Necrotic enteritis (NE) is a significant enteric disease in commercial poultry with considerable economic effect on profitability manifested by an estimated $6 billion in annual losses to the global industry. NE presents a unique challenge, being a complex enteric disease that often leads to either clinical (acute) or subclinical (chronic) form. The latter typically results in poor performance (reduced feed intake, weight gain and eventually higher feed conversion ratio [FCR]) with low mortality rates, and represents the greatest economic impact on poultry production. The use of antibiotic growth promoters (AGPs) has been an effective tool in protecting birds from enteric diseases by maintaining enteric health and modifying gut microbiota, thus improving broilers’ production efficiency and overall health. The removal of AGPs presented the poultry industry with several challenges, including reduced bird health and immunity as well as questioning the safety of poultry products. Consequently, research on antibiotic alternatives that can support gut health was intensified. Probiotics, prebiotics, essential oils, and organic acids were among various additives that have been tested for their efficacy against NE with some being effective but not to the level of AGPs. The focus of this review is on the relationship between NE pathogenesis, microbiome, and host immune responses, along with references to recent reviews addressing production aspects of NE. With a comprehensive understanding of these dynamic changes, new and programmed strategies could be developed to make use of the current products more effectively or build a stepping stone toward the development of a new generation of supplements.

Necrotic enteritis (NE) continues to present major challenges to the poultry industry, and the etiologic agent Clostridium perfringens is the fourth leading cause of bacterially-induced food- borne illnesses in the US. This study was designed to evaluate the effects of a probiotic during naturally occurring NE. On day of hatch, 1080 Cobb 500 male broilers were randomly allocated to three groups (12 replicate pens/treatment, 30 birds/pen) including (1) negative control (NC): corn-soybean meal diet; (2) positive control (PC): NC + 20 mg virginiamycin/kg diet (0.450 kg Stafac^®20/ton); and (3) NC + PrimaLac (1.36 and 0.91 kg/ton from 1–21 and 22–42 days, respectively). One day (d) post placement, all birds were challenged by a commercial live oocyst coccidia vaccine as a predisposing factor to NE. Body weight and feed intake were measured at the onset of NE (d 8) and end of each feeding phase. On d 8, small intestines of two birds/pen were examined for NE lesions, and jejunum samples from one bird were collected for mRNA gene expression analysis of tight junction proteins, cytokines, and nutrient transporters. Data were analyzed using the JMP software and significance between treatments identified by LSD (p < 0.05). Compared to NC, supplementation of probiotic reduced d 1–42 mortality; however, PC was the only group with significantly lower mortality. Despite significantly improved feed conversion ratio (FCR) in PC and probiotic groups during d 1–42, average daily gain was only higher in PC (77.69 g/bird) compared with NC (74.99 g/bird). Furthermore, probiotic and PC groups had significantly reduced lesion scores in the duodenum and jejunum compared to NC. Expression of claudin-3 was higher, while expression of zonula occluden-2 tended (p = 0.06) to be higher in probiotic-supplemented birds compared to NC. Moreover, birds fed the probiotic diet had significantly higher expression of IL-10, IL-17, AMPK-α1, and SGLT1 mRNA compared to NC birds. The expression of PepT1 was higher for the probiotic-supplemented group compared to PC. IFN-γ expression was lower in PC compared to NC, while there was no difference between probiotic and NC. There were no differences in gene expression of sIgA, TNF-α, IL-1β, and IL-22 among treatments. Collectively, these data indicate that in a naturally occurring NE model, supplementation of a probiotic helps to improve FCR and reduce lesions, potentially due to the improvements in mRNA expression of tight junctions, cytokines, and nutrient transporters.

This study assessed the effects of 3 commercial organic acid (OA) preparations on growth performance, intestinal morphology, cecal microbiology, and immunity of Escherichia coli K88-challenged (ETEC) broiler chickens. One thousand one-day-old male broiler chickens were divided into 8 treatments of 5 replicate pens: Negative control (NC) birds received a basal diet (BD) and were not challenged with ETEC; positive control (PC) birds fed the BD and challenged with ETEC; BD + 0.2% (S1) or 0.4% (S2) of an OA mixture (Salkil) from one to 35 d; BD + 0.1, 0.075, and 0.05% (O1) of another OA mixture (Optimax) in the starter (one to 10 d), grower (11 to 24 d), and finisher (25 to 35 d) diets, respectively, or 0.1% (O2) from one to 35 d; BD + 0.07, 0.05, and 0.05% (P1) or 0.1, 0.07, and 0.05% (P2) of a further OA mixture (pHorce) in the starter, grower, and finisher diets, respectively. All groups (not NC) were challenged with one mL of ETEC (1 × 108 cfu/mL) at 7 d of age. The 3 OA mixtures are commercial formic and propionic acid preparations. Birds challenged with ETEC (PC) had reduced (P < 0.05) growth performance, ileal morphological parameters (not crypt depth, which was increased), cecal lactobacilli, and immune responses, and increased cecal E. coli compared with unchallenged, NC birds. The addition of OA to the diets of ETEC challenged birds (S1-P2) either numerically or significantly (P <0.05) improved growth performance, ileal morphology and immune responses, increased cecal lactobacilli, and reduced cecal E. coli. For most OA additions, the assessed parameters were generally enhanced to equivalence to NC birds. The results suggest that dietary OA supplementation can enhance the growth performance, ileal morphology, cecal microbiota, and immunity of ETEC-challenged broilers to an extent that, under such circumstances, the formulations used in this study provided similar performance and assessed parameters as non-challenged birds.

This study evaluated the effects of vitamin E (Vit E) and selenium (Se) supplementation on mRNA abundance of antioxidant, immune response, and tight junction genes, as well as taxonomic and functional profiles of ileal microbiota of broilers exposed to daily 4-h elevated temperature during d 28 to 35. A total of 640-day-old Cobb male broiler chicks were randomly allocated to 32 floor pens in a 2 × 2 factorial arrangement that included ambient temperature (thermoneutral [TN] or heat stress [HS]) and dietary treatments (basal diet or Vit E + Se). Vit E and organic Se were added to the basal diet at the rate of 250 mg/kg and 1 mg/kg, respectively. Liver and jejunum tissue samples were taken on d 27 (1 bird/pen), d 28 and d 35 (2 birds/pen) from birds for qPCR analysis. Data were subjected to a 2-way ANOVA using the GLM procedure of JMP. Ileal contents were taken on d 27 and d 35 for microbial profiling. Microbiota data were analyzed in QIIME 2 and significance between treatments identified linear discriminant analysis effect size (LEfSe, P < 0.05). Dietary Vit E/Se significantly downregulated the mRNA levels of HSPs in liver and jejunal tissues of the HS-challenged birds both on d 28 and d 35. Moreover, mRNA abundance of TLR2, TNFα, IFNγ, IL-1β, IL-10, and iNOS in the liver were significantly downregulated in birds fed the Vit E/Se diet on d 35. However, dietary treatment had no significant impact on oxidative stress, immunity, and gut integrity related genes analyzed in jejunal tissues on d 28 and d 35, except downregulation of IFNγ on d 35 (P = 0.052). LEfSe analysis revealed that Lachnospiraceae FE2018 and Ruminococcaceae NK4A214 groups was enriched in the Vit E/Se birds on d 35. Moreover, PICRUSt analysis predicted significant functional differences among the treatment groups. In conclusion, dietary supplementation of Vit E/Se mitigated the negative effects of HS potentially via improving antioxidant status, regulating cytokine responses and modifying ileal microbiota and its function.