The Role of an Early Salmonella Typhimurium Infection as a Predisposing Factor for Necrotic Enteritis in a Laboratory Challenge Model

Abstract

Necrotic enteritis (NE) caused by Clostridium perfringens (CP) in poultry is an important bacterial disease in terms of economic implications. The disease is multifactorial and is invariably associated with predisposing factors. In the present experiments, we investigated the potential predisposing role of neonatal Salmonella Typhimurium (ST) infection for NE-associated mortality in a laboratory challenge model. In two experiments, day-of-hatch chicks were randomly assigned to four groups: Group 1, nonchallenged control; Group 2, chickens received Eimeria maxima (EM) and CP; Group 3, chickens received EM and CP and were also challenged with ST at day 1 of age; Group 4, chickens received EM and CP and were also challenged with ST at day 17 of age. Challenged groups received an oral dose of EM at 18 days of age and CP (10(8) colony-forming units/chick) at 22-23 days of age. When compared to EM and CP, chicks challenged with ST (day 1) had increased NE-associated mortality and CP-associated lesion scores (P < 0.05) in both experiments. Furthermore, body weight and body weight gain were lower (P < 0.05) in chicks infected with ST (day 1) in the first experiment, even though no differences (P > 0.05) were observed in weight gain in the second experiment. Chicks challenged with ST (day 17) were similar to the EM and CP group in all of the above-mentioned parameters, indicating that a paratyphoid infection in younger chicks remarkably alters the susceptibility to secondary bacterial infections. Based on this work, the authors suggest that an ST infection early in the age of a chick may be important for altering susceptibility to NE, an observation that may be useful from the perspective of experimental reproduction of this disease and, perhaps, as an economically important reason to address the problem of paratyphoid Salmonella infections in young chicks.

Selection of Bacillus spp. for Cellulase and Xylanase Production as Direct-Fed Microbials to Reduce Digesta Viscosity and Clostridium perfringens Proliferation Using an in vitro Digestive Model in Different Poultry Diets

“…It is caused by type A strains of Clostridium perfringens that are specific to poultry with toxin types alpha and NetB ( 2 , 3 ). Coccidia infections are the most common pre-requisite for NE to occur ( 4 ), however, dysbacteriosis associated with diet ingredients, changes in feed ration, immunosuppression, Salmonella infections, and/or removal of the use of quimioterapeutics are known to predispose birds to NE ( 1 – 5 ). Antibiotic growth promoters (AGPs) are commonly used to mitigate the incidence of enteric diseases, such as NE.…”

The Use of Probiotics in Poultry Production for the Control of Bacterial Infections and Aflatoxins

“…Based on the previous results, the effect of Bacillus-DFM candidate spores formed by an isolate of Bacillus subtilis and two of Bacillus amyloliquefaciens on growth performance, intestinal integrity, necrotic enteritis (NE) lesions, and ileal microbiota in broiler chickens using a previously established NE-challenged model [90] was evaluated [24]. This study consisted of three experimental groups: negative control (NC), positive control (PC), and Bacillus-DFM group (DFM).…”

Necrotic enteritis predisposing factors in broiler chickens

“…Elwinger et al, 1992;La Ragione et al, 2004;Layton et al, 2013;Tactacan et al, 2013). These microbial interactions are protective rather than predisposing but there are examples of bacterial infections that have been found to predispose to greater NE development; for example, early infection with a Salmonella enterica serovar Typhimurium isolate increased NE-related mortality and lesion scores, perhaps resulting from a change in host immune response (Shivaramaiah et al, 2011). It is clear that bacteria in the GIT can have profound effects on C. perfringens-induced disease development, either by directly affecting the way that C. perfringens can colonize and proliferate or by modulation of the chicken immune system.…”