Alphamune, a yeast extract antibiotic alternative, has been shown to stimulate the immune system, increase BW in pigs, and reduce Salmonella colonization in chickens. The influence of Alphamune on gastrointestinal tract development has not been reported. Two trials were conducted to evaluate the effects of Alphamune on gut maturation of 7- and 21-d-old turkey poults. Poults were fed a standard control unmedicated turkey starter diet or the same diet supplemented with either 1 or 2 lb/ton of Alphamune (n = 18/group). Poults were weighed on d 7 and 21, euthanized, and a 2-cm section was collected from the midpoint of the duodenum, jejunum, and ileum of each bird (9 poults/d per treatment) and fixed in a 10% formalin solution for 72 h and then stained. Twenty measurements of villus height, villus surface area, lamina propria thickness, crypt depth, and density of neutral, sialomucin, and sulfomucin goblet cells were taken per section per poult. On d 7, BW were higher for the poults given the Alphamune treatments compared with control poults; however, no differences were observed on d 21. Alphamune supplementation influenced intestinal morphology differently based on gut location. Ileum villus height, surface area, lamina propria thickness, crypt depth, and neutral, sialomucin, and sulfomucin goblet cell density were enhanced with Alphamune treatments on d 7 and 21 (P < 0.05) and in a dose-dependent manner for many of the parameters evaluated. Jejunum results were mixed. Surface area, crypt depth, and sialomucin and sulfomucin goblet cells were consistently higher for the 2 lb/ton of Alphamune groups compared with the control group on d 7 and 21. Duodenum villus height, surface area, and goblet cell density were higher for the 2 lb/ton of Alphamune groups on d 7; however, intestinal morphology of the duodenum was not different between the control and treated birds on d 21. These results suggest that feed supplemented with Alphamune can accelerate gastrointestinal maturation in turkey poults and is more pronounced in the ileum than in other portions of the small intestine.

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 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.

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.