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The gastrointestinal tract provides the biological environment for nutrient digestion and absorption. Its physical and chemical barriers are crucial to protect from invading pathogens and toxic substances. On this basis, the intactness of the gastrointestinal tract, with its multiple functions and impacts, is one of the key prerequisites for human and animal health. Undoubtedly, the functions of a healthy gut system also largely benefit the welfare and performance of animals in farming systems such as poultry industries. Broiler chickens grow rapidly, as a result of rigorous genetic programs, due to the high absorption capacity of intestinal epithelia for nutrients, the quick transport of nutrients to the muscle, and their efficient conversion into energy and biomass. Due to oxygen metabolism or enteric commensal bacteria, intestinal epithelial cells create reactive oxygen and nitrogen species physiologically. However, increased generation of these oxidants goes along with the formation of free radicals resulting in oxidative stress causing lipid peroxidation and dramatic molecular changes in the structure and function of the cell and mitochondrial membranes. These effects contribute to chronic oxidative stress and inflammation of the gastrointestinal tract and generally affect all chicken organs, tissues, and cells. Hence, all forms of chronic stress, regardless of the origin, negatively impact the chicken's overall performance, health, and welfare. This review article highlights some enteric inflammation models and biomarkers to evaluate gut integrity in chickens and discusses the repercussions that chronic stress and intestinal inflammation have on the health and performance of commercial poultry

The goal of this research was to assess cyclic heat stress on gut permeability, bone mineralization, and meat quality in chickens. Two separate trials were directed. 320 day-of-hatch Cobb 500 male chicks were randomly assigned to four thermoneutral (TN) and four cyclic heat stress (HS) chambers with two pens each, providing eight replicates per treatment in each trial (n = 20 chicks/replicate). Environmental conditions in the TN group were established to simulate commercial production settings. Heat stress chickens were exposed to cyclic HS at 35 °C for 12 h/day from days 7–42. Performance parameters, intestinal permeability, bone parameters, meat quality, and leukocyte proportions were estimated. There was a significant (p < 0.05) reduction in body weight (BW), BW gain, and feed intake, but the feed conversion ratio increased in chickens under cyclic HS. Moreover, HS chickens had a significantly higher gut permeability, monocyte and basophil levels, but less bone mineralization than TN chickens. Nevertheless, the TN group had significant increases in breast yield, woody breast, and white striping in breast fillets compared to HS. These results present an alternative model to our previously published continuous HS model to better reflect commercial conditions to evaluate commercially available nutraceuticals or products with claims of reducing the severity of heat stress.

Histomonas meleagridis, the etiological agent of histomonosis, is a poultry parasite primarily detrimental to turkeys. Characteristic lesions occur in the liver and ceca, with mortalities in turkey flocks often reaching 80–100%. Chickens and other gallinaceous birds can be susceptible but the disease was primarily considered sub-clinical until recent years. Treating and preventing H. meleagridis infection have become more difficult since 2015, when nitarsone was voluntarily removed from the market, leaving the poultry industry with no approved prophylactics, therapeutics, or vaccines to combat histomonosis. Phytogenic compounds evaluated for chemoprophylaxis of histomonosis have varied results with in vitro and in vivo experiments. Some recent research successes are encouraging for the pursuit of antihistomonal compounds derived from plants. Turkeys and chickens exhibit a level of resistance to re-infection when recovered from H. meleagridis infection, but no commercial vaccines are yet available, despite experimental successes. Safety and stability of live-attenuated isolates have been demonstrated; furthermore, highly efficacious protection has been conferred in experimental settings with administration of these isolates without harming performance. Taken together, these research advancements are encouraging for vaccine development, but further investigation is necessary to evaluate proper administration age, dose, and route. A summary of the published research is provided in this review.

Chronic stress is recognized as a secret killer in poultry. It is associated with systemic inflammation due to cytokine release, dysbiosis, and the so-called leaky gut syndrome, which mainly results from oxidative stress reactions that damage the barrier function of the cells lining the gut wall. Poultry, especially the genetically selected broiler breeds, frequently suffer from these chronic stress symptoms when exposed to multiple stressors in their growing environments. Since oxidative stress reactions and inflammatory damages are multi-stage and long-term processes, overshooting immune reactions and their down-stream effects also negatively affect the animal’s microbiota, and finally impair its performance and commercial value. Means to counteract oxidative stress in poultry and other animals are, therefore, highly welcome. Many phytogenic substances, including flavonoids and phenolic compounds, are known to exert anti-inflammatory and antioxidant effects. In this review, firstly, the main stressors in poultry, such as heat stress, mycotoxins, dysbiosis and diets that contain oxidized lipids that trigger oxidative stress and inflammation, are discussed, along with the key transcription factors involved in the related signal transduction pathways. Secondly, the most promising phytogenic substances and their current applications to ameliorate oxidative stress and inflammation in poultry are highlighted. Simple Summary Chronic stress and inflammation, known also as “secret killers” in animals, can lead to lipid peroxidation, protein oxidation and nitration, DNA damage, and finally apoptosis. This is due to an imbalance between free radical generation and endogenous antioxidant defense, which in turn possess detrimental impacts on the health and performance of animals. In this review, we discuss the mechanistic pathways of oxidative stress and inflammation associated with the main secret killers in poultry, namely heat stress, dysbiosis, leaky gut syndrome, and mycotoxins. Additionally, we shed light on the potential use, challenges, and future prospects of phytogenic bioactive substances in mitigating oxidative stress and inflammation in poultry.

The purpose of this pilot study was to evaluate and determine the concentration of prostaglandin GF2α (PGF2α) and isoprostane 8‐iso‐PGF2α in plasma and intestine of specific pathogen-free (SPF) Leghorn chickens challenged with Eimeria maxima, with or without dietary supplementation of curcumin using solid‐phase microextraction and ultra‐performance liquid chromatography/tandem mass spectrometry. Eighty 1-day-old male SPF chickens were randomly allocated to one of four groups with four replicates (n = 5 chickens/replicate). Groups consisted of: (1) Control (no challenge), (2) Curcumin (no challenge), (3) Eimeria maxima (challenge), and (4) Eimeria maxima (challenge) + curcumin. At day 28 of age, all chickens in the challenge groups were orally gavaged with 40,000 sporulated E. maxima oocysts. No significant differences (P > 0.05) were observed in the groups regardless of the treatment or challenge with E. maxima. Enteric levels of both isoprostane 8‐iso‐PGF2α and PGF2α at 7 days and 9 days post-challenge were significantly increased (P E. maxima. At 9 days post-challenge, only levels of isoprostane 8‐iso‐PGF2α in the enteric samples were significantly reduced in chickens challenged with E. maxima supplemented with curcumin, compared with E. maxima challenge chickens. No differences of isoprostane 8‐iso‐PGF2α or PGF2α were observed in plasma at both days of evaluation. Similarly, no significant differences were observed between the challenge control or chickens challenge with E. maxima and supplemented with curcumin at both times of evaluation. The results of this pilot study suggests that the antioxidant anti-inflammatory properties of curcumin reduced the oxidative damage and subsequent intestinal mucosal over-production of lipid oxidation products. Further studies to confirm and extend these results in broiler chickens are required.

The purpose of this study was to evaluate and determine the concentration of isoprostane 8‐iso‐PGF2α and prostaglandin GF2α (PGF2α) from plasma and intestine in specific pathogen-free (SPF) chickens challenged with Eimeria maxima (EM) using solid‐phase microextraction and ultra‐performance liquid chromatography/tandem mass spectrometry. Forty one-day-old male SPF chickens were randomly allocated to one of two groups with four replicates (n=5 chickens/replicate). Groups consisted of Control (no challenge) or the Challenge group EM (40,000 sporulated oocysts/bird). At day 7 and 9 post-challenge, half of the chickens were euthanized in both groups to determine plasmatic and enteric concentrations of isoprostane 8‐iso‐PGF2α and PGF2α. Enteric levels of both 8‐iso‐PGF2α and PGF2α were significantly increased at 7 (8‐iso‐PGF2α P=0.0000252; PGF2α P=0.00000268) and 9 days (8‐iso‐PGF2α P=0.000000717; PGF2α P=0.00000222) post-challenge compared to non-challenge control chickens. However, plasma levels of isoprostane 8‐iso‐PGF2α and PGF2α were similar in both groups. A significant reduction (P=0.0000095) in oocyst excretion was observed in chickens at 9 days post-challenge compared to 7 days. Chickens challenged with EM showed an inflammatory response associated with significant increases in enteric PGF2α and 8-Iso-PGF2α, suggesting that the active disease phase was accompanied by inflammation and oxidative stress within the intestinal layer.

The purpose of this research was to isolate and identify non-temperature sensitive (ts-) (≥39.5 °C insulation), vaccine Mycoplasma synoviae (MS) strains from laying breeder hens vaccinated with temperature sensitive (ts+) strains ( 0.05). This investigation demonstrated the reversal of the thermosensitivity, pathogenicity, and vertical transmission of the MS−H strain.

Mycoplasma synoviae (MS) and Mycoplasma gallisepticum (MG) strains were isolated at 39.5 &deg, C to rule out temperature-sensitive strains (ts+) and identified using random amplification of polymorphic DNA. Then, their minimum inhibitory concentrations (MIC100) were calculated in isolated strains from broiler breeders and laying hens vaccinated with ts+ MS-H and ts+ MG TS-11 vaccines in Mexico. We sampled 631 lots of hens. A total of 28 of the 123 MS isolates and 12 of the 23 MG isolates were analyzed using random amplification of polymorphic DNA, of which 24 and 3 matched the DNA banding patterns of the MS-H and MG-F strains, respectively. The isolated MS and MG strains were sensitive to tiamulin and tylosin and showed intermediate sensitivity or resistance to lincomycin, florfenicol, erythromycin, enrofloxacin, and curcumin. Although both the MS and MG strains were sensitive to the same antibiotics (MIC100 lower than 1 mg mL&minus, 1), the MG strains were 5 to 10 times more sensitive than the MS strains. MS is the most frequently isolated mycoplasma in Mexican poultry production. The MS vaccine used (ts+ MS-H) could reverse its thermosensitivity and therefore could regain its virulence. MS was less sensitive to tiamulin and tylosin compared to MG.

The objectives of the present study were to evaluate the risks involved in the use of Enrofloxacin for Salmonella Enteritidis (SE) or Salmonella Heidelberg (SH) in commercial poultry and determine the effects of a probiotic as an antibiotic alternative. Two experiments were conducted to evaluate the risks involved in the use of Enrofloxacin for SE or SH in commercial poultry. Experiment 1 consisted of two trials. In each trial, chickens were assigned to one of three groups; control + SE challenged; Enrofloxacin 25 mg/kg + SE; and Enrofloxacin 50 mg/kg + SE. Chickens received Enrofloxacin in the drinking water from days 1 to 5 of age. On day 6, all groups received fresh water without any treatment. All chickens were orally gavaged with 10(7) cfu/chick of SE at 7 days of age and euthanized on 8 days of age. In Experiment 2, turkey poults were assigned to one of the three groups; control + SH; probiotic + SH; and Enrofloxacin 50 mg/kg + SH. Poults received probiotic or Enrofloxacin in the drinking water from days 1 to 5 of age. On day 6, poults received fresh water without any treatment. Poults were orally gavaged with 10(7) cfu/poult of SH at 7 days of age. Poults were weighed and humanely killed 24 h post-SH challenge to evaluate serum concentration of fluorescein isothiocyanate-dextran to evaluate intestinal permeability, metagenomics, and SH infection. In both trials of Experiment 1, chickens treated with Enrofloxacin were more susceptible to SE organ invasion and intestinal colonization when compared with control non-treated chickens (P 0.05). In Experiment 2, poults treated with 50 mg/kg of Enrofloxacin showed an increase in body weight, however, this group also showed an increase in SH susceptibility, intestinal permeability, and lower proportion of Firmicutes and Bacteroidetes, but with control group had the highest proportion of Proteobacteria. By contrast, poults that received the probiotic had the highest proportion of Firmicutes and Bacteroidetes, but lowest Proteobacteria. The results of the present study suggest that prophylactic utilization of Enrofloxacin at five times the recommended dose in poultry increases the susceptibility to salmonellae infections, and confirms that probiotics may be an effective tool in salmonellae infections.