Abstract
Bovine necrohemorrhagic enteritis is a major cause of mortality in veal calves. Clostridium perfringens is considered as the causative agent, but there has been controversy on the toxins responsible for the disease. Recently, it has been demonstrated that a variety of C. perfringens type A strains can induce necrohemorrhagic lesions in a calf intestinal loop assay. These results put forward alpha toxin and perfringolysin as potential causative toxins, since both are produced by all C. perfringens type A strains. The importance of perfringolysin in the pathogenesis of bovine necrohemorrhagic enteritis has not been studied before. Therefore, the objective of the current study was to evaluate the role of perfringolysin in the development of necrohemorrhagic enteritis lesions in calves and its synergism with alpha toxin. A perfringolysin-deficient mutant, an alpha toxin-deficient mutant and a perfringolysin alpha toxin double mutant were less able to induce necrosis in a calf intestinal loop assay as compared to the wild-type strain. Only complementation with both toxins could restore the activity to that of the wild-type. In addition, perfringolysin and alpha toxin had a synergistic cytotoxic effect on bovine endothelial cells. This endothelial cell damage potentially explains why capillary hemorrhages are an initial step in the development of bovine necrohemorrhagic enteritis. Taken together, our results show that perfringolysin acts synergistically with alpha toxin in the development of necrohemorrhagic enteritis in a calf intestinal loop model and we hypothesize that both toxins act by targeting the endothelial cells.
Highlights
Since the ban on antimicrobial growth promoters in Europe, necrohemorrhagic enteritis emerged as a major cause of mortality in veal calves in Belgium, causing important economic losses [1,2,3]
To elucidate the relative contribution of perfringolysin and alpha toxin in the induction of necrohemorrhagic enteritis a wild-type strain and its ΔpfoA Δplc mutant was used in combination with the ΔpfoA Δplc mutant complemented with either the pfoA or the plc gene or both (Figure 2)
These results suggest that the causative toxin is one of the toxins produced by all C. perfringens type A strains
Summary
Since the ban on antimicrobial growth promoters in Europe, necrohemorrhagic enteritis emerged as a major cause of mortality in veal calves in Belgium, causing important economic losses [1,2,3]. A more recent study isolated only beta2-negative type A strains from calves with necrohemorrhagic enteritis and these strains were able to induce pathological changes in inoculated intestinal loops [10]. We recently developed an experimental intestinal loop model that mimics the typical lesions of calf necrohemorrhagic enteritis both macroscopically and microscopically [20] In this model, it was demonstrated that type A strains from bovine and non-bovine origin, including both beta2-negative and -positive strains, were able to induce necrohemorrhagic lesions [20]. It was demonstrated that type A strains from bovine and non-bovine origin, including both beta2-negative and -positive strains, were able to induce necrohemorrhagic lesions [20] These results suggest that the causative toxin should be present in all the tested C. perfringens strains. The importance of perfringolysin in the pathogenesis of bovine necrohemorrhagic enteritis is not reported before
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