Abstract
Using seven experimental approaches, we attempted to solve the question of possible participation of colicinogeny and colicin-sensitivity in the pathology of the post-weaning diarrhoeic enteritis of piglets. In our research, both enterotoxic E. coli strains (ETEC) and normal, commensal E. coli strains in the intestinal microflora of 803 weaned piglets were followed. In diarrhoeic piglets, colicinogeny was more frequent in the ETEC strains than in the simultaneously isolated commensal ones. ETEC strains were largely insensitive to the most frequently appearing colicin types and the inhibitive effect of their colicins on commensal E. coli was less likely than the opposite (inhibition of ETEC strains by colicins of the commensal ones). Bolstering the diet of healthy piglets with a mixture of symbiotic colicinogenic strains and colicin-sensitive ETEC strains could not prevent diarrhoeic enteritis due to established dominance of ETEC. In all parts of the intestinal tract during the post-weaning diarrhoea (PWD), mostly non-colicinogenic strains of the commensal flora survived. In six serotypes of ETEC strains, the frequency of colicinogenic strains ranged from 7% (in the serotype O139) to 66% (in serotype O141). From 9 frequent colicin types, colicin V (mainly against the serotypes O8 and O147), E2 (against O139 and O8), D (mainly against O8) and E3 (mainly against O138) met most sensitive strains among ETEC. Hence, colicinogeny was no pathogenetic factor of PWD. Nevertheless, colicinogenic commensal strains gradually regained dominance during the decline phase of the disease in surviving piglets.
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