de Repentigny L, Phaneuf M, Mathieu L G
Department of Microbiology and Immunology, Faculty of Medicine, University of Montreal, Quebec, Canada.
Infect Immun. 1992 Nov;60(11):4907-14. doi: 10.1128/iai.60.11.4907-4914.1992.
Gastrointestinal colonization and systemic dissemination by Candida albicans and Candida tropicalis were compared in intact and immunocompromised mice. Five-day-old CFW mice were inoculated by the oral-intragastric route with 1.0 x 10(7) CFU of two C. albicans and two C. tropicalis strains isolated from the blood of patients with acute leukemia and with C. albicans 4918 and its cerulenin-resistant mutant 4918-10. C. albicans and C. tropicalis spread to the lungs, liver, and kidneys within 30 min postinoculation, and organ CFU of the two species were comparable over the following 10 days. Close association of blastoconidia with the villous surface of the small intestine resulted in lysis of microvilli and then progressive invasion of villi. Blastoconidia within villi were surrounded by a conspicuous zone of clearing. Persistent colonization of the small and large intestines by C. albicans blood isolates and strains 4918 and 4918-10 was similar for 31 days after inoculation, but consistently exceeded that of C. tropicalis. In mice colonized with C. albicans, immunosuppression with cortisone acetate and cyclophosphamide on days 30 and 33 after inoculation increased stomach CFU 40- to 370-fold and intestinal CFU 30- to 80-fold. In contrast, persistent colonization by C. tropicalis was undetectable before immunosuppression and only became apparent after treatment. C. albicans disseminated more frequently and with higher organ CFU than C. tropicalis. Despite this fact, 20% of mice infected with C. tropicalis died, compared with 4% infected with C. albicans blood isolates. Indirect immunofluorescence revealed penetrative growth by Candida hyphae exclusively in the mucosa and submucosa of the stomach from immunosuppressed, persistently colonized mice. Taken together, the data indicate that C. tropicalis appears to be more virulent than C. albicans and that factors responsible for gastrointestinal colonization, systemic dissemination, and mortality in immunocompromised mice may not be identical.
在完整和免疫受损小鼠中比较了白色念珠菌和热带念珠菌的胃肠道定植及全身播散情况。将5日龄的CFW小鼠通过口服灌胃途径接种1.0×10⁷CFU的两种从急性白血病患者血液中分离出的白色念珠菌和两种热带念珠菌菌株,以及白色念珠菌4918及其对浅蓝菌素耐药的突变株4918 - 10。接种后30分钟内,白色念珠菌和热带念珠菌扩散至肺、肝和肾,在接下来的10天里这两种菌的器官CFU相当。芽生孢子与小肠绒毛表面紧密相连,导致微绒毛溶解,随后绒毛逐渐被侵袭。绒毛内的芽生孢子被一个明显的清亮区包围。接种后31天内,白色念珠菌血液分离株、4918和4918 - 10菌株在小肠和大肠的持续定植情况相似,但始终超过热带念珠菌。在白色念珠菌定植的小鼠中,接种后第30天和第33天用醋酸可的松和环磷酰胺进行免疫抑制,使胃CFU增加40至370倍,肠CFU增加30至80倍。相比之下,热带念珠菌在免疫抑制前未检测到持续定植,仅在治疗后才变得明显。白色念珠菌比热带念珠菌更频繁地发生播散且器官CFU更高。尽管如此,感染热带念珠菌的小鼠中有20%死亡,而感染白色念珠菌血液分离株的小鼠死亡率为4%。间接免疫荧光显示,在免疫抑制且持续定植的小鼠中,念珠菌菌丝仅在胃黏膜和黏膜下层穿透性生长。综合来看,数据表明热带念珠菌似乎比白色念珠菌更具毒力,并且在免疫受损小鼠中,导致胃肠道定植、全身播散和死亡的因素可能并不相同。