Viability of Listeria monocytogenes on commercially-prepared hams surface treated with acidic calcium sulfate and lauric arginate and stored at 4°C.

We demonstrated the effectiveness of delivering an antimicrobial purge/fluid into shrink-wrap bags immediately prior to introducing the product and vacuum sealing, namely the "Sprayed Lethality In Container" (SLIC™) intervention delivery method. The pathogen was Listeria monocytogenes, the antimicrobials were acidic calcium sulfate (ACS; calcium sulfate plus lactic acid; 1:1 or 1:2 in dH(2)O) and lauric arginate (LAE; Ethyl-N-dodecanoyl-l-arginate hydrochloride; 5% or 10% in dH(2)O), and the product was commercially prepared "table brown" ham (ca. 3 pounds each). Hams were surface inoculated with a five-strain cocktail of L. monocytogenes (ca. 7.0 log(10) CFU per ham), added to shrink-wrap bags that already contained ACS or LAE, vacuum-sealed, and stored at 4°C for 24h. Pathogen levels decreased by 1.2, 1.6, 2.4, and 3.1 log(10) CFU/ham and 0.7, 1.6, 2.2, and 2.6 log(10) CFU/ham in samples treated with 2, 4, 6, and 8mL of a 1:1 and 1:2 solution of ACS, respectively. In samples treated with 2, 4, 6, and 8mL of a 5% solution of LAE, pathogen levels decreased by 3.3, 6.5, 5.6, and 6.5 log(10) CFU/ham, whereas when treated with a 10% solution of LAE pathogen levels decreased ca. 6.5 log(10) CFU/ham for all application volumes tested. The efficacy of ACS and LAE were further evaluated in shelf-life studies wherein hams were surface inoculated with either ca. 3.0 or 7.0 log(10) CFU of L. monocytogenes, added to shrink-wrap bags that contained 0, 4, 6, or 8mL of either a 1:2 solution of ACS or a 5% solution of LAE, vacuum-sealed, and stored at 4°C for 60 days. For hams inoculated with 7.0 log(10) CFU, L. monocytogenes levels decreased by ca.1.2, 1.5, and 2.0 log(10) CFU/ham and 5.1, 5.4, and 5.5 log(10) CFU/ham within 24h at 4°C in samples treated with 4, 6, and 8mL of a 1:2 solution of ACS and a 5% solution of LAE, respectively, compared to control hams that were not treated with either antimicrobial. Thereafter, pathogen levels remained relatively unchanged (±1.0 log(10) CFU/ham ) after 60 days at 4°C in hams treated with 4, 6, and 8mL of a 1:2 solution of ACS and increased by ca. 2.0-5.0 log(10) CFU/ham in samples treated with 4, 6, and 8mL of a 5% solution of LAE. For hams inoculated with 3.0 log(10) CFU, L. monocytogenes levels decreased by 1.3, 1.9, and 1.8 log(10) CFU/ham within 24h at 4°C in samples treated with 4, 6, and 8mL of a 1:2 solution of ACS, respectively, compared to control hams that were not treated. Likewise, levels of the pathogen were reduced to below the limit of detection (i.e., 1.48 log(10) CFU/ham) in the presence of 4, 6, and 8mL of a 5% solution of LAE within 24h at 4°C. After 60 days at 4°C, pathogen levels remained relatively unchanged (±0.3 log(10) CFU/ham) in hams treated with 4, 6, and 8mL of a 1:2 solution of ACS. However, levels of L. monocytogenes increased by ca. 2.0 log(10) CFU/ham in samples treated with 4 and 6mL of a 5% LAE solution within 60 days but remained below the detection limit on samples treated with 8mL of this antimicrobial. These data confirmed that application via SLIC™ of both ACS and LAE, at the concentrations and volumes used in this study, appreciably reduced levels of L. monocytogenes on the surface of hams within 24h at 4°C and showed potential for controlling outgrowth of the pathogen over 60 days of refrigerated storage.