Fate of Shiga toxin-producing O157:H7 and non-O157:H7 Escherichia coli cells within refrigerated, frozen, or frozen then thawed ground beef patties cooked on a commercial open-flame gas or a clamshell electric grill.

Both high-fat and low-fat ground beef (percent lean:fat = ca. 70:30 and 93:7, respectively) were inoculated with a 6-strain cocktail of non-O157:H7 Shiga toxin-producing Escherichia coli (STEC) or a five-strain cocktail of E. coli O157:H7 (ca. 7.0 log CFU/g). Patties were pressed (ca. 2.54 cm thick, ca. 300 g each) and then refrigerated (4°C, 18 to 24 h), or frozen (-18°C, 3 weeks), or frozen (-18°C, 3 weeks) and then thawed (4°C for 18 h or 21°C for 10 h) before being cooked on commercial gas or electric grills to internal temperatures of 60 to 76.6°C. For E. coli O157:H7, regardless of grill type or fat level, cooking refrigerated patties to 71.1 or 76.6°C decreased E. coli O157:H7 numbers from an initial level of ca. 7.0 log CFU/g to a final level of ≤1.0 log CFU/g, whereas decreases to ca. 1.1 to 3.1 log CFU/g were observed when refrigerated patties were cooked to 60.0 or 65.5°C. For patties that were frozen or freeze-thawed and cooked to 71.1 or 76.6°C, E. coli O157:H7 numbers decreased to ca. 1.7 or ≤0.7 log CFU/g. Likewise, pathogen numbers decreased to ca. 0.7 to 3.7 log CFU/g in patties that were frozen or freeze-thawed and cooked to 60.0 or 65.5°C. For STEC, regardless of grill type or fat level, cooking refrigerated patties to 71.1 or 76.6°C decreased pathogen numbers from ca. 7.0 to ≤0.7 log CFU/g, whereas decreases to ca. 0.7 to 3.6 log CFU/g were observed when refrigerated patties were cooked to 60.0 or 65.5°C. For patties that were frozen or freeze-thawed and cooked to 71.1 or 76.6°C, STEC numbers decreased to a final level of ca. 1.5 to ≤0.7 log CFU/g. Likewise, pathogen numbers decreased from ca. 7.0 to ca. 0.8 to 4.3 log CFU/g in patties that were frozen or freeze-thawed and cooked to 60.0 or 65.5°C. Thus, cooking ground beef patties that were refrigerated, frozen, or freeze-thawed to internal temperatures of 71.1 and 76.6°C was effective for eliminating ca. 5.1 to 7.0 log CFU of E. coli O157:H7 and STEC per g.

Fate of Shiga toxin-producing O157:H7 and non-O157:H7 Escherichia coli cells within blade-tenderized beef steaks after cooking on a commercial open-flame gas grill.

We compared the fate of cells of both Shiga toxin-producing Escherichia coli O157:H7 (ECOH) and Shiga toxin-producing non-O157:H7 E. coli (STEC) in blade-tenderized steaks after tenderization and cooking on a gas grill. In phase I, beef subprimal cuts were inoculated on the lean side with about 5.5 log CFU/g of a five-strain mixture of ECOH or STEC and then passed once through a mechanical blade tenderizer with the lean side facing up. In each of two trials, 10 core samples were removed from each of two tenderized subprimals and cut into six consecutive segments starting from the inoculated side. Ten total cores also were obtained from two nontenderized (control) subprimals, but only segment 1 (the topmost segment) was sampled. The levels of ECOH and STEC recovered from segment 1 were about 6.0 and 5.3 log CFU/g, respectively, for the control subprimals and about 5.7 and 5.0 log CFU/g, respectively, for the tenderized subprimals. However, both ECOH and STEC behaved similarly in terms of translocation, and cells of both pathogen cocktails were recovered from all six segments of the cores obtained from tenderized subprimals, albeit at lower levels in segments 2 to 6 than those found in segment 1. In phase II, steaks (2.54 and 3.81 cm thick) cut from tenderized subprimals were subsequently cooked (three steaks per treatment) on a commercial open-flame gas grill to internal temperatures of 48.9, 54.4, 60.0, 65.6, and 71.1°C. Regardless of temperature or thickness, we observed 2.0- to 4.1-log and 1.5- to 4.5-log reductions in ECOH and STEC levels, respectively. Both ECOH and STEC behaved similarly in response to heat, in that cooking eliminated significant numbers of both pathogen types; however, some survivors were recovered due, presumably, to uneven heating of the blade-tenderized steaks.

Inactivation of Shiga toxin-producing O157:H7 and non-O157:H7 Shiga toxin-producing Escherichia coli in brine-injected, gas-grilled steaks.

We quantified translocation of Escherichia coli O157:H7 (ECOH) and non-O157:H7 verocytotoxigenic E. coli (STEC) into beef subprimals after brine injection and subsequently monitored their viability after cooking steaks cut therefrom. Beef subprimals were inoculated on the lean side with ca. 6.0 log CFU/g of a five-strain cocktail of rifampin-resistant ECOH or kanamycin-resistant STEC, and then passed once through an automatic brine-injector tenderizer, with the lean side facing upward. Brine solutions (9.9% ± 0.3% over fresh weight) consisted of 3.3% (wt/vol) of sodium tripolyphosphate and 3.3% (wt/vol) of sodium chloride, prepared both with (Lac(+), pH = 6.76) and without (Lac(-), pH = 8.02) a 25% (vol/vol) solution of a 60% potassium lactate-sodium diacetate syrup. For all samples injected with Lac(-) or Lac(+) brine, levels of ECOH or STEC recovered from the topmost 1 cm (i.e., segment 1) of a core sample obtained from tenderized subprimals ranged from ca. 4.7 to 6.3 log CFU/g; however, it was possible to recover ECOH or STEC from all six segments of all cores tested. Next, brine-injected steaks from tenderized subprimals were cooked on a commercial open-flame gas grill to internal endpoint temperatures of either 37.8 °C (100 °F), 48.8 °C (120 °F), 60 °C (140 °F), or 71.1 °C (160 °F). Regardless of brine formulation or temperature, cooking achieved reductions (expressed as log CFU per gram) of 0.3 to 4.1 of ECOH and 0.5 to 3.6 of STEC. However, fortuitous survivors were recovered even at 71.1 °C (160 °F) for ECOH and for STEC. Thus, ECOH and STEC behaved similarly, relative to translocation and thermal destruction: Tenderization via brine injection transferred both pathogens throughout subprimals and cooking highly contaminated, brine-injected steaks on a commercial gas grill at 71.1 °C (160 °F) did not kill all cells due, primarily, to nonuniform heating (i.e., cold spots) within the meat.