Leprosy pathophysiology
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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 immune response towards the my bacteria. Therefore, tuberculoid and lepromatous patients will show different histopathologic findings:
- 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:
Pathophysiology
References
- ↑ 1.0 1.1 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.