Abstract
BackgroundPoultry necrotic enteritis (NE) is an economically important disease caused by C. perfringens. The disease causing ability of this bacterium is linked with the production of a wide variety of toxins. Among them, necrotic enteritis B-like (NetB) toxin is reported to be involved in the pathogenesis of NE; in addition there is some circumstantial evidence that tpeL toxin may enhance virulence, but this is yet to be definitely shown. The situation becomes more complicated in the presence of a number of predisposing factors like co-infection with coccidia, type of diet and use of high protein diet. These co-factors alter the intestinal environment, thereby favoring the production of more toxins, leading to a more severe disease. The objective of this study was to develop a successful animal model that would induce clinical signs and lesions of NE using C. perfringens type G strains obtained from field outbreaks. A separate trial was simultaneously considered to establish the role of dietary factor with coccidial co-infection in NE.ResultsThe results have shown that use of net-B positive C. perfringens without predisposing factors induce moderate to severe NE (Av. Lesion score 1.79 ± 1.50). In a separate trial, addition of fish meal to a feed of C. perfringens challenged birds produced higher number of NE cases (Av. Lesion score 2.17 ± 1.28). However, use of less virulent E. necatrix strain along with fish meal in conjunction with net-B positive strain did not alter the severity of NE lesions in specific pathogen free chicken (Av. Lesion score 2.21 ± 1.13).ConclusionsThis study suggests that virulent C. perfringens type G strains can induce NE lesions in the absence of other predisposing factors. Birds in the clostridia challenged group showed moderate to severe NE lesions. Use of less virulent coccidia strain contributed to a lesser extent in increasing the severity of disease. Maize based diet along with fishmeal (1:1) increased the severity of lesions but statistically it was non-significant. The NE lesions in all experimental groups were found to be present more frequently in the duodenum. In this way, this study provided an effective model for in vivo production of NE in poultry birds.
Highlights
Necrotic enteritis (NE), a reemerging threat to the poultry industry, has been well controlled for many years by the use of in-feed antibiotics and antimicrobial growth promoters (AGPs) [1]. These were the most effective strategies, until a few years ago, to overcome huge losses to what has been called a $6 billion disease [2]. This spike in the incidence of necrotic enteritis (NE) has resulted from the ban Mohiuddin et al Gut Pathogens (2021) 13:68 in many countries on the use of antibiotics and AGPs [3]
With the discovery of new toxin in 2008, it was found that the presence of netB toxin is essential [6] and the toxinotype having netB toxin gene in addition to alpha gene was named as C. perfringens type G in 2018 [5]
The present study has established the fact that type G alone can be a major contributor in causing NE
Summary
Necrotic enteritis (NE), a reemerging threat to the poultry industry, has been well controlled for many years by the use of in-feed antibiotics and antimicrobial growth promoters (AGPs) [1]. These were the most effective strategies, until a few years ago, to overcome huge losses to what has been called a $6 billion disease [2]. The situation becomes more complicated in the presence of a number of predisposing factors like co-infection with coccidia, type of diet and use of high protein diet These co-factors alter the intestinal environment, thereby favoring the production of more toxins, leading to a more severe disease. A separate trial was simultaneously considered to establish the role of dietary factor with coccidial co-infection in NE
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
