A Poultry Subclinical Necrotic Enteritis Disease Model Based on Natural Clostridium perfringens Uptake

He W, Goes EC, Wakaruk J, Barreda DR, Korver DR. A Poultry Subclinical Necrotic Enteritis Disease Model Based on Natural Clostridium perfringens Uptake. Front Physiol. 2022 Jun 8;13:788592. doi: 10.3389/fphys.2022.788592

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Necrotic enteritis (NE) in poultry is an opportunistic infection caused by Clostridium perfringens. Well-known as a multifactorial disease, NE development is under the influence of a wide range of environmental risk factors that promote the proliferation of pathogenic C. perfringens at the expense of nonpathogenic strains. Current in vivo NE challenge models typically incorporate pre-exposure to disease risk factors, in combination with exogenous C. perfringens inoculation. Our objective was to validate a natural, subclinical NE challenge model. Aiming to optimize the current natural NE model, we incorporated a novel stressor, a 24-h feed withdrawal at day 18 post-hatch, apart from other commonly used risk factors for inducing experimental NE.

Approach

Ross 708 broilers (n=752) were divided into three experimental flocks. Animals in flocks 1 and 3 were randomly assigned to two dietary treatments to evaluate the impact of antibiotic removal on NE development (antibiotic treatment and drug-free treatment). Animals in flock 2 were used for evaluating the immunomodulation effect of ß-glucan and were randomly assigned to three injection treatments (each with 5 cages of 8 birds). All three flocks were treated with a natural NE challenge procedure but with different levels of coccidiosis challenge intensity. Our goal was to enhance current models using a natural uptake of C. perfringens from the barn environment to produce a subclinical infection. We incorporated access to litter, coccidial exposure (either 10× or 15× of the manufacturer-recommended Coccivac B52 Eimeria vaccine challenge; provided unspecified doses of E. acervulina, E. mivati, E. tenella, and two strains of E. maxima), feed composition, and feed withdrawal stress, and achieved the commonly observed NE infection peak at 3 weeks post-hatch. NE severity was evaluated based on gut lesion pathology, clinical signs, and mortality rate.

Analysis of Results

Under cage-reared conditions, 15× coccidial vaccine-challenged birds showed overall NE lesion prevalence that was 8-fold higher than 10× coccidial vaccine-challenged birds. NE-associated mortality was observed only in a floor-reared flock after a 15× coccidial vaccine challenge. Our results suggested timely application of stress factors resulted in a consistent NE infection similar to the field situation, characterized by a high incidence of gut lesions in the flock with a low mortality rate.

Application

The NE infection model presented in this study is based on the natural uptake of C. perfringens presented in the housing environment by the chicken. We incorporated multiple NE-associated risk factors to promote the natural development of pathogens, and successfully reproduce subclinical NE. This will contribute to future research aiming at understanding and preventing this disease, by mimicking the natural development of NE in commercial poultry production.

Abstract

Necrotic enteritis (NE) in poultry is an opportunistic infection caused by Clostridium perfringens. Well-known as a multifactorial disease, NE development is under the influence of a wide range of environmental risk factors that promote the proliferation of pathogenic C. perfringens at the expense of nonpathogenic strains. Current in vivo NE challenge models typically incorporate pre-exposure to disease risk factors, in combination with exogenous C. perfringens inoculation. Our goal was to enhance current models using a natural uptake of C. perfringens from the barn environment to produce a subclinical infection. We incorporated access to litter, coccidial exposure (either 10× or 15× of the manufacturer-recommended Coccivac B52 Eimeria vaccine challenge; provided unspecified doses of E. acervulina, E. mivati, E. tenella, and two strains of E. maxima), feed composition, and feed withdrawal stress, and achieved the commonly observed NE infection peak at 3 weeks post-hatch. NE severity was evaluated based on gut lesion pathology, clinical signs, and mortality rate. Under cage-reared conditions, 15× coccidial vaccine-challenged birds showed overall NE lesion prevalence that was 8-fold higher than 10× coccidial vaccine-challenged birds. NE-associated mortality was observed only in a floor-reared flock after a 15× coccidial vaccine challenge.