Evaluation of post-fermentation heating times and temperatures for controlling Shiga toxin-producing Escherichia coli cells in a non-dried, pepperoni-type sausage.

Coarse ground meat was mixed with non-meat ingredients and starter culture (Pediococcus acidilactici) and then inoculated with an 8-strain cocktail of Shiga toxin-producing Escherichia coli (ca. 7.0 log CFU/g). Batter was fine ground, stuffed into fibrous casings, and fermented at 35.6°C and ca. 85% RH to a final target pH of ca. pH 4.6 or ca. pH 5.0. After fermentation, the pepperoni-like sausage were heated to target internal temperatures of 37.8°, 43.3°, 48.9°, and 54.4°C and held for 0.5 to 12.5 h. Regardless of the heating temperature, the endpoint pH in products fermented to a target pH of pH 4.6 and pH 5.0 was pH 4.56±0.13 (range of pH 4.20 to pH 4.86) and pH 4.96±0.12 (range of pH 4.70 to pH 5.21), respectively. Fermentation alone delivered ca. a 0.3- to 1.2-log CFU/g reduction in pathogen numbers. Fermentation to ca. pH 4.6 or ca. pH 5.0 followed by post-fermentation heating to 37.8° to 54.4°C and holding for 0.5 to 12.5 h generated total reductions of ca. 2.0 to 6.7 log CFU/g.

Outbreaks caused by sprouts, United States, 1998-2010: lessons learned and solutions needed.

After a series of outbreaks associated with sprouts in the mid-1990s, the U.S. Food and Drug Administration (FDA) published guidelines in 1999 for sprouts producers to reduce the risk of contamination. The recommendations included treating seeds with an antimicrobial agent such as calcium hypochlorite solution and testing spent irrigation water for pathogens. From 1998 through 2010, 33 outbreaks from seed and bean sprouts were documented in the United States, affecting 1330 reported persons. Twenty-eight outbreaks were caused by Salmonella, four by Shiga toxin-producing Escherichia coli, and one by Listeria. In 15 of the 18 outbreaks with information available, growers had not followed key FDA guidelines. In three outbreaks, however, the implicated sprouts were produced by firms that appeared to have implemented key FDA guidelines. Although seed chlorination, if consistently applied, reduces pathogen burden on sprouts, it does not eliminate the risk of human infection. Further seed and sprouts disinfection technologies, some recently developed, will be needed to enhance sprouts safety and reduce human disease. Improved seed production practices could also decrease pathogen burden but, because seeds are a globally distributed commodity, will require international cooperation.

Survival rate of salmonella on cooked pig ear pet treats at refrigerated and ambient temperature storage.

Pet treats, including pig ears, have been implicated as vehicles of human salmonellosis, and Salmonella has been isolated on commercially produced pig ears. Therefore, behavior of the pathogen on this very low water activity (aw) pet treat is of interest. The survival of Salmonella serotypes Newport and Typhimurium DT104 was measured on natural (aw 0.256) and smoked (aw 0.306) pig ear pet treat products inoculated at ca. 6.5 log CFU per sample and stored at 4.4 or 22°C for 365 days. Surviving populations of Salmonella were enumerated periodically, and a modified Weibull model was used to fit the inactivation curves for log populations. After 14 days, the decline of Salmonella was significantly (P < 0.05) greater at 22°C than at 4.4°C. By 365 days of storage at 4.4°C, Salmonella Typhimurium DT104 declined by 2.19 log on smoked pig ears and 1.14 log on natural pig ears, while Salmonella Newport declined by 4.20 log on smoked pig ears and 2.08 log on natural pig ears. Populations of Salmonella Typhimurium DT104 on refrigerated natural pig ears rebounded between day 152 (3.21 log CFU per sample) and day 175 (4.79 log CFU per sample) and rose gradually for the duration of the study to 5.28 log CFU per sample. The model fits for survival rate of Salmonella on pig ears at 4.4°C show a rapid initial decline followed by a long tailing effect. Salmonella Typhimurium DT104 on natural pig ears at 4.4°C had the slowest rate of reduction. At 22°C Salmonella declined nonlinearly by >4.5 log for each combination of serotype and pig ear type at 22°C but remained detectable by enrichment. The model parameter for days to first decimal reduction of Salmonella on pig ears was two to three times higher at 4.4°C compared with 22°C, demonstrating that Salmonella slowly declines on very low aw refrigerated pet treats and more rapidly at room temperature. This information may be useful for pet treat safety assessments.

Implications of salt and sodium reduction on microbial food safety.

Excess sodium consumption has been cited as a primary cause of hypertension and cardiovascular diseases. Salt (sodium chloride) is considered the main source of sodium in the human diet, and it is estimated that processed foods and restaurant foods contribute 80% of the daily intake of sodium in most of the Western world. However, ample research demonstrates the efficacy of sodium chloride against pathogenic and spoilage microorganisms in a variety of food systems. Notable examples of the utility and necessity of sodium chloride include the inhibition of growth and toxin production by Clostridium botulinum in processed meats and cheeses. Other sodium salts contributing to the overall sodium consumption are also very important in the prevention of spoilage and/or growth of microorganisms in foods. For example, sodium lactate and sodium diacetate are widely used in conjunction with sodium chloride to prevent the growth of Listeria monocytogenes and lactic acid bacteria in ready-to-eat meats. These and other examples underscore the necessity of sodium salts, particularly sodium chloride, for the production of safe, wholesome foods. Key literature on the antimicrobial properties of sodium chloride in foods is reviewed here to address the impact of salt and sodium reduction or replacement on microbiological food safety and quality.

Transfer of Escherichia coli O157:H7 to iceberg lettuce via simulated field coring.

The field-core (cut and core) harvesting technique used for iceberg lettuce was evaluated as a potential means of cross-contamination with Escherichia coli O157:H7. Chlorinated water treatment was evaluated for its efficacy in removing or inactivating the pathogen on the blade portion of the field coring device and on cored lettuce. Field coring devices inoculated by immersing blades in soil containing E. coli O157:H7 at 3.74 or 6.57 log CFU/g contained 3.13 and 4.97 log CFU per blade, respectively. Treatment of inoculated field coring device blades by immersing in chlorinated water (200 microg/ml total chlorine) for 10 s resulted in a reduction of 1.56 log CFU per blade, which was 1.42 log CFU per blade greater than that achieved using water, but insufficient to eliminate the pathogen on blades. Field coring devices inoculated by contacting soil containing E. coli O157:H7 at 2.72 and 1.67 log CFU/g, then repeatedly used to cut and core 10 lettuce heads, transferred the pathogen to 10 and 5 consecutively processed heads, respectively. Lettuce cores remained positive for the pathogen after spraying with 100 microg/ml free chlorine for 120 s at 2.81 kg/cm2 (40 lb/in2), regardless of the inoculum level. The number of E. coli O157:H7 recovered from inoculated lettuce cores treated for 10 s with chlorine was significantly (P < or = 0.05) different from the number recovered from tissues treated with water. Dipping contaminated field coring devices in chlorinated water may not be effective in killing the pathogen and controlling cross-contamination from head to head. Spraying contaminated lettuce with chlorinated or untreated water reduces but does not eliminate E. coli O157:H7.

Evaluation of hot-water and sanitizer dip treatments of knives contaminated with bacteria and meat residue.

Hot water (HW; 82.2 degrees C, 180 degreesF) is used for sanitation of meat cutting implements in most slaughter facilities, but validation of actual practices against meat-borne bacterial pathogens and spoilage flora is lacking. Observed implement immersions in HW in two large pork processing plants were found to typically be < or = 1 s. Impact of these practices on bacteria on metal surfaces was assessed in the laboratory, and alternative treatments were investigated. Knives were inoculated with raw pork residues and Escherichia coli O157:H7, Salmonella Typhimurium DT104, Clostridium perfringens, and Lactobacillus spp. and were sampled before and after 1- or 15-s dips of blades in HW, warm water (48.9 degrees C), or warm sanitizers (neutral or acid quaternary ammonium compounds [QAC] at 400 ppm, or peroxyacetic acid at 700 ppm H2O2 and 165 ppm peroxyacetic acid). Simultaneous scrubbing and 15-s dipping in HW or acid QAC was also evaluated. Reductions on knives dipped for 1 s were usually < 1 log and were not significantly different (P > 0.05) between treatments. Reductions of E. coli O157:H7 after 15 s in HW, neutral QAC, acid QAC, or peroxyacetic acid were 3.02, 2.38, 3.04, and 1.52 log, respectively. Reductions of other bacteria due to HW were not significantly different from sanitizers and were significantly greater than warm water for all bacteria except C. perfringens. Combined scrubbing and 15-s dipping in HW resulted in a 2.91- and 2.25-log reduction of E. coli O157:H7 and Salmonella Typhimurium DT104, respectively, whereas reduction caused by acid QAC was significantly less at about 1.7 log each. Brief dip treatments of contaminated knives have limited efficacy, but longer immersions cause greater reductions that were not enhanced by scrubbing. QAC is a suitable alternative to HW in this application.

Validation of bacon processing conditions to verify control of Clostridium perfringens and Staphylococcus aureus.

It is unclear how rapidly meat products, such as bacon, that have been heat treated but not fully cooked should be cooled to prevent the outgrowth of spore-forming bacterial pathogens and limit the growth of vegetative cells. Clostridium perfringens spores and vegetative cells and Staphylococcus aureus cells were inoculated into ground cured pork bellies with and without 1.25% liquid smoke. Bellies were subjected to the thermal profiles of industrial smoking to 48.9 degrees C (120 degrees F) and normal cooling of bacon (3 h) as well as a cooling phase of 15 h until the meat reached 7.2 degrees C (45 degrees F). A laboratory-scale bacon smoking and cooling operation was also performed. Under normal smoking and cooling thermal conditions, growth of C. perfringens in ground pork bellies was <1 log regardless of smoke. Increase of S. aureus was 2.38 log CFU/g but only 0.68 log CFU/g with smoke. When cooling spanned 15 h, both C. perfringens and S. aureus grew by a total of about 4 log. The addition of liquid smoke inhibited C. perfringens, but S. aureus still achieved a 3.97-log increase. Staphylococcal enterotoxins were detected in five of six samples cooled for 15 h without smoke but in none of the six samples of smoked bellies. In laboratory-scale smoking of whole belly pieces, initial C. perfringens populations of 2.23 +/- 0.25 log CFU/g were reduced during smoking to 0.99 +/- 0.50 log CFU/g and were 0.65 +/- 0.21 log CFU/g after 15 h of cooling. Populations of S. aureus were reduced from 2.00 +/- 0.74 to a final concentration of 0.74 +/- 0.53 log CFU/g after cooling. Contrary to findings in the ground pork belly system, the 15-h cooling of whole belly pieces did not permit growth of either pathogen. This study demonstrates that if smoked bacon is cooled from 48.9 to 7.2 degrees C (120 to 45 degrees F) within 15 h, a food safety hazard from either C. perfringens or S. aureus is not likely to occur.

Growth potential of Clostridium perfringens during cooling of cooked meats.

Many meat-based food products are cooked to temperatures sufficient to inactivate vegetative cells of Clostridium perfringens, but spores of this bacterium can survive, germinate, and grow in these products if sufficient time, temperature, and other variables exist. Because ingestion of large numbers of vegetative cells can lead to concomitant sporulation, enterotoxin release in the gastrointestinal tract, and diarrhea-like illness, a necessary food safety objective is to ensure that not more than acceptable levels of C. perfringens are in finished products. As cooked meat items cool they will pass through the growth temperature range of C. perfringens (50 to 15 degrees C). Therefore, an important step in determining the likely level of C. perfringens in the final product is the estimation of growth of the pathogen during cooling of the cooked product. Numerous studies exist dealing with just such estimations, yet consensual methodologies, results, and conclusions are lacking. There is a need to consider the bulk of C. perfringens work relating to cooling of cooked meat-based products and attempt to move toward a better understanding of the true growth potential of the organism. This review attempts to summarize observations made by researchers and highlight variations in experimental approach as possible explanations for different outcomes. An attempt is also made here to identify and justify optimal procedures for conducting C. perfringens growth estimation in meat-based cooked food products during cooling.

Incidence of Clostridium perfringens in commercially produced cured raw meat product mixtures and behavior in cooked products during chilling and refrigerated storage.

A total of 445 whole-muscle and ground or emulsified raw pork, beef, and chicken product mixtures acquired from industry sources were monitored over a 10-month period for vegetative and spore forms of Clostridium perfringens. Black colonies that formed on Shahidi-Ferguson perfringens (SFP) agar after 24 h at 37 degrees C were considered presumptive positive. Samples that were positive after a 15-min heat shock at 75 degrees C were considered presumptive positive for spores. Of 194 cured whole-muscle samples, 1.6% were positive; spores were not detected from those samples. Populations of vegetative cells did not exceed 1.70 log10 CFU/g and averaged 1.56 log10 CFU/g. Of 152 cured ground or emulsified samples, 48.7% were positive, and 5.3% were positive for spores. Populations of vegetative cells did not exceed 2.72 log10 CFU/g and averaged 1.98 log10 CFU/g; spores did not exceed 2.00 log10 CFU/g and averaged 1.56 log10 CFU/g. Raw bologna (70% chicken), chunked ham with emulsion, and whole-muscle ham product mixtures were inoculated with C. perfringens spores (ATCC 12916, ATCC 3624, FD1041, and two product isolates) to ca. 3.0 log10 CFU/g before being subjected either to thermal processes mimicking cooking and chilling regimes determined by in-plant temperature probing or to cooking and extended chilling regimes. Populations of C. perfringens were recovered on SFP from each product at the peak cook temperatures, at 54.4, 26.7, and 7.2 degrees C, and after up to 14 days of storage under vacuum at 4.4 degrees C. In each product, populations remained relatively unchanged during chilling from 54.4 to 7.2 degrees C and declined slightly during refrigerated storage. These findings indicate processed meat products cured with sodium nitrite are not at risk for the growth of C. perfringens during extended chilling and cold storage.

Survival and growth of alkali-stressed Listeria monocytogenes on beef frankfurters and thermotolerance in frankfurter exudates.

Cells of Listeria monocytogenes exposed at 4 degrees C to 1% solutions of two alkaline cleaners or alkali-adapted in tryptose phosphate broth (pH 10.0) at 37 degrees C for 45 min, followed by 4 degrees C for 48 h, were inoculated onto beef frankfurters containing high fat (16 g) and high sodium (550 mg) or low fat (8 g) and low sodium (250 mg) per 57-g serving. Frankfurters were surface inoculated (2.0 log10 CFU/g), vacuum packaged, stored at -20, 4, or 12 degrees C, and analyzed for populations of L. monocytogenes at 2-day to 2-week intervals. Populations did not change significantly on frankfurters stored at -20 degrees C for up to 12 weeks. After storage at 4 degrees C for 6 weeks (I week before the end of shelf life), populations of control cells and cells exposed to alkaline cleaners were ca. 6.0 log10 CFU/g of low fat, low sodium (LFLS) frankfurters and ca. 3.5 log10 CFU/g of high fat, high sodium (HFHS) frankfurters. Growth of alkali-adapted cells on both types of frankfurters was retarded at 4 degrees C. Growth of L. monocytogenes on frankfurters stored at 12 degrees C was more rapid than at 4 degrees C, but a delay in growth of alkali-adapted cells on HFHS and LFLS frankfurters was evident during the first 9 and 6 days, respectively. Alkali-adapted cells had a significantly (P < or = 0.05) lower logistic D59 degrees C-value (decimal reduction time) than alkaline cleaner-exposed cells, but the D59 degrees C-value was not different from that of control cells. Cells exposed to a nonbutyl alkaline cleaner, and then heated in LFLS frankfurter exudates, had a significantly lower D62 degrees C-value than cells that had been exposed to some of the other treatments. Growth characteristics of L. monocytogenes inoculated onto the surface of frankfurters may be altered by previous exposure to alkaline environments. Differences in growth characteristics of L. monocytogenes on HFHS versus LFLS beef frankfurters stored at refrigeration temperatures indicate that composition influences the behavior of both alkaline-stressed and control cells.