Diarrhea remains one of the most common diseases of suckling and postweaning piglets worldwide and is responsible for approximately 10.8% of preweaning mortality in certain geographic regions (1). During the last few years, we have observed that in an increasing number of cases suspected of enteric colibacillosis in piglets, it has not proven possible to determine the etiological agent by standard slide agglutination techniques, using anti-fimbrial sera. Our objectives were: (i) To determine the prevalence of E. coli pathotypes among diarrheic and non-diarrheic piglets, using DNA hybridization and polymerase chain reaction (PCR), in order to identify potential emerging diarrhea-causing pathotypes, (ii) to examine the ability of relevant pathotypes to induce diarrhea in newborn pigs, and (iii) to assess an antibiotic sensitivity profile of isolates.
Our data showed that approximately 22.9% of E. coli isolates from diarrheic piglets could be attributed to E. coli infection and that 20.5% of these appeared to be associated with ne E. coli, pathotypes AIDA/STb/EAST1 and AIDA/STb. Selected isolates of these pathotypes induced diarrhea in experimentally infected piglets, suggesting a role for the AIDA-I factor in the pathogenesis of diarrhea in piglets. In contrast, the EAST1 pathotype was common among E. coli isolates from both diarrheic and non-diarrheic piglets. An isolate of this pathotype failed to produce diarrhea in piglets, suggesting that EAST1 alone is probably not a significant marker of pathogenic E. coli isolated from piglets with diarrhea. Antibiotic sensitivity testing showed that isolates of the AIDA-I/STb/EAST1 and AIDA-I/STb pathotypes were frequently sensitive to enrofloxacin, gentamicin, neomycin and trimethroprim-sulfamethoxazole, suggesting that these drugs may be useful for treatment of related infections.
Enterotoxigenic E. coli (ETEC) has been commonly incriminated as one of the most important etiological agents of the disease, but other groups of E. coli such as Shiga toxin-producing E. coli (STEC) and enteropathogenic E. coli (EPEC) are important enteric pathogens in piglets (reviewed in 2). ETEC strains express F4 (K88), F5 (K99), F6 (987P), F18 or F41 fimbriae and can produce heat labile (LTI and LTII) or heat stable [STa (or STI) and STb (or STII)] enterotoxins. STEC strains, of which enterohemorrhagic E. coli (EHEC) is a subset, express the E. coli attaching and effacing (EAE) factor and produce the shiga-like toxins 1 and 2 (Stx1 and Stx2) associated with hemorrhagic colitis and hemolytic uremic syndrome in humans. F18 fimbriae-positive strains may produce a shiga-like toxin variant (Stx2e) and are thus referred to as porcine STEC responsible for edema disease or they may produce enterotoxins and are referred to as ETEC causing postweaning diarrhea. EPEC strains produce the EAE adhesin; some of these isolates from humans are further characterized by the expression of “localized adherence (LA)” to Hep-2 cells in vitro. Although many E. coli isolates originally classified as EPEC are EAE- and LA-negative, they exhibit a pattern of diffuse adherence (DA) to Hep-2 cells, distinguishing them as a separate diarrheagenic group known as the diffusely adhering E. coli (DAEC), isolated mainly from diarrheic infants. Isolates of this group express various fimbrial and non-fimbrial adhesins, including the adhesin involved in diffuse adherence (AIDA-I). Although originally detected in E. coli isolates from humans with diarrhea, the AIDA-I system has also been detected recently in E. coli strains isolated from pigs with edema disease and postweaning diarrhea. Another group, the enteroaggregative E. coli (EAggEC), expresses the aggregative adherence fimbriae I (AAF/I) and produces the enteroaggregative heat-stable enterotoxin 1 (EAST1). Strains of the EAggEC have been associated with an episode of persistent diarrhea in children and they exhibit an aggregative adherence pattern to cultured human epithelial cells in vitro. EAST1 has been suggested to play an important role in the pathogenesis of diarrhea in pigs.
Footnotes
Acknowledgments
This work was supported by the Saskatchewan Agricultural Development Fund. The author acknowledges the contribution of Drs. Jane Pritchard, Dorothy Middleton, Greg Appleyard, and John M. Fairbrother.
This information first appeared in the Prairie Diagnostic Service Expositor and is reprinted here with permission.
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References
- 1.Tubbs RC, Hurd HS, Dargatz N, Hill G. Preweaning morbidity and mortality in the United States swine herd. Swine Health Prod 1993;1:21–28.
- 2.DebRoy C, Maddox CW. Identification of virulence attributes of gastrointestinal Escherichia coli isolates of veterinary significance. Ann Health Res Rev 2001;1:129–140. [PubMed]
