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 in the physical properties of the gut, the immunological status of birds, and the disruption of 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.

This work discusses the present-day limitations of current commercial Salmonella vaccines for broilers and layers and explores a novel approach towards poultry vaccination using biodegradable nanoparticle vaccines against Salmonella. With the increasing global population and poultry production and consumption, Salmonella is a potential health risk for humans. The oral administration of killed or inactivated vaccines would provide a better alternative to the currently commercially available Salmonella vaccines for poultry. However, there are currently no commercial oral killed-vaccines against Salmonella for use in broilers or layers. There is a need for novel and effective interventions in the poultry industry. Polymeric nanoparticles could give way to an effective mass-administered mucosal vaccination method for Salmonella. The scope of this work is limited to polymeric nanoparticles against Salmonella for use in broilers and layers. This review is based on the information available at the time of the investigation.

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.

The objective of this study was to identify the effects of experimental necrotic enteritis (NE) infection on the production performance, gut microbiome, and cecal tonsil transcriptome in broiler birds. A total of 192 chicks were not-induced (control) or induced with NE. NE was induced by inoculating Eimeria maxima at 14 d of age and Clostridium perfringens at 19, 20, and 21 d of age. NE challenge increased (p < 0.01) NE lesion score at 7 days post-E.maxima infection (dpi), decreased (p < 0.01) average weight gain and increased (p < 0.01) mortality at 7 and 14 dpi. NE challenge increased (p < 0.05) gut permeability at 5, 6, and 7 dpi and increased ileal C. perfringens load at 5 dpi. NE challenge increased (p < 0.01) Eimeria oocyst shedding at 5, 6, 7, 8 and 14 dpi. NE challenge decreased (p < 0.05) the relative abundance of Lactobacillaceae and increased (p < 0.05) the relative abundance of Campylobacteriaceae, Comamonadaceae, and Ruminococcaceae at 6 dpi. NE challenge upregulated (p < 0.05) genes related to immune response and downregulated (p < 0.05) genes related to lipid metabolism at 6 dpi. It can be concluded that NE infection decreased beneficial bacteria and increased gut permeability.

No abstract