In addition to acid stress, it is possible that bacterial cells may be exposed to elevated temperatures as well as oxidative stress during infection. Yuk and Marshall (2003) reported that heat adap- tation of E. coli O157: H7 reduced the total amount of Stx toxin production due to decreased intracellular toxin concentration. However, enhanced membrane fluidity by heat adaptation increased Stx toxin secretion in E. coli O157: H7. In E. coli, proteins associated with thermotolerance played a role in macrophage sur- vival, which suggested that HSPs contributed to bacterial survival and virulence during infection (Delaney and others 1993).