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A fluoroquinolone induces a novel mitogen-encoding bacteriophage in Streptococcus canis
Keely T Ingrey1, Jun Ren, John F Prescott
1Department of Pathobiology, University of Guelph, Ontario N1G 2W1, Canada.
Infection and Immunity
|May 23, 2003
Summary
Fluoroquinolone antibiotics may contribute to canine toxic shock syndrome by inducing bacteriophages in Streptococcus canis. These phages carry a gene, scm, that enhances superantigen production, potentially explaining disease emergence in dogs.
Area of Science:
- Veterinary Medicine
- Microbiology
- Molecular Biology
Background:
- Emergence of canine streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (NF) in dogs.
- Potential link between fluoroquinolone use and increased severity of canine STSS/NF.
Purpose of the Study:
- To investigate if fluoroquinolones contribute to canine STSS/NF by inducing bacteriophages in Streptococcus canis.
- To identify and characterize potential virulence genes encoded by these bacteriophages.
Main Methods:
- Treatment of S. canis with mitomycin and enrofloxacin to induce bacteriophage lysis.
- Construction and screening of a bacteriophage (phisc1) gene library for mitogenic activity using canine lymphocytes.
- Sequencing of identified mitogenic phage inserts and PCR analysis of the scm gene in S. canis isolates.
Main Results:
- Enrofloxacin induced bacteriophage-mediated lysis of S. canis at therapeutic concentrations.
- A novel gene, scm, was identified within the induced bacteriophage, showing similarity to known mitogens.
- The scm gene was present in most S. canis isolates and its expression significantly increased upon bacteriophage induction.
Conclusions:
- Fluoroquinolone-induced bacteriophage activation in S. canis may contribute to canine STSS and NF.
- The identified scm gene, a potential streptococcal superantigen, is a key factor in this process.
- Findings suggest a mechanism linking antibiotic use to the emergence of severe streptococcal infections in dogs.