Component release after exposure of Staphylococcus aureus cells to pulsed electric fields

The objective of this work was to get further insights on the mechanism of inactivation of bacterial cells by pulsed electric fields (PEF) through the study of the release of intracellular components after exposing Staphylococcus aureus cells in McIvlaine buffer (pH 7.0, 2 mS/cm) to PEF treatments of different intensity (18 and 25 kV/cm) and treatment times (from 20 to 400 mu s). Release of most compounds, except proteins, was almost immediate after the treatment, but the relative amount released depended on the molecule studied. A good correlation between the release of the smallest components studied (particularly ions) and membrane permeabilization (as measured by NaCl sensitization and PI entry) was observed. On the other hand, results obtained suggested that S. aureus inactivation by PEF would be related to the exit of cytoplasmic proteins of a molecular weight higher than 6 kDa. Results obtained in this work indicated that increasing PEF treatment time would reduce the capability of S. aureus cells to repair the electropores formed and suggested that this might be due to the formation of pores of a larger size, which S. aureus cells would be unable to reseal in a situation of homeostasis loss. Industrial relevance: Results reported here can help to design more effective treatments for microbial inactivation using PEF on food, and therefore facilitate its industrial implementation.

Automated summary

This study aimed to investigate the mechanism of bacterial cell inactivation by pulsed electric fields (PEF) through studying the release of intracellular components of Staphylococcus aureus cells. The results showed that the release of certain components, such as ions, correlated with membrane permeabilization, while the inactivation of S. aureus by PEF was related to the release of cytoplasmic proteins above a certain molecular weight. Additionally, increasing PEF treatment time was found to reduce the cell's ability to repair electropores, potentially due to the formation of larger pores.