Barral A, Petersen E A, Sacks D L, Neva F A
Am J Trop Med Hyg. 1983 Mar;32(2):277-85. doi: 10.4269/ajtmh.1983.32.277.
BALB/c, C57B1/6 and (BALB/c x C57B1/6)F1 mice all proved susceptible to infection by a strain of Leishmania isolated from a Central Brazilian with espundia. The course of disease differed markedly between BALB/c and C57B1/6 mice. BALB/c mice suffered from a rapidly progressive and widely metastatic, but non-ulcerative, disease resembling diffuse cutaneous leishmaniasis. In contrast, C57B1/6 mice initially contained parasite multiplication effectively and appeared clinically cured. However, the parasite could persistently be cultured up to about 1 year post-infection. At that time, the parasite load in the infected footpad increased and a patent disease developed characterized by distinctive ulcerative metastases with destruction of soft-tissue in the nasal region similar to the one observed in espundia. Development of disease in both strains of mice was associated with depression of cell-mediated immunity as monitored by delayed-type hypersensitivity in vivo and lymphocyte transformation in vitro. Thus, our study suggests that diffuse cutaneous leishmaniasis and espundia can be caused by the same strain of parasite, and that the particular clinical expression in the individual mouse is determined by the host response.
BALB/c、C57B1/6和(BALB/c×C57B1/6)F1小鼠均被证明对从巴西中部一名患有粘膜皮肤利什曼病的患者身上分离出的一株利什曼原虫敏感。BALB/c小鼠和C57B1/6小鼠的病程明显不同。BALB/c小鼠患有一种快速进展且广泛转移但无溃疡的疾病,类似于弥漫性皮肤利什曼病。相比之下,C57B1/6小鼠最初能有效抑制寄生虫增殖,临床上似乎已治愈。然而,感染后长达约1年仍可持续培养出寄生虫。此时,感染足垫中的寄生虫载量增加,出现了明显的疾病,其特征为独特的溃疡性转移,伴有鼻部软组织破坏,类似于在粘膜皮肤利什曼病中观察到的情况。通过体内迟发型超敏反应和体外淋巴细胞转化监测发现,两种品系小鼠的疾病发展均与细胞介导免疫的抑制有关。因此,我们的研究表明,弥漫性皮肤利什曼病和粘膜皮肤利什曼病可能由同一株寄生虫引起,并且单个小鼠的特定临床表型由宿主反应决定。