Russell R G, O'Donnoghue M, Blake D C, Zulty J, DeTolla L J
Department of Pathology, School of Medicine, University of Maryland, Baltimore.
J Infect Dis. 1993 Jul;168(1):210-5. doi: 10.1093/infdis/168.1.210.
Experimental challenge studies with Campylobacter jejuni were conducted in 3.5-month-old infant Macaca mulatta. One infant monkey (92-1) was challenged with 2.7 x 10(10) cfu of strain 78-37. A second infant was infected intentionally by natural transmission. The infants developed diarrhea 32 h after challenge of infant 92-1. Electron microscopic observations indicate that cell invasion is the primary mechanism of colon damage and diarrheal disease caused by C. jejuni. Intracellular C. jejuni were located in membrane-bound vacuoles and were free in the cytoplasm. Damaged epithelial cells exhibited premature apoptosis and were exfoliated into the lumen of the colon. C. jejuni were also located extracellularly in the mucosa and submucosa. Some cells had dilated endoplasmic reticulum, indicating possible alteration in ion and water transport.
对3.5个月大的婴猴猕猴进行了空肠弯曲菌的实验性激发研究。一只婴猴(92 - 1)用2.7×10¹⁰ cfu的78 - 37菌株进行激发。第二只婴猴通过自然传播被故意感染。在对婴猴92 - 1进行激发后32小时,这些婴猴出现腹泻。电子显微镜观察表明,细胞侵袭是空肠弯曲菌引起结肠损伤和腹泻病的主要机制。细胞内的空肠弯曲菌位于膜结合的液泡中,也游离于细胞质中。受损的上皮细胞表现出过早凋亡,并脱落到结肠腔内。空肠弯曲菌也存在于黏膜和黏膜下层的细胞外。一些细胞的内质网扩张,表明离子和水运输可能发生改变。