Influence of RecA on in vivo virulence and Shiga toxin 2 production in Escherichia coli pathogens

The enterohemorrhagic Escherichia coli (EHEC) O157:H7 strains 933 and 86-24 as well as the uropathogenic E. coli (UPEC) strain 536 were compared with their isogenic recA mutants and recA trans-complemented strains in intravenous lethality and lung toxicity assays in mice. While the wild-type EHEC strains were fully virulent, the virulence of the recA mutants was strongly reduced. Complementation of the EHEC recA mutants with the cloned E. coli recA gene restored their virulence capacity. The stx(2) EHEC mutant TUV86-2 as well as its isogenic recA mutant were completely avirulent in both assays. In contrast, RecA had no influence on the virulence of UPEC strain 536. We conclude that the lethality observed with EHEC is presumably mainly due to Shiga toxin, which is severely down-regulated in the recA mutants as a result of lacking spontaneous phage induction. Therefore, the EHEC recA(+) strains 933 and 86-24 were compared for their Shiga toxin 2 (Stx2) production with the respective recA(-) counterparts. The recA mutants of the EHEC strains were significantly reduced in toxin synthesis and were devoid of Stx2 specific phage production. Complementation of the EHEC recA mutants with the cloned recA gene enabled the recA mutants to restore toxin and phage production. These results suggest that the higher level of Stx2 synthesis in the EHEC strains is the result of a higher level of spontaneous Stx2 specific phage induction, which is controlled by RecA. (C) 1999 Academic Press.