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.

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Fumonisins (FB) and deoxynivalenol (DON) are mycotoxins which may predispose broiler chickens to necrotic enteritis (NE). The objective of this study was to identify the effects of subclinical doses of combined FB and DON on NE. A total of 480 day-old male broiler chicks were divided into four treatment groups; 1) control group (basal diet + Clostridium perfringens); 2) necrotic enteritis group (basal diet + Eimeria maxima + C. perfringens); 3) FB + DON group (basal diet + 3 mg/kg FB + 4 mg/kg DON + C. perfringens); and 4) FB + DON + NE group (basal diet + 3 mg/kg FB + 4 mg/kg DON + E. maxima + C. perfringens). Birds in NE and FB + DON + NE groups received 2.5 × 103E. maxima on day 14. All birds were inoculated with C. perfringens on days 19, 20, and 21. On day 35, birds in the NE, FB + DON, and FB + DON + NE groups had 242, 84, and 339 g lower BWG and a 19-, 2-, and 22-point increase in FCR respectively, than in the control group. Subclinical doses of FB + DON increased (p < 0.05) the NE lesion scores compared to the control group on day 21. On day 21, birds in the NE, FB + DON, and FB + DON + NE groups had increased (p < 0.05) serum FITC-D, lower (p < 0.05) jejunal tight junction protein mRNA, and increased (p < 0.05) cecal tonsil IL-1 mRNA compared to control group. On day 21, birds in the NE group had decreased (p < 0.05) villi height to crypt depth ratio compared to the control group and the presence of FB + DON in NE-induced birds further decreased the villi height to crypt depth ratio. Birds in the NE, FB + DON, and FB + DON + NE groups had increased (p < 0.05) C. perfringens, lower (p < 0.05) Lactobacillus loads in the cecal content, and a lower (p < 0.05) CD8+: CD4+ cell ratio in the cecal tonsils compared to the control group. It can be concluded that subclinical doses of combined FB and DON predispose C. perfringens-inoculated birds to NE, and the presence of FB + DON in NE-induced birds exacerbated the severity of NE.

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