Influence of RecA onin vivovirulence and Shiga toxin 2 production inEscherichia colipathogens

Abstract

The enterohemorrhagicEscherichia coli(EHEC) O157:H7 strains 933 and 86–24 as well as the uropathogenicE. coli(UPEC) strain 536 were compared with their isogenicrecA mutants andrecAtrans-complemented strains in intravenous lethality and lung toxicity assays in mice. While the wild-type EHEC strains were fully virulent, the virulence of therecA mutants was strongly reduced. Complementation of the EHECrecA mutants with the clonedE. colirecA gene restored their virulence capacity. Thestx2EHEC mutant TUV86-2 as well as its isogenicrecA 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 therecA mutants as a result of lacking spontaneous phage induction. Therefore, the EHECrecA+strains 933 and 86–24 were compared for their Shiga toxin 2 (Stx2) production with the respectiverecA−counterparts. TherecA mutants of the EHEC strains were significantly reduced in toxin synthesis and were devoid of Stx2 specific phage production. Complementation of the EHECrecA mutants with the clonedrecA gene enabled therecA 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.