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In the pharmaceutical, cosmetic, chemical, and food industries high-pressure homogenization is used for the preparation or stabilization of emulsions and suspensions, or for creating physical changes, such as viscosity changes, in products. Another well-known application is cell disruption of yeasts or bacteria in order to release intracellular products such as recombinant proteins. The development over the last few years of homogenizing equipment that operates at increasingly higher pressures has also stimulated research into the possible application of high-pressure homogenization as a unit process for microbial load reduction of liquid products. Several studies have indicated that gram-negative bacteria are more sensitive to high-pressure homogenization than gram-positive bacteria supporting the widely held belief that high-pressure homogenization kills vegetative bacteria mainly through mechanical disruption. However, controversy exists in the literature regarding the exact cause(s) of cell disruption by high-pressure homogenization. The causes that have been proposed include spatial pressure and velocity gradients, turbulence, cavitation, impact with solid surfaces, and extensional stress. The purpose of this review is to give an overview of the existing literature about microbial inactivation by high-pressure homogenization. Particular attention will be devoted to the different proposed microbial inactivation mechanisms. Further, the different parameters that influence the microbial inactivation by high-pressure homogenization will be scrutinized.

We have studied sublethal injury in Salmonella enterica serovar Typhimurium caused by mild heat and by different emerging nonthermal food preservation treatments, i.e., high-pressure homogenization, high hydrostatic pressure, pulsed white light, and pulsed electric field. Sublethal injury was determined by plating on different selective media, i.e., tryptic soy agar (TSA) plus 3% NaCl, TSA adjusted to pH 5.5, and violet red bile glucose agar. For each inactivation technique, at least five treatments using different doses were applied in order to cover an inactivation range of 0 to 5 log units. For all of the treatments performed with a technique, the logarithm of the viability reductions measured on each of the selective plating media was plotted against the logarithm of the viability reduction on TSA as a nonselective medium, and these points were fined by a straight line. Sublethal injury between different techniques was then compared by the slope and the y intercept of these regression lines. The highest levels of sublethal injury were observed for the heat and high hydrostatic pressure treatments. Sublethal injury after those treatments was observed on all selective plating media. For the heat treatment, but not for the high-pressure treatment, sublethal injury occurred at low doses, which were not yet lethal. The other nonthermal techniques resulted in sublethal injury on only some of the selective plating media, and the levels of injury were much lower. The different manifestations of sublethal injury were attributed to different inactivation mechanisms by each of the techniques, and a mechanistic model is proposed to explain these differences.

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A detailed study of the inactivation of Staphylococcus aureus and Yersinia enterocolitica by high-pressure homogenisation was performed at, respectively, 25 and 35 different combinations of process temperature and process pressure covering a range of 5-50 degrees C and 100-300 MPa. It appeared that in the entire studied pressure-temperature domain, S. aureus was more resistant to high-pressure homogenisation than Y. enterocolitica. Furthermore, the effect of the process pressure on the inactivation of S. aureus was considerably smaller than on the inactivation of Y. enterocolitica. Also, temperature between 5 and 40 degrees C did not affect inactivation of S. aureus by high-pressure homogenisation, while Y. enterocolitica inactivation was affected by temperature over a much wider range. Different mathematical models were compared to describe the inactivation of both bacteria under the experimental conditions applied. Such pressure-temperature inactivation models form the engineering basis for design, evaluation and optimisation of high-pressure homogenisation processes as a new preservation technique.