The lactoperoxidase system (LPS) enhanced thermal destruction of Listeria monocytogenes and Staphylococcus aureus. After LPS activation, biphasic survival curves were observed for L. monocytogenes at 57.8°C and for S. aureus at 55.2°C. The data were consistent with a model that assumed two bacterial populations differing in heat sensitivity. The more heat-sensitive fractions (93% of the L. monocytogenes, 92% of the S. aureus) were killed almost instantly. For these biphasic survival curves, D values were based on the much smaller, less-heat-sensitive fractions. For L. monocytogenes, the D522°C values were 30.2 min (untreated milk) and 10.7 min (LPS activated); corresponding D552°C values were 8.2 and 1.6 min; corresponding D57.8.c values were 2.3 and 0.5 min. For S. aureus, the D522°C values were 33.3 min (untreated milk) and 2.2 min (LPS activated), and the corresponding D55s2°C values were 7.6 and 1.1 min, respectively. The most rapid killing of L. monocytogenes occurred when samples were heated soon after activation of the LPS. Activation of the LPS followed by heating can increase the margin of safety with respect to milkborne pathogens.
The lactoperoxidase system (LPS) was activated by addition of thiocyanate (SCN−) and hydrogen peroxide (H2O2) and utilizing the inherent milk lactoperoxidase (LP). For Listeria monocytogenes studies, initial concentrations of 2.4 mM SCN− and 0.6 mM H2O2 were added. The corresponding concentrations were 1.2 mM SCN− and 0.3 mM H2O2 for Staphylococcus aureus studies. The LPS increased the predicted time to reach half the maximum attainable CFU/ml by 326 h for L. monocytogenes at 10°C and by 6.3 h at 35°C. For S. aureus, the corresponding increases were 36 h at 10°C and 2.4 h at 37°C. During the initial period after activation of the LPS, bactericidal effects against L. monocytogenes at 35°C and S. aureus at 37°C were observed. After recovery from the effects of the LPS, growth rate of each pathogen was of similar magnitude as in the H2O2-treated and untreated milk, with the exception of L. monocytogenes at 10°C.
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