Synergy between Nisin and Select Lactates against Listeria monocytogenes Is Due to the Metal Cations

2003 ◽  
Vol 66 (9) ◽  
pp. 1631-1636 ◽  
Author(s):  
JENNIFER CLEVELAND McENTIRE ◽  
THOMAS J. MONTVILLE ◽  
MICHAEL L. CHIKINDAS
Keyword(s):  
Lactic Acid ◽  
Listeria Monocytogenes ◽  
Resistant Strain ◽  
Foodborne Pathogen ◽  
Metal Cations ◽  
Resistant Mutant ◽  
Wild Type ◽  
Atp Levels ◽  
Potassium Lactate ◽  
Lactic Acids

Listeria monocytogenes, a major foodborne pathogen, has been responsible for many outbreaks and recalls. Organic acids and antimicrobial peptides (bacteriocins) such as nisin are produced by lactic acid bacteria and are commercially used to control pathogens in some foods. This study examined the effects of lactic acid (LA) and its salts in combination with a commercial nisin preparation on the growth of L. monocytogenes Scott A and its nisin-resistant mutant. Because of an increase in its activity at a lower pH, nisin was more active against L. monocytogenes when used in combination with LA. Most of the salts of LA, including potassium lactate, at up to 5% partially inhibited the growth of L. monocytogenes and had no synergy with nisin. Zinc and aluminum lactate, as well as zinc and aluminum chloride (0.1%), worked synergistically with 100 IU of nisin per ml to control the growth of L. monocytogenes Scott A. No synergy was observed when zinc or aluminum lactate was used with nisin against nisin-resistant L. monocytogenes. The nisin-resistant strain was more sensitive to Zn lactate than was wild-type L. monocytogenes Scott A; however, the cellular ATP levels of the nisin-resistant strain were not significantly affected. Changes in the intracellular ATP levels of the wild-type strain support our hypothesis that pretreatment with zinc lactate sensitizes cells to nisin. The similar effects of the salts of hydrochloric and lactic acids support the hypothesis that metal cations are responsible for synergy with nisin.

Growth, Inhibition, and Survival of Listeria monocytogenes as Affected by Acidic Conditions

1990 ◽  
Vol 53 (8) ◽  
pp. 652-655 ◽  
Author(s):  
DONALD E. CONNER ◽  
VIRGINIA N. SCOTT ◽  
DANE T. BERNARD
Keyword(s):  
Lactic Acid ◽  
Listeria Monocytogenes ◽  
Growth Inhibition ◽  
Propionic Acid ◽  
Cell Populations ◽  
Growth And Survival ◽  
Viable Cells ◽  
Acidic Conditions ◽  
Ph Range ◽  
Lactic Acids

Growth and survival of four strains of Listeria monocytogenes under acidic conditions were investigated. Tryptic soy broth with yeast extract (TSBYE) was acidified with acetic, citric, hydrochloric, lactic, or propionic acid to pH 4.0–6.0, inoculated with L. monocytogenes and incubated at 30 or 4°C. The minimum test pH at which L. monocytogenes did not grow (inhibitory pH) was determined for each acid. In the pH range tested, this inhibitory pH was 5.0 for propionic acid, 4.5 for acetic and lactic acids, and 4.0 for citric and hydrochloric acids. All four strains gave similar results. Subsequent studies were conducted at 10 and 30°C to determine changes in cell populations in TSBYE adjusted to each inhibitory pH. Initial populations of viable cells (104 CFU/ml) were reduced to <10 CFU/ml within 1–3 weeks at 30°C, whereas at 10°C, L. monocytogenes survived for 11–12 weeks in acetic, citric, or propionic acid-adjusted media and for 6 weeks in media adjusted with hydrochloric or lactic acid. The concentration of undissociated lactic acid was 0.002 M at pH 4.5.

Effect of Age of Cook-in-Bag Delicatessen Meats Formulated with Lactate-Diacetate on the Behavior of Listeria monocytogenes Contamination Introduced When Opening the Packages during Storage

2013 ◽  
Vol 76 (7) ◽  
pp. 1274-1278 ◽  
Author(s):  
IFIGENIA GEORNARAS ◽  
DARREN TOCZKO ◽  
JOHN N. SOFOS
Keyword(s):  
Lactic Acid ◽  
Listeria Monocytogenes ◽  
Lactic Acid Bacteria ◽  
Meat Products ◽  
Potential Effect ◽  
Meat Industry ◽  
Storage Product ◽  
Potassium Lactate ◽  
Yeasts And Molds ◽  
Effect Of Age

This study evaluated the potential effect of age of cook-in-bag ham and turkey breast delicatessen meats formulated with lactate-diacetate on survival and/or growth of Listeria monocytogenes introduced after opening of packages and slicing of product. Commercially prepared cured ham and turkey breast products formulated with potassium lactate and sodium diacetate were stored at 1.7°C unsliced, in their original cook-in-bags, and without postlethality exposure. On days 5, 90, 120, and 180 of storage, product slices (10.2 by 7.6 cm) were surface inoculated (1 to 2 log CFU/cm2) with a 10-strain mixture of L. monocytogenes, vacuum packaged (seven slices per bag), and stored at 4°C for up to 13 weeks. Inoculated levels of L. monocytogenes on both products were 1.4 to 1.5 log CFU/cm2. Irrespective of product age at slicing and inoculation, after 13 weeks of vacuum-packaged storage (4°C), pathogen counts on product slices were 1.5 to 2.3 (ham) and 2.3 to 2.5 (turkey) log CFU/cm2. Overall, the results of the study showed that the age of the cook-in-bag products prior to slicing and inoculation with the pathogen did not (P ≥ 0.05) affect the behavior of L. monocytogenes during vacuum-packaged storage (4°C, up to 13 weeks) of ham and turkey slices. Mean counts of lactic acid bacteria and yeasts and molds, when detected, did not exceed approximately 1 and 2 log CFU/cm2, respectively, among all stored samples. Findings of the study will be useful to the meat industry and risk assessors in their efforts to control L. monocytogenes in ready-to-eat meat products.

Behavior of Listeria monocytogenes at 7, 13, 21, and 35°C in Tryptose Broth Acidified with Acetic, Citric, or Lactic Acid

1989 ◽  
Vol 52 (10) ◽  
pp. 688-695 ◽  
Author(s):  
NORMAH AHAMAD ◽  
ELMER H. MARTH
Keyword(s):  
Acetic Acid ◽  
Lactic Acid ◽  
Statistical Analysis ◽  
Listeria Monocytogenes ◽  
Dissociation Constants ◽  
Interactive Effects ◽  
Lactic Acids

Inhibition of Listeria monocytogenes CA and V7 by of acetic, citric, and lactic acids at 7, 13, 21, and 35°C was investigated. Statistical analysis showed interactive effects between temperature, types, and concentration of acids and strains of the pathogen. Presence of up to 0.1% of acetic, citric and lactic acids in the medium (tryptose broth) inhibited growth; the degree of inhibition increased as the temperature of incubation decreased (no growth occurred in the presence of 0.1% acetic acid at 7°C). L. monocytogenes was inactivated at all temperatures when acid concentrations in the medium were 0.3% or greater. Acetic acid was most detrimental to L. monocytogenes followed in order by lactic and citric acids. The antilisterial activity of these acids coincided with their degree of undissociation. Citric and lactic acids, with larger dissociation constants, were less detrimental to the pathogen than was acetic acid.

Alternative Sigma Factor σB Is Not Essential for Listeria monocytogenes Surface Attachment

2005 ◽  
Vol 68 (2) ◽  
pp. 311-317 ◽  
Author(s):  
UTE SCHWAB ◽  
YUEWEI HU ◽  
MARTIN WIEDMANN ◽  
KATHRYN J. BOOR
Keyword(s):  
Stainless Steel ◽  
Listeria Monocytogenes ◽  
Single Cells ◽  
Foodborne Pathogen ◽  
Plate Count ◽  
Initial Surface ◽  
Wild Type ◽  
Surface Attachment ◽  
Steel Analysis ◽  
Static Conditions

Listeria monocytogenes is a foodborne pathogen frequently isolated from the food processing environment. Multiple lines of evidence suggested a possible role for the L. monocytogenes alternative transcription factor sigma B (σB) in surface attachment and biofilm formation. Therefore, through plate count and microscopic techniques, the L. monocytogenes 10403S strain and an otherwise isogenic ΔsigB strain were tested for attachment to stainless steel. Analysis of microscopic images revealed that after 72 h at 24°C under static conditions the tested L. monocytogenes strains attached uniformly to surfaces as single cells. Both strains were capable of rapid attachment (i.e., numbers of attached cells were essentially the same after either 5 min or 24 h of incubation). Numbers of attached ΔsigB cells were significantly lower than those of the wild-type strain after 48 and 72 h of incubation at 24°C (P = 0.001). Similar numbers of the ΔsigB strain attached to stainless steel regardless of temperature (24 or 37°C); however, ΔsigB cells attached at higher relative numbers in the presence of 6% NaCl after 48 and 72 h. Furthermore, in the presence of Pseudomonas fluorescens, similarly high numbers of wild-type and ΔsigB cells attached to the surfaces, forming mixed biofilms. Our data suggest that σB is not required for initial surface attachment of L. monocytogenes.

Growth and Survival of Listeria monocytogenes in Vacuum-Packaged Ground Beef Inoculated with Lactobacillus alimentarius FloraCarn L-2

1998 ◽  
Vol 61 (5) ◽  
pp. 551-556 ◽  
Author(s):  
BENJAMIN J. JUVEN ◽  
SUSAN F. BAREFOOT ◽  
MERLE D. PIERSON ◽  
LINDA H. McCASKILL ◽  
BRIAN SMITH
Keyword(s):  
Hydrogen Peroxide ◽  
Lactic Acid ◽  
Listeria Monocytogenes ◽  
Ground Beef ◽  
Resistant Mutant ◽  
Antibiotic Resistant ◽  
Growth And Survival ◽  
Ca 50 ◽  
Psychrotrophic Strain

A culture of the psychrotrophic strain FloraCarn L-2 of Lactobacillus alimentarius was added to ground beef (pH 5.4) inoculated with two isolates of Listeria monocytogenes able to grow in refrigerated ground beef. The ground beef was vacuum-packaged and stored for 9 weeks at 4°C. Populations of inoculated L. monocytogenes initially were 6.3 to 6.4 log10 CFU/g and increased to 7.4 log10 CFU/g in ground beef with no added lactobacilli. Addition of L. alimentarius L-2 or its antibiotic-resistant mutant SRL-2 reduced the final populations of L. monocytogenes to 4.3 or 4.1 log10 CFU/g, respectively. L. alimentarius L-2 did not produce bacteriocins or hydrogen peroxide in vitro. The antilisterial effect of L. alimentarius observed in laboratory media and ground beef is attiibuted to lactic acid (ca. 50 mM) produced by growing cultures.

scholarly journals Increased ATPase Activity Is Responsible for Acid Sensitivity of Nisin-Resistant Listeria monocytogenes ATCC 700302

2004 ◽  
Vol 70 (5) ◽  
pp. 2717-2721 ◽  
Author(s):  
Jennifer Cleveland McEntire ◽  
George M. Carman ◽  
Thomas J. Montville
Keyword(s):  
Cell Death ◽  
Listeria Monocytogenes ◽  
Foodborne Pathogen ◽  
Spontaneous Mutant ◽  
Wild Type ◽  
Cell Cytoplasm ◽  
Acid Sensitivity ◽  
In The Wild ◽  
Increased Activity

ABSTRACT The growth of the foodborne pathogen Listeria monocytogenes can be controlled by nisin, an antimicrobial peptide. A spontaneous mutant of L. monocytogenes shows both resistance to nisin and increased acid sensitivity compared to the wild type. Changes in the cell membrane correlated with nisin resistance, but the mechanism for acid sensitivity appears unrelated. When hydrochloric or lactic acid is added to cultures, intracellular ATP levels drop significantly in the mutant (P < 0.01) compared to the results seen with the wild type. Characterization of the F0F1 ATPase, which hydrolyzes ATP to pump protons from the cell cytoplasm, shows that the enzyme is more active in the mutant than in the wild type. These data support a model in which the increased activity of the mutant ATPase upon acid addition depletes the cells' supply of ATP, resulting in cell death.

Viability of a Five-Strain Mixture of Listeria monocytogenes in Vacuum-Sealed Packages of Frankfurters, Commercially Prepared with and without 2.0 or 3.0% Added Potassium Lactate, during Extended Storage at 4 and 10° C†‡

2002 ◽  
Vol 65 (2) ◽  
pp. 308-315 ◽  
Author(s):  
ANNA C. S. PORTO ◽  
BERNADETTE D. G. M. FRANCO ◽  
ERNANI S. SANT'ANNA ◽  
JEFFREY E. CALL ◽  
ANDREA PIVA ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Listeria Monocytogenes ◽  
Lactic Acid Bacteria ◽  
Proximate Composition ◽  
Potassium Lactate ◽  
Polyethylene Bags

The viability of Listeria monocytogenes was monitored on frankfurters containing added potassium lactate that were obtained directly from a commercial manufacturer. Eight links (ca. 56 g each) were transferred aseptically from the original vacuum-sealed bulk packages into nylon-polyethylene bags. Each bag then received a 4-ml portion of a five-strain mixture of the pathogen. Frankfurters containing 2.0 or 3.0% potassium lactate were evaluated using 20 CFU per package, and frankfurters containing 3.0% potassium lactate were evaluated using 500 CFU per package. The packages were vacuum-sealed and stored at 4 or 10°C for up to 90 or 60 days, respectively. During storage at 4°C, pathogen numbers remained at about 1.6 log10 CFU per package over 90 days in packages containing frankfurters with 2.0% potassium lactate that were inoculated with about 20 CFU. In packages containing frankfurters with 3.0% potassium lactate that were inoculated with about 20 CFU and stored at 4°C, pathogen numbers remained at about 1.4 log10 CFU per package over 90 days. In packages containing frankfurters with 3.0% potassium lactate that were inoculated with about 500 CFU and stored at 4°C, pathogen numbers remained at about 2.4 log10 CFU per package over 90 days. However, in the absence of any added potassium lactate, pathogen numbers increased to 4.6 and 5.0 log10 CFU per package after 90 days of storage at 4°C for starting levels of 20 and 500 CFU per package, respectively. During storage at 10°C, pathogen numbers remained at about 1.4 log10 CFU per package over 60 days in packages containing frankfurters with 2.0% potassium lactate that were inoculated with about 20 CFU. In packages containing frankfurters with 3.0% potassium lactate that were inoculated with about 20 CFU and stored at 10°C, pathogen numbers remained at about 1.1 log10 CFU per package over 60 days of storage. In the absence of any added potassium lactate, pathogen numbers increased to 6.5 log10 CFU per package after 28 days and then declined to 5.0 log10 CFU per package after 60 days of storage at 10°C. In packages containing frankfurters with 3.0% potassium lactate that were inoculated with about 500 CFU per package, pathogen numbers remained at about 2.4 log10 CFU per package over 60 days of storage at 10°C, whereas in the absence of any added potassium lactate, pathogen numbers increased to about 6.6 log10 CFU per package within 40 days and then declined to about 5.5 log10 CFU per package after 60 days of storage. The viability of L. monocytogenes in frankfurter packages stored at 4 and 10°C was influenced by the pH and the presence or levels of lactate but not by the presence or levels of indigenous lactic acid bacteria or by the proximate composition of the product. These data establish that the addition of 2.0% (P &lt; 0.0004) or 3.0% (P &lt; 0.0001) potassium lactate as an ingredient in frankfurters can appreciably enhance safety by inhibiting or delaying the growth of L. monocytogenes during storage at refrigeration and abuse temperatures.

Radiation (Gamma) Resistance and Postirradiation Growth of Listeria monocytogenes Suspended in Beef Bologna Containing Sodium Diacetate and Potassium Lactate†

2003 ◽  
Vol 66 (11) ◽  
pp. 2051-2056 ◽  
Author(s):  
CHRISTOPHER SOMMERS ◽  
XUETONG FAN ◽  
BRENDAN A. NIEMIRA ◽  
KIMBERLY SOKORAI
Keyword(s):  
Listeria Monocytogenes ◽  
Radiation Dose ◽  
Ionizing Radiation ◽  
Foodborne Pathogen ◽  
Meat Products ◽  
Radiation Doses ◽  
Refrigerated Storage ◽  
Potassium Lactate ◽  
Sodium Diacetate

Listeria monocytogenes, a psychrotrophic foodborne pathogen, is a frequent postprocessing contaminant of ready-to-eat (RTE) meat products, including frankfurters and bologna. Ionizing radiation can eliminate L. monocytogenes from RTE meats. When they are incorporated into fine-emulsion sausages, sodium diacetate (SDA) and potassium lactate (PL) mixtures inhibit the growth of L. monocytogenes. The radiation resistance of L. monocytogenes, and its ability to proliferate during long-term refrigerated storage (9°C), when inoculated into beef bologna that contained 0% SDA–0% PL, 0.07% SDA–1% PL, and 0.15% SDA–2% PL, were determined. The radiation doses required to eliminate 90% of the viable L. monocytogenes cells were 0.56 kGy for bologna containing 0% SDA–0% PL, 0.53 kGy for bologna containing 0.07% SDA–1% PL, and 0.46 kGy for bologna containing 0.15% SDA–2% PL. L. monocytogenes was able to proliferate on bologna containing 0% SDA–0% PL during refrigerated storage, but the onset of proliferation was delayed by the addition of the SDA-PL mixtures. An ionizing radiation dose of 3.0 kGy prevented the proliferation of L. monocytogenes and background microflora in bologna containing 0.07% SDA–1% PL and in bologna containing 0.15% SDA–2% PL over 8 weeks of storage at 9°C. Little effect on lipid oxidation and color of the control bologna, or bologna containing SDA-PL mixtures, was observed upon irradiation at either 1.5 or 3.0 kGy.

Effectiveness of Acidic Calcium Sulfate with Propionic and Lactic Acid and Lactates as Postprocessing Dipping Solutions To Control Listeria monocytogenes on Frankfurters with or without Potassium Lactate and Stored Vacuum Packaged at 4.5°C

2004 ◽  
Vol 67 (5) ◽  
pp. 915-921 ◽  
Author(s):  
MARYURI T. NUÑEZ de GONZALEZ ◽  
JIMMY T. KEETON ◽  
GARY R. ACUFF ◽  
LARRY J. RINGER ◽  
LISA M. LUCIA
Keyword(s):  
Lactic Acid ◽  
Listeria Monocytogenes ◽  
Calcium Sulfate ◽  
Limit Of Detection ◽  
Meat Products ◽  
Bactericidal Effect ◽  
Antimicrobial Substances ◽  
Potassium Lactate ◽  
Residual Nitrite ◽  
Plate Counts

The safety of ready-to-eat meat products such as frankfurters can be enhanced by treating with approved antimicrobial substances to control the growth of Listeria monocytogenes. We evaluated the effectiveness of acidic calcium sulfate with propionic and lactic acid, potassium lactate, or lactic acid postprocessing dipping solutions to control L. monocytogenes inoculated (ca. 108 CFU/ml) onto the surface of frankfurters with or without potassium lactate and stored in vacuum packages at 4.5° C for up to 12 weeks. Two frankfurter formulations were manufactured without (control) or with potassium lactate (KL, 3.3% of a 60% [wt/wt] commercially available syrup). After cooking, chilling, and peeling, each batch was divided into inoculated (four strains of L. monocytogenes mixture) and noninoculated groups. Each group was treated with four different dips: (i) control (saline solution), (ii) acidic calcium sulfate with propionic and lactic acid (ACS, 1:2 water), (iii) KL, or (iv) lactic acid (LA, 3.4% of a 88% [wt/wt] commercially available syrup) for 30 s. Noninoculated frankfurters were periodically analyzed for pH, water activity, residual nitrite, and aerobic plate counts (APCs), and L. monocytogenes counts (modified Oxford medium) were determined on inoculated samples. Surface APC counts remained at or near the lower limit of detection (&lt;2 log CFU per frank) on franks with or without KL and treated with ACS or LA throughout 12 weeks at 4.5° C. L. monocytogenes counts remained at the minimum level of detection on all franks treated with the ACS dip, which indicated a residual bactericidal effect when L. monocytogenes populations were monitored over 12 weeks. L. monocytogenes numbers were also reduced, but not to the same degree in franks made without or with KL and treated with LA. These results revealed the effectiveness of ACS (bactericidal effect) or LA (bacteriostatic effect) as postprocessing dipping solutions to inhibit or control the growth of L. monocytogenes on vacuum-packaged frankfurters stored at 4.5° C for up to 12 weeks.

scholarly journals Increased Listeria monocytogenes Dissemination and Altered Population Dynamics in Muc2-Deficient Mice

2021 ◽  
Vol 89 (4) ◽  
Author(s):  
Ting Zhang ◽  
Jumpei Sasabe ◽  
Karthik Hullahalli ◽  
Brandon Sit ◽  
Matthew K. Waldor
Keyword(s):  
Population Dynamics ◽  
Listeria Monocytogenes ◽  
Systemic Disease ◽  
Foodborne Pathogen ◽  
Major Constituent ◽  
Infection Model ◽  
Wild Type ◽  
Content Type ◽  
Oral Infections ◽  
Founding Population

ABSTRACT The mucin Muc2 is a major constituent of the mucus layer that covers the intestinal epithelium and creates a barrier between epithelial cells and luminal commensal or pathogenic microorganisms. The Gram-positive foodborne pathogen Listeria monocytogenes can cause enteritis and also disseminate from the intestine to give rise to systemic disease. L. monocytogenes can bind to intestinal Muc2, but the influence of the Muc2 mucin barrier on L. monocytogenes intestinal colonization and systemic dissemination has not been explored. Here, we used an orogastric L. monocytogenes infection model to investigate the role of Muc2 in host defense against L. monocytogenes. Compared to wild-type mice, we found that Muc2−/− mice exhibited heightened susceptibility to orogastric challenge with L. monocytogenes, with higher mortality, elevated colonic pathology, and increased pathogen burdens in both the intestinal tract and distal organs. In contrast, L. monocytogenes burdens were equivalent in wild-type and Muc2−/− animals when the pathogen was administered intraperitoneally, suggesting that systemic immune defects related to Muc2 deficiency do not explain the heightened pathogen dissemination observed in oral infections. Using a barcoded L. monocytogenes library to measure intrahost pathogen population dynamics, we found that Muc2−/− animals had larger pathogen founding population sizes in the intestine and distal sites than observed in wild-type animals. Comparisons of barcode frequencies suggested that the colon becomes the major source for seeding the internal organs in Muc2−/− animals. Together, our findings reveal that Muc2 mucin plays a key role in controlling L. monocytogenes colonization, dissemination, and population dynamics.

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