Topic
Visceral leishmaniasis
About: Visceral leishmaniasis is a research topic. Over the lifetime, 7486 publications have been published within this topic receiving 184865 citations. The topic is also known as: Kala-Azar & viscus leishmaniasis.
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TL;DR: Patients with PKDL are considered as reservoirs of VL, linking its eradication to effective control of PKDL and future functional investigations on Tregs and their interaction with lesional effector lymphocytes would be indispensable for development of immunomodulatory therapies against Leishmania infection.
Abstract: Post-kala-azar dermal leishmaniasis (PKDL) is a dermal sequela of visceral leishmaniasis (VL), reported mainly from two regions - Sudan in eastern Africa and the Indian subcontinent, with incidences of 50-60% and 5-10%, respectively. Importantly, patients with PKDL are considered as reservoirs of VL, linking its eradication to effective control of PKDL. The etiopathogenesis of PKDL is presumably due to an immunological assault on latent dermal parasites. Immunological markers include IL-10, whose expression in skin and plasma of Sudanese patients with VL predicted onset of PKDL. Cell-mediated immune responses, notably restoration of IFN-γ production by antigen-stimulated lymphocytes are well documented in Sudanese PKDL, but remain ambiguous in the Indian form; recently, antigen-specific IL-10-producing CD8+ lymphocytes have been implicated in pathogenesis. In Indian PKDL, upregulation of intralesional IFN-γ and TNF-α is counterbalanced by IL-10 and TGF-β together with downregulated IFN-γ R1. Although IL-10 curtails excessive IFN-γ-mediated reactivity and ensures parasite survival, its cellular source remains to be confirmed, with infiltrating regulatory T cells (Tregs) being a likely candidate. Future functional investigations on Tregs and their interaction with lesional effector lymphocytes would be indispensable for development of immunomodulatory therapies against Leishmania infection.
88 citations
TL;DR: Cats living in endemic areas of visceral leishmaniasis are significantly more likely to be coinfected with FIV, which may present confounding clinical signs and therefore cats in such areas should be always carefully screened for coinfections.
87 citations
TL;DR: This study is the first report of VL that is caused by L. tropica in Iran, and the dominant strain of Leishmania was L. infantum (63 out of the 64 cases), but one case of L.tropica was also detected.
Abstract: Visceral leishmaniasis (VL) is caused by various strains of Leishmania donovani, Leishmania infantum, and Leishmania chagasi with different geographical distribution. The aim of this study was to identify the strains of Leishmania that can cause VL in southern Iran. DNA of Leishmania were extracted from the slides of bone marrow aspirates (#42) and spleen punctures (#22), which were positive for leishman body from the patients who were referred to the hospitals affiliated with Shiraz University of Medical Sciences. Differences in Leishmania strains were determined by size difference of the polymerase chain reaction (PCR) amplification as visualized on agarose gel. PCR results and smears had 100% correlation. The dominant strain of Leishmania was L. infantum (63 out of the 64 cases), but one case of L. tropica was also detected. VL mostly involves children below 2 years of age in Iran, therefore infection with L. infantum was expected, but this study is the first report of VL that is caused by L. tropica in Iran.
87 citations
TL;DR: Both naturally and experimentally infected dogs developed the same histopathological reaction, but to differing degrees, and the main feature of the immune response was the lack of specific T-cell response to leishmanial antigen.
87 citations
Journal Article•
TL;DR: Through immunostaining, it was established that sialoadhesin-positive stromal bone marrow macrophages contain parasites; such long-lived mononuclear phagocytes could be the host cells where the parasite can find "safe targets" unreactive to the dominant effector immune mechanism triggered by the replicative stage of the parasites.
Abstract: Human visceral leishmaniasis is mainly due to intracellular protozoan parasites of the Leishmania donovani complex, i.e., L. donovani and L. infantum (or L. chagasi). A mouse model has been established to monitor 1) the parasitic process initiated by L. infantum in three tissues they invade, and 2) parameters of the acquired immune response they trigger. Mice congenic at the Lsh locus and mice of inbred strains differing at the MHC locus have been inoculated by the i.v. route with L. infantum. The parasitic process has been evaluated by the follow-up of the parasitic load in the liver, the spleen, and, for the first time, in the bone marrow using a very sensitive limiting dilution assay. As previously established for L. donovani, the early outcome of L. infantum is also under the control of the Lsh locus in the liver; genes of the MHC complex are involved in the development of the subsequent acquired immune response. "Cure" or "noncure" haplotypes are the same for the two species of Leishmania; as far as the cure haplotype is concerned, whatever the tissues being screened, the parasites are never totally cleared, although the liver is the tissue in which the best parasite load reduction is achieved. Through immunostaining, it was established that sialoadhesin-positive stromal bone marrow macrophages contain parasites; such long-lived mononuclear phagocytes could be the host cells where the parasite can find "safe targets" unreactive to the dominant effector immune mechanism triggered by the replicative stage of the parasites.
87 citations