P2-167 Mechanisms of Resistance to High Pressures by Vibrio parahaemolyticus

Tuesday, July 24, 2012
Exhibit Hall (Rhode Island Convention Center)
Haixia Lu, Zhejiang Gongshang University, Hangzhou, China
Yu Tong, Zhejiang Gongshang University, Hangzhou, China
Jianrong Li, Zhejiang Gongshang University, Hangzhou, China
Jinru Chen, The University of Georgia, Griffin, GA
Introduction:  High pressure has been used to control Vibrio parahaemolyticus in seafood.  Although a >300 MPa pressure can kill the pathogen, it adversely affects seafood texture.  Pressures lower than this level have been shown to be ineffective in eliminating pressure-resistant V. parahaemolyticus from seafood.

Purpose: The objective of this project was to observe changes in cell membrane protein and fatty acid profiles as well as Na+K+ATPase activity of V. parahaemolyticus as influenced by high pressure treatments.

Methods: A pressure-sensitive strain of V. parahaemolyticus (ZJGSMC001) was repeatedly treated with hydrostatic pressures ranging from 80 to 250 MPa, and cells that survived the 250 MPa treatments were selected.  Soluble cell member protein and fatty acid profiles of the pressure resistant derivates and their sensitive parent strains were determined using the SDS-PAGE electrophoresis and GC-MS method, respectively. The Na+K+ATPase activity of the strains were determined using a commercial assay.

Results: Results indicated that when exposed to a pressure of 250 MPa culturable cell counts of pressure-resistant strains was ca. 3 logs higher than that of pressure-sensitive strains.  The pressure-resistant strains appeared to have a greater amount of soluble cell membrane protein of 35 KDa.  The Na+K+ATPase was 83.3% more active than that of pressure-sensitive strains.  The ratio of unsaturated vs. saturated fatty acids of cell membranes was 1.03 in the pressure-resistant strains comparing to 1.17 in the pressure-sensitive strains.

Significance: Results suggest that cell membranes of V. parahaemolyticus were damaged when exposed to a 250 MPa pressure.  Cell membrane protein and fatty acid profiles as well as Na+K+ATPase activity may have played a role in mediating the resistance of V. parahaemolyticus to high pressures.  Pressure-resistant strains may have survived the treatments through degradating soluble cell membrane proteins, enhancing the activity of Na+K+ATPase, and increasing the expression of saturated fatty acids.