21The fate of five different E. coli strains, including three Shiga-toxin producing E. coli (STEC) 22 strains, was analyzed during the production and ripening of semi-hard raw milk cheese. The 23 strains, that were previously isolated from raw milk cheese, were spiked into raw milk prior to 24 cheese production at two different levels (about 10 1 CFU/ml and 10 3 CFU/ml, respectively). 25Two cheese types were produced, that differed in cooking temperatures (40 and 46°C). The 26 cheeses were sampled during manufacture and the 16 week ripening period. An increase in E. 27coli counts of about 3.5 log 10 CFU/g occurred from raw milk to fresh cheese at day 1, which 28 is attributed to a concentration effect during cheese production and growth of the strains. 29During ripening over 16 weeks a slow continuous decrease was observed for all strains. 30However, significant differences were found between the E. coli strains at the applied spiking 31 levels, while the inactivation was similar in the two different cheese types. The two generic E.

The ability of foodborne pathogens to survive in certain foods mainly depends on stress response mechanisms. Insight into molecular properties enabling pathogenic bacteria to survive in food is valuable for improvement of the control of pathogens during food processing. Raw milk cheeses are a potential source for human infections with Shiga toxin-producing Escherichia coli (STEC). In this review, we focused on the stress response mechanisms important for allowing STEC to survive raw milk cheese production processes. The major components and regulation pathways for general, acid, osmotic, and heat shock stress responses in E. coli and the implications of these responses for the survival of STEC in raw milk cheeses are discussed.