Carcase chilling is an integral component of meat processing needed for microbial safety and quality. Microbes on the carcase surface encounter a reduction in temperature and a lowering of water activity as the carcase exterior dries from exposure to cold air blown over it. In vitro studies with STEC E. coli O157:H7 Sakai show a significant (1000-fold) decrease in culturable cell numbers when shifted to a non-lethal combination of low temperature and water activity. However cells recover viability rapidly, before losing culturability again. Eventually, the cells recover, and growth resumes at the rate expected for the conditions after an extended lag phase. While this phenomenon is being exploited for novel technologies for carcase disinfection, for acceptance of those processes and better scientific understanding is required.
The initial increase in cells is thought to be due to recovery of culturability, rather than growth of survivors, because the rate of increase of culturable cells is far higher than the rate at which the cells can replicate under the treatment conditions. This hypothesis was tested by reducing the treatment temperature so that cells could not replicate. Nonetheless, CFU continued to rise after the shift in growth conditions, indicating recovery of culturability of cells rather than growth.
It was hypothesised that damage to the cell membrane could explain the results: both cold and osmotic shock are known to cause membrane disruption. To test this, flow cytometry was used to assess several aspects of cell physiology using different stains: PI (membrane integrity), DiBAC (membrane potential) and CFDAse (cellular respiration). The data suggested membrane damage (PI and DiBAC) after the application of the shock, as well as an increase in metabolism (CFDase), suggesting that that repair of damage requires biosynthesis of new cell materials and proteins, rather than simple reorganization of existing structures and molecular systems.