Enteropathogenic Escherichia coli enteritis: evaluation of the gnotobiotic piglet as a model of human infection.

Abstract

SUMMARY The pathogenicity of classical enteropathogenic Escherichia coli strains of human origin was investigated in gnotobiotic piglets. One to two day old piglets in groups of four were infected perorally with approximately 10 colony forming units of one of eight enteropathogenic E coli strains or a non-pathogenic control strain. Animals were necropsied 24 or 48 hours after infection and their intestines were subjected to histological examination, quantitative bacterial culture and estimation of lactase activity. Four enteropathogenic E coli strains caused mild to moderate diarrhoea in nine of the 16 piglets inoculated with them. Piglets given two of these strains later became moribund. One enteropathogenic E coli strain caused a severe illness unaccompanied by diarrhoea. Inflammation of the intestinal mucosa occurred with all eight enteropathogenic E coli strains, but not with the control strain. Pathological changes were most pronounced in the distal ileum and colon and adherent bacteria were seen on the surface of the inflamed mucosa. The extent of the inflammatory response in infected piglets for the most part paralleled the severity of the clinical signs, the degree of bacterial colonisation and the reduction in lactase activity. Electron microscopic examination of tissue from piglets infected with three different strains showed that bacterial adherence to the apical plasma membrane of epithelial cells was accompanied by distinctive ultrastructural changes. These included degeneration of the microvillous brush border, together with cupping and pedestal formation of the plasma membrane at sites of bacterial attachment. The same changes have been seen in naturally occuring enteropathogenic E coli diarrhoea in humans and rabbits. The combined clinical and pathological findings indicate that the neonatal gnotobiotic piglet is a suitable model of infection with enteropathogenic E coli.Escherichia coli is both the predominant member of the normal aerobic colonic flora and a prominent cause of gastroenteritis.

A Novel Developmental Process of Intestinal Epithelial Lesions in a Calf Infected with Attaching and Effacing Escherichia coli.

“…Elongated microvilli adjacent to the attachment sites have previously been reported in pigs [6], rabbits [4] and chicks [5]. The developmental mechanism of AE lesions in these animals also seemed to be consistent with that in humans.…”

“…It colonizes the intestinal tract and adheres intimately to the enterocytes, resulting in the effacement of microvilli and formation of pedestals [3]. Although there have been many reports on attaching and effacing (AE) lesions in several species with AEEC infection [4][5][6], only one report dealt with the developmental process of AE lesions [2]. We investigated AE lesions on the enterocytes in a one-month-old calf and a piglet, and we found the developmental process of AE lesions in the calf was different from that in the piglet.…”

Mouse Model of Enteropathogenic Escherichia coli Infection

“…(68). Others have demonstrated that EPEC induces A/E lesions in other hosts, such as rabbits and piglets (41,50,67), and that REPEC colonizes the mouse intestinal epithelium as well (49). In contrast, Frankel et al reported that no EPEC colonies could be cultured from the intestine of Swiss NIH mice at 15 days postinfection (21).…”

Animal Models of EnterohemorrhagicEscherichia coliInfection

“…In these early studies, no other signs of ASMscience.org/MicrobiolSpectrumdisease were reported. As was found in human infections, histologic abnormalities were detected in the cecum and colon, and primarily consisted of destruction of the mucosal brush border and inflammation (51). These first investigations recognized that E. coli O157:H7 caused intestinal lesions that were morphologically similar to those previously described for EPEC (52), and thus EHEC was considered a member of the same pathotype group (53).…”