Effects of Eimeria brunetti Infection and Dietary Zinc on Experimental Induction of Necrotic Enteritis in Broiler Chickens

Abstract

Broilers infected with Eimeria brunetti and given dietary zinc were examined for experimental induction of necrotic enteritis. Inoculation with sporulated E. brunetti oocysts at 7 days of age was followed by 5 consecutive days of oral inoculation with cultured Clostridium perfringens. Feed was supplemented with zinc at 1000 ppm. Upon necropsy of broilers 6 days after coccidial inoculation, necrotic enteritis was found in 20% (2/10) of birds given both organisms and dietary zinc. Coccidial lesion scores were also highest in that group. Birds infected with E. brunetti and C. perfringens with no dietary zinc had significantly higher coccidiosis lesion scores (P less than 0.05) than groups inoculated with E. brunetti only, regardless of zinc supplementation. Alpha toxin levels in intestinal contents were low in groups infected with both organisms, regardless of zinc supplementation. Zinc was tested for effects of alpha toxin production in vitro. In the mid-log phase (6 hours incubation), a high level of alpha toxin was produced in zinc-supplemented media, but this was lost quickly in the presence of trypsin. Addition of zinc partly protected the toxin from the action of trypsin.

Alpha-Toxin ofClostridium perfringensIs Not an Essential Virulence Factor in Necrotic Enteritis in Chickens

“…The inactivation of the chromosomal plc gene had no effect on the virulence of the resultant strains in chickens. As the wild-type isolate was obtained from a clinical case of chicken NE and produced a disease pathology similar to that reported in many other disease induction models (6,14,32,34,44,47), we conclude that our results can be readily extrapolated to other virulent strains.…”

The effect of commonly used anticoccidials and antibiotics in a subclinical necrotic enteritis model

“…Several field cases have been reported in which coccidiosis preceded or coincided with necrotic enteritis, although clinical coccidiosis will not always result in the development of necrotic enteritis (Long, 1973;Broussard et al, 1986;Droual et al, 1994;Dhillon et al, 2004;Hermans & Morgan, 2007). Combined experimental infection with species of Eimeria and C. perfringens leads to higher intestinal lesion scores, increased intestinal numbers of C. perfringens, increased mortality and reduced weight gain compared to infection with C. perfringens alone (Al-Sheikhly & Al-Saieg, 1980;Shane et al, 1985;Kageyama et al, 1987;Baba et al, 1992;Baba et al, 1997;Williams et al, 2003;Gholamiandehkordi et al, 2007;Park et al, 2008).…”

Analysis of Core Housekeeping and Virulence Genes Reveals Cryptic Lineages ofClostridium perfringensThat Are Associated With Distinct Disease Presentations

“…While virulence genes are not usually considered to be part of the core genome, there are exceptions. In this study, we examined two such exceptions: the plc gene, which encodes the a-toxin, a phospholipase C that is also a primary determinant of C. perfringens virulence (Long and Truscott 1976;Baba et al 1992;Awad et al 1995;Rood 1998); and the colA gene, which encodes the k-toxin, a collagenase that facilitates tissue necrosis (Bryant and Stevens 1997;Rood 1998;Petit et al 1999).…”