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Chapter 6 : Listeria monocytogenes High Hydrostatic Pressure Resistance and Survival Strategies
Category: Applied and Industrial Microbiology
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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.
Reductions in viable numbers of wild-type L. monocytogenes cells after exposure to different pressures for 20 min at 20°C. Cells were grown in brain heart infusion broth at 30°C with shaking (160 rpm). Cells were harvested (i) in mid-exponential phase and resuspended in N-(2-acetamido)2-aminoethanesulfonic acid (ACES) buffer before treatment (●), (ii) in stationary phase and resuspended in ACES buffer before treatment (○), and (iii) in mid-exponential phase and resuspended in semiskimmed milk before treatment (▲). Data are also presented in reference 43 .
Visualization of exponentially grown cells of wild-type L. monocytogenes Scott A (A) and the piezotolerant mutant AK01 (B) with electron microscopy. Bars, 500 nm (A) and 200 nm (B). Reprinted from reference 43 .
Protein and DNA sequences of the glycine-rich region of ctsR of L. monocytogenes. The piezotolerant mutant strain AK01 lacks a GGT codon sequence in the glycine-rich region ( 42 ). Mutations in this region were found at relatively high frequencies in other piezotolerant L. monocytogenes isolates ( 41 ).