The heat resistance of Listeria monocytogenes

Mackey, B.M.; Bratchell, N.

doi:10.1111/j.1472-765x.1989.tb00298.x

Cited by 129 publications

(60 citation statements)

References 20 publications

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“…For example, D 60 values were reported as 1.46 to 16.7 min and Z values as 4.6 to 8.4 for meat, chicken, and fish (12). Similarly, Z values were reported as 4.3 to 9.9 in various foods (33). In the present study, the heating coil apparatus yielded results that were in the general range of those reported in the above-mentioned studies and that were very reproducible from run to run.…”

Section: Discussionsupporting

confidence: 71%

“…L. monocytogenes is frequently isolated from food because of its widespread occurrence in the environment and its ability to grow at refrigerated temperatures (39). Furthermore, it possesses constitutive resistance to heat inactivation that is at least as great as those of most vegetative food-borne pathogens, such as the common Salmonella enterica serotypes (12,21,33). Like many bacteria, L. monocytogenes may respond to several sublethal stress factors by increasing its heat tolerance.…”

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confidence: 99%

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Cold Shock Induction of Thermal Sensitivity in Listeria monocytogenes

Miller

Bayles

Eblen

2000

Appl Environ Microbiol

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Cold shock at 0 to 15°C for 1 to 3 h increased the thermal sensitivity of Listeria monocytogenes. In a model broth system, thermal death time at 60°C was reduced by up to 45% after L. monocytogenes Scott A was cold shocked for 3 h. The duration of the cold shock affected thermal tolerance more than did the magnitude of the temperature downshift. The Z values were 8.8°C for controls and 7.7°C for cold-shocked cells. The D values of cold-shocked cells did not return to control levels after incubation for 3 h at 28°C followed by heating at 60°C. Nine L. monocytogenes strains that were cold shocked for 3 h exhibited D 60 values that were reduced by 13 to 37%. The D-value reduction was greatest in cold-shocked stationary-phase cells compared to cells from cultures in either the lag or exponential phases of growth. In addition, cold-shocked cells were more likely to be inactivated by a given heat treatment than nonshocked cells, which were more likely to experience sublethal injury. The D values of chloramphenicol-treated control cells and chloramphenicol-treated cold-shocked cells were no different from those of untreated cold-shocked cells, suggesting that cold shock suppresses synthesis of proteins responsible for heat protection. In related experiments, the D values of L. monocytogenes Scott A were decreased 25% on frankfurter skins and 15% in ultra-high temperature milk if the inoculated products were first cold shocked. Induction of increased thermal sensitivity in L. monocytogenes by thermal flux shows potential to become a practical and efficacious preventative control method.

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Section: Discussionsupporting

confidence: 71%

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confidence: 99%

Cold Shock Induction of Thermal Sensitivity in Listeria monocytogenes

Miller

Bayles

Eblen

2000

Appl Environ Microbiol

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“…Sub-lethal injury has been studied in many bacteria, for example similar observations of the effect of heat treatment have been made with L. monocytogenes (e.g. Mackey and Bratchell 1989;. These reports cast doubt on the validity of the mechanism that underlies the use of first-order reaction kinetics (and D-values) to describe thermal inactivation of E. coli 0157:H7.…”

Section: Discussion Of the Most Appropriate Function To Describe The mentioning

confidence: 96%

“…Although measured heat resistance can vary considerably with test conditions, none of the published data suggests that E. coli 0157:H7 is unusually heat-resistant as compared with other nonspore-forming foodborne pathogens such as Listeria monocytogenes (Mackey and Bratchell 1989;. In the UK, the ACMSF report on VTEC recommends that minced beef and minced beef products, including beefburgers, should be heated to an internal temperature of 70°C for 2 min or its equivalent (Table 2).…”

Section: Review Of Published Datamentioning

confidence: 99%

Thermal inactivation ofEscherichia coliO157:H7

Stringer

George

Peck

2000

Journal of Applied Microbiology

104

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SUMMARY Verotoxin‐producing Escherichia coli O157:H7 is a cause of serious foodborne illness. It has a very small infectious dose and so it is vital to eliminate this pathogen from food. As heat treatment is the method of bacterial destruction most frequently used in food processing, accurate prediction of thermal death rates is necessary to achieve desired safety margins whilst minimizing processing. In most studies thermal inactivation has been described using first‐order reaction kinetics and D‐values. Whilst this approach does not seem justified on a theoretical basis, and may increase inaccuracy, there is no doubt that it is convenient and in many cases provides an adequate description of thermal death. A review of published data on the measured thermal inactivation of E. coli O157:H7 shows no strong evidence that a heat treatment of 70°C for 2 min (or equivalent) fails to deliver a 6‐decimal reduction in cell numbers.

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“…1b. It was reported by many early scientists that LTLT (Mackey and Bratchell, 1989) and HTST (Bunning et al 1992) treatments are adequate to destroy Listeria in milk. Numerous conflicting reports concerning the unusual heat resistance of L. monocytogenes in milk can be found in the early literature.…”

Section: Evaluation Of the Most Effective Pasteurization Temperature-mentioning

confidence: 99%