Background Poultry 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. Results The 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). Conclusions This 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.

Multi-drug resistant (MDR) diarrheagenic Escherichia coli has rapidly spread worldwide and represents the most serious threat to management of diarrhea in developing countries. We investigated an outbreak of severe diarrhea in a neonatal ward during 1 Apr-30 Jul 2012, where 60 suspected cases were found. To identify possible sources of infection, we conducted a case-control study through which we identified the increased infection risk of 4.6 fold for each liter of bottle milk feeding (OR = 4.6, 95%CI = 1.50-14.70). E. coli serotype O128:H45 with virulence gene stIb was found in 14 out of 18 stool or diaper swab samples and were MDR. This was a neonatal diarrhea outbreak caused by multi-drug resistant E. coli while bottle milk feeding was the possible vehicle in facilitating the transmission. This outbreak reinforces that enterotoxigenic Escherichia coli (ETEC) should be considered when the clinical picture is consistent and common gastrointestinal pathogens are not found.