Growth and Metabolic Activities of Heat Treated <i>Staphylococcus aureus</i>

Allwood, M. C.; Russell, A. D.

doi:10.1111/j.1365-2672.1969.tb02191.x

Cited by 14 publications

(5 citation statements)

References 13 publications

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“…The stock solution was sterilized by filtration through a 0.45-rm membrane. Stock solutions were stored no longer than 1 week at 4°C. Volumes of BS stock solution and predetermined volumes of TSA were mixed aseptically APPL.…”

Section: Methodsmentioning

confidence: 99%

Thermal injury of Yersinia enterocolitica

Restaino¹,

Jeter²,

Hill³

1980

Appl Environ Microbiol

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Procedures were developed to evaluate thermal injury to three strains of Yersinia enterocolitica (serotypes 0:3, 0:8, and 0:17). Serotype 0:17 (atypical strain) was more sensitive to bile salts no. 3 (BS) 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 P04 buffer, pH 7.0, at 470C for 70, 60, and 12 mi, 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 for serotypes 0:3 and 0:8 and TSA plus 0.16% BS for 0:17. Heat injury of serotype 0: 17 cells for 15 min in 0.1 M P04 buffer caused an approximate 1,000-fold reduction in cell numbers on selective media as compared with cells heated in pork infusion (PI), BHI broth, and 10% nonfat dry milk (NFDM). The extended lag and resuscitation period in BHI broth was 2.5 times greater for 0:17 cells injured in 0.1 M P04 than for cells injured in BHI or PI. 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 synthesis was required for repair, whereas deoxyribonucleic, cell wall, and protein synthesis were not necessary for recovery of 0:17 cells injured in 0.1 M P04 buffer, BHI, or PI. Inhibition of respiration by 2,4-dinitrophenol slowed repair only for 0:17 cells injured in 0.1 M P04 buffer, not for cells injured in PI or BHI. Yersinia enterocolitica and Y. enterocoliticalike organisms (atypical strains) have been isolated from a wide variety of foods as well as from environmental sources. In an extensive European survey, Leistner et al. (43) identified Y. enterocolitica in chicken meat, pork, and beef. Strains have been isolated from vacuum-packaged beef, lamb, and dark firm meat (pH 2 6.5) held under refrigeration (20, 26, 54), raw and pasteurized milk (32, 52), cheeses (51), mussels, ice cream, bananas, fish, ham, and sausage (41). They have also been isolated from pond and well water (11), streams, lakes (28), and drinking water (39). Only one foodborne outbreak caused by Y. enterocolitica has been documented (14), although food sources were implicated in other outbreaks (15, 29, 59). In 1976, an illness occurred among school children in Oneida County, New York (5). Chocolate milk was determined to be the common vector of transmission. Serotype 0:8 was isolated from an unopened carton of the milk and from the hospitalized children. Thirty-three children were hospitalized for suspected appendicitis, and 13 appendectomies were performed. Many treatments used in food processing and combinations of treatments may induce suble-thal damage to cells or spores (12). In addition, the production of bacterial end products such as organic acids in foods may cause sensitive bacterial cells to become stressed or injured. Therefore, unprocessed as well as pr...

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Section: Methodsmentioning

confidence: 99%

Thermal injury of Yersinia enterocolitica

Restaino¹,

Jeter²,

Hill³

1980

Appl Environ Microbiol

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“…In thermally stressed cells, alteration of permeability and degradation of RNA, especially of ribosomal RNA, have been reported (1,11,27). During repair, the heat-stressed cells restore their altered permeability and synthesize ribosomal RNA and protein (16,21).…”

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confidence: 99%

Repair of Injury in Freeze-Dried Salmonella anatum1

Ray

Jezeski

Busta

1971

Applied Microbiology

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Repair of injury induced by freeze-drying Salmonella anatum in nonfat milk solids occurred rapidly after rehydration. Injury in surviving cells was defined as the inability to form colonies on a plating medium containing deoxycholate. Death was defined as inability to form colonies in the same medium without this selective agent. The rate of repair of injury was reduced by lowering the temperature from 35 C to 10 C and was extremely low at 1 C. Repair was independent of influence of pH between 6.0 and 7.0. Repair did not require synthesis of protein, ribonucleic acid, or cell wall mucopeptide, but did require energy in the form of adenosine triphosphate (ATP) synthesized through oxidative phosphorylation. The requirement for ATP was based on dinitrophenol or cyanide interference with repair. Dinitrophenol activity was pH-dependent; no repair occurred at pH 6.0 and some repair was observed at pH 6.5 and above. Injured cells were extremely sensitive to low concentrations of ethylenedinitrilotetraacetate. This indicated that freezedrying injury of S. anatum may involve the lipopolysaccharide portion of the cell wall and that repair of this damage requires ATP synthesis.

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“…Harris (1963) referring to 'inimical environments' mentions natural waters, dessication, sunlight and antibiotic therapy as areas which could be categorized as more or less damaging. Heat and toxic chemicals are more overtly harmful, but whatever the treatment, to the extent that it constitutes damage, the subsequent treatment will involve a recovery period (Allwood & Russell 1969) which may be sensitive to temperature variations. Therefore, our results bear consideration when looking at tests involving toxic chemicals, and for similar tests carried out in different laboratories.…”

Section: Resultsmentioning

confidence: 99%