The domestic chicken is a common model organism for human biological research and of course also forms the basis of a global protein industry. Recent methodological advances have spurred the recognition of microbiomes as complex communities with important influences on the health and disease status of the host. In this minireview, we provide an overview of the current state of knowledge of the chicken gastrointestinal microbiome focusing on spatial and temporal variability, the presence and importance of human pathogens, the influence of the microbiota on the immune system, and the importance of the microbiome for poultry nutrition. Review and meta-analysis of public data showed cecal communities dominated by Firmicutes and Bacteroides at the phylum level, while at finer levels of taxonomic resolution, a phylogenetically diverse assemblage of microorganisms appears to have similar metabolic functions that provide important benefits to the host as inferred from metagenomic data. This observation of functional redundancy may have important implications for management of the microbiome. We foresee advances in strategies to improve gut health in commercial operations through management of the intestinal microbiota as an alternative to in-feed subtherapeutic antibiotics, improvements in pre- and probiotics, improved management of polymicrobial poultry diseases, and better control of human pathogens via colonization reduction or competitive exclusion strategies.

BackgroundPoultry remains a major source of foodborne bacterial infections. A variety of additives with presumed anti-microbial and/or growth-promoting effects are commonly added to poultry feed during commercial grow-out, yet the effects of these additives on the gastrointestinal microbial community (the GI microbiome) as the bird matures remain largely unknown. Here we compared temporal changes in the cecal microbiome to the effects of formic acid, propionic acid, and medium-chain fatty acids (MCFA) added to feed and/or drinking water.ResultsCecal bacterial communities at day of hatch (n = 5 birds), 7d (n = 32), 21d (n = 27), and 42d (n = 36) post-hatch were surveyed using direct 454 sequencing of 16S rRNA gene amplicons from each bird in combination with cultivation-based recovery of a Salmonella Typhimurium marker strain and quantitative-PCR targeting Clostridium perfringens. Treatment effects on specific pathogens were generally non-significant. S. Typhimurium introduced by oral gavage at day of hatch was recovered by cultivation from nearly all birds sampled across treatments at 7d and 21d, but by 42d, S. Typhimurium was only recovered from ca. 25% of birds, regardless of treatment. Sequencing data also revealed non-significant treatment effects on genera containing known pathogens and on the cecal microbiome as a whole. In contrast, temporal changes in the cecal microbiome were dramatic, highly significant, and consistent across treatments. At 7d, the cecal community was dominated by three genera (Flavonifractor, Pseudoflavonifractor, and a Lachnospiracea sequence type) that accounted for more than half of sequences. By 21d post-hatch, a single genus (Faecalibacterium) accounted for 23-55% of sequences, and the number of Clostridium 16S rRNA gene copies detected by quantitative-PCR reached a maximum.ConclusionsOver the 42 d experiment, the cecal bacterial community changed significantly as measured by a variety of ecological metrics and increases in the complexity of co-occurrence networks. Management of poultry to improve animal health, nutrition, or food safety may need to consider the interactive effects of any treatments with the dramatic temporal shifts in the taxonomic composition of the cecal microbiome as described here.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-014-0282-8) contains supplementary material, which is available to authorized users.

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The influence of fructooligosaccharide (FOS) on the ability of Salmonella typhimurium to grow and colonize the gut of chickens was investigated. In vitro studies showed that Salmonella did not grow when FOS was the sole carbon source. When FOS was fed to chicks at the .375% level, little influence on Salmonella colonization was observed. At the .75% level, 12% fewer FOS-fed birds were colonized with Salmonella compared with control birds. When chicks given a partially protective competitive exclusion (CE) culture were fed diets supplemented with .75% FOS, only 4 of 21 (19%) chickens challenged with 10(9) Salmonella cells on Day 7 became colonized as compared with 14 of 23 (61%) chickens given CE alone. When chickens were stressed by feed and water deprivation on Day 13 and challenged with 10(9) Salmonella on Day 14, 33 of 36 (92%) chickens fed a control diet were colonized compared with only 9 of 36 (25%) chickens fed a .75% FOS diet. Chickens treated with FOS had a fourfold reduction in the level of Salmonella present in the ceca. Feeding FOS in the diet of chickens may lead to a shift in the intestinal gut microflora, and under some circumstances may result in reduced susceptibility to Salmonella colonization.

A study was conducted of 32 broiler flocks on eight different farms, belonging to four major U.S. producers. The farms were studied over I complete calendar year. Overall, 28 (87.5%) of the flocks became Campylobacter positive, and only four (12.5%) remained negative throughout the 6- to 8-week rearing period. In the majority of flocks, sampled every 2 weeks throughout production, Campylobacter-positive fecal and cecal samples were not detected until 4 to 8 weeks of age. In only six of the flocks were environmental samples found to be positive before shedding of Campylobacter was detected in the birds. Even in some of the Campylobacter-negative flocks, contamination of the rearing environment was positive for Campylobacter but did not result in the birds subsequently excreting the organism. These findings are discussed in relation to U.S. husbandry practices and present uncertainty about sources of Campylobacter infection for poultry flocks. Birds were often transported to the processing plant in coops that were already contaminated with Campylobacter, and the organisms were sometimes found in samples of scald water and chill water. After chilling, the proportions of Campylobacter-positive carcasses from different producers ranged from 21.0 to 40.9%, which is lower than in other studies, and possible reasons are considered.

Campylobacter isolates from diverse samples within broiler production and processing environments were typed by using flaA short variable region DNA sequence analysis. Sixteen flocks from four different farms representing two broiler producers in Arkansas and California were analyzed. Fourteen of the flocks (87.5%) were Campylobacter-positive; two remained negative throughout the 6-week rearing period. In general, multiple clones were present within a flock. Additionally, clones found within a flock were also present on the final product, although the diversity of Campylobacter spp. on the final product appeared to be reduced relative to that observed within the flock. Comparison of clones between flocks on the same farm revealed that some clones of Campylobacter persisted in multiple flocks. Furthermore, some clones were identified across the two farms that were under the same management. In two sampling periods, environmental isolates were positive for Campylobacter prior to flock shedding. Environmental samples associated with five additional flocks were positive for Campylobacter concomitantly with recovery of Campylobacter from the birds. Analysis of the environmental isolates that were positive prior to flock shedding demonstrated that in some instances the environmental isolates possessed genotypes identical to those of isolates originating from the flock, while in other cases the environmental isolates possessed genotypes that were distantly related to isolates obtained from the flock. Analyses of environmental isolates that tested positive concurrently with the positive isolates from the flocks demonstrated varied results; in some instances the environmental isolates possessed genotypes identical to those of isolates originating from the flock, while in other cases the environmental isolates possessed genotypes that were distantly related to isolates obtained from the flock. These data suggest that the external environment may contribute to Campylobacter contamination during poultry production and processing. However, environmental contamination with Campylobacter does not appear to be the sole contributing factor.

The presence of salmonellae in fertile broiler hatching eggs has been clearly identified as a critical control point in the salmonellae contamination of broiler chickens. This paper reviews the published research studies on a) the penetration and proliferation of salmonellae in hatching eggs, b) the consequences of this contamination on the contamination of the final product, and c) the egg's defenses against invading salmonellae. A better understanding of the material in this review paper will assist poultry researchers and the poultry industry in continuing to make progress in reducing and eliminating salmonellae from fertile hatching eggs, hatcheries, and breeder flocks.

Colonization of the ceca and contamination on carcasses of chickens by Campylobacter spp. was investigated. Samples were taken on the farm and after transport and holding. In the first set of experiments, 20 chickens, obtained from each of 10 broiler farms, were collected from houses containing 6- to 7-wk-old birds. Half of the birds were slaughtered at the farm; the other half were transported (10 birds per chicken coop) to a holding facility and killed within 16 to 18 h. The levels of Campylobacter spp. on the carcass and in the ceca were assessed. Ceca from birds in 9 of the 10 farms sampled were positive for Campylobacter spp. Colonization levels ranged from 10(4.11) to 10(7.28) cfu Campylobacter spp./g cecal matter, except on one farm, where the organism was not isolated. The mean count on the farm was 10(5.44) cfu Campylobacter spp./g cecal material, and after transport the mean was 10(6.15) cfu/g. Significant increases (P = .0085) in levels of Campylobacter spp. on the chicken carcasses occurred after transport. Levels of Campylobacter spp. enumerated from unprocessed chicken carcasses after transport averaged 10(7.11) per carcass, up from an average of 10(3.66) cfu per carcass of the farm. To further verify this observation, field trials were conducted to assess levels on carcasses before and after commercial transport. Employing five farms and 200 6-wk-old chickens, the above observations were confirmed: prior to transport 12.1% of the chickens harbored an average of 10(2.71) cfu per carcass, but after transport 56.0% of the chicken exteriors harbored an average of 10(5.15) cfu per carcass. The results of this study indicate that transport and holding prior to processing contributes to the Campylobacter spp. of > 10(4) cfu normally found on processed poultry carcasses.