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Salmonella typhimurium strains which are deficient in uridine diphosphate (UDP)-galactose-4-epimerase (gal E mutants) owe their outstanding protective capacity when used as live vaccine to the fact that when galactose is supplied exogenously, such as occurs in vivo, smooth cell wall lipopolysaccharides are synthesized. The mutants lose most of their protective capacity when this phenotypic curing is prevented by a second mutation of the kind found in strains LT2 M1 A (deficient in galactokinase) or E32 (deficient in UDP-galactose-lipopolysaccharide transferase). Despite such phenotypic reversion, thegal E mutants are rendered avirulent as a result of galactose-induced bacteriolysis. Secondary mutants have been isolated which differ from each other with respect to the extent of galactose-induced lysis. The differences in galactose sensitivity are attributable to different activities of the other Leoloir pathway enzymes, namely, galactokinase and galactose-1-phosphate-uridyl transferase. The influence of these enzymes on lipopolysaccharide composition and galactose sensitivity and thus on virulence and immunogenicity ofgal E mutants has been studied.

Immunity in Experimental Salmonellosis II. Basis for the Avirulence and Protective Capacity of gal E Mutants of Salmonella typhimurium