Abstract
Clostridium perfringens causes enteric diseases in animals and humans. In poultry, avian-specific C. perfringens strains cause necrotic enteritis, an economically significant poultry disease that costs the global industry over $2 billion annually in losses and control measures. With removal of antibiotic growth promoters in some countries this disease appears to be on the rise. In experimental conditions used to study disease pathogenesis and potential control measures, reproduction of the disease relies on the use of predisposing factors such as Eimeria infection and the use of high protein diets, indicating complex mechanisms involved in the onset of necrotic enteritis. The mechanisms by which the predisposing factors contribute to disease progression are not well understood but it has been suggested that they may cause perturbations in the microbiota within the gastrointestinal tract. We inspected changes in cecal microbiota and short chain fatty acids (SCFA) induced by Eimeria and fishmeal, in birds challenged or not challenged with C. perfringens. C. perfringens challenge in the absence of predisposing factors did not cause significant changes in either the alpha or beta diversity of the microbiota nor in concentrations of SCFA. Moreover, there was no C. perfringens detected in the cecal microbiota 2 days post-challenge without the presence of predisposing factors. In contrast, both fishmeal and Eimeria caused significant changes in microbiota, seen in both alpha and beta diversity and also enabled C. perfringens to establish itself post challenge. Eimeria had its strongest influence on intestinal microbiota and SCFA when combined with fishmeal. Out of 6 SCFAs measured, including butyric acid, none were significantly influenced by C. perfringens, but their levels were strongly modified following the use of both predisposing factors. There was little overlap in the changes caused following Eimeria and fishmeal treatments, possibly indicating multiple routes for progressing towards clinical symptoms of necrotic enteritis.
Highlights
It has been more than half a century since necrotic enteritis (NE) was first reported in chickens by Parish et al [1]
The results produced in the present study suggest that, by itself, the pathogenic C. perfringens strain was unable to cause any significant changes in the cecal microbiota, and it demonstrated a total inability to establish itself and remain in the microbial community 2 days post-challenge, without the help of predisposing factors
This study identified microbiota and short chain fatty acids (SCFA) changes that correlated with the use of predisposing factors, which may be important in the successful induction of NE in the experimental systems
Summary
It has been more than half a century since necrotic enteritis (NE) was first reported in chickens by Parish et al [1]. In experimental disease challenge trials it is necessary to introduce predisposing factors, such as Eimeria co-infection, high protein feed (including fishmeal), indigestible non-starch polysaccharides, controlled immunosuppression or deliberate stressing of birds, to produce clinical symptoms in a substantial proportion of challenged birds [4]. Healthy birds often carry strains of C. perfringens without showing any clinical symptoms of NE. It has been suggested that other bacteria may play a role in disease onset: for instance a significant reduction in Weissella confusa has been noted in C. perfringens challenged birds while uncultured mollicutes associated with human intestinal problems increased by 3.7 fold in NE birds [5]. Reduction of Lactobacillus johnsonii by NE [5] and independently by fishmeal [6] has been reported
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