Leprosy

Download as pptx, pdf, or txt
Download as pptx, pdf, or txt
You are on page 1of 26

Leprosy

Mycobacterium leprae is the organism


causes leprosy.
M. leprae has not been grown in the
laboratory, either on artificial media or in cell
culture.
It can be grown in the mouse footpad or in
the armadillo.
Armadillo
Humans are the natural hosts, although the
armadillo may also be a reservoir for human
infection.
The optimal temperature for growth is 30°C
lower than body temperature; it is therefore
grows preferentially in the skin and
superficial nerves.
It is the slowest-growing human bacterial
pathogen.
Transmission:
Infection is acquired by prolonged contact
with patients with leprosy, who discharge M.
leprae in large numbers in nasal secretions
and from skin lesions.
The disease occurs worldwide, with most
cases in the tropical areas of Asia and Africa.
Pathogenesis:

The organism replicates intracellularly,


typically within skin histiocytes, endothelial
cells, and the Schwann cells of nerves.
There are two distinct forms:
1.tuberculoid leprosy
2.lepromatous leprosy
There is several intermediate forms between
the two extremes.
Tuberculoid leprosy:
The cell-mediated immune (CMI) response to
the organism limits its growth, very few acid-
fast bacilli are seen, and granulomas
containing giant cells form.
The CMI response consists primarily of CD4-
positive cells and a Th-1 profile of cytokines,
namely, -interferon, interleukin-2, and
interleukin-12.
It is the CMI response that causes the nerve
damage seen in tuberculoid leprosy.
The lepromin skin test result is positive.
An extract of M. leprae is injected
intradermally, and induration is observed 48
hours later in those in whom a cell-mediated
immune response against the organism
exists.
Lepromatous leprosy:
The cell-mediated response to the organism
is poor, the skin and mucous membrane
lesions contain large numbers of organisms,
foamy histiocytes rather than granulomas are
found, and the lepromin skin test result is
negative.
Note that in lepromatous leprosy, only the
cell-mediated response to M. leprae is
defective.
The cell-mediated response to other
organisms is unaffected, and the humoral
response to M. leprae is intact.
However, these antibodies are not
protective.
Clinical Findings:
1.The incubation period averages several
years, and the onset of the disease is gradual.
2.In tuberculoid leprosy:
Hypopigmented macular or plaque-like skin
lesions, thickened superficial nerves, and
significant anesthesia of the skin lesions
occur.
3.In lepromatous leprosy:
Multiple nodular skin lesions occur,
resulting in the typical leonine (lionlike)
facies.
Leonine facies
After the onset of therapy, patients with
lepromatous leprosy often develop erythema
nodosum leprosum (ENL).
ENL is characterized by painful nodules,
especially along the extensor surfaces of the
tibia and ulna.
Erythema nodosum leprosum
The disfiguring appearance of the disease
results from several factors:
(1) The skin anesthesia results in traumas,
which often become infected.
(2) Resorption of bone leads to loss of
features such as the nose and fingertips.
(3) Infiltration of the skin and nerves leads to
thickening and folding of the skin.
Patients with forms of the disease
intermediate between tuberculoid and
lepromatous can progress to either extreme.
Laboratory Diagnosis:

1.In lepromatous leprosy:


The bacilli are easily demonstrated by
performing an acid-fast stain of skin lesions
or nasal scrapings.
2.In the tuberculoid form:
Very few organisms are seen and the
appearance of typical granulomas is sufficient
for diagnosis.
3.Cultures are negative because the
organism does not grow on artificial media.
4.No serologic tests are useful.
Treatment:
The therapy used is dapsone
(diaminodiphenylsulfone).

Because resistance to the drug has emerged,


combination therapy is now recommended,
e.g., dapsone, rifampin, and clofazimine for
lepromatous leprosy and dapsone and
rifampin for the tuberculoid form.
Treatment is given for at least 2 years or
until the lesions are free of organisms.
Prevention:

Isolation of all lepromatous patients, coupled


with chemoprophylaxis with dapsone for
exposed children, is required.
There is no vaccine.

You might also like