Researchers show that the global epidemic of Clostridium difficile 027/NAP1/BI in the early to mid-2000s was caused by the spread of two different but highly related strains of the bacterium rather than one as was previously thought. The spread and persistence of both epidemics were driven by the acquisition of resistance to a frontline antibiotic.
Unlike many other healthcare-associated bacteria, C. difficile produces highly resistant and infectious spores. These spores can promote the transmission of C. difficile and potentially facilitates its spread over greater geographical distances, even across continents.
This study highlights the ease and rapidity with which the hospital bacterium, C. difficile, can spread throughout the world, emphasising the interconnectedness of the global healthcare system.
"Between 2002 and 2006, we saw highly publicised outbreaks of C. difficile in hospitals across the UK, USA, Canada and Europe," says Dr Miao He, first author from the Wellcome Trust Sanger Institute. "We used advanced DNA sequencing to determine the evolutionary history of this epidemic and the subsequent pattern of global spread.
"We found that this outbreak came from two separate epidemic strains or lineages of C. difficile, FQR1 and FQR2, both emerging from North America over a very short period and rapidly spread between hospitals around the world."
The team used the genetic history to map both epidemic strains of C. difficile using a global collection of samples from hospital patients between 1985 and 2010. They demonstrated that the two C. difficile strains acquired resistance to this antibiotic, fluoroquinolone, separately, a key genetic change that may have instigated the epidemics in the early 2000s.
"Up until the early 2000s, fluoroquinolone was an effective treatment for C. difficile infection," says Professor Brendan Wren, author from
|Contact: Aileen Sheehy|
Wellcome Trust Sanger Institute