Timing of predisposing factors is important in necrotic enteritis models

Abstract

Since the ban of antimicrobial growth promotors, the importance of necrotic enteritis in broilers increases. Reliable and reproducible infection models are required for pathogenesis studies and product screening. Two major predisposing factors in necrotic enteritis models are fishmeal supplementation to feed and Eimeria infection. However, many unsolved issues regarding these predisposing factors still exist. Therefore, the influence of timepoint of fishmeal administration (onset on day 8 or day 18), timing of coccidiosis challenge (day 15 or day 19) and strain of coccidiosis challenge (field strain vs. commercial vaccine) on the induction of necrotic enteritis lesions was investigated. The birds were inoculated with Clostridium perfringens three times per day for four consecutive days (day 17 until day 20) and were scored for the presence of necrotic enteritis on days 22, 23, 24, 25 and 26. Supplementation of the diet with fishmeal from day 8 onwards increased the likelihood of necrotic enteritis compared to supplementation from day 18 onwards. Birds challenged on day 19 with coccidiosis were more likely to have necrotic enteritis on scoring days 23 and 24 compared to birds challenged on day 15. Differences on other scoring days were less pronounced. Finally, the strain of coccidiosis challenge had little influence on the induction of necrotic enteritis. Findings of this study can help researchers to set up successful necrotic enteritis infection models.

Experimental induction of necrotic enteritis in chickens by a <i>netB</i>-positive Japanese isolate of <i>Clostridium perfringens</i>

“…have been considered to be the important predisposing factors in reproducing the disease experimentally. Recently published studies showed that lesions of NE were observed when either Eimeria spp., fishmeal or the combination of both was administered as predisposing factors [ 25 , 30 , 35 ]. NE lesions induced by Eimeria spp.…”

“…At day 26 of age, the chickens were euthanized with inhaled carbon dioxide gas, and their digestive tracts were examined for gross necrotic lesions. The gross necrotic lesions in the small intestine (duodenum to ileum) were scored as described previously [ 10 , 35 ] as follows: 0=no gross lesion; 1=thin or friable walls with roughened mucosa; 2 =focal necrosis or ulceration (1–5 foci); 3=focal necrosis or ulceration (6–15 foci); 4=focal necrosis or ulceration (16 or more foci); 5=patches of necrosis 2–3 cm long; and 6=diffuse necrosis typical of field cases. Chickens with lesion scores of 2 or more were considered as NE positive.…”

Role of Clostridium perfringens Toxins in Necrotic Enteritis in Poultry

“…NE produced by C. perfringens is a complex and multifactorial disease difficult to reproduce experimentally (Shojadoost et al 2012;Prescott et al 2016b;Van Waeyenberghe et al 2016). Several factors should be considered for a successful reproduction of experimental NE, including induction of intestinal damage with a coccidial infection, genetic background of the animals, size of feed particles, animal protein content and non-starch polysaccharides in the birds'diet, and C. perfringens strains used in the challenge, as well as the route, dose, and frequency of the infection (Stanley et al 2014;Rodgers et al 2015;Prescott et al 2016b;Van Waeyenberghe et al 2016;Oh and Lillehoj 2016).…”

Probiotics mitigating subclinical necrotic enteritis (SNE) as potential alternatives to antibiotics in poultry

“…There are many predisposing factors, such as viscosity of digesta, the presence of non-digestible polysaccharides, the gastrointestinal tract transit time and the intestinal pH, which are responsible for the ability of bacteria to cause the disease (Moore 2016;Yang et al 2019). One of the important factors is the coccidiosis caused by Eimeria species, which creates a suitable environment for the proliferation of CP (Si et al 2007;Van Waeyenberghe et al 2016). Due to coccidiosis, perforations are made in the intestinal epithelial lining, and plasma proteins accumulate in these holes.…”