We surveyed chicken livers from various sources for the presence and levels of Salmonella. The pathogen was recovered from 148 (59.4%) of 249 chicken livers purchased at retail stores in Delaware, New Jersey, and Pennsylvania over about a 9-month period. Positive samples harbored Salmonella at levels of 6.4 most probable number (MPN)/g to 2.4 log CFU/g. The percentage of Salmonella-positive livers purchased at retail outlets in New Jersey (72%, 59 of 82 livers) was significantly higher (P < 0.05) than the percentage for livers purchased in Delaware (48%, 36 of 75 livers); however, this percentage was not significantly different (P > 0.05) from that for livers purchased in Pennsylvania (57.6%, 53 of 92 livers). The pathogen was also recovered more often (P = 0.019) from livers that were packaged by retailers (81 of 121 livers, 66.9%) than from livers packaged directly by processors (67 of 128 livers, 52.3%). In related studies, 12 (5.8%) of 207 chicken livers harvested from birds on a research farm tested positive for Salmonella at levels of 0.4 to 2.2 MPN/g. The recovery rate of Salmonella was 4.4% (6 of 135 livers) from livers with the gall bladder attached and 8.3% (6 of 72 livers) from livers when the gall bladder was removed at harvest on the research farm. We also quantified the levels of a nine-strain cocktail (ca. 6.5 log CFU/g) of Salmonella strains inoculated externally onto or internally into livers both before and after extended cold storage. Storage for at least 2 days at 4°C or 15 days at −20°C resulted in a decrease of about 1.0 log CFU/g in pathogen levels. Given the relatively high recovery rate (ca. 6.0 to 60.0%) and high (possibly illness causing) levels (0.4 MPN/g to 2.4 CFU/g) of Salmonella associated with chicken livers in the present study, further interventions for processors are needed to lower the prevalence and levels of this pathogen on poultry liver.
The viability of Shiga toxin–producing Escherichia coli (STEC), Salmonella, and Listeria monocytogenes within plant- and beef-based burgers was monitored during storage and cooking. When inoculated (ca. 3.5 log CFU/g) into 15-g portions of plant- or beef-based burgers, levels of STEC and Salmonella decreased slightly (≤0.5-log decrease) in both types of burgers when stored at 4°C, but increased ca. 2.4 and 0.8 log CFU/g, respectively, in plant-based burgers but not beef-based burgers (≤1.2-log decrease), after 21 days at 10°C. For L. monocytogenes, levels increased by ca. 1.3 and 2.6 log CFU/g in plant burgers after 21 days at 4 and 10°C, respectively, whereas pathogen levels decreased slightly (≤0.9-log decrease) in beef burgers during storage at 4 and 10°C. Regarding cooking, burgers (ca. 114 g each) were inoculated with ca. 7.0 log CFU/g STEC, Salmonella, or L. monocytogenes and cooked in a sauté pan. Cooking plant- or beef-based burgers to 62.8°C (145°F), 68.3°C (155°F), or 73.9°C (165°F) delivered reductions ranging from ca. 4.7 to 6.8 log CFU/g for STEC, ca. 4.4 to 7.0 log CFU/g for L. monocytogenes, and ca. 3.5 to 6.7 log CFU/g for Salmonella. In summary, the observation that levels of all three pathogens increased by ca. 1.0 to ca. 2.5 log CFU/g in plant-based burgers when stored at an abusive temperature (10°C) highlights the importance of proper storage (4°C) to lessen risk. However, because all three pathogens responded similarly to heat in plant-based as in beef-based burgers, well-established cooking parameters required to eliminate STEC, Salmonella, or L. monocytogenes from ground beef should be as effective for controlling cells of these same pathogens in a burger made with plant-sourced protein. HIGHLIGHTS
We investigated the effects of deep-frying or oven cooking on inactivation of Shiga toxin-producing cells of Escherichia coli (STEC) in meatballs. Finely ground veal and/or a finely ground beef-pork-veal mixture were inoculated (ca. 6.5 log CFU/g) with an eight-strain, genetically marked cocktail of rifampin-resistant STEC strains (STEC-8; O111:H, O45:H2, O103:H2, O104:H4, O121:H19, O145:NM, O26:H11, and O157:H7). Inoculated meat was mixed with liquid whole eggs and seasoned bread crumbs, shaped by hand into 40-g balls, and stored at -20°C (i.e., frozen) or at 4°C (i.e., fresh) for up to 18 h. Meatballs were deep-fried (canola oil) or baked (convection oven) for up to 9 or 20 min at 176.7°C (350°F), respectively. Cooked and uncooked samples were homogenized and plated onto sorbitol MacConkey agar with rifampin (100 μg/ml) followed by incubation of plates at 37°C for ca. 24 h. Up to four trials and three replications for each treatment for each trial were conducted. Deep-frying fresh meatballs for up to 5.5 min or frozen meatballs for up to 9.0 min resulted in reductions of STEC-8 ranging from ca. 0.7 to ≥6.1 log CFU/g. Likewise, reductions of ca. 0.7 to ≥6.1 log CFU/g were observed for frozen and fresh meatballs that were oven cooked for 7.5 to 20 min. This work provides new information on the effect of prior storage temperature (refrigerated or frozen), as well as subsequent cooking via deep-frying or baking, on inactivation of STEC-8 in meatballs prepared with beef, pork, and/or veal. These results will help establish guidelines and best practices for cooking raw meatballs at both food service establishments and in the home.
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