A deadly bug that has claimed thousands of lives around the world began in North America, a study has found.
Scientists traced the origins of 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. However, the scientists said they didn’t know if the bug spread due to international travel as they were following the trail of the pathogen rather than infected people.
The strains, FQR1 and FQR2, went on to spark a global epidemic in the early to mid 2000s.
C.diff is a bacterium that infects the gut, causing diarrhoea, fever and cramps. In some cases, infection can lead to life-threatening complications.
Those most at risk are people in hospital taking broad-spectrum antibiotics, those with serious underlying conditions and the elderly.
However, at the height of the outbreak in 2006, Nicola Redfern, 32, became the first healthy young person to die from the infection in Britain. The mother from Staffordshire died less than two weeks after having a son after a series of doctors failed to diagnose the superbug, which she picked up in hospital.
By 2007, there were almost 53,000 reported cases of C.diff infection in England. Urgent counter measures taken against the bug saw the number of English cases fall dramatically to 17,414 in 2011.
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 Cambridgeshire, said: ‘Between 2002 and 2006, we saw highly publicised outbreaks of C. difficile in hospitals across the UK, USA, 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.
‘We’ve seen that since these strains acquired resistance to this frontline antibiotic, not only is it now virtually useless against this organism, but resistance seems to have been a major factor in the continued evolution and persistence of these strains in hospitals and clinical settings,’ said Prof Wren.
The first outbreak strain of C.diff, FQR1, originated in the Pittsburgh area of the U.S in 2001 and quickly spread across the country, before jumping to south Korea and Switzerland.
It was followed by FQR2 which emerged in 2003 from the Montreal area in Canada, and spread rapidly over a much wider area, covering the whole of North America and reaching out to Europe and Australia.
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 scale C.diff outbreaks in many UK hospitals.
‘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.’