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.

The gut of warm-blooded animals is colonized by microbes possibly constituting at least 100 times more genetic material of microbial cells than that of the somatic cells of the host. These microbes have a profound effect on several physiological functions ranging from energy metabolism to the immune response of the host, particularly those associated with the gut immune system. The gut of a newly hatched chick is typically sterile but is rapidly colonized by microbes in the environment, undergoing cycles of development. Several factors such as diet, region of the gastrointestinal tract, housing, environment, and genetics can influence the microbial composition of an individual bird and can confer a distinctive microbiome signature to the individual bird. The microbial composition can be modified by the supplementation of probiotics, prebiotics, or synbiotics. Supplementing these additives can prevent dysbiosis caused by stress factors such as infection, heat stress, and toxins that cause dysbiosis. The mechanism of action and beneficial effects of probiotics vary depending on the strains used. However, it is difficult to establish a relationship between the gut microbiome and host health and productivity due to high variability between flocks due to environmental, nutritional, and host factors. This review compiles information on the gut microbiota, dysbiosis, and additives such as probiotics, postbiotics, prebiotics, and synbiotics, which are capable of modifying gut microbiota and elaborates on the interaction of these additives with chicken gut commensals, immune system, and their consequent effects on health and productivity. Factors to be considered and the unexplored potential of genetic engineering of poultry probiotics in addressing public health concerns and zoonosis associated with the poultry industry are discussed.

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.

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