Coccidia-induced mucogenesis promotes the onset of necrotic enteritis by supporting Clostridium perfringens growth

Efficacy of early treatment with toltrazuril in prevention of coccidiosis and necrotic enteritis in chickens

“…a varying mortality rate occurs (Williams, 1996). It has been shown to increase the risk of NE occurrence (Al-Sheikhly & Al-Saieg, 1980) by damage of epithelia (Williams, 2005), protein leakage and increase of mucus secretion allowing C. perfringens to replicate and produce toxins (Van Immerseel et al, 2004, 2009Collier et al, 2008;Cooper & Songer, 2010). NE was effectively prevented by mixing antimicrobial growth promoters in the broiler feed (Elwinger et al, 1998;Lanckriet et al, 2010).…”

Xylanase supplementation to a wheat-based diet alleviated the intestinal mucosal barrier impairment of broiler chickens challenged byClostridium perfringens

“…The increased epithelial apoptosis might result from local inflammatory response in the small intestine caused by C. perfringens infection (Zhou et al, 2009). Previous studies showed that cytokine and chemokine responses appeared and pro-inflammatory cytokines such as tumour necrosis factor-a, interferon-g and IL-1b expression were up-regulated in the intestinal tissues during C. perfringens challenge (Collier et al, 2008;Park et al, 2008;Zhou et al, 2009) . Epithelial cell apoptosis, rather than necrosis, may limit the host inflammatory response early after infection.…”

“…In support of this view, it was observed that the plasma endotoxin levels were increased in the challenged birds. Although endotoxin is produced by Gram-negative bacteria and C. perfringens is Gram-positive, C. perfringens infection could cause the overgrowth of many Gram-negative bacteria, particularly E. coli, in the ileum (McReynolds et al, 2004;Liu et al, 2010) and bacteria translocation to the liver, spleen and blood (Collier et al, 2008;Liu et al, 2010), thereby leading to endotoxin translocation into the blood circulation. Xylanase supplementation in wheat-based diets is known to enhance dietary nutrient utilization by the chickens, which may reduce microbial activity as a result of substrate limitation in the ileum (Choct et al, 1999).…”

“…The disease causes severe necrosis of the intestinal tract, disrupts villusÁcrypt micro-architecture, and increases intestinal permeability and translocation of intestinal bacteria, thus compromising the integrity of mucosal barrier function (Collier et al, 2003(Collier et al, , 2008Liu et al, 2010;Golder et al, 2011) and lowering nutrient absorption and bird performance (Xu et al, 2003;Jia et al, 2009). The major factors for NE are the proliferation of the enteric bacterium Clostridium perfringens type A or C and production of exotoxins (Keyburn et al, 2008).…”

Clostridium perfringens: a review of the disease in pigs, horses and broiler chickens

“…Coccidiosis is also a well-known predisposing factor due to mucosal damage, which leads to plasma leakage into the gut. Additionally, the immune response to coccidial infection increases the amount of mucus in the intestinal tract; both mucus and plasma are used as a substrate by C. perfringens (COLLIER et al, 2008).…”