Competitive exclusion between non-pathogenic type A and type E strains of Clostridium perfringens.

REDONDO, L M; PEREYRA, A; DOMINGUEZ, J E; FERNANDEZ MIYAKAWA, ME

Palm Cove

Congreso; 8º ClostPath International Meetings on the Molecular Biology and Pathogenesis of Clostridia.; 2013

Clostridium perfringens (CP) type E is responsible for hemorrhagic enteritis in cattle. By definition produces alpha and iota toxin, this last a binary toxin which induces the disruption of the cytoskeletal architecture. In natural cases of type E enteritis there is a predominance of a single clone as it was shown by MLST studies. The objective of the present study was to clarify some competitive traits inherent to type E isolates which could be able to improve their fitness within the bovine gut environment. CP type A isolates from healthy bovine and type E isolates from natural cases of adult cattle enteritis were analysed. Inter-strain differences regarding oxygen tolerance, growth rate, toxin production, adhesive properties, and intra-specific inhibition were determined. The adhesive properties were evaluated using Caco-2 cells treated either with filtered type E supernatants or purified iota toxin. Growth rates and production of alpha and theta toxins were not statistically different between commensal type A and type E strains. Adhesions assays on CaCo-2 including bacteriology, optical and confocal microscopy, and scanning electronic microscopy showed that iota toxin and supernatants treatment decrease adherence of type A strains but increase type E, suggesting that this strain would be particularly suited to exploit the changes induced by the effect of iota toxin. These type E strains were also able to inhibit the growth of commensal strains by means of a secreted factor. This substance showed bacteriostatic effect on tested CP isolates and had no effect on all of the gram negative bacteria used, suggesting a selection for intra specific competence for specific resources. These results suggests that iota toxin enterocytes disruption increase type E cell adhesion and facilitate the displacement of commensal strains during colonization by pathogenic strains, together with intra-specific growth inhibition of other strains.