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. 1966 Jan;91(1):134–142. doi: 10.1128/jb.91.1.134-142.1966

Repair of Thermal Injury of Staphylococcus aureus1

John J Iandolo a,2, Z John Ordal a
PMCID: PMC315922  PMID: 5903089

Abstract

Iandolo, John J. (University of Illinois, Urbana), and Z. John Ordal. Repair of thermal injury of Staphylococcus aureus. J. Bacteriol. 91:134–142. 1966.—Exposure of Staphylococcus aureus MF 31 to sublethal temperatures produced a temporary change in the salt tolerance and growth of the organism. After sublethal heat treatment at 55 C for 15 min, more than 99% of the viable population was unable to reproduce on media containing 7.5% NaCl. The data presented demonstrate that thermal injury, in part, occurred owing to changes in the cell membrane, which allowed soluble cellular components to leak into the heating menstruum. When the cells were placed in a limiting medium, complete recovery did not occur, regardless of the incubation time. The temperature and the pH which produced the optimal rate of recovery were similar to those described previously for the multiplication of uninjured cells. However, the rate of recovery as well as the unchanging total count during recovery indicated that cell multiplication was not a factor during the recovery process. The nutrient requirements for the complete recovery of injured cells consisted of a solution containing an energy source, such as glucose, a mixture of amino acids, and phosphate. The use of the metabolic inhibitors, penicillin, cycloserine, 2,4-dinitrophenol, and chloramphenicol, did not inhibit recovery. Actinomycin D, however, completely suppressed recovery. This result implied that ribonucleic acid synthesis was particularly involved; this inference was substantiated by radio tracer experiments. The rate at which label was incorporated in the nucleic acid fraction paralleled that of recovery and the return of salt tolerance.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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