UC Davis

Despite being able to attain commercial sterility, thermal processing can promote reactions that could lower the overall quality of foods. Non-thermal processing was developed to solve some of the fundamental constraints of thermal processing, which reduces food nutrition and sensory quality. Non-thermal processing systems do, however, have some inherent limitations, such as a low rate of bacterial inactivation and the necessity for a lengthy treatment period. To increase the efficacy and shorten the treatment time needed of non-thermal processing, this study assessed the combination of two common non-thermal processing techniques, namely UV light irradiation and ultrasound treatment with food grade antimicrobial compounds.This study evaluated a synergistic antimicrobial treatment using a combination of ultrasound in a low frequency (LFU, 40kHz) or a high-frequency domain (HFU, 1 MHz) and a food-grade antioxidant, propyl gallate (PG, 10 mM), against a model gram-positive (Listeria innocua) and the gram-negative bacteria (Escherichia coli O157:H7) in water and a model beverage (apple juice). Treatment times ranged from 5 to 15 minutes for HFU and 5 to 45 minutes for LFU. Bacterial inactivation kinetic measurements were complemented by characterization of biophysical changes in liposomes, changes in bacterial membrane permeability, morphological changes in bacterial cells, and intracellular oxidative stress upon treatment with LFU/HFU, PG, and a combination of LFU/HFU + PG. This study also evaluated the effects of a synergistic antimicrobial combination of high-frequency ultrasounds and the food-grade antioxidant, propyl gallate, against mono-species biofilms from L. innocua and multispecies biofilms formed using a raw milk sample and L. innocua. This study also examines the antibacterial activity of combining UV-A light treatment or high-frequency (HFU) ultrasound treatment with three different classes of phenolic compounds (gallate derivatives, cinnamic acid derivatives, and other polyphenolic compounds such as quercetin, flavone, and grape seed extract) against E. coli O157:H7 and L. innocua. This study was motivated by the need to develop compounds that can work synergistically with UV-A light treatment or HFU. The result of this study indicated that the combination of ultrasound, both LFU and HFU, with PG resulted in a significant enhanced bacterial inactivation of 5 log CFU/mL, P<0.05, within 10 (HFU) to 30 minutes (LFU) of treatment time. The inactivation kinetic of HFU is significantly faster compared to LFU with the same PG concentration. Combined treatment of HFU + PG also significantly (> 5 log CFU/mL, P < 0.05) enhanced the inactivation of both L. innocua and multispecies biofilm as compared to single treatments of HFU or PG, after 30 minutes of treatment time. Upon extended treatment of cells with LFU/HFU and PG, a significant increase in membrane damage was observed compared to LFU/HFU or PG single treatments. Although oxidative stress was not the primary mechanism responsible for synergistic inactivation by LFU+PG, it was one of the factors contributing to bacterial inactivation in HFU+PG treatment. Overall, the study illustrates synergistic inactivation of various bacteria targets using a combination of LFU/HFU and PG based on enhanced membrane damage, oxidative stress and metabolic activity suppression and its potential for applications in the food and environmental systems. On the screening study, six photo-activated compounds were found to have a synergistic interaction with UV-A inactivating E. coli O157:H7, and four compounds were confirmed in the case of L. innocua, all of which belong to cinnamic acid derivatives. Of six photosensitizers confirmed in UV-A treatment, there were four retained their antimicrobial effectiveness when combined with HFU. Sinapic acid (SA) demonstrated the highest bacterial inactivation efficiency of the 18 chemicals tested when combined with either UV-A or HFU treatment. A "cause and effect" relationship between the physiochemical responses of the targeted bacteria to the combined treatments was observed, where intracellular oxidative stress could be a direct result of membrane damage, and membrane damage could also contribute to the inactivation of membrane-associated dehydrogenase enzyme families.