leprosy
leprosy Leprosy may briefly be defined as a chronic, potentially disabling disease, mainly affecting the nerves, skin, and eyes, caused by a bacillus, Mycobacterium leprae, which microscopically resembles the organism of tuberculosis. However, a better understanding of this complex disease calls for attention to (i) the long incubation period (usually 2–5 years); (ii) the remarkable diversity of clinical findings, apparently related to the level of immunity of different individuals; (iii) the frequency of adverse (damaging) immunological reactions, based on either cell-mediated or humoral (antigen–anitbody) mechanisms (iv) its propensity to produce disability and deformity, which in some cases may be severe and widespread, affecting eyes, face, or limbs; and (v) the social and psychological consequences of leprosy for the patient, the family, and the community, sometimes leading to outright stigmatization and rejection.
Leprosy is generally believed to have originated in Asia. From India, it probably spread to China in about 500 bc and then to Japan. It may have been carried from India in the fourth century bc by returning soldiers and camp followers of the Greek wars of conquest in Asia. In Europe, leprosy was active between the tenth and fifteenth centuries and then, for reasons largely unknown, steadily declined. Fear, stigma, and awareness of the disease also declined, but reappeared a few centuries later when the imperialist and colonialist activities of the countries in Western Europe revealed large numbers of cases in Africa, Asia, and Polynesia. Chaulmoogra (hydnocarpus) oil was introduced as treatment in the nineteenth century, but its beneficial effects were short-lived and it was not until the 1940s that effective chemotherapy became available. Dr G. H. Faget of the National Leprosarium at Carville, Louisiana, US, showed that a sulphone, ‘Promin’ (glucosulphone sodium) was effective intravenously in the treatment of leprosy, and this led to the use of dapsone (di-amino di-phenyl sulphone), given as tablets by mouth, on a wide scale.
The number of registered cases in the world has decreased from 5.4 million in 1985 to 700 000 recently. They are mainly in South and Cental America, Africa and the Far East. These remarkable changes have come about largely as a result of the widespread implementation of regimens of multiple drug therapy for all cases of leprosy as recommended by (WHO) in 1982. The enormous success of these regimens led to the establishment by WHO in 1994 of an Action Programme for the Elimination of Leprosy, aimed at reducing the prevalence of leprosy worldwide to less then one case per 10 000 of the population, and thus eliminating the disease as a public health problem.
A glance at the world map of prevalence suggests that the current distribution is somewhat tropical, but in the past leprosy has been quite widespread in Europe, Scandinavia, China, Korea, and Japan. The likelihood is that its development and spread are favoured by poverty and a range of poor socio-economic conditions, including over-crowding, malnutrition, illiteracy, lack of clean water, and inadequate (or non-existent) basic health services, including immunization.
For reasons which are not understood and which are in stark contrast to the situation with tuberculosis, the current HIV/AIDS pandemic has not, as yet, had an adverse effect on diagnosis, clinical management, treatment, or the control of leprosy. Coincident cases (HIV infection and leprosy in the same patient) have been reported from various countries, but there is no general evidence that HIV infection alters the clinical course of the disease or response to treatment.
Despite much research through the years, it is still impossible to grow the causative organism, Mycobacterium leprae, in laboratory culture in an artificial medium. A breakthrough was however achieved by Charles Shepard of the US Public Health Service in 1960, when he demonstrated that the bacillus could be grown in the foot-pads of laboratory mice, thus providing for the first time a model to establish the biological identity of the bacillus, assess the value of new drugs, and study drug resistance. In 1971, Eleanor Storrs and Waldemar Kirchheimer in the US reported that the 9-banded armadillo, Dasypus novemcinctus Linn., was susceptible to inoculation with bacilli of human origin, and the model was rapidly developed in the US and elsewhere to provide enormous numbers of bacilli for vaccine research and other projects. Although these endeavours have not entirely escaped the attention of animal rights activists, the general public has remained sympathetic to the importance of research and the use of animal models in order to pursue studies aimed at the prevention and treatment of leprosy in human beings.
Somewhat disappointingly, no specific vaccine against leprosy has yet been developed. It has, however, been shown that armadillo-derived, killed leprosy bacilli, in combination with BCG (Bacille Calmette-Guérin, the standard anti-tuberculosis vaccine) offers a high degree of protection, as shown in field trials in India, though not confirmed in trials in Venezuela and Malawi. Despite impressive progress, much remains to be done in the ‘final’ push towards elimination. The WHO has recently summarized the situation as follows:
‘Leprosy elimination stands at a critical and extremely difficult juncture. This is partly because the commitment to eliminate leprosy in many endemic countries is beginning to slacken (among decision-makers and in the field). Moreover, those areas that are easy to reach and to work in, have been effectively covered. The residual problem is far more difficult — from all perspectives — and is further complicated by structural inadequacies in local health services. Even today, people in many areas do not have ready access to diagnosis and MDT (including those with long-standing disease). Therefore, achievements will no longer be sustainable if significant numbers of hidden cases remain undetected and accessibility to treatment services remains difficult’
Leprosy is generally believed to have originated in Asia. From India, it probably spread to China in about 500 bc and then to Japan. It may have been carried from India in the fourth century bc by returning soldiers and camp followers of the Greek wars of conquest in Asia. In Europe, leprosy was active between the tenth and fifteenth centuries and then, for reasons largely unknown, steadily declined. Fear, stigma, and awareness of the disease also declined, but reappeared a few centuries later when the imperialist and colonialist activities of the countries in Western Europe revealed large numbers of cases in Africa, Asia, and Polynesia. Chaulmoogra (hydnocarpus) oil was introduced as treatment in the nineteenth century, but its beneficial effects were short-lived and it was not until the 1940s that effective chemotherapy became available. Dr G. H. Faget of the National Leprosarium at Carville, Louisiana, US, showed that a sulphone, ‘Promin’ (glucosulphone sodium) was effective intravenously in the treatment of leprosy, and this led to the use of dapsone (di-amino di-phenyl sulphone), given as tablets by mouth, on a wide scale.
The number of registered cases in the world has decreased from 5.4 million in 1985 to 700 000 recently. They are mainly in South and Cental America, Africa and the Far East. These remarkable changes have come about largely as a result of the widespread implementation of regimens of multiple drug therapy for all cases of leprosy as recommended by (WHO) in 1982. The enormous success of these regimens led to the establishment by WHO in 1994 of an Action Programme for the Elimination of Leprosy, aimed at reducing the prevalence of leprosy worldwide to less then one case per 10 000 of the population, and thus eliminating the disease as a public health problem.
A glance at the world map of prevalence suggests that the current distribution is somewhat tropical, but in the past leprosy has been quite widespread in Europe, Scandinavia, China, Korea, and Japan. The likelihood is that its development and spread are favoured by poverty and a range of poor socio-economic conditions, including over-crowding, malnutrition, illiteracy, lack of clean water, and inadequate (or non-existent) basic health services, including immunization.
For reasons which are not understood and which are in stark contrast to the situation with tuberculosis, the current HIV/AIDS pandemic has not, as yet, had an adverse effect on diagnosis, clinical management, treatment, or the control of leprosy. Coincident cases (HIV infection and leprosy in the same patient) have been reported from various countries, but there is no general evidence that HIV infection alters the clinical course of the disease or response to treatment.
Despite much research through the years, it is still impossible to grow the causative organism, Mycobacterium leprae, in laboratory culture in an artificial medium. A breakthrough was however achieved by Charles Shepard of the US Public Health Service in 1960, when he demonstrated that the bacillus could be grown in the foot-pads of laboratory mice, thus providing for the first time a model to establish the biological identity of the bacillus, assess the value of new drugs, and study drug resistance. In 1971, Eleanor Storrs and Waldemar Kirchheimer in the US reported that the 9-banded armadillo, Dasypus novemcinctus Linn., was susceptible to inoculation with bacilli of human origin, and the model was rapidly developed in the US and elsewhere to provide enormous numbers of bacilli for vaccine research and other projects. Although these endeavours have not entirely escaped the attention of animal rights activists, the general public has remained sympathetic to the importance of research and the use of animal models in order to pursue studies aimed at the prevention and treatment of leprosy in human beings.
Somewhat disappointingly, no specific vaccine against leprosy has yet been developed. It has, however, been shown that armadillo-derived, killed leprosy bacilli, in combination with BCG (Bacille Calmette-Guérin, the standard anti-tuberculosis vaccine) offers a high degree of protection, as shown in field trials in India, though not confirmed in trials in Venezuela and Malawi. Despite impressive progress, much remains to be done in the ‘final’ push towards elimination. The WHO has recently summarized the situation as follows:
‘Leprosy elimination stands at a critical and extremely difficult juncture. This is partly because the commitment to eliminate leprosy in many endemic countries is beginning to slacken (among decision-makers and in the field). Moreover, those areas that are easy to reach and to work in, have been effectively covered. The residual problem is far more difficult — from all perspectives — and is further complicated by structural inadequacies in local health services. Even today, people in many areas do not have ready access to diagnosis and MDT (including those with long-standing disease). Therefore, achievements will no longer be sustainable if significant numbers of hidden cases remain undetected and accessibility to treatment services remains difficult’
A. Colin McDougall
Bibliography
Action Programme for the Elimination of Leprosy. Status Report, 1996. WHO/LEP/96.5 World Health Organisation, Geneva, Switzerland.
Hastings, R. C. (ed.) (1985). Leprosy, ‘Medicine in the Tropics Series’. Churchill Livingstone, Edinburgh, London, Melbourne, and New York.
Jopling, W. H. and and McDougall, A. C. (1996). Handbook of Leprosy, (5th edn) CBS Publishers and Distributors, 4596/1-A, 11-Daryaganj, New Delhi, 110 002, India.
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leprosy