Clostridium perfringens type A and C are the primary etiological agents associated with necrotic enteritis (NE) in poultry. The predisposing factors implicated in the incidence of NE changes the physical properties of the gut, immunological status of birds, and disrupt the gut microbial homeostasis, causing an over-proliferation of C. perfringens. The principal virulence factors contributing to the pathogenesis of NE are the α-toxin, β-toxin, and NetB toxin. The immune response to NE in poultry is mediated by the Th1 pathway or cytotoxic T-lymphocytes. C. perfringens type A and C are also pathogenic in humans, and hence are of public health significance. C. perfringens intoxications are the third most common bacterial foodborne disease after Salmonella and Campylobacter. The restrictions on the use of antibiotics led to an increased incidence of NE in poultry. Hence, it is essential to develop alternative strategies to keep the prevalence of NE under check. The control strategies rely principally on the positive modulation of host immune response, nutritional manipulation, and pathogen reduction. Current knowledge on the etiology, pathogenesis, predisposing factors, immune response, effect on the gut microbial homeostasis, and preventative strategies of NE in this post-antibiotic era is addressed in this review.

C. jejuni is the leading cause of human foodborne illness associated with poultry, beef, and pork consumption. C. jejuni is highly prevalent in commercial poultry farms, where horizontal transmission from the environment is considered to be the primary source of C. jejuni. As an enteric pathogen, C. jejuni expresses virulence factors regulated by a two-component system that mediates C. jejuni’s ability to survive in the host. C. jejuni survives and reproduces in the avian intestinal mucus. The avian intestinal mucus is highly sulfated and sialylated compared with the human mucus modulating C. jejuni pathogenicity into a near commensal bacteria in poultry. Birds are usually infected from two to four weeks of age and remain colonized until they reach market age. A small dose of C. jejuni (around 35 CFU/mL) is sufficient for successful bird colonization. In the U.S., where chickens are raised under antibiotic-free environments, additional strategies are required to reduce C. jejuni prevalence on broilers farms. Strict biosecurity measures can decrease C. jejuni prevalence by more than 50% in broilers at market age. Vaccination and probiotics, prebiotics, synbiotics, organic acids, bacteriophages, bacteriocins, and quorum sensing inhibitors supplementation can improve gut health and competitively exclude C. jejuni load in broilers. Most of the mentioned strategies showed promising results; however, they are not fully implemented in poultry production. Current knowledge on C. jejuni’s morphology, source of transmission, pathogenesis in poultry, and available preharvest strategies to decrease C. jejuni colonization in broilers are addressed in this review.

To evaluate the efficacy of synbiotic during a necrotic enteritis (NE) infection, a total of 360 day-old chicks were randomly assigned into 4 experimental groups in a 2 × 2 factorial setup: control, challenge, synbiotic (1 g/kg), and challenge + synbiotic, with 6 replicates. NE was induced by gavaging 1 × 10⁴Eimeria maxima oocysts and 1 × 10⁸ CFU/mL of Clostridium perfringens on d 14 (D14) and D19, 20, and 21, respectively. At D35, the NE challenge decreased the BW gain (P < 0.001) and increased feed conversion ratio (P = 0.03), whereas synbiotic supplementation decreased the feed intake (P = 0.04). At D21, NE challenge increased gut permeability (P < 0.001), decreased regulatory T cells (Tregs) in the cecal tonsil (CT) (P = 0.02), increased Tregs in the spleen (P = 0.02), decreased nitric oxide (NO) production in the spleen (P = 0.04) and decreased IL-10 expression in CT (P = 0.02), whereas synbiotic supplementation increased CD4+:CD8+ T cells in the spleen (P < 0.001) and decreased interferon (IFN)-γ expression in the jejunum (P = 0.07), however, synbiotic supplementation during NE challenge decreased mid-gut lesion score (P < 0.001), increased CD4+:CD8+ T cells in CT and decreased IgA production in bile (P < 0.001), compared to the control group. At D28, synbiotic supplementation decreased CD4+:CD8+ T cells in CT (P < 0.001), whereas synbiotic supplementation during NE challenge decreased Tregs in CT (P < 0.001) and increased NO production in the spleen (P = 0.04), compared to the control group. At D35, the NE challenge decreased CD4+:CD8+ T cells in the spleen (P = 0.03), decreased IgA production in bile (P = 0.02), decreased IL-10 expression in CT (P = 0.04), and decreased IL-10 (P = 0.009), IFN-γ (P = 0.03) and inducible nitric oxide synthase (P = 0.02) expression in the jejunum, whereas synbiotic supplementation increased Tregs in the spleen (P = 0.04), compared to control group. Synbiotic supplementation during the NE challenge decreased both IL-1β (P = 0.02) and IFN-γ (P = 0.001) expression in CT, compared to the control group. It can be concluded that synbiotic supplementation increases production performance by decreasing mid-gut lesions and enhancing protective immunity against NE, and efficiency of synbiotic could be improved by blending additional probiotics and prebiotics.

The gut is home to more than millions of bacterial species. The gut bacteria coexist with the host in a symbiotic relationship that can influence the host’s metabolism, nutrition, and physiology and even module various immune functions. The commensal gut microbiota plays a crucial role in shaping the immune response and provides a continuous stimulus to maintain an activated immune system. The recent advancements in high throughput omics technologies have improved our understanding of the role of commensal bacteria in developing the immune system in chickens. Chicken meat continues to be one of the most consumed sources of protein worldwide, with the demand expected to increase significantly by the year 2050. Yet, chickens are a significant reservoir for human foodborne pathogens such as Campylobacter jejuni. Understanding the interaction between the commensal bacteria and C. jejuni is essential in developing novel technologies to decrease C. jejuni load in broilers. This review aims to provide current knowledge of gut microbiota development and its interaction with the immune system in broilers. Additionally, the effect of C. jejuni infection on the gut microbiota is addressed.

The objective of this study was to evaluate the effect of 25% arginine supplementation as a functional amino acid in partially alleviating the detrimental effects of necrotic enteritis (NE) on the growth performance, serum biochemistry, gut integrity, and the relative gene expression of tight junction proteins and inflammatory cytokines in broilers during NE. Three hundred and sixty 1-day-old chicks were randomly allocated to 4 treatments in a 2 x 2 factorial arrangement -basal diet and 125% arginine diet, with or without NE challenge. NE was induced by inoculating 1 x 10(4) Eimeria maxima sporulated oocysts on d 14 and 1 x 10(8) CFU/bird C. perfringens on d 19, 20, and 21. The NE challenge had a significant effect on the BWG (p < 0.05), FCR (p < 0.05), serum AST (p < 0.05), GLU (p < 0.05), and K+ (p < 0.05) levels, and intestinal permeability (p < 0.05) and jejunal lesion score (p < 0.05). A significant challenge x diet interaction effect was observed in the cecal tonsil CD8(+): CD4(+) T-cell ratio on d 21 (p < 0.05) and 28 (p < 0.05) and spleen CD8(+): CD4(+) T-cell ratio on d 21 (p < 0.05) and 35 (p < 0.05). Arginine supplementation significantly increased the CD8(+): CD4(+) T-cell ratio in uninfected birds but decreased the CD8(+): CD4(+) T-cell ratio in infected birds. On d 21, a significant interaction effect was observed on the relative expression of the iNOS gene (p < 0.05). Arginine supplementation significantly downregulated the expression of the iNOS gene in infected birds. A significant effect of the challenge (p < 0.05) was observed on the relative gene expression of the ZO-1 gene in the jejunum. NE challenge significantly downregulated the expression of the ZO-1 gene on d 21. In conclusion, arginine supplementation did not alleviate the depression in growth performance and disease severity during the NE challenge. However, arginine downregulated the expression of inflammatory cytokines and enzymes, preventing inflammatory injury to the tissues during NE. Hence, arginine might be supplemented with other alternatives to downregulate inflammatory response during NE in poultry.