Adhesive properties of an outer structure of Clostridium perfringens type A isolated from piglets with with catarrhal enteritis

• Autor(a) principal: Teixeira,Elizabeth Pelosi
• Data de Publicação: 1999
• Outros Autores: Serafim,Marlene Braide, Höfling,Maria Alice Cruz, Yamada,Aureo T., Castro,Antonio Fernando Pestana de
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Revista de Microbiologia
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37141999000300010
• topic: Cl. perfringens type A; adherence; fibrillar structure; enteritis; piglets

One strain (S32) of Clostridium perfringens type A was isolated from a case of catarrhal enteritis of piglets. This strain was able to adhere to HeLa cells showing an adherence index (AI) of 25.15 ± 1.26 (mean ± 1 standard error of the mean). Treatment of the bacterial cells with trypsin (0.25mg/ml) decreased in 70%-80% the AI and metaperiodate (10mg/ml) abolished completely the adherence, suggesting that the structure responsible for this phenomenon was probably a glycoprotein. Heating of bacterial suspensions (100ºC/5 min) before carrying out the adhesion test decreased the AI rendering it equal to the negative controls. Rabbit homologous S32 antiserum inhibited the adherence up to dilutions of 1: 640, at least. The piglet ileal loop assay, carried out with strains S32 and Jab-1 (negative control) demonstrated that the strain S32 was able to adhere to the intestinal epithelial cells when examined after Gram staining. Transmission electron microcopy (TEM) demonstrated that S32 strain displayed a loose fibrillar material not seen with Jab-1. Stabilization of the bacterial cells with homologous antiserum of strain S32, followed by staining with rhuteniun red, revealed loose long fibrillar material on the outer surface of the cells, that sometimes could be seen spreading out from the cells and linking bacterial cells. The question whether this structure might be an adhesin for this strain of Cl. perfringes type A, perhaps playing a role in the pathogenesis of the catarrhal enteritis of piglets, is dependent on further studies.