Science

English

Investigations were performed on shedding of C. perfringens in sows from four different pig farms. In two farms where no outbreaks of necrotizing enteritis had been observed, no strains of C. perfringens producing beta-toxin were detected in the faeces of sows. In contrast, C. per fringens strains producing beta-toxin were detected in sows on both farms suffering outbreaks of acute necrotizing enteritis. Strains of C. perfringens producing beta-toxin were invariably positive for the beta2-toxin gene. However, strains carrying the beta2-toxin gene only (i.e. negative for beta-toxin) were present in animals on all farms with roughly similar frequencies (mean 28.2% carriers). Some sows carried C. perfringens strains of both toxin genotypes simultaneously. Whereas these data further support the role of betatoxin as a cause of necrotizing enteritis, the role of beta2-toxin in intestinal disease of piglets remains unclear. To establish the role of faecal shedding vs. environmental contamination as reservoirs of C. perfringens type C, strains were isolated from teats and feedlot trough swabs (toxin genotype beta/beta2), as well as from fodder (genotype beta2). However, sows carried this pathogen intermittently and in small numbers. This renders an individual, reliable diagnosis of carrier sows very difficult. Ribotyping of 34 C. perfringens isolates of different toxin genotypes showed five distinct profiles. Different toxin genotypes can belong to the same ribotype, and the same toxin genotype can be present in different ribotypes. Thus, even if a majority (79.4%) of strains investigated in a limited geographic region belonged to ribotype 1, ribotyping offered discrimination of strains beyond toxin typing.

Keywords: Clostridium perfringens type C,enteritis,piglet,molecular epidemiology,toxin genotypes,ribotyping

Deutsch

In vier Schweinebetrieben wurden molekular epidemiologische Bestandesuntersuchungen bei Muttersauen auf Clostridium perfringens durchgeführt. In zwei Beständen ohne Clostridienenteritisfälle wurden in Faeces von Sauen C. perfringens ohne Beta-, aber mit Beta2-Toxingenen gefunden. In zwei Beständen mit stationär auftretender Clostridienenteritis konnten C. perfringens der Toxingenotypen Beta und Beta2 sowie Beta2 allein nachgewiesen werden. Einige Sauen schieden gleichzeitig beide Toxingenotypen aus. Das Toxin Beta gilt als Hautptvirulenzfaktor, die Bedeutung des Beta2-Toxins bleibt somit fraglich. Die Tatsache, dass Sauen intermittierend und quantitativ wenig Erreger ausscheiden, erschwert eine individuelle, zuverlässige Diagnostik des Trägertums. Bei Umgebungsuntersuchungen wurden C. perfringens in Zitzen- und Futtertrogabstrichen (Toxingenotyp Beta/Beta2) sowie in Ferkelwühlerde (Toxingenotyp Beta2) festgestellt. Bei der Ribotypisierung von 34 C. perfringens Stämmen mit unterschiedlichen Toxingenotypen konnten fünf verschiedene Ribotypen, davon einer dominierend (79.4%), festgestellt werden. Unterschiedliche Toxingenotypen können zum gleichen Ribotyp, aber auch gleiche Toxingenotypen zu unterschiedlichen Ribotypen gehören.

Schlüsselwörter: Clostridium perfringens Typ C,Enteritis,Ferkel,Molekularepidemiologie,Toxingenotypen,Ribotypisierung

Français

Une étude épidémiologique de l´entérite à Clostridium perfringens type C a été conduite chez des truies de quatre porcheries. Dans deux élevages exempt d´entérite nécrosante du porcelet, nous avons décelé C. perfringens avec le gène de la toxine beta2 dans les fèces de truies, mais pas celui de la toxine beta. Dans deux troupeaux avec entérite nécrosante chronique, nous avons isolé C. perfringens, soit avec les gènes des toxines beta et beta2, soit de la toxine beta2 seule. Certaines truies excrétaient simultanément les deux génotypes de toxine. On admet que la toxine beta est le facteur de virulence majeur, le rôle de la toxine beta2 reste ainsi incertain. Le fait que les truies excrètent l´agent pathogène en faible quantité et d´une manière intermittente rend difficile le diagnostic individuel de portage. Lors d´investigations environnementales, des souches de C. perfringens ont été isolées sur les mamelles, dans les mangeoires (génotype beta/beta2), de même que dans un aliment (génotype beta2). L´analyse ribotypique de 34 souches de différents génotypes de toxine a révélé cinq ribotypes, dont l´un d´eux est prédominant (79,4%). Différents génotypes de toxine peuvent se retrouver dans le même ribotype, respectivement les mêmes génotypes peuvent être présents dans différents ribotypes.

Italiano

Per approfondire le conoscenze epidemiologiche riguardanti l´enterite necrotizzante sono stati effettuati degli studi sul patogeno C. perfringens in scrofe e suinetti provenienti da quatro diversi allevamenti suini. Nelle feci di due allevamenti senza casi dichiarati di enterite da clostridio sono stati identificati dei ceppi di C. perfringens senza il gene della tossina beta, ma con il gene della tossina beta2. Negli altri due allevamenti sono stati riscontrarti casi acuti di enterite necrotizzante e i ceppi di C. perfringens ivi isolati presentano entrambi i geni delle tossine beta e beta2 o unicamente il gene della tossina beta2. Alcuni suini possedevano patogeni di entrambi i genotipi tossinici. La tossina beta rappresenta un importante fattore di virulenza, quindi il ruolo della tossina beta2 in assenza di produzione della tossina beta rimane poco chiaro. Dal momento che il patogeno è presente in dosi minime nei suini e si manifesta inoltre con intermittenza, una diagnosi accurata per ogni individuo portatore risulta essere difficoltosa. Studi epidemiologici sulla provenienza di questi ceppi di C. perfringens sono stati fatti sulle mammelle e su campioni di cibo dalle mangiatoie (genotipo tossinico beta/beta2), come pure su campioni di lettiera per suinetti (genotipo tossinico beta2). In totale, tramite l´analisi ribotipica applicata a 34 ceppi di C. perfringens aventi genotipi tossinici diversi, sono stati identificati cinque ribotipi differenti, di cui uno prevalente sugli altri 4 (79.4% del totale). Questa ricerca ha potuto evidenziare come genotipi tossinici diversi possono appartenere allo stesso ribotipo, così come ceppi di uno stesso genotipo tossinico possono appartenere a ribotipi diversi.