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. 1989 Jan;57(1):82–87. doi: 10.1128/iai.57.1.82-87.1989

Age-specific colonization of porcine intestinal epithelium by 987P-piliated enterotoxigenic Escherichia coli.

E A Dean 1, S C Whipp 1, H W Moon 1
PMCID: PMC313044  PMID: 2562837

Abstract

Neonatal (less than 1-day-old), 3- and 7-day old, and older (3-week-old postweaning) pigs were challenged by intragastric inoculation with 987P-piliated (987P+) enterotoxigenic Escherichia coli (ETEC) 987. Neonatal pigs were colonized (i.e., there were greater than or equal to 10(8) CFU of test strain per 10-cm ileal segment) and developed diarrhea. Intestinal colonization and the incidence and severity of diarrhea were lower in 3- and 7-day old pigs than in neonates. Older pigs were not colonized and did not develop diarrhea following oral inoculation with five strains of 987P+ ETEC. Strain 987 (987P+) adhered in vitro to intestinal epithelial cell brush borders isolated from both neonatal (sensitive) and older (resistant) pigs. The in vivo growth and expression of 987P pilus by strain 987 in ligated ileal loops created in neonatal and older pigs were similar. The in vivo adherence of 987P+ ETEC to intestinal epithelium in ligated ileal loops in neonatal and older pigs was compared. In neonatal pigs, most of the bacteria were in layers associated with the villous epithelium. In older pigs, most of the bacteria were associated with mucus-like material in the intestinal lumen. We concluded that swine develop an innate resistance to 987P+ ETEC by 3 weeks of age. This resistance does not appear to be due to an absence of 987P-specific receptors in the intestines of the older pig or to an inability of 987P+ bacteria to grow and express pili in the older pig. We hypothesized that the resistance of older pigs to 987P-mediated disease is due to release of 987P-specific receptors into the intestinal lumen, where these receptors facilitate bacterial clearance rather than bacterial adherence to intestinal epithelium and colonization.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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