What is the pathogenesis of leishmaniasis?

Updated: Feb 18, 2020
  • Author: Craig G Stark, MD, FACP, FFTM, RCPS(Glasg), FISTM; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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Answer

After inoculation by sandflies, the flagellated promastigotes bind to macrophages in the skin. Two of the parasite surface molecules appear to play a prominent role in parasite-phagocyte interactions. The extent and presentation of disease depend on several factors, including the humoral and cell-mediated immune response of the host, the virulence of the infecting species, and the parasite burden. Infections may heal spontaneously or may progress to chronic disease, often resulting in death from secondary infection.

Promastigotes activate complement through the alternate pathway and are opsonized. The most important immunologic feature is a marked suppression of the cell-mediated immunity to leishmanial antigens. In persons with asymptomatic self-resolving infection, T-helper (Th1) cells predominate, with interleukin 2 (IL-2), interferon-gamma, and IL-12 as the prominent cytokines that induce disease resolution, although immune suppression years later can result in disease. An overproduction of both specific immunoglobulins and nonspecific immunoglobulins also occurs. The increase in gamma globulin leads to a reversal of the albumin-globulin ratio commonly associated with this disease.

As noted earlier, leishmaniasis involves the reticuloendothelial system. Parasitized macrophages disseminate infection to all parts of the body but more so to the spleen, liver, and bone marrow. The spleen is enlarged, with a thickening of the capsule, and is soft and fragile; its vascular spaces are dilated and engorged with blood. The reticular cells of Billroth are markedly increased and packed with the amastigote forms of the parasite. However, no evidence of fibrosis is present. In the liver, the Kupffer cells are increased in size and number and infected with amastigote forms of Leishmania. Bone marrow turns hyperplastic, and parasitized macrophages replace the normal hemopoietic tissue.


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