Microbiological Safety of Cheese Made from Heat-Treated Milk, Part II. Microbiology

1990 ◽  
Vol 53 (6) ◽  
pp. 519-540 ◽  
Author(s):  
ERIC A. JOHNSON ◽  
JOHN H. NELSON ◽  
MARK JOHNSON

A review of epidemiological literature identified six illness outbreaks transmitted via U.S. produced cheese during 40 years, 1948–1988. During these four decades, the United States cheese industry produced over 100 billion pounds of natural cheese (not including cottage and related varieties). The most frequent causative factor in U.S. and Canadian cheese-related outbreaks was post-pasteurization contamination. Faulty pasteurization equipment or procedures were implicated in one outbreak each in the U.S. and Canada. Use of raw milk was a factor in one outbreak in each country. Inadequate time-temperature combinations used for milk heat treatment were not implicated. The epidemiology of cheese-related outbreaks in the U.S., Canada, and Europe demonstrated that soft surface-ripened cheese, e.g. Camembert and Brie, are at significantly greater risk to transmit pathogens than other cheeses. No outbreaks were linked to hard Italian varieties, e.g. Parmesan, Romano, and Provolone. Varieties such as Cheddar and Swiss were infrequently involved. A variety of pathogens have been isolated from raw milk. Some, including Salmonella, Listeria, and enteropathogenic Escherichia coli can survive and grow in some cheeses. In one of the few published studies of milk heat-treatment for cheesemaking, multistrain or species mixtures of pathogens were inoculated into raw milk at levels of 105/ml which was heat-treated in a commercial HTST pasteurizer — mean holding time 17.6 s, minimum 16.2 s. All strains of Yersinia enterocolitica, Campylobactersp., Escherichia coli 0157:H7, and all but one Salmonella species were destroyed at 65°C (149°F). Salmonella senftenberg (rarely isolated from cheese) was inactivated at 69°C (156.2°F). Listeria monocytogenes in naturally contaminated milk at levels of 104 organisms per ml was inactivated at 66°C (150.8°F); laboratory-cultured inoculum at levels of 105 organisms per ml required 69.0°C (156.2°F). A multiplicity of practices other than pasteurization or heat-treatment contribute significantly to the microbiological safety of cheese. Some, such as milk quality management, lactic culture management, pH control, salt addition, and controlled curing conditions are established technologies. Others represent potential opportunities, such as natural inhibitory substances in milk, antibacterial substances, e.g. nisin and lysozyme.

1990 ◽  
Vol 53 (7) ◽  
pp. 610-623 ◽  
Author(s):  
ERIC A JOHNSON ◽  
JOHN H. NELSON ◽  
MARK JOHNSON

Heat treatment or pasteurization does not adversely affect the cheesemaking process or the resulting physical properties of the cheese. Both types of heat-treatments can correct chemical changes that occur in cold stored raw milk. Thermization on the farm may help control psychrotrophic bacteria in cold stored milk. Some denaturation of whey protein does occur during pasteurization. Heat treatments slightly above current minimum pasteurization requirements can cause body/texture and moisture control problems in cheese. Loss of functionality can adversely affect the marketing of whey protein products. Cheeses made from pasteurized milk ripen more slowly and usually do not exhibit the flavor intensity of cheeses made from raw or heat-treated milk. Swiss and hard Italian type cheese, whose traditional flavor results in part from native milk enzymes and microflora, would also be adversely affected if milk pasteurization for cheesemaking were mandatory. The quality of cheese made from pasteurized milk is consistently better than cheese made from raw milk as evidenced by fewer body and flavor defects consequent to the growth of undesirable bacteria. Either pasteurization or heat-treatment enables improved uniform process control and quality during cheesemaking. Pathogens were prioritized as high, medium, or low risk in cheese. Three organisms, Salmonella, Listeria monocytogenes and enteropathogenic Escherichia coli were judged to be high risk threats to the cheese industry. Staphylococcus aureus was listed as low risk because growth and toxin production is readily suppressed by lactic cultures and acidity (pH) control in cheese. Three actions are recommended:Establish a guideline for minimum heat-treatment of milk for cheesemaking: 64.4°C (148°F) for 16 s or equivalent with adequate process control.Evaluate current safety technology and practices used for cheese manufacture. Support research with primary emphasis on the combined effect of heat-treatment and other current cheese technologies.Evaluate technologies not currently utilized in cheese manufacture for safety potential.


1982 ◽  
Vol 45 (6) ◽  
pp. 513-515 ◽  
Author(s):  
G. F. SENYK ◽  
R. R. ZALL ◽  
W. F. SHIPE

Raw milk was heat-treated under subpasteurization and suprapasteurization conditions, cooled and stored for up to 72 h at 4.4 and 6.7°C. Milk lipase activity and bacteria counts were monitored in both unheated and heated milks. Inhibition of milk lipase activity ranged from 42 to 98% for treatments of 57.2°C for 10 sec to 73.9°C for 10 sec, respectively. The logs of Standard Plate Count after 72 h of storage at 6.7°C were 6.56, 4.86, 4.31, 4.00 and 2.82 for unheated and 10-sec heat treatments at 57.2, 65.6, 73.9 and 82.2°C, respectively. Psychrotrophic Bacteria Counts were also lower in the heated milks than in the unheated milk. The logs of Psychrotrophic Bacteria Counts after 72 h of storage at 6.7°C were 6.21, 2.45, 2.27, 1.33 and 1.00 for unheated and 10-sec heat treatments at 57.2, 65.6, 73.9 and 82.2°C, respectively. Heat treatment of raw milk supplies would result in limiting action of the milk lipase system and growth of bacteria.


2008 ◽  
Vol 71 (5) ◽  
pp. 1023-1027 ◽  
Author(s):  
R. N. COBBOLD ◽  
M. A. DAVIS ◽  
D. H. RICE ◽  
M. SZYMANSKI ◽  
P. I. TARR ◽  
...  

A survey for Shiga toxigenic Escherichia coli in raw milk and beef was conducted within a defined geographic region of the United States. Prevalence rates based on detection of Shiga toxin gene (stx) were 36% for retail beef, 23% for beef carcasses, and 21% for raw milk samples, which were significantly higher than were Shiga toxigenic E. coli isolation rates of 7.5, 5.8, and 3.2%, respectively. Seasonal prevalence differences were significant for stx positivity among ground beef and milk samples. Distribution of stx subtypes among isolates varied according to sample type, with stx1 predominating in milk, stx2 on carcasses, and the combination of both stx1 and stx2 in beef. Ancillary virulence markers eae and ehx were evident in 23 and 15% of isolates, respectively. Pulsed-field gel electrophoresis demonstrated associations between food isolates and sympatric bovine fecal, and human clinical isolates. These data demonstrate that non-O157 Shiga toxigenic E. coli is present in the food chain in the Pacific Northwest, and its risk to health warrants critical assessment.


1996 ◽  
Vol 63 (1) ◽  
pp. 35-48 ◽  
Author(s):  
Andrew J. R. Law

SummaryThe effects of heat treatment and subsequent acidification of milk on the distribution of proteins, Ca and Pi, between the serum and micellar phases were examined using ultracentrifugation. After heating milk at 85 °C for 10 min, and storing for 22 h at 4, 20 or 30 °C, there was a marked increase in the concentration of κ-casein in the serum. At 4 and 20 °C there was also slightly more β-casein in the serum from heat-treated milk than in that from the corresponding raw milk. The whey proteins were extensively denatured, and were almost equally distributed between the supernatants and micellar pellets. After storage for 22 h the distribution of Ca and Pi between soluble and colloidal phases in heat-treated milk was similar to that in raw milk. After acidifying heat-treated milk by the addition of glucono-δ-lactone and storing for 22 h at 4, 20 or 30 °C there was progressive solubilization of colloidal calcium phosphate with decreasing pH, and at pH 5·0 almost all of the Ca and Pi was present in the serum. At 20 °C, and even more so at 4 °C, serum concentrations of the individual caseins increased considerably with decreasing pH, reaching maximum levels of about 25 and 40% of the total casein at pH 5·7 and 5·5 respectively, and then decreasing rapidly at lower pH. Compared with raw milk, maximum dissociation in heat-treated milks stored at 4 and 20 °C occurred at higher pH, and the overall levels of dissociation of individual caseins from the micelles were lower. At 30 °C, the concentrations of individual caseins in the serum of heat-treated milk decreased steadily as the pH was reduced, and did not show the slight increase found previously for raw milk. The role of the denatured whey proteins in interacting with κ-casein and in promoting aggregation of the micelles on acidification is discussed.


1993 ◽  
Vol 56 (7) ◽  
pp. 568-572 ◽  
Author(s):  
ELSA A. MURANO ◽  
MERLE D. PIERSON

Escherichia coli serotype O157:H7 cells were grown at 30°C for 6 h and subjected to a heat stress, or heat shock, at 42°C for 5 min. Heat-shocked and nonheat-shocked controls were heat treated at 55°C for up to 60 min. The number of injured cells was significantly higher in heat-shocked cells than in controls, and the rate of release of cell components was higher in heat-shocked cells. Anaerobic plating resulted in higher recovery of injured cells, when compared with aerobic plating, regardless of whether the cells were heat shocked or not. In addition, heat shocking resulted in lower catalase and superoxide dismutase activities when compared with controls. It also resulted in greater survivability after exposure to hydrogen peroxide, suggesting that heat shocking somehow enables the cells to survive exposure to toxic substances in addition to heat. The heat-shock response, coupled with anaerobic conditions, increased the ability of E. coli O157:H7 cells to recover after a heat treatment. Thus, heat shock did not afford protection to the cells against injury, but rather enhanced their ability to recover during storage.


1978 ◽  
Vol 45 (3) ◽  
pp. 391-403 ◽  
Author(s):  
Haytham A. Jaddou ◽  
John A. Pavey ◽  
Donald J. Manning

SummaryThe effect of heat treatment of milk on low molecular weight, volatile compounds was studied in order to relate changes in the flavour of milks to changes in chemical composition. Milks were heat treated in a UHT plant for 3 or 90 s at 140 °C and stored at ambient temperature for periods up to 112 d. Volatile compounds in raw milk and in heated milks were isolated by a low temperature spray distillation technique and identified using gas chromatography and mass spectrometry. Cabbagey defects in heated milks are correlated with total volatile sulphur and it is concluded that the compounds H2S, COS, CH3SH, CS2 and (CH3)2S could be responsible for this defect.


1977 ◽  
Vol 40 (12) ◽  
pp. 857-862 ◽  
Author(s):  
LANA S. WECKBACH ◽  
B. E. LANGLOIS

Grade A raw milk which had initial psychrotrophic counts of less than 103/ml was inoculated with an antibiotic-resistant Pseudomonas sp. to a final cell concentration of 102, 104, or 106/ml. The inoculated milk was held at 4 C for 14 h and then exposed to the following time-temperature treatments: 72 C for 15 sec, 79 C for 15 sec, 88 C for 10 sec, and 95 C for < 5 sec. An uninoculated raw milk control was handled and analyzed along with inoculated samples. Aliquots of milk were analyzed for marked Pseudomonas sp., total psychrotrophic counts, numbers of Pseudomonas, and for distribution of nitrogen before and after each heat treatment and after storage of non-heat-treated raw milk and heat-treated samples for 7 and 14 days at 7 C. Psychrotrophic counts were significantly affected by heat treatment, initial cell inoculum, days stored, and plating media. Non-casein N, non-casein protein, total albumin, β-lactoglobulin, proteose-peptone, and globulin N were significantly decreased by heat treatment. Non-casein N, non-casein protein, β-lactoglobulin, and proteose-peptone were significantly increased by days of storage.


2011 ◽  
Vol 74 (5) ◽  
pp. 759-768 ◽  
Author(s):  
JO ANN S. VAN KESSEL ◽  
JEFFREY S. KARNS ◽  
JASON E. LOMBARD ◽  
CHRISTINE A. KOPRAL

The zoonotic bacteria Salmonella enterica, Listeria monocytogenes, and Escherichia coli are known to infect dairy cows while not always causing clinical signs of disease. These pathogens are sometimes found in raw milk, and human disease outbreaks due to these organisms have been associated with the consumption of raw milk or raw milk products. Bulk tank milk (BTM) samples (536) and in-line milk filters (519) collected from dairy farms across the United States during the National Animal Health Monitoring System's Dairy 2007 study were analyzed by real-time PCR for the presence of S. enterica and pathogenic forms of E. coli and by culture techniques for the presence of L. monocytogenes. S. enterica was detected in samples from 28.1% of the dairy operations, primarily in milk filters. Salmonella was isolated from 36 of 75 PCR-positive BTM samples and 105 of 174 PCR-positive filter samples, and the isolates were serotyped. Cerro, Kentucky, Muenster, Anatum, and Newport were the most common serotypes. L. monocytogenes was isolated from 7.1% of the dairy operations, and the 1/2a complex was the most common serotype, followed by 1/2b and 4b (lineage 1). Shiga toxin genes were detected in enrichments from 15.2% of the BTM samples and from 51.0% of the filters by real-time PCR. In most cases, the cycle threshold values for the PCR indicated that toxigenic strains were not a major part of the enrichment populations. These data confirm those from earlier studies showing significant contamination of BTM by zoonotic bacterial pathogens and that the consumption of raw milk and raw milk products presents a health risk.


2011 ◽  
Vol 74 (1) ◽  
pp. 13-17 ◽  
Author(s):  
V. LORUSSO ◽  
A. DAMBROSIO ◽  
N. C. QUAGLIA ◽  
A. PARISI ◽  
G. LASALANDRA ◽  
...  

Verocytotoxin-producing Escherichia coli (VTEC) O26 is an emergent pathotype that has caused an increasing number of sporadic cases and outbreaks of gastroenteritis, hemorrhagic colitis, and hemolytic uremic syndrome in the United States and Europe. Many cases are associated with the consumption of milk and undercooked or fermented meats. The stx2 strains of VTEC O26 seem to be more likely to cause human infections than isolates expressing only stx1. The isolation and identification of VTEC O26 from foods is labor intensive and time-consuming. We developed a multiplex PCR (M-PCR) assay for the identification and characterization of E. coli O26 VTEC and its detection in raw milk and ground beef. The method is based on the amplification of the wzx, stx1, and stx2 genes for the simultaneous detection of the O26 antigen and verocytotoxin types 1 and 2. This M-PCR assay had a sensitivity of 108 CFU/ml when applied to a bacterial suspension and of 106 CFU/ml or g when applied to both inoculated milk and minced beef samples. This M-PCR assay also was highly specific, and results were consistently negative for negative controls (nonpathogenic E. coli strains, uninoculated milk and beef samples, and samples inoculated with the nontarget microorganisms). This method could be used for the rapid detection of E. coli O26 VTEC from foods and for the rapid identification and characterization of clinical and environmental isolates.


2003 ◽  
Vol 66 (3) ◽  
pp. 382-389 ◽  
Author(s):  
JOHN S. NOVAK ◽  
JAMES T. C. YUAN

The threat of pathogen survival following ozone treatment of meat necessitates careful evaluation of the microorganisms surviving under such circumstances. The objective of this study was to determine whether sublethal aqueous ozone treatment (3 ppm of O3 for 5 min) of microorganisms on beef surfaces would result in increased or decreased survival with respect to subsequent heat, alkali, or NaCl stress. A mild heat treatment (55°C for 30 min) was used for comparison. Reductions in three-strain cocktails of Clostridium perfringens, Escherichia coli O157:H7, and Listeria monocytogenes on beef following the heat treatment were 0.14, 0.77, and 1.47 log10 CFU/g, respectively, whereas reductions following ozone treatment were 1.28, 0.85, and 1.09 log10 CFU/g, respectively. C. perfringens cells exhibited elevated heat resistance at 60°C (D60 [time at 60°C required to reduce the viable cell population by 1 log10 units or 90%] = 17.76 min) following heat treatment of beef (55°C for 30 min) but exhibited reduced viability at 60°C following ozone treatment (D60 = 7.64 min) compared with the viability of untreated control cells (D60 = 13.84 min). The D60-values for L. monocytogenes and E. coli O157:H7 following heat and ozone exposures were not significantly different (P > 0.05). C. perfringens cells that survived ozone treatment did not exhibit increased resistance to pH (pH 6 to 12) relative to non-ozone-treated cells when grown at 37°C for 24 h. The heat treatment also resulted in decreased numbers of surviving cells above and below neutral pH values for both E. coli O157:H7 and L. monocytogenes relative to those of non-heat-treated cells grown at 37°C for 24 h. There were significant differences (P < 0.05) in C. perfringens reductions with increasing NaCl concentrations. The effects of NaCl were less apparent for E. coli and L. monocytogenes survivors. It is concluded that pathogens surviving ozone treatment of beef are less likely to endanger food safety than are those surviving sublethal heat treatments.


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