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Leprosy ROBERT C CLINICAL MICROBIOLOGY REVIEWS, JUly 1988, p. 330-348 Vol. 1, No. 3 0893-8512/88/030330-19$02.00/0 Copyright X 1988, American Society for Microbiology Leprosy ROBERT C. HASTINGS,* THOMAS P. GILLIS, JAMES L. KRAHENBUHL, AND SCOTT G. FRANZBLAU Laboratory Research Branch, Gillis W. Long Hansen's Disease Center, U.S. Public Health Service, Carville, Louisiana 70721 OVERVIEW OF LEPROSY................................................................ 330 Epidemiology ................................................................ 330 Clinical Aspects ................................................................ 331 Indeterminate leprosy ................................................................ 331 LL ................................................................ 331 TT ................................................................ 331 Borderline leprosy ................................................................ 331 Reactions................................................................ 332 Patient Management ................................................................ 332 CELL WALL STRUCTURE AND ASSOCIATED ANTIGENS OF M. LEPRAE ................................333 Cell Wall of M. leprae ............................................................. 333 Protein Antigens of M. leprae ................................................................ 333 Molecular Biology of M. leprae ................................................................ 334 IMMUNOLOGY................................................................ 335 Immunologic Research ................................................................ 335 Goals................................................................ 335 Obstacles to research ................................................................ 335 Major breakthroughs ................................................................ 335 Clinical Immunology ................................................................ 336 Lepromin test................................................................ 336 Humoral immunity and serodiagnosis in leprosy ................................................................ 336 CMI in Leprosy ................................................................ 336 Mechanisms of Specific Anergy in LL................................................................ 337 Genetic control of CMI in leprosy................................................................ 337 Role of the lymphocyte in specific anergy in leprosy ...............................................................337 The Macrophage in Host Resistance to Leprosy ................................................................ 337 Leprosy Vaccine ................................................................ 338 MICROBIOLOGY ............................................................. 339 Metabolism ............................................................. 339 Catabolic activity ............................................................. 339 Amino acid metabolism ............................................................ 340 Nucleic acid metabolism ............................................................ 340 Lipid metabolism ............................................................ 340 Iron ............................................................. 340 Biophysical parameters............................................................. 340 In Vivo Drug Testing ............................................................. 340 In Vitro Drug Testing ............................................................. 341 ACKNOWLEDGMENTS ............................................................ 342 LITERATURE CITED............................................................. 342 OVERVIEW OF LEPROSY person. There is evidence that transmission of leprosy can occur through (i) intact skin, (ii) inhalation and deposition Leprosy or Hansen's disease is a chronic infectious dis- of bacilli onto intact nasal mucosa, and (iii) penetrating ease caused by Mycobacterium leprae. wounds, such as thorns or biting arthropods. Which of these mechanisms is most common is unknown. Perhaps the most Epidemiology popular view is that the leprosy bacilli are expelled from the The total number of leprosy patients in the world has been nose of a patient with active disease and impact on the nasal estimated to be about 10.6 million (199). Of these, about 62% mucosa of another individual. are in Asia and 34% are in Africa (170). Expressed in terms Although the disease is predominantly one of humans, of the intensity of the disease in a population, i.e., as mean since 1975 it has been demonstrated to be a natural infection prevalence, the disease is about three times as intense in of wild armadillos (Dasypus novemcinctus) in Louisiana and Africa as it is in Asia. Texas (236, 237). Spontaneous cases of leprosy have also Transmission of leprosy is thought to be from person to been described in two mangabey monkeys (78), and experi- mental leprosy has been transmitted to the rhesus monkey * Corresponding author. (10). The disease has been present in wild armadillos since at 330 VOL. 1, 1988 LEPROSY 331 least 1961 (232). The relationship between leprosy in wild medians at the wrist, common peroneals at the knee, and armadillos and the disease in humans is not clear. There posterior tibials at the ankle) are affected in bacteriologically have been antecdotal reports of leprosy in humans following progressive disease. There is a characteristic pattern of contact with armadillos (132, 230). On the other hand, most sensory loss due to dermal nerve fiber involvement in human leprosy occurs in areas (e.g., India) in which arma- advanced lepromatous leprosy which affects cooler areas of dillos do not exist. If a relationship exists between leprosy in the body surface (194). Despite the widespread involvement wild armadillos and that in humans, it seems to be quantita- in bacteriologically progressive LL, the patient has remark- tively minor. ably few symptoms other than those caused by the bacterial mass and the accumulations of macrophages required to Clinical Aspects contain them. Histopathologically, lepromatous lesions are characterized by massive collections of macrophages con- Leprosy predominantly affects the skin, peripheral taining large numbers of acid-fast bacilli and often containing nerves, and mucous membranes. The clinical features of the large amounts of lipids which create a foamy appearance on disease can be grouped into three parts depending on mech- hematoxylin and eosin staining. These foamy macrophages anism: (i) features due to bacterial proliferation, (ii) features may occupy 90% of the dermis. The dermal foam cell due to the immunologic responses of the host to the leprosy accumulations are separated from the epidermis by a clear bacilli, and (iii) features due to the peripheral neuritis caused zone. by the first two processes (179). Leprosy always involves TT. Polar tuberculoid leprosy (TT) is the localized form of peripheral nerves, almost always involves skin, and fre- the disease. In contrast to uncomplicated LL in which quently involves mucous membranes. The three cardinal bacterial proliferation results in signs and symptoms, much signs of the disease are skin lesion(s), skin anesthesia(s), and of the clinical picture in TT is due to a combination of enlarged peripheral nerve(s). bacterial proliferation and the immunologic responses of the The majority of people effectively resist infection with M. host to the bacilli. Characteristically, TT consists of one or, leprae even in highly endemic areas. It is now thought that as at most, a few well-circumscribed skin lesions with profound many as 200 individuals become infected with M. leprae for anesthesia of the skin lesion itself. There may be an enlarged each overt case which develops and is detected (1). peripheral nerve in the vicinity of the skin lesion(s). Histo- Indeterminate leprosy. For those individuals unable to pathologically, there are very few, if any, demonstrable resist infection with M. leprae, the incubation period varies, acid-fast bacilli. There is a dense, well-organized granuloma but it is usually in the range of 2 to 4 years. The earliest sign consisting of epithelioid cells, surrounded by lymphocytes, of the disease is usually one or a few hypopigmented skin and containing multinucleated Langhans giant cells. The macules with minimal sensory loss confined to the lesion. granuloma involves the basal layer of the epidermis in polar The histopathology of such a lesion may be only that of a TT. nonspecific, chronic dermatitis with scattered round cell Borderline leprosy. Borderline leprosy encompasses those infiltrates of the dermis. The presence of acid-fast bacilli or types of the disease between LL and TT. Mid-borderline is an infiltrate selectively in a nerve bundle in the dermis is rare because it is very unstable. A patient with borderline diagnostic. Indeterminate leprosy has a variable course. In leprosy can develop clinical, bacteriological, and histopatho- approximately three-fourths of such patients, the disease logic features of more tuberculoid disease with time, and this heals spontaneously; some cases remain indeterminate for a is called upgrading. Conversely, developing more leproma- prolonged period of time, and some progress to one of the tous disease with time is called downgrading. As in TT, the established forms of the disease. signs and symptoms of borderline leprosy tend to be due to
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