A NOTORIOUS superbug, that has spread through hospitals around the world, launched its global invasion with a two-pronged attack from North America, research has shown.
Scientists traced the origins of healthcare-associated Clostridium difficile (C diff) to two separate drug-resistant strains that emerged in the US and Canada.
Both produce tough spores that spread easily over long distances – even between continents – and are hard to eradicate.
The strains, FQR1 and FQR2, went on to spark a global epidemic in the early to mid-2000s. Tracking the spread of C diff to the UK, the researchers pinpointed separate transmissions from North America to Exeter, Ayrshire and Birmingham.
Another transmission event brought the bug from continental Europe to Maidstone in Kent. These events triggered large -cale C diff outbreaks in many UK hospitals.
C diff is a bacterium that infects the gut, causing diarrhoea, fever and cramps. In some cases, infection can lead to life-threatening complications.
The superbug affects about 2,000 people in Scotland per year, according to Health Protection Scotland figures. In 2010 it contributed to 270 deaths in Scotland.
Scientists writing in the journal Nature Genetics told how they used a global collection of samples from hospital patients to map the progress of both epidemic C diff strains.
Lead researcher Dr Miao He, from the Wellcome Trust Sanger Institute in Hinxton, Cambridgeshire, said: “Between 2002 and 2006, we saw highly publicised outbreaks of C difficile in hospitals across the UK, US, Canada and Europe. 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.”
Co-author Professor Brendan Wren, from the London School of Hygiene and Tropical Medicine, said until the early 2000s, the antibiotic fluoroquinoline was an effective treatment for C diff. But the North American strains both proved resistant to the drug, making it useless.
“Resistance seems to have been a major factor in the continued evolution and persistence of these strains in hospital and clinical settings,” said Prof Wren.
The first outbreak strain of C diff, FQR1, originated in the US and quickly spread across the country.
It was followed by FQR2 which emerged in Canada, and spread rapidly over a much wider area, covering the whole of North America and reaching out to Europe and Australia.
“We have exposed the ease and rapidity with which these fluoroquinolone-resistant C difficile strains have transmitted across the world,” said Dr Trevor Lawley, another member of the Sanger Institute team.
“Our research highlights how the global healthcare system is interconnected and how we all need to work together when an outbreak such as this occurs.
“Our study heralds a new era of forensic microbiology for the transmission tracking of this major global pathogen and will now help us understand at the genetic level how and why this pathogen has become so aggressive and transmissible worldwide.
“This research will act as a database for clinical researchers to track the genomic changes in C. difficile outbreaks.”