Virulence factors of enterotoxigenic E. coli studied in the infant mouse model.
Enterotoxigenic E. coli (ETEC) strain B41 orally inoculated in infant mice at birth induces lethal diarrheoal disease. This model was used to study virulence factors of ETEC strains of bovine and porcine origins. Strains possessing different plasmid-coded virulence factors were obtained either after spontaneous loss of these factors from the original strain or by plasmid transfer to different E. coli. A clone B41A derived from the strain B41 did not produce K99 antigen, but still produced heat-stable (ST) toxin. This clone B41A was about as pathogenic as the strain B41 in that it caused death of nearly all animals less than 48 h after inoculation with 10(3) bacteria. Plasmids were transferred from the strain B41 to E. coli C600, to nalidixic acid resistant mutants of strains of serotypes O8, O9, O101 and to an E. coli strain isolated from a suckling mouse intestine. K99+ Ent+ transconjuguant clones were either not all or mildly pathogenic. Two strains of porcine origin K88+ Ent+ were mildly pathogenic for mice. Loss of factor K88 did not reduce virulence. In contrast, loss of both K88 and Ent characteristics suppressed virulence. Strain E. coli K12 that had acquired K88 virulence factor possibly with other plasmid-coded characteristics but not the ability to produce ST toxin was non-pathogenic. Hence factors K99 and K88 may not be essential for inducing mortality in the infant mouse model. Other factors may be involved in virulence of the strain B41A. These results were discussed from the viewpoint of pathogenicity for mice and for ETEC natural hosts.