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INTRODUCTION

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Leprosy is a chronic infectious disease caused by Mycobacterium leprae, an acid-fast bacillus (AFB) first recognized by Hansen in 1873 in Bergen, Norway, while examining smears from lepromas of Norwegian patients. Notably, the organism was the first reported bacterium causing chronic disease in humans and principally affects the cooler parts of the body, especially the skin, upper respiratory tract, testes, eyes, and superficial segments of peripheral nerves. The stigma suffered by patients with leprosy has historically been severe. Because of the stigma of leprosy, physicians must carefully consider the social implications of a diagnosis of leprosy, especially in children.

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PATHOGENESIS AND EPIDEMIOLOGY

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M leprae is an AFB in the order Actinomycetales and the family Mycobacteriaceae. The acid fastness of M leprae is weaker than that of other mycobacteria, but as in other mycobacteria, the acid fastness is related to mycolic acids in the cell wall. Viable, undamaged M leprae organisms stain solidly, but degenerating bacilli first stain irregularly, then become granular, and eventually lose acid fastness completely. The persistence of bacillary carcasses can be verified by silver staining techniques. Staining quality, therefore, provides a rapid method for determining the effectiveness of therapy. M leprae still cannot be cultivated in vitro. Therefore, identification depends on criteria other than those used routinely for cultivable mycobacteria. Current criteria for M leprae are the following: (1) it does not grow on routine laboratory media, (2) it infects the footpads of mice in a characteristic manner, (3) acid fastness is abolished by exposure to pyridine, (4) the organism invades nerves of the host, (5) suspensions of dead bacilli produce a characteristic pattern of reactions when injected into the skin of patients (lepromin reaction) in accordance with the various clinical forms of leprosy, (6) it produces the species-specific antigen phenolic glycolipid-1 (GLP-1), and (7) it exhibits species-specific DNA sequences.

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M leprae causes disease by its ability to survive and multiply in macrophages. If macrophages of the host digest the bacilli early, disease is not detectable, or the patient has only minimal lesions. If the macrophages are totally incapable of destroying the organisms, widely disseminated lepromatous leprosy (LL) will follow. Apoptosis of host cells occurs but is not as important in the pathogenesis of leprosy as in some other mycobacterial infections. Survival of M leprae in macrophages depends on the immune response of the patient.

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The role of immunologic processes in damage to nerves in leprosy is poorly understood. Some observations suggest that antineural antibodies in the sera of many patients, especially those with lepromatous disease, are related to such damage. Tumor necrosis factor (TNF) is associated with macrophage infiltration of peripheral nerves in reversal reactions. Infected Schwann cells present antigens to T cells, making them targets for immune attack.

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The highest prevalence of leprosy is in tropical Southeast Asia, South America, and Africa. Approximately 64% of all patients are in Southeast ...

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