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Safety in laboratories

1978, BMJ

Safety in laboratories Only recently has the prevention of infection in clinical laboratories become a matter of public concern. The starting point, in 1973, was the death in London of two people after the accidental infection with smallpox by a laboratory worker at the London School of Hygiene and Tropical Medicine.' This led the DHSS to set up a working party to look at the use of dangerous pathogens in laboratories.2 The Health and Safety at Work Act 1974 stimulated further interest, encouraged for a variety of motives by trade unions and other groups, which culminated this year in leaks and questions in Parliament about the code of practice prepared by another expert working party, chaired by Sir James Howie.3 Yet apart from very rare and grotesque lapses-usually in specialist laboratories handling specifically the exotic viruses, which are the only extremely hazardous (category A) pathogens -there is no evidence that laboratory-acquired infections are still a serious problem in laboratories of hospitals and the PHLS. The main occupational hazard from a grossly infected patient is to his nurses and to a lesser extent the junior doctors, not to technical staff handling small laboratory samples. The exception is tuberculosis, which remains an important risk in routine laboratory work. How, then, does the code of practice produced by the Howie working party differ from its predecessors4-7-to which it acknowledges its indebtedness ? The classification of organisms into categories A, B1, B2, and C is in line with the earlier recommendations of the Godber report.2 Category A organisms -extremely hazardous to laboratory workers-are not normally encountered in routine clinical laboratories. Category B1 includes, for example, Mycobacterium tuberculosis, Salmonella typhi and paratyphi, pathogenic rickettsiae, and materials and reagents known to contain hepatitis B virus; category B2 includes all specimens known to be HBsAg positive. The code of practice sets out in detail the standards of accommodation required if these organisms are to be handled safely and the procedures that should be followed. In his introduction Sir James acknowledges that the financial implications of these exhaustive recommendations make it unlikely that most of them will be implemented. He was asked to pinpoint those hazards to be given priority; these, he thought, should be tuberculosis and hepatitis. The committee also thought that urgent attention should be given to installing exhaust cabinets in laboratories not fitted with them. Some might argue that this recommendation may be somewhat (© BRITISH MEDICAL JOURNAL 1978. All reproduction rights reserved. unrealistic: for, even putting aside the argument that cabinets may have the effect of concentrating an infective hazard instead of dissipating it, we know that there are many bad cabinets available and few of the good ones function optimally most of the time. In an appendix the committee sets out in detail how to install a cabinet and to check that it is working every day. There must also be some doubts about the recommendation that all material that "may contain tubercle bacilli" must be processed in category B1 accommodation in exhaust cabinets. Certainly an authoritative statement is welcome in respect of sputum (even when examination for tubercle is not specified) and will give support to the case already argued by Collins.8 All too often laboratories are sent sputum specimens from patients with open tuberculosis, whether known or hitherto unsuspected, with no indication of their tuberculous origin; sometimes specimens are divided and sent to different laboratories with multiple tentative diagnoses to justify the various requests. Nevertheless, the revised recommendations refer to all specimens-and presumably that could be interpreted as including all urine specimens, accounting for upwards of 4000 of most laboratories' work load. If every urine sample is to be processed as a category B1 specimen the speed of throughput must fall and costs must increase substantially. Again, with fluids, purulent exudates, and biopsy specimens-all of which "may" contain tubercle bacilli-the recommendation is almost certainly unnecessary, because of the small numbers of organisms in such specimens. Anyone who argues that this is an unrealistic interpretation of the code should look at some recent examples of NHS staff "working to rule." There are real problems of safety in laboratories-and paradoxically these are most serious in laboratories other than microbiology departments, especially the haematology and chemical pathology sections. Here hepatitis is a risk; in cytology departments tuberculosis is a particular hazard. No doubt microbiologists of all grades are acutely aware of the risks of their chosen profession, but familiarity breeds contempt. Human nature being what it is, the only way that the hazards will ever be tackled seriously is for statutory requirements to be introduced for the regular inspection of all laboratories by outside bodies. The staff already exist in the form of the community physician and his environmental health officers. They require only a right of access to hospitals No 6117 PAGE 871 Br Med J: first published as 10.1136/bmj.1.6117.871 on 8 April 1978. Downloaded from http://www.bmj.com/ on 16 June 2020 by guest. Protected by copyright. BRITISH MEDICAL JOURNAL LONDON, SATURDAY 8 APRIL 1978 872 to ensure that all is well. Laboratory staff have nothing to fear from such independent inspection. I Hairy-cell leukaemia Leukaemic reticuloendotheliosis accounts for 2% of all leukaemias. It was first recognised in 1958 by Bouroncle et al,' whose investigation of 26 patients identified the cinicopathological features as a unique syndrome. They saw in the blood of their patients cells which they considered to be reticulum cells or histiocytes; they remarked on an unusual feature of these cells, the presence of pseudopodia, shown up especially well in wet preparations and by electron microscopy, which seemed to give an irregular lace-like outline to the cytoplasmic membrane. Some years later Schrek and Donnelly2 noted the presence of numerous short villi around the membrane and imaginatively described them as hairy cells, and so gave the disease its eponym. Hairy-cell leukaemia has attracted considerable interest among haematologists; many case reports have been published as well as studies of the cells by electron microscopy, cytochemistry, and functional and immunological techniques.3-7 The precise nature of the cells is controversial. From studies with specific surface markers they have been identified as B lymphocyte in type, similar to the cells of chronic lymphocytic and prolymphocytic leukaemia.8 Functionally, they behave as lymphocytes rather than histiocytes, though they do show phagocytic potential; some workers believe that they are neither B lymphocytes nor histiocytes but a unique cell type, possibly representing a leukaemic proliferation of monocytes.9 Diagnosis is not always straightforward, and many cases have initially been misdiagnosed as lymphocytic lymphoma, lymphocytic leukaemia, and even myelosclerosis or aplastic anaemia. Hairy-cell leukaemia mainly affects adults over the age of 50, with four times as many men as women. The patient usually presents with an infection or haemorrhage as a consequence of leucopenia and thrombocytopenia. There is also anaemia, which may be severe enough to be the clinically evident feature. Hairy-cell leukaemia can be diagnosed readily when the characteristic cells are found in the blood, where they may constitute up to 95%0 of the circulating leucocytes. They may be absent from the blood, but they will always be seen in the bone marrow. The spleen plays an important and unusual part in this disease. Splenomegaly is commnon, and in at least half the patients the spleen is palpable more than 15 cm below the costal margin. The enlargement is due to a generalised diffuse 8 APRIL 1978 infiltration by mononuclear cells, especially in the red pulp, together with a notable congestion of the spleen with blood, and there will be some red cell sequestration. This pooling and sequestration can be measured with isotope techniques. A normal spleen contains a mere 50 ml of blood (less than 5% of the red cell volume). In hairy-cell leukaemia the spleen may contain one-third or more of the red cell volume, a feature found also in the myeloproliferative disorders.10 Sequestration gives rises to haemolysis, so that the spleen may play an important part in the anaemia, and this should be taken into account when deciding on treatment. Hairy-cell leukaemia is a chronic, steadily progressing disorder. The median survival seems to be between three and five years, but long survival of over ten years has been reported, especially in patients without splenomegaly. Treatment with various cytotoxic drugs has been without obvious effect-not unexpectedly, since the slow proliferative rate of the leukaemic cells makes it unlikely that antimitotic agents would be of value. Splenectomy is probably the treatment of choice in those patients in whom sequestration of cells is important: its value has been well documented. For example, Flandrin et all recently reviewed a series of 111 patients; the median survival in a group of 28 of the patients, all with splenomegaly and all of whom underwent splenectomy, was 45 months, in contrast to a median survival of 29 months in patients with palpable spleens which were not removed. Splenectomy appears to induce remission by removing the large mass of neoplastic cells; it also abolishes the hypersplenism syndrome, thus increasing the numbers of neutrophils and platelets in the peripheral blood. Furthermore, because of the red cell pooling in the spleen, its removal will improve the anaemia and so help the patient's general well being. The value of splenectomy is convincing enough to make it mandatory in patients with splenomegaly. Certain precautions are essential: prophylactic antibiotics and platelet transfusions when thrombocytopenia is present-and, above all, close cooperation between the surgeon and the haematologist. Bouroncle, B A, Wiseman, B K, and Doan, C A, Blood, 1958, 13, 609. Schrek, R, and Donnelly, W J, Blood, 1966, 27, 199. 3Catovsky, D, et al, British Journal of Haematology, 1974, 26, 9. 4Debusscher, L, et al, Blood, 1975, 46, 495. 5 Katayama, I, and Finkel, H E, American Journal of Medicine, 1974, 57, 115. 6 Burke, J S, Byrne, G E, and Rappaport, H, Cancer, 1974, 33, 1399. 7Burke, J S, Mackay, B, and Rappaport, H, Cancer, 1976, 37, 2267. 8 Catovsky, D, et al, British J'ournal of Haematology, 1974, 26, 29. 9 Burns, G F, et al, British Journal of Haematology, 1977, 36, 71. 10 Lewis, S M, et al, British Journal of Haematology, 1977, 35, 351. 1 Flandrin, G, Sebahoun, G, and Bernard, J, in Topics in Haematology, p 872. Amsterdam, Excerpta Medica, 1977. 2 Mechanisms of Parkinson's disease Despite continued research interest in Parkinson's disease, our understanding of the underlying mechanism of the disorder is still far from complete. In 1817 James Parkinson suggested that lesions would be found in the cervical cord and medulla, but in fact we now know that widespread lesions are present in the brain, with the most characteristic finding a loss of melanin-containing cells from the substantia nigra. Nevertheless, the link between these lesions in the substantia nigra and the signs and symptoms of the disease remained obscure until advances in neurochemistry began to provide some answers. In 1960 a striking deficiency of dopa- Br Med J: first published as 10.1136/bmj.1.6117.871 on 8 April 1978. Downloaded from http://www.bmj.com/ on 16 June 2020 by guest. Protected by copyright. Report of the Committee of Inquiry into the Smallpox Outbreak in London in March and April 1973, Cmnd 5626. London, HMSO, 1974. Department of Health and Social Security et al, Report of the Working Party on the Laboratory Use of Dangerous Pathogens, Cmnd 6054. London, HMSO, 1975. 3 Report of the Working Party to Formulate a Code of Practice for the Prevention of Infection in Clinical Laboratories (chairman Sir James Howie). London, 1978: laid in House of Commons Library. 4 Collins, C H, Hartley, E G, and Pilsworth, R, The Prevention of Laboratory Acquired Infection. Public Health Laboratory Service Monograph No 6. London, HMSO, 1977. 5 Department of Health and Social Security et al, Safety in Pathology Laboratories. London, DHSS, 1972. 6 Department of Health and Social Security et al, Safety in the Post-mortem Room. London, DHSS, 1972. Department of Health and Social Security et al, Control of Laboratory Use of Pathogens Very Dangerous to Humans. London, HMSO, 1976. 8 Collins, C H, IMLT Gazette, 1975, 19, 143. 2 BRITISH MEDICAL JOURNAL