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However, fairly large numbers of M. The quantity of bacilli from nasal mucosal lesions in lepromatous leprosy ranges from 10, to 10,, [ 23 ]. Majority of lepromatous patients show leprosy bacilli in their nasal secretions as collected through blowing the nose [ 24 ]. Nasal secretions from lepromatous patients could yield as much as 10 million viable organisms per day [ 25 ].

The entry route of M. The skin and the upper respiratory tract are most likely; however, recent research increasingly favours the respiratory route [ 26 , 27 ]. Measuring the incubation period in leprosy is difficult because of the lack of adequate immunological tools and slow onset of the disease. The minimum incubation period reported is as short as a few weeks and this is based on the very occasional occurrence of leprosy among young infants [ 28 ].

The maximum incubation period reported is as long as 30 years, or over, as observed among war veterans known to have been exposed for short periods in endemic areas but otherwise living in nonendemic areas.

It is generally agreed that the average incubation period is between three and ten years [ 29 ]. Those living in endemic areas with poor conditions such as inadequate bedding, contaminated water, and insufficient diet, or other diseases that compromise immune function are at highest risk for acquiring M. However, HIV infection has not been reported to increase susceptibility to leprosy, impact on immune response to M. On the contrary, initiation of antiretroviral treatment has been reported to be associated with activation of subclinical M.

Schwann cells SCs are a major target for infection by M.

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Binding of M. It has been shown that M. PGL-1, a major unique glycoconjugate on the M. The identification of the M. Macrophages are one of the most abundant host cells to come in contact with mycobacteria. Phagocytosis of M. Nonresponsiveness towards M. Leprosy is classified within two poles of the disease with transition between the clinical forms [ 42 ]. Clinical, histopathological, and immunological criteria identify five forms of leprosy: tuberculoid polar leprosy TT , borderline tuberculoid BT , midborderline BB , borderline lepromatous BL , and lepromatous polar leprosy LL.

It was recommended later that the classification is to be based on the number of skin lesions, less than or equal to five for paucibacillary PB and greater than five for the multibacillary MB form.


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Indeterminate I is a prelude to the determinate forms of leprosy [ 44 , 45 ]. It is characterized by an ill-defined, bizarre hypopigmented macule s with a smooth or scaly surface. The sensations over the macule may or may not be impaired. The nerve proximal to the patch may or may not be thickened. Manifesting with only neural signs without any evidence of skin lesions, polyneuritic leprosy mostly well recognized in the Indian subcontinent. The affected nerves are thickened, tender, or both. Localized involvement of the nerves may form nerve abscesses [ 46 ].

Histoid leprosy is relatively uncommon, distinct clinical, and bacteriologic and histopathologic expression of multibacillary leprosy [ 47 ]. It may occur as a primary manifestation of the disease or in consequence to secondary drug resistance to dapsone following irregular and inadequate monotherapy. It manifests as numerous cutaneous nodules and plaques primarily over the back, buttocks, face, and bony prominences.

Patients show a vigorous-specific immune response to M. The number of bacilli from a newly diagnosed lepromatous patient can reach 10 12 bacteria per gram of tissue. Cell-mediated immunity against M. Leprosy reactions are the acute episodes of clinical inflammation occurring during the chronic course of disease.

They pose a challenging problem because they increase morbidity due to nerve damage even after the completion of treatment. Reactions are interpreted as a shift in patients' immunologic status. Chemotherapy, pregnancy, concurrent infections, and emotional and physical stress have been identified as predisposing conditions to reactions [ 51 ]. Both types of reactions have been found to cause neuritis, representing the primary cause of irreversible deformities.

Type I reaction is characterized by edema and erythema of existing skin lesions, the formation of new skin lesions, neuritis, additional sensory and motor loss, and edema of the hands, feet, and face, but systemic symptoms are uncommon. Type II reaction is characterized by the appearance of tender, erythematous, subcutaneous nodules located on apparently normal skin, and is frequently accompanied by systemic symptoms, such as fever, malaise, enlarged lymph nodes, anorexia, weight loss, arthralgia, and edema.

Additional organs including the testes, joints, eyes, and nerves may also be affected. There may be significant leukocytosis that typically recedes after the reactional state. Type I reaction is a naturally occurring delayed-type hypersensitivity response to M. Immunologically, it is characterized by the development of strong skin test reactivity as well as lymphocyte responsiveness and a predominant Th1 response [ 54 , 55 ]. Pathogenesis of type II reaction is thought to be related to the deposition of immune complexes [ 60 ].


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A massive infiltrate of polymorphonuclear cells PMN in the lesions is only observed during ENL and some patients present with high numbers of neutrophils in the blood as well. Neutrophils may contribute to the bulk of TNF production that is associated with tissue damage in leprosy. Altogether, the data highlight some of the possible mechanisms for thalidomide's efficacy in treating type II reaction. Europe PMC requires Javascript to function effectively. Recent Activity. Leprosy, also known as Hansen's disease, is a chronic infectious disease caused by Mycobacterium leprae, a microorganism that has a predilection for the skin and nerves.

The snippet could not be located in the article text. This may be because the snippet appears in a figure legend, contains special characters or spans different sections of the article. Interdiscip Perspect Infect Dis. Published online Sep 4. PMID: Received May 25; Accepted Jul Bhat and C.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Abstract Leprosy, also known as Hansen's disease, is a chronic infectious disease caused by Mycobacterium leprae , a microorganism that has a predilection for the skin and nerves. Introduction Leprosy, also known as Hansen's disease, is a chronic infectious disease caused by Mycobacterium leprae , a microorganism that has a predilection for the skin and nerves.

Mycobacterium leprae M. Genetic Determinants of Host Response Human genetic factors influence the acquisition of leprosy and the clinical course of disease [ 12 ]. Transmission Two exit routes of M. Your Email:. Colleague's Email:. Separate multiple e-mails with a ;. Send a copy to your email. Some error has occurred while processing your request.

How leprosy is spread

Please try after some time. New findings in the pathogenesis of leprosy and implications for the management of leprosy. Current Opinion in Infectious Diseases26 5 , October Add Item s to:. An Existing Folder. A New Folder.

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The item s has been successfully added to " ". Thanks for registering! This is a thorough review of current treatment options and possible future directions. Lepr Rev. This is a good overview of pathogenesis and mechanism of a PGL-I as a virulence factor. All rights reserved. No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. Login Register. Enjoying our content? Thanks for visiting Infectious Disease Advisor. If you wish to read unlimited content, please log in or register below. Registration is free. Register for free and gain unlimited access to:.