Plasmid carriage and the serum sensitivity of enterobacteria.

The carriage of a range of plasmids by rough, serum-sensitive laboratory strains of Escherichia coli made no difference to their reactivity in human serum as determined by two methods. Plasmid-carrying enterobacteria isolated from polluted river water gave a variety of responses to serum. Smooth E. coli river isolate C8 was killed by serum but only after a delay of 1 h, and curing of antibiotic resistance and colicin determinants from this strain led to a small but significant increase in serum sensitivity. Plasmids from eight strains were transferred by conjugation to a cured derivative of C8 (C8(-)Nal(R)), and in six cases a significant increase in the serum resistance of the progeny was observed. Plasmid-mediated enhancement of resistance was particularly marked with plasmids R1 and NR1, and a round of replication mutant of NR1 conferred greater resistance than did the normal R factor. However, R1 and NR1 were unable to modify the serum response of a cured strain (P21(-)Nal(R)) derived from promptly serum-sensitive isolate P21. These findings suggest that lipopolysaccharide O-side chains, the cell surface components responsible for the delay in serum killing, are essential for the expression of plasmid factors that modify sensitivity to serum. Examination of K(A)(-) variants of two isolates indicated that the K(A) antigen has only a marginal effect on the serum response.