Campylobacter is one of the leading causes of human foodborne illness in the United States, and epidemiological evidence indicates that poultry and poultry products are a significant source of human Campylobacter infections. Reducing Campylobacter in the intestinal tract would reduce contamination of poultry products and eggs. Caprylic acid, an 8-carbon medium-chain fatty acid has been shown to be bactericidal against several pathogenic bacteria. It has, however, not been tested in the control of Campylobacter in chickens. Four trials were carried out to evaluate the efficacy of caprylic acid against cecal Campylobacter jejuni colonization in 10-d-old chicks. In the first 2 trials, day-of-hatch chicks (n=40 per trial) were assigned to negative controls (no Campylobacter, no caprylic acid), positive controls (Campylobacter, no caprylic acid), and a low (0.7%) and a high (1.4%) dose of caprylic acid supplemented in regular chick starter feed (n=10 chicks/treatment). Two more trials were carried out to evaluate a wider range of caprylic acid doses on cecal Campylobacter counts, in which day-of-hatch chicks (n=90 per trial) were assigned to 9 treatments: negative controls (no Campylobacter, no caprylic acid) and caprylic acid doses of 0 (positive controls), 0.35, 0.525, 0.7, 0.875, 1.05, 1.225, and 1.4% (n=10 chicks/treatment). Except for the negative controls, chicks were orally gavaged with approximately 1 x 10(6) cfu Campylobacter on d 3. On d 10, cecal contents were collected and Campylobacter concentrations were determined in each trial. In all 4 trials, the 0.7% dose of caprylic acid consistently reduced Campylobacter content counts compared with the positive control. In trials 3 and 4, doses less than 1.05% consistently reduced cecal Campylobacter content in both trials. At the higher doses, caprylic acid reduced feed consumption and body weight, but did not affect feed conversion when compared with the positive controls. These data suggest that low-dose supplementation with caprylic acid in feed may reduce Campylobacter colonization in young chickens.

Campylobacter causes human foodborne illness, and epidemiological evidence indicates poultry and poultry products as a significant source of human infection. Decreasing Campylobacter in the poultry intestinal tract would decrease contamination of poultry products. Caprylic acid is a medium-chain fatty acid reported to be effective in killing a variety of bacterial pathogens, including Campylobacter jejuni, but its effect has not been investigated in the control of C. jejuni in preslaughter market-aged poultry already colonized with this bacterium. The objective of this study was to determine the therapeutic effect of caprylic acid on C. jejuni counts in the cecal contents of 42-d-old chickens. Four trials were conducted. In the first 2 trials, day-of-hatch chicks (n = 60 per trial) were assigned to 6 treatment groups (n = 10 birds per treatment group): positive controls (Campylobacter, no caprylic acid), 0.7 or 1.4% of caprylic acid in feed for the last 3 d of the trial with or without a 12-h feed withdrawal. Treatments were similar for trials 3 and 4 except the doses used were 0.35 or 0.7% caprylic acid supplementation for the last 7 d of the trial. On d 42, ceca were collected and Campylobacter counts determined. The supplementation of caprylic acid at 0.35 and 0.7% consistently decreased (P < 0.05) the colonization of C. jejuni in the chicken ceca compared with positive control treatment. When these treatments were evaluated after a 12-h feed withdrawal period, 0.7% caprylic acid decreased Campylobacter colonization in the 3-d treatment supplementation. Body weight and feed consumption did not differ between the caprylic acid and control groups. The results suggest that therapeutic supplementation of caprylic acid in the feed can effectively decrease Campylobacter in market-aged chickens and may be a potential treatment for decreasing pathogen carriage in poultry.

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Campylobacter is a leading cause of food-borne illness in the United States. Recent evidence has demonstrated that bacteriocins produced by Bacillus circulans and Paenibacillus polymyxa reduce cecal Campylobacter colonization in broiler chickens infected with Campylobacter jejuni. As Campylobacter coli is the most prevalent Campylobacter isolate recovered in turkeys, the objectives of the present study were to evaluate the efficacy of these bacteriocins against C. coli colonization and their influence on the gastrointestinal architecture of young turkeys. In 3 separate trials, a total of 135 day-of-hatch poults (n = 45/trial) were orally challenged on d 3 with approximately 10(6) cfu of a mixture of 3 C. coli isolates. Immediately before bacteriocin treatment (d 10), cecal Campylobacter concentrations averaged 1.1 x 10(7) cfu/ g of cecal contents (n = 15/trial). On d 10 to 12 posthatch, 2 bacteriocin treatment groups were given free access to feed supplemented with purified, microencapsulated bacteriocins, whereas the positive control treatment group had access to untreated feed (n = 10/treatment group per trial). At the end of the 3-d dosing period, ceca and duodenal loops were collected for analysis. In each of the 3 separate trials, treatment with bacteriocin eliminated detectable ceca Campylobacter concentrations (detection limit, 1 x 10(2) cfu/g of cecal contents) vs. controls (1.0 x 106 cfu of Campylobacter/g of cecal contents). Duodenum crypt depth and goblet cell numbers were also reduced in turkeys treated with either bacteriocin vs. controls (P < 0.05). The dynamic reduction in crypt depth and goblet cell density in turkeys dosed with bacteriocin may provide clues to how bacteriocins inhibit enteric Campylobacter.

Antibiotics are used by veterinarians and producers to treat disease and improve animal production. The federal government, to ensure the safety of the food supply, establishes antibiotic residue tolerances in edible animal tissues and determines the target tissues (e.g., muscle) for residue monitoring. However, when muscle is selected as the target tissue, the federal government does not specify which type of muscle tissue is used for monitoring (e.g., breast versus thigh). If specific muscle tissues incorporate residues at higher concentrations, these tissues should be selected for residue monitoring. To evaluate this possibility in poultry, chickens were divided into four groups and at 33 days of age were dosed with enrofloxacin (Baytril), as per label directions, at either 25 ppm for 3 days, 25 ppm for 7 days, 50 ppm for 3 days, or 50 ppm for 7 days. Breast and thigh muscle tissues were collected from each bird (n = 5 birds per day per group) during the dosing and withdrawal period, and fluoroquinolone concentrations were determined. The results indicate higher overall enrofloxacin concentrations in breast versus thigh muscle for each treatment group (P < 0.05). These data indicate, at least for enrofloxacin, that not all muscle tissues incorporate antibiotics at the same concentrations. These results may be helpful to regulatory agencies as they determine what tissues are to be monitored to ensure that the established residue safety tolerance levels are not exceeded.