Robins-Browne R M, Tzipori S, Gonis G, Hayes J, Withers M, Prpic J K
J Med Microbiol. 1985 Jun;19(3):297-308. doi: 10.1099/00222615-19-3-297.
Yersinia enterocolitica is an important cause of enteritis and mesenteric adenitis in many countries. However the pathogenesis of the disease caused by this organism has not been fully elucidated. Most isolates from clinical material possess two independent properties associated with virulence whose relative contribution to the development of disease is not known. These are the ability to penetrate the intestinal wall, which is thought to be controlled by a plasmid gene, and the production of heat-stable enterotoxin, which is controlled by a chromosomal gene. In this study, we infected neonatal gnotobiotic piglets with strains of Y. enterocolitica expressing these two properties in various combinations. The suitability of the piglet model was shown in experiments in which piglets fed virulent Y. enterocolitica serogroup O3 developed a clinical illness related to the size of the inoculum, which was accompanied by intestinal lesions similar to those reported in naturally and experimentally infected people and animals. The results confirmed the key role of a 47 X 10(6)-mol. wt plasmid in the pathogenicity of Y. enterocolitica, but suggested that penetration of the intestinal wall may be governed by chromosomal rather than plasmid-borne genes. No role for enterotoxin in the pathogenesis of yersiniosis was shown, although there was evidence that enterotoxin may promote intra-intestinal proliferation of Y. enterocolitica, thus favouring increased shedding of bacteria and encouraging their spread between hosts.
小肠结肠炎耶尔森菌是许多国家肠炎和肠系膜腺炎的重要病因。然而,由该生物体引起的疾病发病机制尚未完全阐明。从临床材料中分离出的大多数菌株具有与毒力相关的两种独立特性,但其对疾病发展的相对作用尚不清楚。这些特性包括穿透肠壁的能力(认为由质粒基因控制)和产生热稳定肠毒素(由染色体基因控制)。在本研究中,我们用表达这两种特性不同组合的小肠结肠炎耶尔森菌菌株感染新生无菌仔猪。在实验中显示了仔猪模型的适用性,在这些实验中,喂食强毒小肠结肠炎耶尔森菌O3血清型的仔猪出现了与接种量大小相关的临床疾病,并伴有与自然感染和实验感染的人和动物中报道的类似肠道病变。结果证实了47×10⁶分子量的质粒在小肠结肠炎耶尔森菌致病性中的关键作用,但表明肠壁的穿透可能由染色体而非质粒携带的基因控制。尽管有证据表明肠毒素可能促进小肠结肠炎耶尔森菌在肠道内的增殖,从而有利于细菌排出增加并促进其在宿主间传播,但未显示肠毒素在耶尔森菌病发病机制中的作用。