspective must be seen as an addition and not a replacement. The
actors I have investigated came from different local backgrounds, and it would have
been unobtainable to investigate all of these contexts without building on already
existing literature.
I began the thesis with the unveiling of the bust of Hansen in the park of
Bergen Museum in 1901. My final argument is that this was a more important event
than the observations made by Hansen on February 28, 1873, in that the bust
representeded an international acceptance (although not complete) that Hansen’s
discovery was important and relevant. It was not until the 1880s that the bacillus was
made part of the medical debates on leprosy, and another two decades went by before
its existence was more or less universally accepted. Instead of understanding
discoveries as fixed points in time, perhaps a more appropriate perspective would be
to see them as the outcomes of negotigation that take years or even decades.
 371

APPENDIX 1. "The Discoverer of the Leprosy

Bacillus", 1901

THE DISCOVERY OF THE LEPROSY BACILLUS. [A.uo. 24. 1901.
 
1897-1900 have been prepared by the Imperial Insurance observations and investigations, he published an important
Department, and are placed at the disposal of Congress. They paper in the Norsk Magasin for Lcegevidenskaben (1872), which
relate to 21,176 consumptive persons. The insurance societies gave rise to much discussion in Norwegian medical circles.
intend to ascertain in future the results as to cure for five .tlis researches pointed to the contagious and specific nature
successive years, and only cases in which incapacity for self- of the malady. The Medical Society of Christiania voted a sum
support has not recurred will be regarded as ''successful." of money for him to continue his research. In the course of his
The two published tables express the results of treatment in journeyings through the country he came across instances of
the years 1897, 1898, 1899, and 1900. According to these, the the diseasE, which were more readily explained by contagion
immediate results of the treatment in the four years varied from than by any other theory. An account of his additional in-
68 to 74 per cent. in all the men and from 68 to 73 per cent. in vestigation was published in the Norsk Magasin for Lcegeviden-
all the women under treatment. The three last of the years first skaben (Third Series, vol. iv, 1874), and an abstract of his
referred to show better results than those of 1897, a success paper appeared in The British and Foreign Medico-Chirur-
which is partly due to the more careful selection of cases, and gical Re'Biew (vol. lv, 1875). Unfortunately this important
partly to the experience gained in that year. The beneficial contribution to the subject was but little known outside of
effects of the treatment of 1897 lasted only two years in 27 per Norway. His views confirmed those of Drognat-Landre, who
cent. of the men and 36 per cent. of .the women; whereas of had worked at leprosy in Surinam, and published a book
those treated in 1898, 38 per cent. of men and 44 per cent. of entitled La Contagion:seule cause de la Lepre (Paris, 186g).
women were able to support themselves after the same lapse of This led Hansen to reinvestigate the peculiar bodies (globi-
time. It is worthy of note, however, that of the men treated brown corpuscles);previouslyreferred to, for he held that if the
in 1897, 26 per cent. were still able to work in 1900. Positive disease is contagious there must be some specific virus at work.
conclusions as to the duration of cure cannot yet be drawn, His labours were rewarded by the discovery, in unstained
but the greater success of the> morf' recent years is striking. preparations, of bacilli. These were ultimately stained, and
The effect of the treatment is more lasting in women than in are what we know them to be, the bacilli of leprosy. His dis-
men. covery, be it noted, was made in 1873, that is about ten years
Such are the general results of the efforts to combat con- before the bacillus tuberculosis was made known to the world
sumption of the German compulsory workmen's insurance, by Koch.
aided as it has been by local bodies and institutions for the For years Hansen has repeatedly tried to cultivate and in-
public welfare, as well as by private charity. The experience oculate the bacillus leprre, which is also deservedly known as
of several years shows thab this warfare could not have been Hansen's bacillus, but up to the present fruitlessly. One
successfully waged in Germany without the workmen's insur- great point, however, has been gained, namely, that it is now
ance, but by means of it we feel confident of victory in the practically admitted by all those engaged in the study and
end. observation of leprosy, that the disease is contagious. In
 Norway, practical legislation on this basis has given the best
THE DISCOVERER OF THE LEPROSY BACILLUS. results, ing.
and leprosy there is gradually and surely diminish-
ON August 10th a bust of Dr. G. Armauer Hansen, the dis- Dr. Armauer Hansen has recently (July 29th) celebrated his
coverer of the leprosy bacillus, was unveiled by Professor 6oth birthday, and:the tribute to his lifelong work and devotion
Visdal in the garden of the Museum at Bergen, in the pre- above recorded will be gratifying to all lovers of science.
sence of many Norwegian and foreign medical men. An ad- Norway is a small nation, but while she has such sons she
dress was delivered by Professor 0. Lassar of Berlin, and Drs. may well hold her head high among the proudest.
Sandberg and Lie of Bergen also spoke. Congratulatory
messages were sent from all parts of the world, and a letter
from Professor Virehow was read, in which the veteran

pathologist, after expressing his regret at his inability to be THE PREVENTION OF TUBERCULOSIS.
present, went on to say that Dr. Hansen's work had de- WESTMORLAND.
finitively cleared up a large and difficult field of pathology, and THE accompanying circular may be of use to any sanitary
that his name was known and celebrate<l. throughout the authorities throughout the Kingdom who propose to follow
whole world as a benefactor of mankind. The Kinof Norway the example of the Camberwell Borough Council, the Kendal
conferred on Dr. Armauer Hansen the distinctiOn of Com- Town Council, and the Bowness-on-Windermere and Amble-
mander of the Order of Ola. side Urban District Councils, in examining milk for tubercle
Dr. H. P. Lie, the present Director of the Leprosy Hospitals bacilli, and prosecuting the purveyors who have it for sale.
of Bergen, contributes an interesting biographical sketch of Dr.
Gerhard Henrik Armauer Hansen to the current fasciculus of BOROUGH OF KENDAL.
Lepra (vol. ii, Fase. 3, 1901, p. 121, with portrait). Dr. Hansen TO COWKEEPERS, DAIRYMEN, AND PURVEYORS OF MILK.
was born in Bergen in 1841, and received his early education in D rl ted 2
b ifl!: mtt i; '¥i : k Ys ;;i>lis' of t u 1 a P;
the Cathedral College of that town. After passing his medical
examinations, he became a resident in the Rigshospital of en i o:i Pf ;ld! 1 rf e ':h% ?I1J'1 fuh rfu'b , r; i:
Christiania, and later spent some time as medical officer be found. By Section 6 of the Sale of Food and Drugs Act, 1S75 :-
rr

to the great Lofoten fisheries. In 1868 he became Assistant 1

Medical Officer to the Bergen Leper Hospital (Lungegaards- fog . ;i a el \ ;hneaf:iJ.u g t c ea r f ;; n;:t! fc?!
Hospital), of which Dr. Daniel C. Danielssen was director. demanded by such purchaser, under a penalty not exceeding £2o.
It was under the influence of this enthusiastic teacher and By Article 15 of the Dairies, g:r, h de1JfJ k '!:._ops Order, 1885, as amended
acute observer that Armauer Hansen began his life-long study
of leprosy. His first investigation was to work out the If at any time disease, including in the case of a cow such disease of
significance of the so-called globi, or leprous cells of Virchow. fst:st tfeei' i eddaPi;.ao ! 't 'l, r i ,.t u fd\ e :
These bodies had been already referred to in 1840 by the milk of a diseased cow therein (a) shall not be mixed with other milk;
Danielssen. who thought they were characteristic of the and (b) shall not be sold or used for human food.
Any person guilty of an offence against the above order
disease. This idea he afterwards gave up, and came to the every such offence to a penalty of £5, and in the case of a continuing is liable for
conclusion they were the results of an involutiOn process, offence, to a further penalty of £2 for each day after written notice of the
that is, fatty degeneration. Hansen was not satisfied with offence from the local authority.
the latter explanation; he thought that Danielssen's first idea August, r90r.By order of the Kendal Urban District Council.
JOHN BOLTON, Town Clerk.
was more likely the right one. This led him to investigate
the matter, and in 1869 he published his results in the Nor- AUSTRIA.
wegian Archives of Medicine (Nordisk Mediciniskt Arkiv, Dr. von Kusy, an Under-Secretary in the Austrian Home
vol. i,·1869, No. IJ). Office and Chief of the Sanitary Department of that Ministry,
At this time Hansen spent a year at various universities, is now engaged in drawing up a series of Bills and adminis-
but on his return to Norway he again applied himself to the trative regulations to protect the population of Austria against
difficulties which surrounded the etiology of leprosy. Various tuberculosis. According to the Fremdenblatt the duty of
views were held at that time on this point. As a result of his notification is impressed upon the doctors, while speciP.l


958






958
Editorial. "The Discoverer of the Leprosy Bacillus." The British Medical Journal. August 14, 1901: 494.
 372


APPENDIX 2. International Leprosy Conferences,
resolutions



a) Berlin, 1897


“At the close of the debates of the International Leprosy conference, Berlin 1897, the
Secretaries have the honour to present the following short report of the general
conclusions of the Conference.
They believe that such a resumé will be especially desirable for those members
who have been delegated by their respective Governments, and who have to make
reports on the results of the Conference.
As might be expected, a considerable portion of the discussion has related to
the bacillus Leprae, which the Conference accepts as the Virus of Leprosy, and which
for upwards of 25 years has been known to the scientific world through the important
discovery of Hansen and the able investigations of Neisser.
The conditions under which the bacillus grows and develops are still unknown,
as well as the way of its invasion into the human system; but from the discussions of
the Conference, it seems probable that an unanimity of opinion will soon prevail in
reference to its modes of subsequent dissemination within the human body.
Very interesting observations have been brought forward in connection with
the elimination of the bacilli in large quantities by means of the skin and the nasal and
buccal mucous membranes of lepers; it is desired that such observations be confirmed
where opportunities occur.
The question is of very great importance to those who are entrusted with the
care of the public Health, as leprosy is now acknowledged to be a contagious disease.
Every leper is a danger to his surroundings, the danger varying with the nature
and extent of his relations therewith, and also with the sanitary conditions under
which he lives.
 373

Although among the lower classes, every leper is especially dangerous to his
family and fellow workers, cases of leprosy frequently appear in the higher social
circles.
The theory of heredity of Leprosy is now further shown to have lost ground, in
comparison with the at present generally accepted theory of its contagiousness.
The treatment of Leprosy as only had palliative results up to the present time.
Serum therapy has so far been unsuccessful.
In view of the virtual incurability of Leprosy and the serious and detrimental
effects which its existence in a community causes, and considering the good results
which have followed the adoption of legal measures of isolation in Norway, the
Leprosy Conference, as a logical issue of the theory that the disease is contagious, has
adopted the following resolution proposed by Dr. Hansen and amended by Dr.
Besnier.


1) In such countries, where leprosy forms foci or has a great extension, we
have in isolating the best means of preventing the spread of the disease.
2) The system of obligatory notification of observation and isolation as
carried out in Norway is recommended to all nations with local self-
government and a sufficient number of physicians.
3) It should be left to the legal authorities after consultation with the
medical authorities to take the special measures applicable to the special
social conditions of the districts.”959















959
Abraham, Phin. S; Edward Arning, E. von Bergman, Dubois-Havenith, J. J. Kinyoun and G. Thibierge. “The
Honorary Secretaries’ report from the First International Leprosy Conference” Mitteilungen und
Verhandlungen der internationalen wissenschaftlichen Lepra-Conferenz zu Berlin im October 1897. Bd. 2:
191-192.
 374

b) Bergen, 1909


“1. The Second International Scientific Conference on Leprosy confirms in every
respect the resolutions adopted by the First International Conference of Berlin, 1897.
Leprosy is a disease which is contagious from person to person, whatever may
be the method by which this contagion is effected. Every country, in whatever latitude
it is situated, is within the range of possible infection by Leprosy, and may, therefore,
usefully, undertake measures to protect itself.


2. In view of the success obtained in Germany, Iceland, Norway and Sweden, it
is desirable that other countries with leprosy should proceed to isolate their lepers.


3. It is desirable that lepers should not be permitted to follow certain
occupations which are particularly dangerous in respect to the contagion of leprosy.
In every country and in all cases the strict isolation of leprous beggars and
vagrants is necessary.


4. It is desirable that the healthy children of lepers should be separated from
their leprous parents as soon as possible, and that these children should remain under
observation.


5. An examination should be made from time to time of those who have lived
with lepers by a competent physician.


6. All theories on the etiology and the mode of propagation of leprosy should
be carefully examined to ascertain if they accord with our knowledge of the nature
and the biology of the bacillus of leprosy.
It is desirable that the question of transmissibility of leprosy by insects should
be elucidated, and that the possibility of the existence of leproid diseases among
animals (rats etc.) should receive early study.
 375

7. The clinical study of Leprosy induces the belief that it is not incurable. We
do not at present possess a certain remedy. It is desirable, therefore, to continue the
search for a specific remedy.”960





c) Strasbourg, 1923


“1) Laws governing the anti-leprosy campaign should vary according to the country in
which they are applied, but in all cases foreign lepers should be barred from entering
a country.


2) In countries with little leprosy, the isolation of cases in hospital or in the
leper’s house, is recommended, as practiced in Norway.


3) In endemic centers of leprosy, isolation is necessary; -

a) This isolation should be humane and allow the leper to be near his family, if
this is compatible with efficacious treatment.
b) If cases exist among paupers, nomads or vagabonds and other persons who
cannot be isolated in their homes, isolation should be enforced in a hospital,
sanatorium or agricultural colony, according to circumstances, with suitable
medical treatment.
c) It is advisable to take the children of lepers from their parents and keep them
under constant observation from birth.



4) All members of a leper’s family should be subjected to periodic

examinations.







960
Internationale Wissenschaftlige Lepra-Konferenz. Abgehalten vom 16. bis 19. August 1909 in Bergen
(Norwegen). Mitteilung und Verhandlungen. Bd. 3: 418-419. (Distributed in Lepra Bibliotheca Internationalis.
1910: Fasc. 1)
 376

5) The general public should be informed that leprosy is a contagious disease.



6) Professions liable to spread infection should be barred to lepers, but in that
case the duty arises of helping the sick person and those dependent on him.


Recommendations.

1) Clinical, histological and bacteriological researches should be undertaken
to elucidate the real nature of tuberculous leprosy.
2) Continuous study should be made to establish the connection between
human and nicerine [=rat] leprosy.
3) Research concerning a specific remedy against leprosy should be continued.

4) The League of Nations should resume publication of the periodical “Lepra-
Archives Internationales de la Lèpre”.
5) The League of Nations should establish an international information office
on Leprosy.
6)
The League of Nations should make endeavors to secure statistics on cases


of leprosy throughout the world.”961































961
LNHO: 12B-R898\29272\29272.
 377


APPENDIX 3. "Norwegian Leprosy", 1852


o ' 'f"KIUDLt:proay. 
l"rmn the 1-:cc ugtl•rul r:a!hulic.
BEao, Norway . Sept. '10. 1552. 
llfy D£AR Dn . WAt!<WJ<lUIIT : It w1ll probably 
surprse you to learn that the Oriental leprosy, as
dE'acnhed hy Moss:s and hnalerl by our Sllvinur 
e.xistt!l at tllts morncrrt in Nonvay. It is not :u; 
huur eincc J httvc t>f:llover a hundrt-!d cn.,ttif of
thiM fughtful and loath•ome dt6eaoo, whtch i• here 
exactly the JSamP. that you fnund llt N Ahl ouR Rncl
cbt:9.·here iu Palt-stiuo, aud det crtlJcd. in your 
u P_atb\,·aJs and Abtding Places of our Lord." 
Th•• <li•e""e formerly exi ;ted in Englanrl Rnrl
France, ,,.hence it was finally extirpated by tho 
most severe and tyrannical regulationR, uch "" 
c?n uc,·er Uo Cl forc4:d iu o•.tr - dtt.y Ktlcl C•'•ntry.
f. ·ery person, wtthout exception, that \Vas allhcted 
with lcpros)•, was brought into a puhlic •• lr.: prtlAy 
hou tic.." audutht: di =--t-uBc its nut cuu!.ngiouts l.Jut
hf»red1tary. 1t Vt":\8 thus ahnoat. if not entirety , 
rooh·cl out of th"'"o couutries. It wntt originally
brou ;ht 11110 Fraue by pil!lrims, wb .J had·Inter. 
m:urtcd n l n1eRt!ne; and ll) the ninth Ci!ntury
it watJ carrted luto N or'"·ny, aHer thu oxcur :tiO u'!

of the !'\orthmen imo Norm.,nrt)·; for these 
countries oecm to have bcet mortJ closely 
connected in ,.,.,. c1ent un,cttba u 1n our own.
That tho diseaoe has been importer!iY evitlent 
from tlte foct that it chiclly exid rs upo>n the V.'cllt:
ern coast , bordering upon tbe .Sorth tic•, anti ex 
tends along the whole lin e of it, frum thu Nllzc
to he !liorth Uaf.le. After more than eilht cen.
tet.,Kt\11 fiork 0imts
tUrlht owevrr, Jl has begun tn pc tetirntltl\end, Published:December 27, 1852
hy tlu' det"p furcle and gulfd which oumetion"'d itt· Copyright © The New York Times
tlt:nt the \\" t!Hltn: CuRst of Norwtty, for a dbt:uu e 
of loctwceu ouo lllld two hlltHlrcd miles. It id
l :O\V sometimes fnurut far in the interior, l.lut never 
in th E' Ea bt l'tn part of thP. country, nnrin S werlen. 
lct·l lld ""'"·' t·••Lirt·ly rlopopulatl•d by tho pl r,ue,
and recolor.tzed !rom Norway, and there the dis. 
eat-t':tlt;ts.
Thu Government ha,·o a t '""Sth t:>kt>u tho mat· 
ter _in ha nd, a_nd in addition to a··leprosy hou.•c," 
whic h haH c-xt>te<l for fh·e hunrlrArl yea rs.and nmv
CUIItalll" o11e hullllrcd at,<:! thirty-five t>atiuur.s, they 
h•"·e recenlly built a hospital, tht: fir: t that tht< 
?Curiri C'IJc r knew for the cure of lt!prnsy. It Ha.
been only three years in OfJ£tatiou, under tbem!ln· 
a ;cnol'nt . of Dr . DANU . I .M< KN; anrl tllift g•m tle. 
man loeheves that he ha" succeeded iu curing
eight l el'crs, tho fir,;t tht<t have O''er been cured hy 
nwdu:al n•cantt. lio la1s auah ji,H•l til e hlruul •)f
U1c de<C&tied pcrHOflB aud Jjudtt it to conraiu tuv 
much albun1en, and { hrile nJatter, and uf course in the descendants, though, like other heredit!lry
directti hri-fTorts to c ho
Yplnnvnl of thn ext nsa:.. eflU tions, it often paeses over c:-to gonerttti'ln.
Jle h3s pnhlishcd a scientific work, w1th IJiatus. 111 Owmg to our larger nod increasing population, it
the Frcr.clt ar.d DaniHh la nguages. 1.'hu tuotitu. may become a prcvaleut disease 111 our Western
lion is well pruYidcd with fresh and sea wa:er, and .States. But as yet it i& comparatively in our o•vn
VftpOJ t.,thH. power; Jor IIHlt!-t of the Norwegians are settled
I h vu to-dRy Hcen a uuuolocr of hi patient to•g..thcr, nt;d nhnost every case might now be
\Vhnn• he CO!t tdcrs nearly cured, and th•1e;e wbu found.
h:ne '' "" sont home are going on well. He estt. For the future, I would propose some remcrly of
tuatctJ \hu wholo tJUtnbcr in Norway at thrno tho full owlllg lllltllre : Many veOAelY with Ami-
thousant 1, nltd HS}"B it 11:1 iu'lrcnttlng. null wouhl gla!•ts now sail annually frr.m Norway to tile
hRve hf·en ntuch Luger but fi)r the cht\racter of Urrltctl Stt>tes. They lanri chietlv In N&w-Ynrk.
tho c.uuntry. I have just t avclecl across Norw,.y, et the City or the State enact a law, anrl malta
nnd It lo OIJt' gr""' mouutam or rock, with fruir.fnl It .know_n 111 Norwa.v, appointiug a ph)'oician to
crevicerather thun valle)><, not o11e hr.,.drt,t h t»srt u,qmre tf the diee11se extsts amoug the emigrant"
C•f the whole surface being under cult1va•iuu · Jt iK who enive, onrl if any 11Uch be found, let them
by fer thl! mc>bt thinly inhalHtP.d conntry I' ever have_ their choice between being tranaferred to "
vi•itt!d. The peopldwell eo tar apart. that thu hn"T•1lal or returned to thetr own couutry. The
rliSf'DH\ has &prf'arl ttself but slowly. Yet the in- l..n.P.rly ma y a ct harshly in ""rne inrlividual
crctH.O hos 310\l::'Cfl the Storthing, or Nor\\r egian ens""• hut it is by no means morn tyrannical than
Congresstn grant _35,000 s,rect R ($37,00U). t•>· the Quarantine laws that already oxiH. Jt wilt
:wards lmtldm:; a thJtd hopltal 1n liorgen. 'I'llis h'tld tt' til'curu futuro gt-tu
rutiurut ngalnst one of
ls a very 1:-nge r\\JJn for a country the IIIOHt fc11rful cnlamitiet1 tb:'l t cnn become por-
likA Nor-
'vay, anti the rceulttof Dr. l>A fELL ll•HIItllot Rmong a pcopte.
E="''· ex..
perimPuts arc louked fur with the groa tet anx- Could you h11ve seen, aa indfled you did in the
ter.y , ns the disease is consiUered a great JJ.ational Et< t. tho po.>r creatures, some a-:licterl witb that
cahunirv. L) I'" of tho di••u••• whi ch covers thu face and
JJut the puint to which Iwi:h to call a•.tmltio u is ov"u rltc <:yo:lid, with rerl tubcrd""• and, by the
this: In un1e }Jincr·1 on tho Wc tcrn C•la t of g,ow lh Pf the ttJtme witbin the throat, destrovs
Or\vay tho D';Jnthcr of lopertt nrnoug tht! pue)pln the •pe ch, reduces it to a husky and hoa rse ef.
JS. 11enrly oue 1n tifty. and it is pr cihely fr•J;u tho fort, while the poor leper in a few y ears rt.,scenrls
W Fstern COR!t. that lhc inr.rt·a Jng ctnl g raiivttu to the tomb; or could vou behold tho limb a by
Amcnca. taf.:iiJ plnce. Dr. D.\SII<t-L•a•<r< s11ys "" degrees dropping from tho bod y, and while they
18 ccri:R JHtha[ the dJFease ""Ill ehow it self amoni! n·1u ain tiO dt· tllufc of fl'uling that Ute poor sulfur-
tbcc t:tuigrauts ; fnr ht' k now6 Jcprt)UII individualS llrl<. lreq llNttly lourn them•clvcs with deep scars
,,.·ho ha·vc gone t(l thP lJuitcd Stn.trfll . aud nne ln ht'lurc tbt•y aro cvrm awa re of tho beut, yon would
particular, quite rocr.ntly, wnom he cnrl.,,wo rorl in uot wondtr that r should wish to arouse such at-
"aiu to ditcsuadc, and in wborn the dt:t ::Jiee wa-1 tcntiou, bcloro it be too lnte, as m'ly sec11ro pos-
ouly tJcginuiug to> nppcar. !'lnw, th rmgn it i• tt:rlty 3gutu x t thtR lontbHOtno llffltclinn.
never contagious, ;t is olwavs. •ntl withnnt fail, Et'er most atfc ctionatelv yonre,
hererlnnry, nr.d if there ie the least 9pot in eithar J UIES C. ft!CIIMOND.
of the p:ucuta, it ia absolutely certain lO appea<
 378


APPENDIX 4. The Principles of the Prophylaxis of

Leprosy, 1931






“SUMMARY AND CONCLUSIONS.

1. Prophylaxis of leprosy is not a problem that admits of solution by the
application of any one measure, since the means of dealing with it obviously
vary with geographical, economic, administrative, financial and social
conditions and with the incidence of the disease.
2. There is no reliable system of prophylaxis without treatment, and it is generally
accepted that the earlier the treatment is instituted the better will be the results.
3. Leprosy resembles tuberculosis in being, in certain stages, a contagious but
curable disease : curable at least in the sense that bacteriological examination
becomes negative and other active signs disappear and remain absent
permanently or for an undetermined period.
4. The prophylaxis of leprosy may be achieved by a system of medical, educative
and legislative measures. It should provide for the isolation and treatment of
infectious lepers and particularly for the treatment of early cases in clinics and
dispensaries : also for the periodical examination of suspects. Special measures
should be adopted for dealing with the children of lepers and for patients who
have recovered either after treatment or spontaneously.
5. It is desirable that each country where leprosy exists to an important degree
should have at least one centre for the study of the disease, with research
laboratories and special courses for the medical profession and their assistants.
Where this is not practicable, men should be sent to some foreign centre for
training.
6. Arrangements should be made to include instruction in leprosy in the
curriculum of all medical schools and colleges.
 379

7. It is necessary to educate the public in regard to leprosy by modern methods of
popular teaching and propaganda.
8. Isolation of infectious lepers is a necessary measure in a comprehensive
campaign against leprosy, but it cannot be regarded per se as the sole means of
prophylaxis. Its drawbacks can be mitigated by other measures applied
concurrently. Isolation should be applied only to cases that are considered
infectious.
9. Any form of treatment in order to give satisfactory results required to be
combined with suitable dietetic and general hygienic conditions.
10. For special treatment, oils of the chaulmoogra group and their esters and soaps
are recommended.
11. The system of prophylaxis must be animated by the spirit of preventive


medicine and social hygiene.”962







































962
“League of Nations Health Organisation: The Principles of the Prophylaxis of Leprosy. First General Report
of the Leprosy Commission”, Geneva, April 1931: 9-10.
 380

 381



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