Salmonella continues to be a significant cause of foodborne illnesses in human medicine. The Centers for Disease Control and Prevention reported Salmonella as the second leading cause of foodborne illness in the United States, and the leading cause of both hospitalizations and deaths. Salmonella enterica 4,[5],12:i:- (STM) is a monophasic variant of S. Typhimurium and it is an emerging threat to both human and animal health. STM was first identified in the 1980’s from poultry products and has become increasingly prevalent in meat products including pork. STM has also been identified in swine farms as well as feed manufacturing environments and feed itself. Similar pulse-field gel electrophoresis profiles have been observed between human clinical cases and the STM samples originating from swine feed. These related profiles suggest a link between swine ingesting contaminated feed and the source of foodborne illness in human. The objective of this article was to better understand the history of STM and the possible pathway between swine feed to the household table. Continued research is necessary to better understand how STM can enter both the feed supply chain and the pork production chain to avoid contamination of pork products destined for human consumption.

Salmonella enterica Serotype 4,[5],12:i:- ( STM ) has become an increasing burden for food safety. This strain has been often detected in swine products. STM -contaminated feed, water or air were given to weanling pigs in order to determine possible STM transmission routes. A control group of pigs was also sampled. STM was monitored daily in feces and by rectal and nasal swabs. STM colonization was observed in tissues with the greatest amount in tonsil, lower intestine, and mesenteric lymph nodes. No differences in lesion severity were observed between inoculated and control pigs. Contaminated feed, water, and aerosolized particles were able to cause infection in weaned pigs; however, no STM colonization was observed in skeletal muscle meat destined for human consumption. Based on the results from this study, contaminated pork products most likely stem from cross-contamination of STM from digesta or lymph nodes during processing.

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A total of 350 weanling pigs (DNA 400 × 200; initially, 5.67 ± 0.06 kg BW) were used in a 42-d study with 5 pigs per pen and 14 replicate pens per treatment. At weaning, pigs were allotted to pens in a completely randomized design and pens of pigs were randomly assigned to one of five dietary treatments: 1) negative control (CON; standard nursery diet containing only 150 ppm Zn from trace mineral premix and no acidifier); 2) control diet with 3,000 ppm added zinc from ZnO included in phase 1 and 2,000 ppm added zinc from ZnO included in phase 2 (ZnO); 3) control diet with 0.70% formic acid (FA; Amasil® NA; BASF, Florham, NJ); 4) control diet with 0.18% glycerol monolaurate (GML; Natural Biologics GML, Natural Biologics, Newfield, NY); and 5) control diet with a 1.0% blend of formic acid and glycerol monolaurate (FORMI; FORMI 3G, ADDCON GmbH, Bitterfeld-Wolfen, Germany). Pigs were fed treatment diets from d 0 to d 28 and were then fed a common diet from d 28 to d 42. From d 0 to d 7, pigs fed ZnO or FORMI had increased (P = 0.03) ADG compared to pigs fed CON, with no difference in feed intake (P > 0.05). Overall, pigs fed GML had reduced (P < 0.0001) ADG compared to those fed the CON, ZnO, or FORMI diets. Fecal DM was evaluated from d 7 to d 28 and there was a treatment × day interaction (P = 0.04). Pigs fed GML had a lower fecal DM % on d 7, but a higher fecal DM % on d 14 and 21; however, no differences in fecal DM were observed on d 28. Fresh fecal samples were collected from the same randomly selected pig on d 0 and d 14 (70 pigs total;14 pigs per treatment) for analysis of fecal microbial populations using 16S rDNA sequencing. Dietary treatment did not significantly impact fecal microbiota at the phyla level, but pigs fed ZnO had an increased relative abundance (P < 0.01) of the family Clostridiaceae. A blood sample was also collected from one pig per pen on d 0 and 14 for analysis of serum IgA, IgG, and TNF-α. There was no evidence that dietary treatment effected IgA, IgG, or TNF-α concentrations. The effect of sampling day was significant (P < 0.05), where circulating IgA and TNF-α was increased and IgG was decreased from d 0 to d 14. In summary, there is potential for a blend of formic acid and GML to improve growth performance immediately post-weaning without negatively impacting fecal consistency. Formic acid and GML alone or in combination did not impact fecal microbial populations or serum immune parameters.

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