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A high proportion of invasive strains of Escherichia coli produced colicine V. This property was easily eliminated from 20 of 21 of these strains by 'curing' agents, especially sodium lauryl sulphate, indicating that the genes determining it were located on a plasmid (ColV) which was transmitted from ten of the strains by conjugation. Inoculated intramuscularly, the ColV- forms of all 17 strains tested were less pathogenic for chickens than the corresponding ColV+ forms. The pathogenicity of the ColV- forms of four strains was increased, usually to that of the ColV+ form from which they were derived, by implanting other ColV determinants in them. Much higher concentrations of organisms were found in the blood and liver of chickens infected with ColV+ forms than in chickens infected with ColV- forms. Inoculated intraperitoneally, the ColV+ form of one of the strains, BI88, was more pathogenic for mice than the ColV- form; much higher concentrations of organisms were found in the peritoneal fluid and blood of ColV+-inoculated mice than of ColV--inoculated mice. Inoculated orally and intravenously, ColV+ forms were more pathogenic for colostrum-deprived calves than the corresponding ColV- forms. After mixtures of ColV+ and ColV- organisms of the same strain in ratios of 1:10,1:100 or 1:1000 were given orally, they were found in a similar ratio in the contents of the alimentary tract 1 to 2 days later, when the calves were near to death. Many more ColV+ than ColV- organisms were found in the mesenteric lymph nodes, the deeper tissues and the blood; in the urinary and gall bladders, locations remote from the defence mechanisms of the body, the numbers of ColV- organisms sometimes exceeded those of ColV+ organisms. Colicine V, although demonstrated in the blood at death, did not appear adversely to influence the concentration of ColV- organisms in these calves. Several days after mixtures of ColV+ and ColV- organisms of strain BI88 were taken orally by two human beings, the ColV+ organisms became much more numerous in their faeces than the ColV- ones. Similar results were obtained when colVr organisms of BI88 were included in the inoculum or when a strain whose ColV- form was completely colicine V-resistant was studied. A ColE+ form of BI88 ColV- was no more pathogenic for chickens, mice or colostrum-deprived calves than was a ColE- form of this strain, and it did not persist in the faeces of the two human beings for longer than the ColE- form.

Further Observations on the Association of the Colicine V Plasmid of Escherichia coli with Pathogenicity and with Survival in the Alimentary Tract