SUMMARY: One induced and one spontaneous serum-resistant mutant were derived from smooth serum-sensitive strains. There was little difference in the yield or the O-side-chain-sugar to core-sugar ratio of lipopolysaccharides from the mutants compared with the parental strains. The mutations to serum resistance were not accompanied by increases in either the amount or haemagglutination-inhibiting activity of acidic polysaccharides extracted from the strains.

Two colonially rough forms, designated 17fa and 17gb, were isolated from an aged culture of serum-resistant mutant 17. 17fa appeared to be a mutant and was rapidly killed by serum. 17gb retained sero-logical O-specificity, and 17gb lipopolysaccharide contained a full complement of O-side-chains; the strain was killed by serum but only after a delay of 1 h.

K-negative O8 donor Hfr59, which was serum-resistant, was crossed with rough serum-sensitive strain F470 and recombinants were selected. The majority of recombinants inherited a full complement of lipo-polysaccharide O-side-chains but were killed by serum after a delay of 1 to 2 h.

These results suggest that lipopolysaccharide O-side-chains are responsible for a delay in the killing by normal human serum of smooth strains but that other factors determine full serum resistance. No evidence was found of a role for K-antigens in serum resistance.


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