Development and validation of a surrogate strain cocktail to evaluate bactericidal effects of pressure on verotoxigenic Escherichia coli

Garcia-Hernandez, Rigoberto; McMullen, Lynn M.; Gänzle, Michael G.

doi:10.1016/j.ijfoodmicro.2015.03.028

Cited by 29 publications

(18 citation statements)

References 43 publications

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“…Heat resistance is not related to the phylogenetic group, the serotype, or the virotype of E. coli (Liu et al, 2015; Mercer et al, 2015). Highly heat resistant strains of E. coli exhibit D 60°C values exceeding 10 min (Dlusskaya et al, 2011; Garcia-Hernandez et al, 2015). Genetic determinants of the variability of heat resistance between strains are only partially understood.…”

Section: Variability Of Resistance Of Strains Of E Coli To Heatmentioning

confidence: 99%

“…A reduction in water activity from 0.995 to levels between 0.98 and 0.96 in salt or sucrose solutions significantly enhanced the heat resistance of E. coli (Kaur et al, 1998). The heat resistance of several strains of E. coli was also increased by addition of 2–6% of NaCl (Garcia-Hernandez et al, 2015). Addition of 2% NaCl resulted in the accumulation of amino acids including glycine betaine and proline as major cytoplasmic solutes; accumulation of carbohydrates including glucose and trehalose occurred in response to the addition of 6% NaCl (Pleitner et al, 2012).…”

Section: Effects Of Salt or Sugar Addition In High Moisture Foodsmentioning

confidence: 99%

“…Acquisition of the LHR increases survival after exposure to 60°C for 5 min by more than 7 log(cfu/mL); the LHR is thus one of the most powerful mediators of heat resistance in E. coli ( Table 1 ; Mercer et al, 2015). Loss of the LHR also reduces the pressure resistance in E. coli AW1.7 (Garcia-Hernandez et al, 2015; Liu et al, 2015; Mercer et al, 2015). Remarkably, the presence of a truncated LHR in wild type strains of E. coli , or cloning of fragments of the LHR had little effect on heat resistance, indicating that the 16 genes act in concert to provide heat resistance in LHR-positive strains (Mercer et al, 2015).…”

Section: Lhr and Extreme Resistance To Heatmentioning

confidence: 99%

“…Data shown are log 10 value of D 60 (min) of 144 strains collected from past publications: three values of K-12 strains (Chung et al, 2007; Jin et al, 2008; Dlusskaya et al, 2011), 125 of other strains of E. coli (Juneja and Marmer, 1999; Dlusskaya et al, 2011; Enache et al, 2011; Pleitner et al, 2012; Liu, 2015; Mercer et al, 2015), 2 D-values of strains after overexpression of heat shock proteins (HSP) (Hauben et al, 1997; Ruan et al, 2011), 7 D-values of strains after adaptation to salt or acid stress (Buchanan and Edelson, 1999; Pleitner et al, 2012; Garcia-Hernandez et al, 2015), 5 D-values of LHR positive strains (Pleitner et al, 2012; Mercer et al, 2015), and 2 D-values of strains treated by dry heat (Neetoo and Chen, 2011; Kim et al, 2015). …”

Section: Introductionmentioning

confidence: 99%

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Some Like It Hot: Heat Resistance of Escherichia coli in Food

Gänzle

2016

Front. Microbiol.

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Heat treatment and cooking are common interventions for reducing the numbers of vegetative cells and eliminating pathogenic microorganisms in food. Current cooking method requires the internal temperature of beef patties to reach 71°C. However, some pathogenic Escherichia coli such as the beef isolate E. coli AW 1.7 are extremely heat resistant, questioning its inactivation by current heat interventions in beef processing. To optimize the conditions of heat treatment for effective decontaminations of pathogenic E. coli strains, sufficient estimations, and explanations are necessary on mechanisms of heat resistance of target strains. The heat resistance of E. coli depends on the variability of strains and properties of food formulations including salt and water activity. Heat induces alterations of E. coli cells including membrane, cytoplasm, ribosome and DNA, particularly on proteins including protein misfolding and aggregations. Resistant systems of E. coli act against these alterations, mainly through gene regulations of heat response including EvgA, heat shock proteins, σE and σS, to re-fold of misfolded proteins, and achieve antagonism to heat stress. Heat resistance can also be increased by expression of key proteins of membrane and stabilization of membrane fluidity. In addition to the contributions of the outer membrane porin NmpC and overcome of osmotic stress from compatible solutes, the new identified genomic island locus of heat resistant performs a critical role to these highly heat resistant strains. This review aims to provide an overview of current knowledge on heat resistance of E. coli, to better understand its related mechanisms and explore more effective applications of heat interventions in food industry.

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Section: Variability Of Resistance Of Strains Of E Coli To Heatmentioning

confidence: 99%

Section: Effects Of Salt or Sugar Addition In High Moisture Foodsmentioning

confidence: 99%

Section: Lhr and Extreme Resistance To Heatmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Some Like It Hot: Heat Resistance of Escherichia coli in Food

Gänzle

2016

Front. Microbiol.

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“…While improved RpoH activity can logically increase heat resistance, upregulation of the heat-shock response was previously correlated with improved HHP resistance (17,20). Nevertheless, intrinsic heat and HHP resistance are not necessarily correlated with each other, as the most heat-resistant E. coli strains are not per se the most HHP resistant, and vice versa (13,29). Development of heat resistance through mutational upregulation of the activity of global regulators, such as RpoS and RpoH, seems to comply with the expected pleiotropic systemic impact of heat stress on the cell, although identification of the most important downstream effectors of these extensive stress regulons might help us to better delineate the exact nature of incurred cellular injury.…”

Section: Discussionmentioning

confidence: 99%

Stress-Induced Evolution of Heat Resistance and Resuscitation Speed in Escherichia coli O157:H7 ATCC 43888

Gayán

Cambré

Michiels

et al. 2016

Appl Environ Microbiol

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The development of resistance in foodborne pathogens to food preservation techniques is an issue of increasing concern, especially in minimally processed foods where safety relies on hurdle technology. In this context, mild heat can be used in combination with so-called nonthermal processes, such as high hydrostatic pressure (HHP), at lower individual intensities to better retain the quality of the food. However, mild stresses may increase the risk of (cross-)resistance development in the surviving population, which in turn might compromise food safety. In this investigation, we examined the evolution of Escherichia coli O157:H7 strain ATCC 43888 after recurrent exposure to progressively intensifying mild heat shocks (from 54.0°C to 60.0°C in 0.5°C increments) with intermittent resuscitation and growth of survivors. As such, mutant strains were obtained after 10 cycles of selection with ca. 10 6 -fold higher heat resistance than that for the parental strain at 58.0°C, although this resistance did not extend to temperatures exceeding 60.0°C. Moreover, these mutant strains typically displayed cross-resistance against HHP shock and displayed signs of enhanced RpoS and RpoH activity. Interestingly, additional cycles of selection maintaining the intensity of the heat shock constant (58.5°C) selected for mutant strains in which resuscitation speed, rather than resistance, appeared to be increased. Therefore, it seems that resistance and resuscitation speed are rapidly evolvable traits in E. coli ATCC 43888 that can compromise food safety. IMPORTANCEIn this investigation, we demonstrated that Escherichia coli O157:H7 ATCC 43888 rapidly acquires resistance to mild heat exposure, with this resistance yielding cross-protection to high hydrostatic pressure treatment. In addition, mutants of E. coli ATCC 43888 in which resuscitation speed, rather than resistance, appeared to be improved were selected. As such, both resistance and resuscitation speed seem to be rapidly evolvable traits that can compromise the control of foodborne pathogens in minimal processing strategies, which rely on the efficacy of combined mild preservation stresses for food safety. Minimal processing of foods is based on the combination of mild preservation methods (or hurdles) for maximizing retention of the sensorial and nutritional properties of the food while maintaining the appropriate level of food safety and shelf life (1, 2). Methods such as mild heating, acidification, and the use of natural antimicrobial compounds, high hydrostatic pressure (HHP), pulsed electric fields, ultrasound, and irradiation are some of the techniques commonly used in hurdle approaches (2-4). While the efficacy of minimal processing relies on the additive, or even synergistic, lethal or growth-inhibitory effects of such mild hurdles, the mild intensity might nevertheless pose the risk of increasing resistance to the corresponding treatments. More specifically, rare mutant strains with an increased stress resistance that can spontaneously emerge in a population ...

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Quantitative Microbial Risk Assessment of Hemolytic Uremic Syndrome due to Beef Consumption: Impact of Interventions to Reduce the Presence of Shiga Toxin-Producing Escherichia coli

Brusa

Cap

Leotta

et al. 2023

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Development and validation of a surrogate strain cocktail to evaluate bactericidal effects of pressure on verotoxigenic Escherichia coli

Cited by 29 publications

References 43 publications

Some Like It Hot: Heat Resistance of Escherichia coli in Food

Some Like It Hot: Heat Resistance of Escherichia coli in Food

Stress-Induced Evolution of Heat Resistance and Resuscitation Speed in Escherichia coli O157:H7 ATCC 43888

Quantitative Microbial Risk Assessment of Hemolytic Uremic Syndrome due to Beef Consumption: Impact of Interventions to Reduce the Presence of Shiga Toxin-Producing Escherichia coli

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