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Applied and Environmental Microbiology, January 2006, p. 908-913, Vol. 72, No. 1
0099-2240/06/$08.00+0     doi:10.1128/AEM.72.1.908-913.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Heat Resistance and Mechanism of Heat Inactivation in Thermophilic Campylobacters

Hong T. T. Nguyen, Janet E. L. Corry, and Christopher A. Miles*

Department of Clinical Veterinary Science, University of Bristol, Langford, Bristol BS40 5DU, United Kingdom

Received 21 July 2005/ Accepted 19 September 2005

The heat resistance of Campylobacter jejuni strains AR6 and L51 and the heat resistance of Campylobacter coli strains DR4 and L6 were measured over the temperature range from 50 to 60°C by two methods. Isothermal measurements yielded D55 values in the range from 4.6 to 6.6 min and z values in the range from 5.5 to 6.3°C. Dynamic measurements using differential scanning calorimetry (DSC) during heating at a rate of 10°C/min yielded D55 values of 2.5 min and 3.4 min and z values of 6.3°C and 6.5°C for AR6 and DR4, respectively. Both dynamic and isothermal methods yielded mean D55 values that were substantially greater than those reported previously (0.75 to 0.95 min). DSC analysis of each strain during heating at a rate of 10°C/min yielded a complex series of overlapping endothermic peaks, which were assigned to cell wall lipids, ribosomes, and DNA. Measurement of the decline in the numbers of CFU in calorimetric samples as they were heated showed that the maximum rate of cell death occurred at 56 to 57°C, which is close to the value predicted mathematically from the isothermal measurements of D and z (61°C). Both estimates were very close to the peak m1 values, 60 to 62°C, which were tentatively identified with unfolding of the 30S ribosome subunit, showing that cell death in C. jejuni and C. coli coincided with unfolding of the most thermally labile regions of the ribosome. Other measurements indicated that several essential proteins, including the {alpha} and ß subunits of RNA polymerase, might also unfold at the same time and contribute to cell death.

* Corresponding author. Mailing address: Department of Clinical Veterinary Science, University of Bristol, Langford, Bristol BS40 5DU, United Kingdom. Phone: (44) 117 928 9409. Fax: (44) 117 928 9324. E-mail: chris.miles{at}bristol.ac.uk

Applied and Environmental Microbiology, January 2006, p. 908-913, Vol. 72, No. 1
0099-2240/06/$08.00+0     doi:10.1128/AEM.72.1.908-913.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Miles, C. A. (2006). Relating Cell Killing to Inactivation of Critical Components. Appl. Environ. Microbiol. 72: 914-917 [Abstract] [Full Text]  


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