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Temperature shock, injury and transient sensitivity to nisin in Gram negatives

Aims: The effect of thermal stresses on survival, injury and nisin sensitivity was investigated in Salmonella Enteritidis PT4, PT7 and Pseudomonas aeruginosa. Methods and Results: Heating at 55 degrees C, rapid chilling to 0.5 degrees C or freezing at -20 degrees C produced transient sensitivity to...

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Published in:Journal of applied microbiology 2001-10, Vol.91 (4), p.715-724
Main Authors: Boziaris, I.S, Adams, M.R
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Language:English
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Adams, M.R
description Aims: The effect of thermal stresses on survival, injury and nisin sensitivity was investigated in Salmonella Enteritidis PT4, PT7 and Pseudomonas aeruginosa. Methods and Results: Heating at 55 degrees C, rapid chilling to 0.5 degrees C or freezing at -20 degrees C produced transient sensitivity to nisin. Cells were only sensitive if nisin was present during stress. Resistance recovered rapidly afterwards, though some cells displayed residual injury. Injury was assessed by SDS sensitivity, hydrophobicity changes, lipopolysaccharide release and NPN uptake. LPS release and hydrophobicity were not always associated with transient nisin sensitivity. Uptake of NPN correlated better but persisted longer after treatment. Conclusions: Thermal shocks produce transient injury to the outer membrane, allowing nisin access. After treatment, the permeability barrier is rapidly restored by a process apparently involving reorganization rather than biosynthetic repair. Significance and Impact of the Study: Inclusion of nisin during food treatments that impose sub-lethal stress on Gram negatives could increase process lethality, enhancing microbiological safety and stability.
doi_str_mv 10.1046/j.1365-2672.2001.01433.x
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Methods and Results: Heating at 55 degrees C, rapid chilling to 0.5 degrees C or freezing at -20 degrees C produced transient sensitivity to nisin. Cells were only sensitive if nisin was present during stress. Resistance recovered rapidly afterwards, though some cells displayed residual injury. Injury was assessed by SDS sensitivity, hydrophobicity changes, lipopolysaccharide release and NPN uptake. LPS release and hydrophobicity were not always associated with transient nisin sensitivity. Uptake of NPN correlated better but persisted longer after treatment. Conclusions: Thermal shocks produce transient injury to the outer membrane, allowing nisin access. After treatment, the permeability barrier is rapidly restored by a process apparently involving reorganization rather than biosynthetic repair. Significance and Impact of the Study: Inclusion of nisin during food treatments that impose sub-lethal stress on Gram negatives could increase process lethality, enhancing microbiological safety and stability.</description><identifier>ISSN: 1364-5072</identifier><identifier>EISSN: 1365-2672</identifier><identifier>DOI: 10.1046/j.1365-2672.2001.01433.x</identifier><identifier>PMID: 11576309</identifier><identifier>CODEN: JAMIFK</identifier><language>eng</language><publisher>Oxford UK: Blackwell Science Ltd</publisher><subject>Anti-Bacterial Agents - pharmacology ; Biological and medical sciences ; Cold Temperature ; cold treatment ; Food industries ; Food microbiology ; Freezing ; Fundamental and applied biological sciences. Psychology ; heat ; Heat-Shock Response ; Hot Temperature ; hydrophobicity ; lipopolysaccharides ; microbiological quality ; nisin ; Nisin - pharmacology ; permeability ; Pseudomonas aeruginosa ; Pseudomonas aeruginosa - drug effects ; Pseudomonas aeruginosa - growth &amp; development ; Pseudomonas aeruginosa - physiology ; Salmonella Enteritidis ; Salmonella enteritidis - drug effects ; Salmonella enteritidis - growth &amp; development ; Salmonella enteritidis - physiology ; Staphylococcus aureus ; Surface Properties ; temperature</subject><ispartof>Journal of applied microbiology, 2001-10, Vol.91 (4), p.715-724</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright Blackwell Science Ltd. 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Methods and Results: Heating at 55 degrees C, rapid chilling to 0.5 degrees C or freezing at -20 degrees C produced transient sensitivity to nisin. Cells were only sensitive if nisin was present during stress. Resistance recovered rapidly afterwards, though some cells displayed residual injury. Injury was assessed by SDS sensitivity, hydrophobicity changes, lipopolysaccharide release and NPN uptake. LPS release and hydrophobicity were not always associated with transient nisin sensitivity. Uptake of NPN correlated better but persisted longer after treatment. Conclusions: Thermal shocks produce transient injury to the outer membrane, allowing nisin access. After treatment, the permeability barrier is rapidly restored by a process apparently involving reorganization rather than biosynthetic repair. 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subjects Anti-Bacterial Agents - pharmacology
Biological and medical sciences
Cold Temperature
cold treatment
Food industries
Food microbiology
Freezing
Fundamental and applied biological sciences. Psychology
heat
Heat-Shock Response
Hot Temperature
hydrophobicity
lipopolysaccharides
microbiological quality
nisin
Nisin - pharmacology
permeability
Pseudomonas aeruginosa
Pseudomonas aeruginosa - drug effects
Pseudomonas aeruginosa - growth & development
Pseudomonas aeruginosa - physiology
Salmonella Enteritidis
Salmonella enteritidis - drug effects
Salmonella enteritidis - growth & development
Salmonella enteritidis - physiology
Staphylococcus aureus
Surface Properties
temperature
title Temperature shock, injury and transient sensitivity to nisin in Gram negatives
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