Affiliation:
1. Department of Bacteriology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
Abstract
A previous genetic investigation involving a mouse-nonvirulent
Salmonella abony
donor (high frequency of recombination) and a virulent
S. typhimurium
recipient indicated that two unlinked “low-virulence” loci determined nonvirulence. A nonvirulent recombinant was analyzed to determine the basis for its nonvirulence. The recombinant was smooth (like the parental strains) and prototrophic. The doubling time in mouse serum of the recombinant and the
S. abony
parent (both streptomycin-resistant) was longer than that of the wild-type streptomycin-sensitive ancestor of the
S. typhimurium
recipient. The virulent recipient also grew poorly in serum. However, the nonvirulence of the recombinant was probably not due to its inheritance of the streptomycin-resistance allele from the donor, because other recombinants were streptomycin-resistant but still virulent. Unlike the nonvirulent
S. abony
(but like the
S. typhimurium
), the recombinant was insusceptible to rapid intravenous clearance in normal mice. It therefore appears that neither of the “low-virulence” loci determine diminished virulence by enhancing phagocytosis. Clearance of the recombinant was enhanced by opsonization with immune serum. Counts of viable bacteria in the blood, liver, and spleen of normal mice after intravenous challenge showed that the recombinant, like the
S. abony
donor, failed to proliferate in the tissues, whereas the virulent
S. typhimurium
did so markedly. It is concluded that the nonproliferation of the recombinant was determined by one or both of the “low-virulence” loci from the nonvirulent
S. abony
donor.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
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