Division of Clinical Microbiology, Department of Laboratory Medicine, All India Institute of Medical Sciences, New Delhi, India.
Int J Dermatol. 2011 Sep;50(9):1099-108. doi: 10.1111/j.1365-4632.2011.04925.x.
A substantial number of patients who recover from kala-azar will develop dermatosis [commonly known as post-kala-azar dermal leishmaniasis (PKDL)]. It usually occurs in the Indian subcontinent and East Africa. As many as 10-20% of Indian cases and 50-60% of Sudanese cases develop PKDL after successful treatment of visceral leishmaniasis. Most cases occur after infection with Leishmania donovani and less commonly after Leishmania infantum. However, the PKDL is extremely rare in patients infected with Leishmania chagasi. Though exact pathology is not yet fully known, here we review various evidence, which suggest that the pathogenesis is largely immunologically mediated. Our group has been of the opinion that PKDL disease manifestation is a result of in-vivo generation of quasi-species either as in-vivo hybridization of various circulating and latent populations of the causative species within the host cells or due to external reinfection. We, and other scientists, have recently demonstrated that strains of Leishmania that cause visceral diseases differ genetically from those that cause PKDL. We feel that this review will incite interest in several parasitologists and molecular biologists in the pathogenesis of this important manifestation of the infection, often blamed as the source of outbreaks of leishmaniasis.
相当数量的从黑热病中康复的患者会发展出皮肤病[通常被称为黑热病后皮肤利什曼病(PKDL)]。它通常发生在印度次大陆和东非。在印度,多达 10-20%的病例和在苏丹,多达 50-60%的病例在成功治疗内脏利什曼病后会发展出 PKDL。大多数病例发生在感染杜氏利什曼原虫后,较少发生在感染婴儿利什曼原虫后。然而,在感染恰加斯利什曼原虫的患者中,PKDL 极为罕见。尽管确切的病理学尚未完全了解,但这里我们回顾了各种证据,这些证据表明发病机制在很大程度上是免疫介导的。我们小组一直认为,PKDL 疾病的表现是由于在体内产生准种,无论是由于宿主细胞内各种循环和潜伏种群的体内杂交,还是由于外部再感染。我们和其他科学家最近证明,引起内脏疾病的利什曼原虫菌株在遗传上与引起 PKDL 的菌株不同。我们认为,这篇综述将激发许多寄生虫学家和分子生物学家对这种重要感染表现的发病机制的兴趣,PKDL 常被归咎为利什曼病爆发的源头。
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