Hypervirulent antibiotic-resistant Clostridium difficile in Europe

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Mastrantonio, Paola ; Barbanti, Fabrizio ; Spigaglia, Patrizia (2011)
  • Publisher: Microbial Ecology in Health and Disease
  • Journal: Microbial Ecology in Health and Disease (issn: 1651-2235, eissn: 1651-2235)
  • Related identifiers: doi: 10.3402/mehd.v20i4.7582

Recently, several Clostridium difficile outbreaks due to PCR ribotype 027, associated with increased disease severity and death, have been reported in North America and in several European countries. This strain is toxinA/toxinB-positive, contains the genes for binary toxin and has an 18 bp deletion and a frameshift mutation in the gene tcdC hypothesized to result in a deregulated expression of toxins A and B. These strains are high producers of toxins in vitro compared with other toxinotypes. Moreover, these strains show a high level of resistance to fluoroquinolones, possibly due to the presence of a transition mutation (C to T) in the gyrA, resulting in the amino acid substitution Th82->IIe. A 2 month prospective study was conducted in 38 hospitals in 14 different European countries to get an overview of the phenotypic and genotypic features of C. difficile isolates in 2005. In all, 411 isolates of C. difficile were obtained from diarrhoeic patients with suspected C. difficile-associated diarrhoea (CDAD); the prevalence of the 027 epidemic strain was 6.2%. All 027 strains were positive for binary toxin genes, had an 18 bp deletion in tcdC gene and were resistant to erythromycin and moxifloxacin. Patients infected with an 027 strain were likely to have a more severe disease (OR=2.52, 95% CI 0.92-6.85, p=0.04) and to have been more specifically treated by metronidazole or vancomycin (OR=7.23, CI 0.99-149, p=0.02). Ongoing epidemiological surveillance of CDAD cases with periodic characterization of the strains is needed to detect clustering of cases in time and space and to monitor the emergence of a specific hypervirulent clone.Key words: Clostridium difficile, toxins A and B, hypervirulence, C. difficile-associated diarrhoea
  • References (17)
    17 references, page 1 of 2

    1. Fekety R. Antibiotic-associated diarrhoea and colitis. Curr Opin Infect Dis. 1995;/8:/391 7.

    2. Simor AE, Yake SI, Tsimidis K. Infection due to Clostridium difficile among elderly residents of a long-term care facility. Clin Infect Dis. 1993;/17:/672 8.

    3. Gerding DN, Johnson S, Peterson I, Mulligan M, Silva J. Clostridium difficile associated diarrohea and colitis. Infect Control Hosp Epidemiol. 1995;/16:/459 76.

    4. McFarland LV, Mulligan ME, KwoK RY, Stamm WE. Nosocomial acquisition of Clostridium difficile infection. N Engl J Med. 1989;/320:/204 10.

    5. Cartmill TD, Panigrahi H, Worsley MA, McCann DC, Nice CN, Keith E. Management and control of a large outbreak of diarrhoea due to Clostridium difficile. J Hosp Infect. 1996;/27:/ 1 15.

    6. Muto CA, Pokrywka M, Shutt K, Mendelsohn AB, Nouri K, Posey K, et al. A large outbreak of Clostridium difficileassociated disease with an unexpected proportion of death and colectomies at a teaching hospital following increased fluoroquinolone use. Infect Control Hosp Epidemiol. 2005;/ 26:/273 80.

    7. Voth DE, Ballard JD. Clostridium difficile toxins: mechanism of action and role in disease. Clin Microbiol Rev. 2005;/18:/ 247 63.

    8. Popoff MR, Rubin EJ, Gill DM, Bouquet P. Actin-specific ADP-ribosyltransferase produced by a Clostridium difficile strain. Infect Immun. 1998;/56:/2299 306.

    9. Goncalves C, Decre D, Barbut F, Burghoffer B, Petit JC. Prevalence and characterization of a binary toxin from Clostridium difficile. J Clin Microbiol. 2004;/42:/1933 9.

    10. Rupnik M, Kato N, Grabnar M, Kato H. New types of toxin A negative, toxin B positive strains among Clostridium difficile isolates from Asia. J Clin Microbiol. 2003;/41:/1118 25.

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