Mechanisms of Inactivation of Dry Escherichia coli by High-Pressure Carbon Dioxide

摘要

High-pressure carbon dioxide processing is a promising technology for nonthermal food preservation. However, few studies have determined the lethality of high-pressure CO2 on dry bacterial cells, and the mechanism of inactivation remains unknown. This study explored the mechanisms of inactivation by using Escherichia coli AW1.7 and mutant strains differing in heat and acid resistance, in membrane composition based on disruption of the locus of heat resistance, and in genes coding for glutamate decarboxylases and cyclopropane fatty acid synthase. The levels of lethality of treatments with liquid, gaseous, and supercritical CO2 were compared. The cell counts of E. coli AW1.7 and mutants with a water activity (a(W)) of 1.0 were reduced by more than 3 log(10) (CFU/ml) after supercritical CO2 treatment at 35 degrees C for 15 min; increasing the pressure generally enhanced inactivation, except for E. coli AW1.7 Delta gadAB. E. coli AW1.7 Delta cfa was more susceptible than E. coli AW1.7 after treatment at 10 and 40 MPa; other mutations did not affect survival. Dry cells of E. coli were resistant to treatments with supercritical and liquid CO2 at any temperature. Treatments with gaseous CO2 at 65 degrees C were more bactericidal than those with supercritical CO2 or treatments at 65 degrees C only. Remarkably, E. coli AW1.7 was more susceptible than E. coli AW1.7 Delta cfa when subjected to the gaseous CO2 treatment. This study identified CO2-induced membrane fluidization and permeabilization as causes of supercritical mediated microbial inactivation, and diffusivity was a dominant factor for gaseous CO2.