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dc.contributor.advisorJeter, Wayburn S.en_US
dc.contributor.authorRestaino, Lawrence
dc.creatorRestaino, Lawrenceen_US
dc.date.accessioned2013-04-18T09:39:05Z
dc.date.available2013-04-18T09:39:05Z
dc.date.issued1980en_US
dc.identifier.urihttp://hdl.handle.net/10150/282282
dc.description.abstractProcedures 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.
dc.language.isoen_USen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.subjectYersinia enterocolitica.en_US
dc.titleTHERMAL INJURY OF YERSINIA ENTEROCOLITICAen_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.identifier.oclc7534252en_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.leveldoctoralen_US
dc.identifier.proquest8017809en_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineMicrobiology and Medical Technologyen_US
thesis.degree.namePh.D.en_US
dc.description.noteThis item was digitized from a paper original and/or a microfilm copy. If you need higher-resolution images for any content in this item, please contact us at repository@u.library.arizona.edu.
dc.identifier.bibrecord.b13420434en_US
dc.description.admin-noteOriginal file replaced with corrected file July 2023.
refterms.dateFOA2018-08-19T09:20:37Z
html.description.abstractProcedures 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.


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