Eaton Kathryn A, Friedman David I, Francis Gayle J, Tyler Jessica S, Young Vincent B, Haeger Jennifer, Abu-Ali Galeb, Whittam Thomas S
Unit for Laboratory Animal Medicine, 018 Animal Research Facility, University of Michigan, Ann Arbor, MI 48109-0614, USA.
Infect Immun. 2008 Jul;76(7):3054-63. doi: 10.1128/IAI.01626-07. Epub 2008 Apr 28.
Enterohemorrhagic Escherichia coli (EHEC) is a food-borne pathogen that causes hemorrhagic colitis and acute renal failure. We used a germ-free mouse model to investigate the role of host factors, Shiga toxin 2 (Stx2), and bacterial strain in disease due to EHEC. Germ-free male and female Swiss-Webster mice that were 3 days to 12 weeks old were orally inoculated with 1 of 10 EHEC strains or derivatives of two of these strains with Stx2 deleted. All inoculated mice became infected regardless of the inoculum dose. All bacterial strains colonized the intestines, reaching levels of 10(9) to 10(12) CFU/g of feces by 4 days after inoculation. Seven of the 10 wild-type strains caused disease. However, the two Stx2 deletion mutants, unlike the Stx2(+) parental strains, did not cause disease. The clinical signs of disease in mice included lethargy, dehydration, polyuria, polydypsia, and death. Postmortem examination of affected mice revealed dehydration and luminal cecal fluid accumulation. Histologic examination revealed close adherence of bacteria to the intestinal epithelium in the ileum and cecum but not in the colon. Other lesions included progressive renal tubular necrosis, glomerular fibrin thrombosis, and red blood cell sludging. The severity of disease varied according to the bacterial strain and age, but not sex, of the host. This study demonstrated that EHEC colonizes germ-free mice in large numbers, adheres to the intestinal epithelium, and causes luminal cecal fluid accumulation and progressive renal failure. The disease in mice was Stx2 and bacterial strain dependent. This animal model should be a useful tool for studying the pathogenesis of renal disease secondary to EHEC infection.
肠出血性大肠杆菌(EHEC)是一种食源性病原体,可导致出血性结肠炎和急性肾衰竭。我们使用无菌小鼠模型来研究宿主因素、志贺毒素2(Stx2)和细菌菌株在EHEC所致疾病中的作用。将3日龄至12周龄的无菌雄性和雌性瑞士韦伯斯特小鼠口服接种10株EHEC菌株中的1株或其中两株缺失Stx2的衍生物。无论接种剂量如何,所有接种的小鼠均被感染。所有细菌菌株均在肠道定植,接种后4天粪便中细菌含量达到10⁹至10¹²CFU/g。10株野生型菌株中有7株引起疾病。然而,与Stx2(+)亲本菌株不同,两个Stx2缺失突变体并未引起疾病。小鼠疾病的临床症状包括嗜睡、脱水、多尿、烦渴和死亡。对患病小鼠的尸检显示脱水和盲肠腔内积液。组织学检查显示细菌紧密粘附于回肠和盲肠的肠上皮,但未粘附于结肠。其他病变包括进行性肾小管坏死、肾小球纤维蛋白血栓形成和红细胞淤滞。疾病的严重程度因细菌菌株和宿主的年龄(而非性别)而异。本研究表明,EHEC可在无菌小鼠中大量定植,粘附于肠上皮,并导致盲肠腔内积液和进行性肾衰竭。小鼠疾病依赖于Stx2和细菌菌株。该动物模型应是研究EHEC感染继发肾病发病机制的有用工具。