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. 1993 Aug;61(8):3578–3582. doi: 10.1128/iai.61.8.3578-3582.1993

TnphoA-mediated disruption of K54 capsular polysaccharide genes in Escherichia coli confers serum sensitivity.

T A Russo 1, M C Moffitt 1, C H Hammer 1, M M Frank 1
PMCID: PMC281046  PMID: 8392976

Abstract

To assess whether non-K1, group 2 capsular serotypes are important in conferring serum resistance to extraintestinal isolates of Escherichia coli, a K54 blood isolate (CP9) was evaluated as a model pathogen. Transposon mutagenesis (TnphoA) was used to generate isogenic capsule-negative mutants. CP9 was resistant to the bactericidal effects of serum, growing in 80% serum. In contrast, all of the capsule-negative mutants had an increased sensitivity to 80% normal human serum, undergoing a 2- to 3-log kill over 3 h when starting inocula of 10(4) to 10(7) CFU/ml were used. The killing of the capsule-negative strains was mediated through the alternative complement pathway and not by lysozyme or beta-lysins. The protective effect of the K54 capsule against the bactericidal activity of serum was not through inhibition of the complement cascade, nor did it appear to be through a difference in the binding of C3.

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Selected References

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