The immune system of neonatal chicks is functionally immature during the first week of life. Researchers have previously demonstrated that the avian humoral response can be increased with probiotics. Although the humoral response provides the chick with an effective mechanism to combat pathogens, sufficient antibody titers are not attained until 7 to 10 d postinfection. However, the innate immune system (i.e., heterophils) can respond much more quickly to pathogens. The objective of this study was to determine whether probiotic bacteria can also upregulate heterophil function. Heterophils were isolated from the peripheral blood of neonatal chickens by using a discontinuous density gradient. Oxidative burst and degranulation are bactericidal mechanisms used by heterophils to kill pathogens and were used in this study as indicators of heterophil function. We found that each of the 10 "generally recognized as safe" probiotic isolates (designated G1 to G11) tested in vitro were capable of increasing (P < 0.05) heterophil oxidative burst and degranulation when compared with unstimulated controls. Bacillus subtilis (G3), Lactococcus lactis lactis (G6), and Lactobacillus acidophilus (G8) isolates were determined to elicit the greatest heterophil response in vitro and were subsequently fed to chicks. Phosphate-buffered saline or 1 of these 3 probiotic isolates (approximately 2.5 x 10(8) cfu/chick; 50 chicks/treatment) resuspended in PBS was administered by oral gavage on the day of hatch. Heterophils were isolated from chicks from each of these 4 treatment groups 24 h posttreatment. Significant increases in heterophil degranulation and oxidative burst were observed with the G3-, G6-, and G8-treated chicks when compared with heterophils isolated from birds with no probiotic treatment. These data suggest that probiotic bacteria can significantly improve heterophil oxidative burst and degranulation in broilers. To our knowledge, this is the first study demonstrating a relationship between probiotics and avian heterophil function.
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 is a leading worldwide cause of foodborne illness associated with consumption of poultry products. Unfortunately, most preharvest treatments fail to reduce this enteric foodborne pathogen in poultry. The efficacy of natural plant extracts, such as thymol and carvacrol, has efficacy against other enteric pathogens but has not been evaluated against Campylobacter. To accomplish this, day old broiler chicks (n = 10 chicks/dose) were fed 0% (controls) or thymol or carvacrol or combinations of these compounds in feed in four different trials. Birds were orally challenged with Campylobacter jejuni at day 3 and at day 10, cecal samples were collected for Campylobacter enumeration. Campylobacter counts were reduced for 0.25% thymol (trial 1), 1% carvacrol or 2% thymol (trial 2) treatments, or a combination of both thymol and carvacrol at 0.5% (trial 3) in this study (P < 0.05). These results support supplementation of these compounds in feed to reduce Campylobacter colonization in chickens. PRACTICAL APPLICATIONSCampylobacter is one of the major causes of foodborne enteritis worldwide, and the majority of human campylobacteriosis cases were reported to be associated with improper handling and/or consumption of undercooked poultry . Because poultry are the major contributors for human infections, eliminating or reducing Campylobacter in poultry would greatly reduce the risk of campylobacteriosis in humans. Many strategies have been tried to eliminate Campylobacter with limited success. Considering the increasing consumer demand for natural, safer food products, free from synthetic residues, use of natural compounds with proven antimicrobial efficacy appears to be a promising strategy to control Campylobacter in poultry. In the present study we evaluated the in vivo efficacy of different concentrations and combinations of two natural compounds, thymol and carvacrol, against Campylobacter colonization in broiler chickens. bs_bs_banner Journal of Food Safety
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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