Prevalence of Clostridium perfringens in commercial turkey and layer flocks * Vorkommen von Clostridium perfringens in Puten-und Legehennenherden

Clostridium perfringens is an anaerobic, rod shaped, non-motile bacterium. It is often found in the intestinal tract of chickens, animals, and humans. The presence of C. perfringens, especially in higher numbers or in the small intestines is mostly regarded as an indicator of a disturbed balance of the intestinal flora or “dysbacteriosis”. When C. perfringens proliferates to high numbers in the small intestine and produces toxins damaging the intestinal lining, it can lead to necrotic enteritis (NE), which is an acute disease accompanied with high economic losses (SHANE et al., 1985; LONG and TRUSCOTT, 1976). Mucosal damage by infection with Eimeria spp. (AL-SHEIKHLY and AL-SAIEG, 1980; LANCKRIET et al., 2010) or diets containing a high amount of indigestible, water-soluble non-starch polysaccharides leading to a high viscosity of the intestinal content (KALDHUSDAL and HOFSHAGEN, 1992; CRAVEN, 2000; JIA et al., 2009) are important risk factors for NE. NE has been observed in several domestic and wild birds world wide. Recently several reviews were published (VAN IMMERSEEL et al., 2004; WILLIAMS, 2005; MCDEVITT et al., 2006; OPENGART, 2008; HAFEZ, 2010). Beside clinically manifested disease, subclinical infections may take place and are mostly accompanied with reduction of performance. C. perfringens may also be associated with subclinical cholangiohepatitis and gizzard erosions (ABILDGAARD et al., 2009; NOVOA-GARRIDO et al., 2006). Reports from the field indicate that, after the ban of antimicrobial growth promoters in the European Union in 2006 (EC, 2003), infections of poultry with C. perfringens increased markedly (COOPER and SONGER, 2009; VAN IMMERSEEL et al., 2004, VAN DER SLUIS, 2010). From the economical point of view the estimated cost of NE to the poultry industry globally is nearly 2 billion US every year (MCREYNOLDS et al., 2004). C. perfringens is divided into 5 toxovars A, B, C, D, and E based on the synthesis of four major lethal toxins: alpha (cpa), beta (cpb), epsilon (etx), and iota (iap) (PETIT et al., 1999). Along with these four major toxins, some other toxins like enterotoxin (cpe) and beta2 (cpb2) toxin produced by C. perfringens are considered as important toxins for enteric diseases (MCDONEL, 1986; SONGER, 1996; WATERS et al., 2003, SMEDLEY et al. 2004, MCCLANE et al., 2006). However, it is not clear whether cpe and cpb2 are involved in C. perfringens-associated avian enteric diseases (CRESPO et al., 2007). The infections in poultry are mostly caused by C. perfringens toxovar A, and to a lesser extent by toxovar C (KÖHLER et al., 1974, SONGER and MEER, 1996; ENGSTRÖM et al., 2003). Both toxovars produce cpa while toxovar C strains additionally carry the cpb gene Because C. perfringens toxovar A is highly prevalent in the intestines of healthy animals, controversy exists about its real pathogenic role (SMEDLEY et al., 2004; MCCLANE et al., 2006). Recently, KEYBURN et al. (2008) were able to identify a novel toxin (netB) in a C. perfringens toxovar A strains isolated from chickens suffering from necrotic enteritis. According to the authors this novel toxin is the first definitive virulence factor to be identified in avian C. perfringens strains capable of causing necrotic enteritis. The aim of the present investigation was to determine the prevalence of C. perfringens toxovars in commercial turkey and layer flocks reared in various locations in Germany. *