Thermal inactivation of Listeria monocytogenes within bovine milk phagocytes

Bunning, V K; Donnelly, Catherine W.; Peeler, James T.; Briggs, Elizabeth H.; Bradshaw, J. G.; Crawford, R. G.; Beliveau, Constance M.; Tierney, John T.

doi:10.1128/aem.54.2.364-370.1988

Cited by 77 publications

(39 citation statements)

References 20 publications

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“…Incubation of plates of non-selective media at 25°C for 7 d rather than at 37°C for 48 h improved recoveries of heat-injured cells by up to 10-fold (Bunning et al 1988). A similar improvement was observed when plates were incubated at 30°C for 24 h; held at 5°C for 21 d then re-incubated at 30°C (Beuchat et al 1986).…”

Section: Recovery Of Heat-injured Cellsmentioning

confidence: 61%

“…Following an outbreak of listeriosis associated with the consumption of pasteurized milk, it was suggested that L. monocytogenes might survive pasteurization if located within bovine lymphocytes (Fleming et al 1985). This has been tested directly in two further studies but no evidence of thermal protection was obtained (Bunning et al 1986(Bunning et al , 1988.…”

Section: Milkmentioning

confidence: 99%

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The heat resistance of Listeria monocytogenes

Mackey¹,

Bratchell²

1989

Lett Appl Microbiol

129

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Received 23 M a y 1989 and accepted 31 M a y 1989Heat resistance data for Listeria monocytogenes are reviewed. The organism is appreciably more resistant than common Salmonella serotypes but less resistant than Salmonella senftenbmg 775W. Reports that the organism can survive heating at 80°C have not been substantiated and are incompatible with carefully determined D and z values in milk and a range of foods. Cooking food to an internal temperature of 70°C for 2 min is adequate to ensure destruction of L. monocytogenes. Normal pasteurization procedures will inactivate L. monocytogenes in milk but the margin of safety is greater for vat pasteurization than for high temperature short time treatment.Heat treatment is a critical point for controlling Listeria monocytogenes in many manufactured and prepared foods. Reliable data on heat resistance are therefore essential in defining safe heat treatments, especially as refrigeration cannot be relied upon to prevent growth in the event of underprocessing. An early report of exceptional heat resistance (Beams & Girard 1958) has not been confirmed (Donelly et al. 1987) but the organism does appear to be more heat-resistant than many other non-sporing food-borne pathogens. To assist those involved in the heat processing of food we have summarized published information on heat resistance of L. monocytogenes, though recognizing that data are absent or rudimentary for many products and are actively being sought in many laboratories.General collsideratiollsHeat resistance data for L. monocytogenes taken from papers listed in the References are summarized diagrammatically in Fig. 1 75Temperature ("C) Fig. 1. Heat resistance data for Listmia monocytogenes compiled from papers reviewed in the text and from Bradshaw et a/. (1985, 1987).

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Section: Recovery Of Heat-injured Cellsmentioning

confidence: 61%

Section: Milkmentioning

confidence: 99%

The heat resistance of Listeria monocytogenes

Mackey¹,

Bratchell²

1989

Lett Appl Microbiol

129

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“…As in our previous reports (1)(2)(3)(4), estimates of heat resistance are expressed as D values, thereby assuming that the log1o reduction in bacterial count is linear with respect to time at a constant temperature (first-order kinetics). This estimate of heat resistance was used even when deviations from linearity, e.g., initial short lag (12,17), were observed, because estimates of D are routinely used in designs of processing plants for milk and other foods.…”

Section: Notesmentioning

confidence: 99%

“…For practical milk safety, the potential to induce increased thermotolerance during the lengthy lag or come-up times to temperature for vat or low-temperature long-time pasteurization should not affect the large safety factor (31-D process) determined for L. monocytogenes under worst-case conditions (3,16). However, the low safety factor (4.1-D process) for high-temperature short-time pasteurization, adequate on the basis of certain risk analysis factors (3-5, 9, 11, 19, 27), may be slightly more compromised.…”

Section: Notesmentioning

confidence: 99%

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Thermotolerance of Listeria monocytogenes and Salmonella typhimurium after sublethal heat shock

Bunning

Crawford

Tierney

et al. 1990

Appl Environ Microbiol

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119

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The effect of prior heat shock on thermotolerance of Listeria monocytogenes and Salmonella typhimurium in broth culture was determined. Bacteria were grown at the permissive temperature of 35°C, sublethally heated at 35 (control), 42, 48, and 52°C (nonpermissive control) for various times, and inactivated at either 57.8 or 52°C. The induction of increased thermotolerance by heat shock, although consistent within each experiment, was generally not significant for L. monocytogenes; the increase was significant for S. typhimurium. Temperature shift experiments with L. monocytogenes suggested that induced thermotolerance was not long lived unless the shock temperature was maintained. Exposure to temperatures above the range for normal cell growth (the normal of Arrhenius range) (13) leads to progressive loss of bacterial viability. When bacteria are shifted for a short period from lower to higher temperatures within or slightly above their normal growth range, a degree of protection against the lethal effects of a subsequent shift to a higher temperature or an acquired thermotolerance is achieved (17,20,26).Several investigators (20, 29) concluded that acquired thermotolerance develops during the brief incubation period at elevated but nonlethal temperature as a result of heat shock response, i.e., induction of a specific set of proteins known as heat shock proteins that mediate recovery to stress-induced damage (16,20,26). A direct cause-and-effect relationship between heat shock protein synthesis and acquired thermotolerance, however, is controversial (23, 26).The effect of heat shock response on food safety may be important because certain foods are thermally processed to ensure safety (11). Mackey and Derrick (17, 18) pioneered such studies with Salmonella spp. in broth, liquid whole egg, and reconstituted dried milk and concluded that marginal heat treatments may not be adequate in certain instances. Recent foodborne outbreaks of listeriosis were epidemiologically linked to the consumption of dairy products and meats; hence, the thermal processing parameters of these foods are being reexamined (5,8). This study was undertaken to determine the degree of acquired thermotolerance conferred on Listeria monocytogenes and Salmonella typhimurium by heat shock response and the kinetics and duration of its induction.(Results of this study were presented at the 12th Food Microbiology Research Conference, Chicago, Ill., 8 to 12 November 1989.) L. monocytogenes F5069 was obtained from Robert Weaver, Centers for Disease Control, Atlanta, Ga. This strain belongs to serotype 4b and was isolated from raw bovine milk (3, 4). S. typhimurium 42ScBs was obtained from J. G. Bradshaw, Food and Drug Administration, Cincinnati, Ohio. The strain was isolated from 2% lowfat milk, epidemiologically linked to the 1983 Chicago milk outbreak, and carries the outbreak strain plasmid profile (22).

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Listeria

Czuprynski¹

2004

Pathogenesis of Bacterial Infections in Animals

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Thermal inactivation of Listeria monocytogenes within bovine milk phagocytes

Abstract: Thermal resistance of intracellular and freely suspended Listeria monocytogenes that was associated with a milkborne outbreak of listeriosis was studied by using the sealed tube and slug flow heat exchanger methods. Test temperatures for the former method were 57.

Cited by 77 publications

References 20 publications

The heat resistance of Listeria monocytogenes

The heat resistance of Listeria monocytogenes

Thermotolerance of Listeria monocytogenes and Salmonella typhimurium after sublethal heat shock

Listeria

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