Mechanisms of Thermal Injury in Nonsporulating Bacteria

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

doi:10.1016/s0065-2164(08)70583-5

Cited by 54 publications

(29 citation statements)

References 73 publications

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“…Reversible damages are particularly expected in the case of microorganisms exposed to moderate heating. Thus, the lag in cell destruction, as observed in the present study, could be attributed to the exis- Conversely, curves showing a survivor tail (that are concave upward in the last part of the curves) are also often observed, and are attributed to non-uniform distribution of heat resistance among the individual cells: more resistant ones need more time for destruction (Hansen and Riemann, 1963;Allwood and Russell, 1970). This frequent phenomenon was not observed in the course of the present study probably because too low initial counts (5 x 10 6 CFUlml) and sm ail inocula (100 Ill) were used.…”

Section: Discussionsupporting

confidence: 54%

“…Also, as pointed out by these authors, the heat damaged proteins in the cell can be brought back more or less to their original structure, provided the damage is not too severe, eg if only some of the SoS and hydrogen bonds have not been disrupted. Allwood and Russell (1970) observed that protein denaturation follows other changes within the cell which are responsible for death. According to these authors, the thermal destruction appears to be due to subtlè changes in intracellular labile molecules (enzymes or RNA) and organized systems (ce Il membrane, ribosomes) which are difficult to reverse.…”

Section: Discussionmentioning

confidence: 99%

“…It is weil known that the sensitivity of microorganisms to heat is influenced by many factors such as the nature and concentration of ingredients in the culture medium, the pH of the medium, the physiological state and age of the cells, and their temperature of growth (Hansen and Riemann, 1963;Allwood and Russell, 1970). Thus, it seems possible to find conditions enhancing the effect of heat, so that moderate heat treatment of milk would destroy the undesirable bacterial flora without significantly impairing the biological properties of milk proteins.…”

Section: Introductionmentioning

confidence: 99%

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Combined effect of nisin and moderate heat on destruction of Listeria monocytogenes in milk

Maisnier‐Patin

Tatini

Richard

1995

Lait

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Summary -The kinetics of destruction of two strains of L monocytogenes in skim milk heated at60°C with and without addition of 25 or 50 lU/mi of nisin were studied. The survival curves displayed an initiallag phase followed by an accelerating killing phase. As both the length of the lag phase and the destruction rate depended on the temperature and the presence of nisin, a mathematical model was necessary to compare the survival curves and to determine the time to achieve a given reduction of the Listeria counts. Two models were compared, each allowing satisfactory goodness of fit. However, as they gave verY diverging D-values, the time to achieve a given reduction (3 and 6 10glO)of the numbers of Listeria in milk was calculated using one mode!. Addition of 25 or 50 lU/mi of nisin to milk heated between 54 and 65°C considerably reduced the heat resistance of one of the two strains of Listeria so that the time needed to achieve a 3 and 6 log10 reduction of populations of this bacterium was substantially diminished. For instance, 16 min at 54°C was sufficient to achieve a 103-fold reduction of the number of Listeria in milk containing 25 lU/mi nisin, compared to 77 min in absence of nisin. The cornbined effect of heat and nisin was somewhat enhanced if the bacteria were previously grown in milk at low temperatures. Factors that affect the heat resistance of Listeria are discussed as weil as the possible mode of action of nisin and heat on destruction of bacterial cells.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Combined effect of nisin and moderate heat on destruction of Listeria monocytogenes in milk

Maisnier‐Patin

Tatini

Richard

1995

Lait

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“…The mechanism of thermal inactivation of microorganisms has been widely investigated. Cellular sites of heat injury, such as membranes, nucleic acids, and certain enzymes, have been identified (4,15,26,29). Evaluation of heat inactivation by differential scanning calorimetry suggested that a strong relationship exists between thermal death of bacteria and the first major peak in differential scanning calorimetry thermograms, which is attributed to the unfolding of ribosomes (26).…”

Section: Discussionmentioning

confidence: 99%

Specific Growth Rate Determines the Sensitivity of Escherichia coli to Thermal, UVA, and Solar Disinfection

Berney

Weilenmann

Ihssen

et al. 2006

Appl Environ Microbiol

210

160

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Knowledge about the sensitivity of the test organism is essential for the evaluation of any disinfection method. In this work we show that sensitivity of Escherichia coli MG1655 to three physical stresses (mild heat, UVA light, and sunlight) that are relevant in the disinfection of drinking water with solar radiation is determined by the specific growth rate of the culture. Batch-and chemostat-cultivated cells from cultures with similar specific growth rates showed similar stress sensitivities. Generally, fast-growing cells were more sensitive to the stresses than slow-growing cells. For example, slow-growing chemostat-cultivated cells (D ‫؍‬ 0.08 h ؊1 ) and stationary-phase bacteria from batch culture that were exposed to mild heat had very similar T 90 (time until 90% of the population is inactivated) values (T 90, chemostat ‫؍‬ 2.66 h; T 90, batch ‫؍‬ 2.62 h), whereas T 90 for cells growing at a of 0.9 h ؊1 was 0.2 h. We present evidence that the stress sensitivity of E. coli is correlated with the intracellular level of the alternative sigma factor RpoS. This is also supported by the fact that E. coli rpoS mutant cells were more stress sensitive than the parent strain by factors of 4.9 (mild heat), 5.3 (UVA light), and 4.1 (sunlight). Furthermore, modeling of inactivation curves with GInaFiT revealed that the shape of inactivation curves changed depending on the specific growth rate. Inactivation curves of cells from fast-growing cultures ( ‫؍‬ 1.0 h ؊1 ) that were irradiated with UVA light showed a tailing effect, while for slow-growing cultures ( ‫؍‬ 0.3 h ؊1 ), inactivation curves with shoulders were obtained. Our findings emphasize the need for accurate reporting of specific growth rates and detailed culture conditions in disinfection studies to allow comparison of data from different studies and laboratories and sound interpretation of the data obtained.

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“…2007). One theory to explain the curve shape after applying moderate heat treatment suggests that the survival pattern reflects the inherent phenotypic variation in heat susceptibility of the individual vegetative cells in the population (Allwood and Russell 1970).…”

Section: Discussionmentioning

confidence: 99%

Temperature-assisted high hydrostatic pressure inactivation of Staphylococcus aureus in a ham model system: evaluation in selective and nonselective medium

et al. 2008

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Aims: The purpose of this study was to investigate the inactivation kinetics of Staphylococcus aureus in a ham model system by high hydrostatic pressure at ambient (25°C) and selected temperatures (45, 55°C). Selective [Baird Parker (BP) agar] and nonselective [brain heart infusion (BHI) agar] growth media were used for enumeration in order to count viable and sublethally injured cells. Methods and Results: The micro-organism was exposed to a range of pressures (450, 500, 550, 600 MPa) at ambient temperature (25°C) for up to 45 min. Additionally, the behaviour of the micro-organism was evaluated at mild temperatures in combination with high pressure treatment, namely: (i) 350, 400 and 450 MPa at 45°C; and (ii) 350 and 400 MPa at 55°C, for up to 12 min. Inactivation kinetics were calculated in terms of D p and z p values. Survival curves of S. aureus at ambient temperature were mostly linear, whereas when temperature was applied, tailing was observed in most survival curves. The estimated D p values and therefore the number of surviving cells, were substantially higher on the selective BP agar in the whole range of pressures applied, indicating that S. aureus showed greater recovery in the selective BP agar than the nonselective BHI agar. Samples pressurized at ambient temperature needed higher pressures (over 500 MPa) to achieve a reduction of the population of the pathogen more than 5 log CFU ml )1 . The same level of inactivation was achieved at lower pressure levels when mild heating was simultaneously applied. Indeed, more than 6 log CFU ml )1 reductions were obtained at 400 MPa and 55°C within the first 7 min of the process in BHI medium. Conclusion: Elevated temperatures allowed lower pressure levels and shorter processing times of pathogen inactivation than at room temperature. Greater recovery of the pathogen was observed in the selective (BP agar) medium, regardless of pressure and temperature applied. Significance and Impact of the Study: The obtained kinetics could be employed by the industry in selecting optimum pressure ⁄ temperature processing conditions. Attention must be given to the selection of the enumeration medium, as the use of an inappropriate medium would lead to underestimation of the surviving cells, thus imposing a risk in the microbiological safety of the product.

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Mechanisms of Thermal Injury in Nonsporulating Bacteria

Cited by 54 publications

References 73 publications

Combined effect of nisin and moderate heat on destruction of Listeria monocytogenes in milk

Combined effect of nisin and moderate heat on destruction of Listeria monocytogenes in milk

Specific Growth Rate Determines the Sensitivity of Escherichia coli to Thermal, UVA, and Solar Disinfection

Temperature-assisted high hydrostatic pressure inactivation of Staphylococcus aureus in a ham model system: evaluation in selective and nonselective medium

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