Leprosy pathophysiology: Difference between revisions
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:* High [[bacterial]] index. | :* High [[bacterial]] index. | ||
==References== | ==References== | ||
Revision as of 02:30, 7 July 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Pathogenesis
Genetics
The infection by the mycobacterium leprae and the course of the disease are influenced by certain genetic factors of the host.[1][2] Some single-nucleotide polymorphism have been associated with a higher incidence of leprosy. These include:[1][3][4][5][6]
- Low occurrence of a lymphotoxin-α-producing allele.
- Vitamin D receptor gene.
- TNF-α gene.
- IL-10 gene.
- IFN-γ gene.
- TLR 1 gene.
Another study has also suggested a possible relationship between genetic variants of the NOD2 gene and increased susceptibility to leprosy and the development of type I and II reactions.[7]
Associated Conditions
Gross Pathology
Microscopic Pathology
Histopathology
The manifestations of leprosy depend on the host's immune response towards the mycobacteria. Therefore, tuberculoid and lepromatous patients will show different histopathologic findings:[1][8][9]
- Tuberculoid patients - These patients will show a strong immune response towards the bacteria, with production of IFN-γ and commonly showing a positive lepromin skin test.
- Inflammatory infiltrate with multiple granulomas.
- Granulomas containing giant cells, differentiated macrophages and epithelioid cells.
- Predominance of CD4 cells.
- Low bacterial index.
- Lepromatous patients - These patients will show a weaker immune response towards the bacteria, particularly a weak cell-mediated response.
- Absence of granulomas.
- Straightened skin.
- Predominance of CD8 cells.
- High bacterial index.
References
- ↑ 1.0 1.1 1.2 Bhat, Ramesh Marne; Prakash, Chaitra (2012). "Leprosy: An Overview of Pathophysiology". Interdisciplinary Perspectives on Infectious Diseases. 2012: 1–6. doi:10.1155/2012/181089. ISSN 1687-708X.
- ↑ Alter A, Alcaïs A, Abel L, Schurr E (2008). "Leprosy as a genetic model for susceptibility to common infectious diseases". Hum Genet. 123 (3): 227–35. doi:10.1007/s00439-008-0474-z. PMID 18247059.
- ↑ Alcaïs A, Alter A, Antoni G, Orlova M, Nguyen VT, Singh M; et al. (2007). "Stepwise replication identifies a low-producing lymphotoxin-alpha allele as a major risk factor for early-onset leprosy". Nat Genet. 39 (4): 517–22. doi:10.1038/ng2000. PMID 17353895.
- ↑ Mira MT, Alcais A, di Pietrantonio T, Thuc NV, Phuong MC, Abel L; et al. (2003). "Segregation of HLA/TNF region is linked to leprosy clinical spectrum in families displaying mixed leprosy subtypes". Genes Immun. 4 (1): 67–73. doi:10.1038/sj.gene.6363911. PMID 12595904.
- ↑ Correa-Oliveira, Rodrigo; Misch, Elizabeth A.; Macdonald, Murdo; Ranjit, Chaman; Sapkota, Bishwa R.; Wells, Richard D.; Siddiqui, M. Ruby; Kaplan, Gilla; Hawn, Thomas R. (2008). "Human TLR1 Deficiency Is Associated with Impaired Mycobacterial Signaling and Protection from Leprosy Reversal Reaction". PLoS Neglected Tropical Diseases. 2 (5): e231. doi:10.1371/journal.pntd.0000231. ISSN 1935-2735.
- ↑ Cardoso CC, Pereira AC, Brito-de-Souza VN, Dias-Baptista IM, Maniero VC, Venturini J; et al. (2010). "IFNG +874 T>A single nucleotide polymorphism is associated with leprosy among Brazilians". Hum Genet. 128 (5): 481–90. doi:10.1007/s00439-010-0872-x. PMID 20714752.
- ↑ Berrington WR, Macdonald M, Khadge S, Sapkota BR, Janer M, Hagge DA; et al. (2010). "Common polymorphisms in the NOD2 gene region are associated with leprosy and its reactive states". J Infect Dis. 201 (9): 1422–35. doi:10.1086/651559. PMC 2853728. PMID 20350193.
- ↑ Modlin RL, Hofman FM, Taylor CR, Rea TH (1983). "T lymphocyte subsets in the skin lesions of patients with leprosy". J Am Acad Dermatol. 8 (2): 182–9. PMID 6219136.
- ↑ Wallach D, Flageul B, Bach MA, Cottenot F (1984). "The cellular content of dermal leprous granulomas: an immuno-histological approach". Int J Lepr Other Mycobact Dis. 52 (3): 318–26. PMID 6332791.