Abstract
Listeria innocua micropopulation lag phase and its variability have been modeled as a function of growth temperature, intensity of heat stress, and the number of surviving cells initiating growth. Micropopulation lag phases were found to correlate negatively with inoculum size and growth temperature and positively with heat shock intensity. Validation of the models using experimental milk samples indicated that the average lag phase duration predicted is shorter and more variable than the observed, meaning that they should be considered safe for risk assessment. Our results suggest that the effect of inoculum size on the population lag phase has both stochastic and physiological components.
•Lag is modeled as a function of inoculum size, growth temperature and heat shock.•Lag phases correlate negatively with inoculum size and growth temperature.•Lag phases are directly proportional to previous heat shock–stress-intensity.•Lag phase and lag variability models proposed here are secured.•Predictions of lag phase and its variability must improve QMRA studies.