Costa Carlos H N, Chang Kwang-Poo, Costa Dorcas L, Cunha Francisco Valmor M
Centro de Investigações em Agravos Tropicais Emergentes e Negligenciados, Instituto de Doenças Tropicais Natan Portella, Universidade Federal do Piauí, Rua Artur de Vasconcelos 151-Sul, Teresina 64002-510, PI, Brazil.
Department of Microbiology/Immunology, Center for Cancer Cell Biology, Immunology & Infection, Chicago Medical School, Rosalind Franklin University, North Chicago, IL 60064, USA.
Pathogens. 2023 Jul 24;12(7):969. doi: 10.3390/pathogens12070969.
Kala-azar, also known as visceral leishmaniasis (VL), is a disease caused by and . Patients experience symptoms such as fever, weight loss, paleness, and enlarged liver and spleen. The disease also affects immunosuppressed individuals and has an overall mortality rate of up to 10%. This overview explores the literature on the pathogenesis of preclinical and clinical stages, including studies in vitro and in animal models, as well as complications and death. Asymptomatic infection can result in long-lasting immunity. VL develops in a minority of infected individuals when parasites overcome host defenses and multiply in tissues such as the spleen, liver, and bone marrow. Hepatosplenomegaly occurs due to hyperplasia, resulting from parasite proliferation. A systemic inflammation mediated by cytokines develops, triggering acute phase reactants from the liver. These cytokines can reach the brain, causing fever, cachexia and vomiting. Similar to sepsis, disseminated intravascular coagulation (DIC) occurs due to tissue factor overexpression. Anemia, hypergammaglobulinemia, and edema result from the acute phase response. A regulatory response and lymphocyte depletion increase the risk of bacterial superinfections, which, combined with DIC, are thought to cause death. Our understanding of VL's pathogenesis is limited, and further research is needed to elucidate the preclinical events and clinical manifestations in humans.
黑热病，又称内脏利什曼病（VL），是一种由[具体病原体1]和[具体病原体2]引起的疾病。患者会出现发热、体重减轻、面色苍白以及肝脾肿大等症状。该疾病还会影响免疫功能低下的个体，总体死亡率高达10%。本综述探讨了有关临床前和临床阶段发病机制的文献，包括体外研究和动物模型研究，以及并发症和死亡情况。无症状感染可导致持久免疫。当寄生虫克服宿主防御并在脾脏、肝脏和骨髓等组织中繁殖时，少数受感染个体就会患上VL。肝脾肿大是由寄生虫增殖导致的增生引起的。由细胞因子介导的全身性炎症会发生，从而引发肝脏产生急性期反应物。这些细胞因子可到达大脑，引起发热、恶病质和呕吐。与败血症类似，由于组织因子过度表达会发生弥散性血管内凝血（DIC）。急性期反应会导致贫血、高球蛋白血症和水肿。调节反应和淋巴细胞耗竭会增加细菌二重感染的风险，人们认为细菌二重感染与DIC共同作用会导致死亡。我们对VL发病机制的理解有限，需要进一步研究以阐明人类临床前事件和临床表现。
