Acquisition of genes from an O18:K1:H7 ColV+ strain of Escherichia coli renders intracranially-inoculated E. coli K12 highly virulent for chickens, ducks and guinea-pigs but not mice.

The virulence of intracranially-inoculated mutant forms of an O18ac:K1:H7 ColV+ strain of Escherichia coli (designated MW) that lacked different combinations of its O and K antigens and ColV, and of an E. coli K12 strain to which these characters had been transmitted was studied in mice, chickens, ducks and guinea-pigs. The O18+K1+ColV+ form of MW was highly virulent for chickens and mice but the corresponding form of K12 was only highly virulent for chickens; the O18-K1-ColV- forms of both strains were of low virulence for chickens and mice. K1 was more important than O18 or ColV in determining virulence for both animal species. Ducks and guinea-pigs resembled chickens, not mice, in their response to infection with the O18+K1+ColV+form of K12. Pathogenesis studies revealed that the virulence of the forms of MW and K12 was associated with their ability to proliferate in the central nervous system; only low numbers of organisms were found in the blood and spleen of inoculated animals. The O18+K1+ColV+ form of K12 multiplied in mouse brain and in mouse blood in vitro; its multiplication in chicken blood was partially inhibited. Agglutinins to this and other forms of K12 were found in chicken serum but not in mouse serum. Large doses of mouse serum given to chickens and large doses of chicken serum given to mice did not alter the manner in which these animals responded to K12 O18+K1+ColV+ infection. Vaccination protected chickens and mice against lethal intracranial infection with the O18+K1+ColV+ forms of K12 or MW; it produced a much stronger immunity in mice against intraperitoneal challenge than against intracranial challenge.