An outbreak of necrotic
enteritis (NE) is a complex process requiring one or a number of predisposing factors rather than just the presence of pathogenic Clostridium perfringens. Examples are dietary influences, such as high levels of non-
starch polysaccharides and fishmeal, and factors that evoke epithelial cell damage, such as Fusarium
mycotoxins in feed and Eimeria
infections. Recent studies have shown that different predisposing factors induce similar shifts in the intestinal microbiota composition.
Butyrate-producing-strains of the Ruminococcaceae family are decreased in abundance by both fishmeal and Eimeria. Similarly, a decreased abundance of
butyrate-producing-strains belonging to the Lachnospiraceae family has been induced by fishmeal. Also shifts are observed in the
lactic acid-producing bacteria, such as decreased abundance of Lactobacillus johnsonii or Weissella confusa, when broilers were fed a fishmeal-based diet or a Fusarium
mycotoxin contaminated diet. Finally, the abundance of Candidatus Savagella was decreased in broilers following Eimeria challenge or feeding a
fumonisins contaminated diet. The nature of the microbiota shifts indicate that immune modulatory actions of the intestinal microbiota may play a critical role in the effect on the
necrosis inducing activity of C. perfringens. Indeed, colonization with
butyrate-producing bacteria plays a key role in counteracting
inflammation in the gut and preserving intestinal integrity, while Candidatus Savagella is involved in stimulating Th17 and
immunoglobulin A responses. Lactic acid bacteria stimulate colonization of
lactate-utilizing and
butyrate-producing Lachnospiraceae. Future research needs to clarify the role of the microbiota changes in the pathogenesis of NE.