Emergence of a new epidemic Clostridium difficile strain (ribotype 017) resistant to newer fluoroquinolones in Poland
Abstract number: 1733_553
Pituch H., Wultanska D., Obuch-Woszczatynski P., Nurzynska G., van Leeuwen W., Meisel-Mikolajczyk F., Luczak M., van Belkum A.
Outbreaks due to new hypervirulent C. difficile (ribotype 027, toxinotype III) strains that are highly resistant to fluoroquinolones were detected in The Netherlands between April 2005 and February 2006. One hospital in The Netherlands experienced an outbreak due to a toxin A negative C. difficile strains (ribotype 017 toxinotype VIII). Toxin A negative/toxin B positive C. difficile, PCR ribotype 017 strains lack a part of the toxin A gene and were first recognized as a cause of CDAD in Poland in 1995. Between 2001 and 2005 a growing epidemic of C. difficile-associated diarrhoea (CDAD) caused by toxin variant strains producing only toxin B (A-B+) was noted in our Polish university hospital. All C. difficile strains ribotype 017 isolated before 2001 were susceptible to the newer fluoroquinolones. The new Polish A-B+ isolates belonging to PCR ribotype 017 have a characteristic antimicrobial susceptibility pattern, since they are highly resistant to ciprofloxacin, moxifloxacin, gatifloxacin and show resistance to clindamycin and erythromycin (MLSB type resistance). Macrolide, lincosamide, and streprogramin B resistance is due to the presence of an ermB gene. All PCR ribotype 017 strains were resistant to gatifloxacin and moxifloxacin, but not the historical isolates (obtained before 2001). Exposure of patients to fluoroquinolones in Poland is recognized as a risk factor for CDAD caused by C. difficile strains ribotype 017.
This work was supported by Polish Ministry of Education and Science, Grant No. 2 P05D 074 27.
|Session name:||European Society of Clinical Microbiology and Infectious Diseases|
|Location:||ICC, Munich, Germany|
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