Effect of different purine auxotrophic mutations on mouse-virulence of a Vi-positive strain of Salmonella dublin and of two strains of Salmonella typhimurium.

Ten cfu of a Vi-positive strain of Salmonella dublin, given i.p. to BALB/c mice, caused death. Of transductional derivatives with nutritional requirements expected to reduce virulence, those with complete blocks at aroA (therefore aromatic-dependent) or at purA (therefore adenine-dependent) were non-virulent; no deaths from i.p. inocula of 10(6) or 10(7) cfu, respectively. Transductants with identified blocks at purF, purG, purC or in the purJHD operon, all with purine requirement satisfied by hypoxanthine or any other purine, were of reduced virulence, with some deaths from 10(4) cfu or, for most of the derivatives, from only 10(2) cfu. Blocks at guaA or guaB, causing guanine requirement, likewise resulted only in reduced virulence, with some deaths from inocula of 10(2). Transductional derivatives of two mouse-virulent (LD50, i.p., less than 25 cfu) strains of S. typhimurium were similarly tested, with generally similar results, in that purA and purB (adenine-requiring) transductants were non-virulent, no deaths from 2.5 x 10(7) cfu, and those with purF, purG or purC defects (hypoxanthine-responding) retained partial virulence. However, the guaA and guaB (guanine-requiring) derivatives were of much reduced virulence; all mice survived 2.5 x 10(5) cfu but only one survived 2.5 x 10(7) cfu. In both the S. dublin and the S. typhimurium tests autopsy cultures showed that fatal infections resulted from multiplication of the auxotrophic strain, not from that of non-exacting revertants.