Abstract
Gut microbiota has been demonstrated to be involved in intestinal nutrition, defense, and immunity, as well as participating in disease progression. This study was to investigate gut microbiota changes in chickens challenged with netB-positive Clostridium perfringens strain (CP1) and/or the predisposing Eimeria species (Eimeria) and fed diets with fishmeal supplementation. In addition, the effects of lauric acid, a medium-chain fatty acid (MCFA), on necrotic enteritis (NE) reduction and modulation of microbiota were evaluated. The results demonstrated that microbial communities in the jejunum were distinct from those in the cecum, and the microbial community change was more significant in jejunum. Challenge of CP1 in conjunction with Eimeria significantly reduced species diversity in jejunal microbiota, but cecal microbiota remained stable. In the jejunum, CP1 challenge increased the abundance of the genera of Clostridium sensu stricto 1, Escherichia Shigella, and Weissella, but significantly decreased the population of Lactobacillus. Eimeria infection on its own was unable to promote NE, demonstrating decrements of Clostridium sensu stricto 1 and Lactobacillus. Co-infection with CP1 and Eimeria reproduced the majority of NE lesions with significant increment of Clostridium sensu stricto 1 and reduction in Lactobacillus. The advance of changes on these two taxa increased the severity of NE lesions. Further analyses of metagenomeSeq, STAMP, and LEfSe consistently showed significant overgrowth of Clostridium sensu stricto 1 was associated with NE. The supplementation of lauric acid did not reduce NE incidence and severity but decreased the relative abundance of Escherichia Shigella. In conclusion, significant overgrowth of C. perfringens as well as other Clostridium species in Clostridium sensu stricto 1 with the decrement of Lactobacillus in the jejunum is the featured microbiota correlated with NE. Controlling proliferation of Clostridium sensu stricto 1 and manipulation of Lactobacillus in the jejunum should be the strategy to prevent NE.
Highlights
Necrotic enteritis (NE) as the result of proliferations of Clostridium perfringens (C. perfringens) type A and their associated toxins in the small intestine of chickens is a devastating enteric disease, characterized by sudden diarrhea, unexpected mortality, and mucosal necrosis [1, 2]
C. perfringens-associated NE in poultry has been well-controlled by in-feed antimicrobial growth promoters (AGPs), low levels of antibiotics acting as growth promoters to improve the growth performance of animals [5]
Co-infection with CP1 and Eimeria led to significant increment of Clostridium sensu stricto 1 (71.89%), increased relative abundance of Escherichia Shigella (4.68%), but the decrements of Lactobacillus (16.99%), Weissella (0.44%) and Staphylococcus (0.40%)
Summary
Necrotic enteritis (NE) as the result of proliferations of Clostridium perfringens (C. perfringens) type A and their associated toxins in the small intestine of chickens is a devastating enteric disease, characterized by sudden diarrhea, unexpected mortality, and mucosal necrosis [1, 2]. In the case of human necrotizing enterocolitis, an enteric disease in infants associated with C. perfringens [21], a recent study found that Bacteroides dorei, an opportunist pathogenic bacterium in anaerobic infections, was associated with an increased mortality of this disease [22]. Several studies have demonstrated that the increment of bacteria belong to a genus of Escherichia-Shigella was associated with C. perfringens infection [5, 20]. This evidence raised the possibility that certain microbes or microbiota in the gut may contribute to the virulence or development of enteric disease in chickens, for NE
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