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• W1501930257 abstract "This chapter highlights aspects of hydrostatic pressure (HHP) inactivation and survival strategies of the human pathogen Listeria monocytogenes. The resistance of L. monocytogenes to the damaging effects of freezing, drying, and heat is remarkable for a non-spore-forming bacterium. The majority of all major food-borne outbreaks of listeriosis appear to be caused by serovar 4b strains. The major regulator of virulence genes in L. monocytogenes is PrfA. PrfA binds to a palindromic recognition sequence (PrfA box) located in the promoter region of regulated genes. The underlying mechanism has been identified for a number of isolates and is described in this chapter. Clearly, the variability in HHP resistance of different species, strains, and even cells within a population makes the proper design of HHP treatments that would allow for adequate reductions of bacteria a challenging task. Bacteria have several stress responses that provide ways to specifically produce mutations and respond to selective pressure. These include the SOS response, the general stress response, the heat shock response, and the stringent response. The underlying mechanisms can be a DNA polymerase that synthesizes errorcontaining DNA, recombination-dependent generation of mutations, or recombinationin dependent generation of mutation (e.g., strand slippage). Extensive application of functional genomics tools may rapidly increase one's knowledge of bacterial stress responses and survival mechanisms, including the characterization of stress-induced mutator phenotypes and the occurrence of stable subpopulations of pathogens that are more resistant to inactivation treatments than the wild-type population." @default.
• W1501930257 created "2016-06-24" @default.
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• W1501930257 date "2014-04-30" @default.
• W1501930257 modified "2023-09-26" @default.
• W1501930257 title "Listeria monocytogenes High Hydrostatic Pressure Resistance and Survival Strategies" @default.
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• W1501930257 doi "https://doi.org/10.1128/9781555815646.ch6" @default.
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