A model describing the relationship between regrowth lag time and mild temperature increase for Listeria monocytogenes

In order to comply with the consumer demand for ready-to-eat and look 'fres h' products, mild heat treatment will be used more and more in the agrofood industry. Nonetheless there is no tool to define the most appropriate mild heat treatment. In order to build this tool, it is necessary to study and describe the response of a bacterial population to a mild increase in tempe rature, from the dynamic point of view. The response to a mild increase in temperature, defined by stress duration and temperature, consisted in a mor tality phase followed by the lag time of the survivors and their exponentia l growth. The effect of the mild increase in temperature on the mortality p hase was described in a previous paper (Breand et al., Int. J. Food Microbi ol., in press). The effect of the stress duration on the lag was presented in a previous paper (Breand et al., Int. J. Food Microbiol. 38 (1997) 157-1 67). In particular, the biphasic relationship between the lag and the stres s duration was observed and modelled with a four parameter nonlinear model: the primary model (Breand et al., Int. J. Food Microbiol. 38 (1997) 157-16 7). The study presented in this paper deals with the effect of the stress t emperature on the biphasic relationship between the lag time and the stress duration. The secondary models describing the effect of the stress tempera ture on this biphasic relationship, were empirically built from our experim ental data concerning Listeria monocytogenes. This work pointed out that th e higher the stress temperature, the narrower the range of stress duration for which the lag time increased. Since the primary and the secondary model s of the lag time were available, the global model describing the effect of the mild increase duration and temperature directly on the lag was fitted. This model allowed an improvement of the parameter estimator precision. Th e potential contribution in mild heat treatment optimization of this global model and the one built for the mortality phase (Breand et al., Int. J. Fo od Microbiol., in press) is discussed. (C) 1999 Elsevier Science B.V. All r ights reserved.