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Advisor(s)
Abstract(s)
C. difficile infection (CDI) is the cause of an intestinal disease mediated by two potent cytotoxins, TcdA and
TcdB. Symptoms of CDI can range from asymptomatic colonization or mild diarrhea, to life-threatening
inflammatory lesions such as pseudomembraneous colitis, toxic megacolon or bowel perforation. In part because
of the recent emergence of so-called hypervirulent strains, especially (but not exclusively) those belonging to
ribotype 027, C. difficile is now considered a main nosocomial enteric pathogen.
Hypervirulent epidemic strains have been associated with more severe disease conditions, with higher relapse
rates and increased mortality. Health care-associated CDI develops in hospitalized patients undergoing antibiotic
treatment because C. difficile can colonize the gut if the normal intestinal microbiota is disturbed. However, C.
difficile is also emerging as an important pathogen in the community, as well as in animal husbandry. The
organism is an obligate anaerobe, and has the ability to form spores. Spores are extremely resilient and can
accumulate and remain viable in the environment or in the host for long periods of time. Spores that remain
latent in the gut are responsible for the recurrence of C. difficile-associated disease (CDAD) when antibiotic
therapy is stopped. At least some of the hypervirulent epidemic strains show a greater sporulation capacity in
vitro, as well as robust toxin production.
The first detection of C. difficile 027 hypervirulent epidemic strains implicated in a hospital outbreak in Portugal
dates from January 2012, involving 12 patients, with a crude mortality rate of 50%. Here we report on the genetic
characterization of those strains as well as the antibiotic resistance profile, toxin production, and rate and
efficiency of spore formation. In parallel, C. difficile 027 non-outbreak strains isolated from other Portuguese
health care facilities are also investigated.
Description
Keywords
Clostridium difficile Outbreak Sporulation Antibiotic resistance
