Biomedical subjects

E H Marth

Publications and source records attributed to E H Marth.

At least 19 recordsLinked to original sources

PubMed1992

Antagonism between Listeria monocytogenes and lactococci during fermentation of products from ultrafiltered skim milk.

Tyndallized samples of unfiltered skim milk and retentate (concentrated fivefold or twofold by volume) and permeate from UF skim milk were inoculated with 5.5 x 10(3) to 1.5 x 10(5) cfu/ml of Listeria monocytogenes strains California or V7 together with 4 x 10(7) to 2.3 x 10(8) cfu/ml of mesophilic lactic acid bacteria. Numbers of L. monocytogenes (McBride Listeria agar) and lactic acid bacteria (all purpose Tween agar) were determined after 0, 6, 12, 24, 30, and 36 h of incubation at 30 degrees C. Lactic acid bacteria significantly inhibited or inactivated L. monocytogenes in all three products. Inactivation was greater in permeate (6.77 orders of magnitude) than in unfiltered skim milk (3.67 orders of magnitude) or in retentate (4.21 orders of magnitude). Degree of inactivation in retentate was related to the extent of concentration. Inactivation was not complete, and L. monocytogenes survived in these products during fermentation for up to 36 h. When fermented products were refrigerated (4 degrees C), L. monocytogenes survived for 4 to 6 wk in skim milk, 3 to 5 wk in retentate, and 1 wk in permeate. At refrigeration temperature, length of survival was dependent on type of product and strain of the pathogen.

Animals↗

PubMed1992

Survival of Listeria monocytogenes during the manufacture and ripening of Swiss cheese.

Rindless Swiss cheese was made from a mixture of pasteurized whole and skim milk that was inoculated to contain 10(4) to 10(5) cfu of Listeria monocytogenes (strain Ohio, California, or V7)/ml. During clotting of milk, numbers of L. monocytogenes remained nearly unchanged. When the curd was heated gradually to attain the cooking temperature (50 degrees C), numbers of L. monocytogenes increased by approximately 40 to 45% over those in inoculated milk. Cooking curd at 50 degrees C (122 degrees F) for 30 to 40 min resulted in resilient curd having a pH of 6.40 to 6.45 and decreased L. monocytogenes by 48% compared with numbers of the pathogen in inoculated milk. After curd was pressed under whey, numbers of L. monocytogenes increased by approximately 52% over those in inoculated milk and reached their maxima at the end of this stage. A sharp decrease in numbers of L. monocytogenes occurred during brining of cheese blocks (7 degrees C for 30 h). The population of L. monocytogenes continued to decrease during cheese ripening. Average D values for strains California, Ohio, and V7 were 29.2, 24, and 22.5 d, respectively. Listeria was not detected (direct plating, and cold enrichment) after 80, 77, and 66 d of ripening of Swiss cheese made from milk inoculated with strains California, Ohio, and V7, respectively. Thus, Swiss cheese made in this study did not permit extended survival of L. monocytogenes.

Animals↗

PubMed1992

Salmonellae, salmonellosis, and dairy foods: a review.

Salmonellae continue to be a major concern for the dairy industry because these bacteria have caused recent outbreaks of illness and have been isolated from various dairy products in the market place. Salmonellae are generally not heat resistant and normally grow at 35 to 37 degrees C, but they can grow at much lower temperatures, provided that the incubation time is suitably extended. To minimize problems, foods should be held at or below 2 to 5 degrees C at all times. Both conventional and rapid methods are available to isolate salmonellae from dairy foods and to identify the bacteria. Salmonellae behave differently in different kinds of cheese: they survived in ripening Cheddar cheese for up to 7 mo at 13 degrees C and for 10 mo at 7 degrees C; in coldpack cheese food for several weeks, depending on the pH and preservative used; and in Domiati cheese 13 to 36 d, depending on the manufacturing process used. When Mozzarella cheese was made, temperatures of stretching and molding (60 degrees C) killed all salmonellae present, but, in cottage cheese, survival of the pathogen depended on the cooking temperature of curd. Spray drying of skim milk killed substantial numbers of salmonellae, but some survivors remained. Butter readily supported growth of salmonellae at room temperature, and neither freezing nor refrigeration for brief periods eliminated salmonellae from butter. Use of appropriate hygienic procedures, e.g., Hazard Analysis Critical Control Point system, during processing should reduce the likelihood of salmonellosis outbreaks associated with dairy foods.

Animals↗

PubMed1992

Characteristics of sodium benzoate injury of Listeria monocytogenes.

Over 99% of viable cells of Listeria monocytogenes were injured after exposure to a solution of 8.5% sodium benzoate (pH 7.0) for 1 h. Injury was evident by the inability of the bacterium to tolerate 6% NaCl in tryptose agar (TA) and the ability to grow on TA with no added salt. The colony-forming ability of the injured cells was restored when they recovered in tryptose broth containing sublethal amounts of metabolic or synthetic inhibitors. Synthesis of mRNA was critical for restoration of salt tolerance. Inhibition of electron transport, protein synthesis, or repair of the cell wall did not suppress recovery of the cells. Changes in the cell membrane which may have occurred did not allow soluble proteins or nucleotides to leak during the course of benzoate injury.

Anti-Bacterial Agents↗

PubMed1991

Borrelia burgdorferi: another cause of foodborne illness?

Borrelia burgdorferi was identified as the etiological agent of Lyme disease in 1982. This Gram-negative spirochete is classified in the order Spirochaetales and the family Spirochaetaceae. The pathogen is fastidious, microaerophilic, mesophilic and metabolises glucose through the Embden-Meyerhof pathway. A generation time of 11 to 12 h at 37 degrees C in Barbour-Stoenner-Kelly medium has been reported. Lyme disease, named after Lyme in Connecticut, is distributed globally. It is the most commonly reported vector-borne disease in the United States, where the incidence is highest in the eastern and midwestern states. Since establishment of national surveillance in 1982, there has been a nine-fold increase in the number of cases reported to the U.S. Centers for Disease Control. The deer tick of the genus Ixodes is the primary vector of Lyme borreliosis. The tick may become infected with B. burgdorferi, by feeding on an infected host, at any point in its 2-year life cycle which involves larval, nymphal and adult stages. The infection rate in deer ticks may be as high as 40% in endemic areas. The primary vertebrate reservoirs for Ixodes are the white-footed mouse (Peromyscus leucopus) and the white-tailed deer (Odocopileus virginianus). Dairy cattle and other food animals can be infected with B. burgdorferi and hence some raw foods of animal origin might be contaminated with the pathogen. Recent findings indicate that the pathogen may be transmitted orally to laboratory animals, without an arthropod vector. Thus, the possibility exists that Lyme disease can be a food infection. In humans, the symptoms of Lyme disease, which manifest themselves days to years after the onset of infection, may involve the skin, cardiac, nervous and/or muscular systems, and so misdiagnosis can occur.

Animals↗

PubMed1991

Survival of Listeria monocytogenes in a food colorant derived from red beets.

Three commercial lots of the red beet colorant were inoculated to contain circa 10(3) to 10(7) Listeria monocytogenes strains California, V7, or Scott A per milliliter and stored for 56 d at 7 degrees C. McBride listeria agar was used to determine numbers of survivors. Selected colonies thought to be L. monocytogenes were confirmed biochemically. When necessary, samples were tested by cold enrichment (up to 8 weeks). Samples of colorant initially containing 10(3) to 10(4) strain California/ml were always free of the pathogen after 56 d, and sometimes after 42 d. Samples with high initial numbers (10(5) to 10(6)/ml) were not free of the pathogen after 8 wk at 7 degrees C. Strains V7 and Scott A, regardless of size of initial population, always survived beyond 56 d. Before inoculation, all test samples of colorant were free of L. monocytogenes (direct plating or cold enrichment).

Colony Count, Microbial↗

PubMed1991

Injury and death of frozen Listeria monocytogenes as affected by glycerol and milk components.

A cell suspension of Listeria monocytogenes strain Scott A in phosphate buffer solution alone or with added glycerol, milk fat, lactose, or casein was frozen and stored at -18 degrees C. At suitable intervals, samples of cell suspensions were thawed at 35 degrees C and plated on suitable media to distinguish between surviving injured and noninjured cells of L. monocytogenes. Glycerol (2 or 4%) protected L. monocytogenes from death and injury during frozen storage for up to 6 mo; however, when 2% glycerol was present, 30 min of frozen storage had to elapse after completion of freezing before protection against death was evident. During short-term (2 wk or less) frozen storage, lactose, milk fat, and casein, each at 2%, provided better protection to L. monocytogenes than did 2% glycerol. During long-term frozen storage, milk components, each at 2%, protected L. monocytogenes against death and injury, but less than that provided by glycerol. Protection by lactose and milk fat against death during frozen storage was observed during 4 wk and against injury during 5 mo and 4 wk of frozen storage, respectively. Protection by casein against death and injury occurred during frozen storage for up to 6 mo. Salts that simulate milk ultrafiltrate provided almost no protection to L. monocytogenes during freezing and frozen storage. Increasing the concentration of milk fat from 2 to 4% resulted in almost no change in death of L. monocytogenes, but in a decrease in injury only during the first 24 h of frozen storage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Strains and suspending menstrua as factors affecting death and injury of Listeria monocytogenes during freezing and frozen storage.

Cell suspensions of Listeria monocytogenes strains V7, California, and Ohio in phosphate buffer solution, tryptose broth, or milk were frozen and stored at -18 degrees C. At appropriate intervals during storage, a sample was thawed at 35 degrees C and surface-plated on suitable media to allow colony formation by noninjured or noninjured plus injured cells. Degrees of death and injury were calculated from the data. Cells of L. monocytogenes were more resistant to death and injury when they were suspended in milk or tryptose broth rather than phosphate buffer solution. There was a significant (two-way ANOVA) difference in resistance to death and injury during frozen storage among strains of L. monocytogenes suspended in tryptose broth. The difference was nonsignificant when the cells were suspended in phosphate buffer solution or milk. Listeria monocytogenes strain Ohio was more resistant to death and injury during frozen storage when cells were suspended in tryptose broth rather than milk. The opposite was true for strains V7 and California. Death and injury of L. monocytogenes strains V7, California, and Ohio suspended in phosphate buffer solution were 98.7, 97.9, and 91.2% and 77.5, 51.6, and 70.2%, respectively, after 4 wk of frozen storage. The values were 67.3, 91.6, and 42.3% and 44.4, 65.6, and 32.6%, respectively, when cells were suspended in tryptose broth, and they were 37.8, 40, and 60.7% and 10.8, 66.8, and 46%, respectively, when cells were suspended in milk.

Animals↗

PubMed1990

Purification and Partial Characterization of a Prolyl-Dipeptidyl Aminopeptidase from Lactobacillus helveticus CNRZ 32.

X-prolyl-dipeptidyl aminopeptidase, which hydrolyzed Gly-Pro-p-nitroanilide (relative activity [RA] = 100%) and Arg-Pro-p-nitroanilide (RA, 130%), was purified to homogeneity from the cell extract of Lactobacillus helveticus CNRZ 32. The enzyme also hydrolyzed Ala-Pro-Gly (RA, 11%) and Ala-Ala-p-nitroanilide (RA, 2%) but was not active on Ala-Leu-Ala, dipeptides, and endopeptidase and carboxypeptidase substrates. The enzyme was purified 145-fold by streptomycin sulfate precipitation, ammonium sulfate fractionation, and a series of column chromatographies on DEAE-cellulose, arginine-Sepharose 4B, and glycyl-prolyl-AH-Sepharose 4B. The purified enzyme appeared as a single band on native polyacrylamide gel and sodium dodecyl sulfate-polyacrylamide gel electrophoreses and had a molecular weight of 72,000. Optima for activity by the purified enzyme were pH 7.0 and 40 degrees C. The enzyme was incubated at 40 degrees C for 15 min with various metal ions. It was activated by Mg (2.5 mM), Ca (0.1 to 2.5 mM), Na (10 to 50 mM), and K (10 to 50 mM) and was inhibited by Hg (0.1 to 2.5 mM), Cu (0.1 to 2.5 mM), and Zn (0.1 to 2.5 mM). Enzyme activity was partially inhibited by EDTA (1.0 mM, 20 h at 40 degrees C), 1,10-phenanthroline (1.0 mM, 15 min at 40 degrees C), phenylmethylsulfonyl fluoride (1.0 mM), N-ethylmaleimide (1.0 mM), and iodoacetate (1.0 mM). It was completely inhibited by diisopropyl fluorophosphate (1.0 mM, 2 h at 40 degrees C) and p-chloromercuribenzoate (1.0 mM, 15 min at 40 degrees C). The enzyme was not affected by dithioerythritol (1.0 to 10 mM).

Journal Article↗

PubMed1990

Listeria monocytogenes--threat to a safe food supply: a review.

Listeria monocytogenes can cause circling disease, encephalitis, meningitis, septicemia, and mastitis in dairy cattle. Shedding of the pathogen from the udder or contamination from the environment can lead to presence of L. monocytogenes in raw milk. Surveys indicate the pathogen is in about 4% of US raw milks. Although HTST pasteurization commonly inactivates L. monocytogenes, evidence suggests that under unusual circumstances minimal survival is possible. The pathogen grows well in liquid dairy products at 4 to 35 degrees C and achieves higher populations in chocolate than in unflavored milks. When present in cheese milk, growth of L. monocytogenes may be retarded but not stopped by lactic starter cultures. The pathogen is concentrated in the curd with only a small fraction of cells in milk appearing in whey. Once in curd, the behavior of the pathogen ranges from growth (feta cheese making) to death of most but not all cells (cottage cheese making). During ripening of cheese, the numbers of L. monocytogenes decrease gradually (as in Cheddar or Colby cheese), decrease precipitously early during ripening, and then stabilize (as in blue cheese) or increase markedly (as in Camembert cheese). Consumption of foods containing L. monocytogenes can lead to listeriosis in susceptible humans (adults with a compromised immune system), pregnant women, and infants). In large outbreaks of human listeriosis, mortality rates of ca. 30% are common.

Animals↗

PubMed1990

Behavior of Listeria monocytogenes in the presence of gluconic acid and during preparation of cottage cheese curd using gluconic acid.

Unrestricted or minimally restricted growth of Listeria monocytogenes strain V7 occurred 1) at 13 degrees C in tryptose broth with .125 or .25% gluconic acid or .1 to .3% glucono-delta-lactone, 2) at 13 degrees C in milk with .125 to 1.0% gluconic acid or .5 or 1.0% glucono-delta-lactone, 3) at 35 degrees C in tryptose broth with .125 to .5% gluconic acid or .1 to 5% glucono-delta-lactone, and 4) at 35 degrees C in milk with .125 to 1.0% gluconic acid or .5 to 1.5% glucono-delta-lactone. Limited growth of L. monocytogenes occurred 1) at 13 degrees C with .375 or .5% gluconic acid or .3 or .4% glucono-delta-lactone, 2) at 13 degrees C in milk with 1.5% glucono-delta-lactone, 3) at 35 degrees C in tryptose broth with .75% glucono-delta-lactone, and 4) at 35 degrees C in milk with 2.0% glucono-delta-lactone. Partial to complete inactivation of L. monocytogenes occurred 1) at 13 degrees C in tryptose broth with .75 to 1.5% gluconic acid or .75 or 1.0% glucono-delta-lactone, 2) at 13 degrees C in milk with 1.5% gluconic acid or 2.0 to 3.0% glucono-delta-lactone, 3) at 35 degrees C in tryptose broth with .75 to 1.5% gluconic acid or 1.0% glucono-delta-lactone, and 4) at 35 degrees C in milk with 1.5% gluconic acid or 2.5 or 3.0% glucono-delta-lactone. Milk containing L. monocytogenes was coagulated with gluconic acid, HCl, or rennet, and cottage cheese curd was prepared. After cooking, numbers of the pathogen in curd or whey from rennet-coagulated milk were reduced by ca. 1.5 and 2.5 orders, respectively. Small numbers of survivors appeared in curd but not in whey of HCl-coagulated milk. No survivors were detected in curd or whey of gluconic acid-coagulated milk.

Animals↗

PubMed1990

Fate of Listeria monocytogenes during the manufacture and ripening of Parmesan cheese.

Parmesan cheese was made from a mixture of pasteurized whole and skim milk that was inoculated to contain ca. 10(4) to 10(5) cells of Listeria monocytogenes/ml. Curd was cooked at 51 degrees C (124 degrees F) for ca. 45 min. During cheese making, maximum numbers of L. monocytogenes appeared just before cooking; at this point, the increase over initial numbers was a .61 to 1.0 order of magnitude. During cooking of curd, the average decrease in numbers of L. monocytogenes was a .22 order of magnitude. During cheese ripening, numbers of L. monocytogenes decreased almost linearly and faster than reported for other hard cheeses. Listeria monocytogenes strain California died faster than did strain V7. Listeria monocytogenes were not detected in cheese after 2 to 16 wk of ripening, depending on the strain of the pathogen and the lot of cheese. Parmesan cheese made in this study was not a favorable medium for survival of L. monocytogenes.

Animals↗

PubMed1990

Changes in populations of Listeria monocytogenes in a medium with internal pH control containing Streptococcus cremoris.

Behavior of Listeria monocytogenes in a commercial starter culture medium with internal pH control was examined. The IPCM-1 medium was inoculated with L. monocytogenes (strain V7, Scott A, or California) at ca. 10(3) cfu/ml and Streptococcus cremoris (.25%, 1.6 x 10(5) or 1.0%, 8.6 x 10(5) cfu/ml) and was incubated at 21 or 30 degrees C for 30 h. The pH of the uninoculated medium and control (L. monocytogenes only) was between 6.8 and 7.0 before and after incubation. The area on a figure between control and treatment curves for numbers of L. monocytogenes was calculated, designated as area of inhibition, and used to quantitate inhibition of L. monocytogenes caused by S. cremoris. No significant difference was found in area of inhibition or pH values at 6, 24, and 30 h of incubation among the three strains of L. monocytogenes for a given set of conditions (percentage of S. cremoris added and temperature). Inhibition of the pathogen increased with an increase in amount of S. cremoris inoculum used and with higher rather than lower incubation temperature. Populations of L. monocytogenes in IPCM-1 medium without S. cremoris after 30 h of incubation were 10(6) to 10(7)/ml at 21 degrees C and 10(8)/ml at 30 degrees C. At 21 degrees C inhibition of Listeria began after 18 and 24 h and at 30 degrees C after 12 and 15 h of incubation in samples inoculated with 1.0 and .25% S. cremoris, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Enzyme activities of cell-free extracts from mutant strains of lactic streptococci subjected to sublethal heating or freeze-thawing.

Two mutant lactose-negative (Lac-), proteinase-negative (Prt-) strains of lactic streptococci, Streptococcus lactis 25Sp and S. cremoris KHA2, and their parents, S. lactis C2 and S. cremoris KH Lac+ Prt+, were grown in a suitable medium with the pH maintained at 6.5 by addition of NH4OH. Cells were harvested by centrifugation, resuspended, and then heated sublethally at 54 or 69 degrees C for 15 sec. Cells also were frozen and stored for 1 week at -20 or -100 degrees C. Cell-free extracts of cells heated at 54 degrees C had more proteinase and aminopeptidase activities than did a similar extract of cells heated at 69 degrees C. The greatest enzyme activities occurred in the cell-free extracts prepared from cells frozen and stored at -100 degrees C. Specific activities of proteinase and dipeptidase generally decreased in extracts of freeze-shocked cells compared to those in extracts of untreated cells. Enzyme activity of extracts also decreased in the presence of 5% NaCl at pH 5.0. Cell-free extracts at pH values of 5 to 8 were heated at 69 degrees C for 1.5, or 10 min. Heating them for 10 min caused a loss of dipeptidase activity which was most pronounced at pH 5.0 and least pronounced at pH 7.0.

Aminopeptidases↗

PubMed1989

Behavior of Listeria monocytogenes in the presence of sodium propionate.

Survival or growth of Listeria monocytogenes in Tryptose Broth supplemented with 0, 0.05, 0.1, 0.15, 0.2, 0.25 or 0.3% sodium propionate was determined when the pH of the medium was 5.0 or 5.6 and incubation was at 4, 13, 21 and 35 degrees C. The pathogen grew in all controls, propionate-free broth, except at 4 degrees C and pH 5.0. At pH 5.6 and 4, 13, 21 and 35 degrees C the bacterium grew in the presence of all propionate concentrations used in this study. The higher concentrations permitted only minimal growth with smallest ultimate populations and longest generation times. Reducing the pH to 5.0 served to minimize growth further at 13, 21 and 35 degrees C than that observed at the same temperatures but at pH 5.6. The extent of growth was directly proportional to the propionate concentrations; at high concentrations, propionate caused a gradual decrease in populations and/or prolonged the lag phase. At 35 degrees C, a concentration of 0.25% did not allow growth, whereas 0.3% caused inactivation of the pathogen after 80 h of incubation. At 4 degrees C and pH 5.0, all concentrations of sodium propionate caused a gradual decrease in populations during the incubation period.

Animals↗

PubMed1989

Simple Method To Detect beta-Galactosidase.

A simple and rapid method was developed to detect beta-galactosidase by using alpha- or beta-naphthyl-beta-d-galactopyranoside as substrate and fast garnet GBC as a dye coupler following polyacrylamide gel electrophoresis. This method was specific for beta-galactosidase but not for phospho-beta-galactosidase.

Journal Article↗

PubMed1989

Behavior of Listeria monocytogenes during manufacture and ripening of brick cheese.

Brick cheese was made by the washed-curd procedure from pasteurized whole milk inoculated to contain ca. 1 x 10(2) to 1 x 10(3) Listeria monocytogenes [strain Scott A, Ohio, V7, or California]/ml. Cheeses were ripened (15 degrees C/95% relative humidity) with a surface smear for 2, 3, or 4 wk to simulate production of mild, aged, or "Limburger-like" brick cheese, respectively, and then stored an additional 20 to 22 wk at 10 degrees C. Populations of strains Scott A, Ohio, V7, and California increased 1.89, 1.72, .83, and .86 orders of magnitude, respectively, following completion of brining ca. 32 h after the start of cheese making. All four L. monocytogenes strains leached from cheese into brine during 24 h and survived in brine at 10 degrees C at least 5 d after removal of cheese. Strains Scott A and Ohio grew rapidly during the initial 2 wk of smear development and attained maximum populations of ca. 6.6 and 6.2, 7.0 and 6.9, and 5.6 and 5.1 log10/g in 4-wk-old slice (pH 6.0 to 6.5), surface (pH 6.5 to 6.9), and interior (pH 5.6 to 6.2) samples of cheese, respectively. Numbers of strains Scott A and Ohio generally decreased 1- to 7-fold during 20 to 22 wk at 10 degrees C. Strains V7 and California failed to grow appreciably in any cheese during or after smear development, despite pH of 6.8 to 7.4 in fully ripened cheese; the strains were never isolated from 2- and 3-wk-old cheese and with direct plating were detected sporadically at levels generally less than or equal to 4.0 log10/g in cheese aged greater than or equal to 4 wk. Cold enrichment of slice, surface, and interior samples of cheeses aged greater than or equal to 4 wk generally yielded positive results for L. monocytogenes; strains V7 and California were detected in all cheeses after 20 to 22 wk at 10 degrees C. At 10 ppm, methyl sulfide, dimethyl disulfide, or methyl trisulfide (compounds commonly produced during ripening of brick and Limburger cheese) failed to inhibit appreciably growth of L. monocytogenes.

Cheese↗

PubMed1989

Loss of viability by Listeria monocytogenes in commercial bovine pepsin-rennet extract.

Loss of viability by Listeria monocytogenes strains California, V7, and Scott A in commercial bovine pepsin-rennet extract was determined during storage for 56 d at 7 degrees C. Four levels (10(3) to 10(6)/ml) of L. monocytogenes were added to the coagulant, and McBride listeria agar was used to determine numbers of survivors. Selected colonies thought to be L. monocytogenes were confirmed biochemically. Samples also were tested during and after completion of cold enrichment (up to 8 wk at 4 degrees C). Coagulant inoculated with 10(3) to 10(4) L. monocytogenes/ml usually was free of viable cells of the pathogen after 28 d and sometimes after 14 d, as determined by direct plating and cold enrichment. When the inoculum was 10(5) to 10(6) cells/ml, samples of coagulant usually were free of viable L. monocytogenes after 42 d and sometimes after 28 d. The three strains of L. monocytogenes behaved similarly, although strain California was somewhat less hardy in the environment of the coagulant than were the other two strains. Bovine pepsin-rennet extract, before inoculation, was free of L. monocytogenes (direct plating and cold enrichment).

Animals↗