THERMAL INJURY OF YERSINIA ENTEROCOLITICA

Abstract

Procedures were developed to evaluate thermal injury to three strains of Yersinia enterocolitica (serotype 0:3, 0:8 and 0:17). Serotype 0:17 (atypical strain) was more sensitive to bile salts (BS) #3 and to sublethal heat treatment than the typical strains, 0:3 and 0:8. When the 0:3, 0:8 and 0:17 serotypes were thermally stressed in 0.1 M PO₄ buffer, pH=7.0, at 47C for 70, 60 and 12 min, respectively, greater than 99% of the total viable cell population was injured. Injury was determined by the ability of cells to form colonies on Brain heart infusion (BHI) agar, but not on Trypticase soy agar (TSA) plus 0.6% BS #3 for serotypes 0:3 and 0:8 and TSA plus 0.16% BS #3 for 0:17. Heat injury of serotype 0:17 cells for 15 min in 0.1 M PO₄ buffer caused an approximate 1000-fold reduction in cell numbers on selective media as compared to cells heated in PI, BHI broth and 10% nonfat dry milk (NFDM). The extended lag and resuscitation period on BHI broth was 2.5 times greater for 0:17 cells injured in 0.1 M PO₄ than for cells injured in BHI or PI menstruums. The rate and extent of repair of Y. enterocolitica 0:17 cells in three recovery media were directly related to the heating menstruum used for injury. The use of metabolic inhibitors demonstrated that ribonucleic acid (RNA) synthesis was required for repair, whereas deoxyribonucleic (DNA), cell wall and protein synthesis were not necessary for recovery of 0:17 cells injured in 0.1 M PO₄ buffer, BHI or PI menstruums. Inhibition of respiration by 2,4-dinitrophenol slowed repair only for 0:17 cells injured in 0.1 M PO₄ buffer, but not cells injured in PI or BHI menstruums.