Bondarenko V M, Potaturkina-Nesterova N I, Iakushenko O S, Tararak T Ia, Nesterov A S
Gamaleya Research Institute of Epidemiology and Microbiology, Moscow, Russia.
Zh Mikrobiol Epidemiol Immunobiol. 1998 Jan-Feb(1):3-6.
Acute enteric infection was reproduced in rabbits, used as an experimental model, receiving Aspergillus flavus metabolites with food for 15 days and inoculated rectally with enterotoxigenic strain Klebsiella pneumoniae K24 6723. Pathomorphological study revealed the penetration of Klebsiella into microplicate cells of the intestinal epithelium, the proliferation of bacteria in the lamina propria and in the cupolas of Peyer's patches, as well as in phagolysosomes of leukocytes and macrophages. The lesion of the mucous membrane in both large and small intestine, accompanied by the hyperplasia of lymphoid follicles, was noted. As a rule, surface epithelium was dystrophically changed and peeled off into the lumen of the intestine. The specificity of such lesion was confirmed by the detection of Klebsiella in Coons' direct immunofluorescence test. The experimental model confirmed the role of a decrease in immunological protective reactions of the body, caused the action of A.flavus metabolites, in the development of the infectious process, initiated by opportunistic enterobacteria.
以家兔作为实验模型，使其连续15天经食物摄入黄曲霉代谢产物，然后经直肠接种产肠毒素肺炎克雷伯菌K24 6723，从而引发急性肠道感染。病理形态学研究显示，肺炎克雷伯菌可侵入肠道上皮的微皱细胞，在固有层、派伊尔结穹窿以及白细胞和巨噬细胞的吞噬溶酶体中增殖。观察到大肠和小肠黏膜均有病变，伴有淋巴滤泡增生。通常，表面上皮发生营养不良性改变并脱落至肠腔内。通过库恩氏直接免疫荧光试验检测到肺炎克雷伯菌，证实了此类病变的特异性。该实验模型证实了机体免疫保护反应降低（由黄曲霉代谢产物作用所致）在由机会性肠道细菌引发的感染过程发展中的作用。
