Thermal inactivation of a single strain each of serotype O26:H11, O45:H2, O103:H2, O104:H4, O111:H⁻, O121:H19, O145:NM, and O157:H7 cells of Shiga toxin-producing Escherichia coli in wafers of ground beef.

For each of two trials, freshly ground beef of variable fat content (higher: 70:30 %lean:%fat; lower: 93:7 %lean:%fat) was separately inoculated with ca. 7.0 log CFU/g of a single strain of Escherichia coli serotypes O26:H11, O45:H2, O103:H2, O104:H4, O111:H⁻, O121:H19, O145:NM, and O157:H7. Next, ca. 3-g samples of inoculated beef were transferred into sterile filter bags and then flattened (ca. 1.0 mm thick) and vacuum sealed. For each temperature and sampling time, three bags of the inoculated wafers of beef were submerged in a thermostatically controlled water bath and heated to an internal temperature of 54.4°C (130°F) for up to 90 min, to 60°C (140°F) for up to 4 min, or to 65.6°C (150°F) for up to 0.26 min. In lower fat wafers, D-values ranged from 13.5 to 23.6 min, 0.6 to 1.2 min, and 0.05 to 0.08 min at 54.4, 60.0, and 65.6°C, respectively. Heating higher fat wafers to 54.4, 60.0, and 65.6°C generated D-values of 18.7 to 32.6, 0.7 to 1.1, and 0.05 to 0.2 min, respectively. In addition, we observed reductions of ca. 0.7 to 6.7 log CFU/g at 54.4°C after 90 min, ca. 1.1 to 6.1 log CFU/g at 60.0°C after 4 min, and 0.8 to 5.8 log CFU/g at 65.6°C after 0.26 min. Thus, cooking times and temperatures effective for inactivating a serotype O157:H7 strain of E. coli in ground beef were equally effective against the seven non-O157:H7 Shiga toxin-producing strains investigated herein.

Validation of food-grade salts of organic acids as ingredients to control Listeria monocytogenes on pork scrapple during extended refrigerated storage.

This study was conducted to investigate control of Listeria monocytogenes on pork scrapple during storage at 4°C. In phase I, scrapple was formulated, with or without citrate-diacetate (0.64%), by a commercial processor to contain various solutions or blends of the following antimicrobials: (i) lactate-diacetate (3.0 or 4.0%), (ii) lactate-diacetate-propionate (2.0 or 2.5%), and (iii) levulinate (2.0 or 2.5%). Regardless of whether citrate-diacetate was included in the formulation, without the subsequent addition of the targeted antimicrobials pathogen levels increased ca. 6.4 log CFU/g within the 50-day storage period. In the absence of citrate-diacetate but when the targeted antimicrobials were included in the formulation, pathogen numbers increased by ca. 1.3 to 5.2 log CFU/g, whereas when citrate-diacetate was included with these antimicrobials, pathogen numbers increased only by ca. 0.7 to 2.3 log CFU/g. In phase II, in the absence of citrate-diacetate, when the pH of the lactate-diacetate-propionate blend (2.5%) was adjusted to pH 5.0 or 5.5 pathogen numbers remained unchanged (≤0.5 log CFU/g increase) over 50 days, whereas when citrate-diacetate was included with the lactate-diacetate-propionate blend adjusted to pH 5.0 or 5.5, pathogen numbers decreased by 0.3 to 0.8 log CFU/g. In phase III, when lower concentrations of the lactate-diacetate-propionate blend (1.5 or 1.94%) were adjusted to pH 5.5, pathogen numbers increased by ca. 6.0 and 4.7 log CFU/g, respectively, whereas when the mixture was adjusted to pH 5.0, pathogen numbers increased by ≤0.62 log CFU/g. Thus, scrapple formulated with lactate-diacetate-propionate (1.5 and 1.94% at pH 5.0) is an unfavorable environment for outgrowth of L. monocytogenes.