| Autor: |
Vilei, Edy M., Schlatter, Yvonne, Perreten, Vincent, Straub, Reto, Popoff, Michel R., Gibert, Maryse, Gröne, Andrea, Frey, Joachim |
| Předmět: |
|
| Zdroj: |
Molecular Microbiology; Sep2005, Vol. 57 Issue 6, p1570-1581, 12p |
| Abstrakt: |
The cpb2 gene of β2-toxigenic Clostridium perfringens isolated from horses, cattle, sheep, human and pigs was sequenced. The cpb2 gene of equine and other non-porcine isolates differed from porcine isolates by the absence of an adenine in a poly A tract immediately downstream of the start codon in all non-porcine C. perfringens strains. This deletion involved formation of a cryptic gene harbouring a premature stop codon after only nine amino acid codons, while the full β2-toxin protein consists of 265 amino acids. Immunoblots carried out with antibodies directed against a recombinant β2-toxin showed the absence of expression of the β2-toxin in equine and the other non-porcine strains under standard culture conditions. However, treatment of C. perfringens with the aminoglycosides gentamicin or streptomycin was able to induce expression of the cpb2 gene in a representative equine strain of this group, presumably by frameshifting. The presence of the β2-toxin was revealed by immunohistology in tissue samples of small and large intestine from horses with severe typhlocolitis that had been treated before with gentamicin. This result may explain the finding that antibiotic treatment of horses affected by β2-toxigenic C. perfringens leads to a more accentuated and fatal progression of equine typhlocolitis. Clinical observations show a reduced appearance of strong typhlocolitis in horses with intestinal complications admitted to hospital care since the standard use of gentamicin has been abandoned. This is the first report on expression of a bacterial toxin gene by antibiotic-induced ribosomal frameshifting. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
Plný text