Clostridium difficile — what is the Australian story?

Have distance and preparedness helped our hospitals dodge the C. difficile bullet?

In his acclaimed book The tyranny of distance, Geoffrey Blainey argued that Australia's history has been deeply shaped by distance and isolation.1

Isolation is not necessarily bad if you are responsible for controlling infectious diseases. Once Australia could rapidly access information from the outside world via telegraph, distance and isolation could be turned to our advantage. When news of Spanish influenza came down the wire in 1918, the Commonwealth Director of Quarantine had sufficient warning to stop the boats (which were, on that occasion, carrying sick Australian soldiers).2 As a result, Australia dodged the most virulent first wave of H1N1 influenza, and our case-fatality rate was about 50% lower than that observed in Europe and the United States.

Times have changed; the tyranny of distance is now just a line in a Split Enz song.3 We have email, mobile phones and Twitter; people and perishable goods arrive every hour from everywhere. From the public health perspective, there is less chance now of keeping emerging pathogens out of Australia, particularly if they are carried in the gastrointestinal tracts of healthy travellers returning from overseas.

During the early 2000s, hospitals in North America, the United Kingdom and Europe experienced large outbreaks of Clostridium difficile infection.4,5 One strain in particular, fluoroquinolone-resistant polymerase chain reaction (PCR) ribotype 027, caused devastating illness in otherwise healthy people.4 At international conferences, we heard chilling tales of patients admitted for elective joint replacement developing severe diarrhoea and then toxic megacolon, and only surviving after total colectomy, or not surviving at all. PCR ribotype 027 spread quickly within hospitals, between hospitals and between continents.5 C. difficile infection became a national news story in the UK, and rates of C. difficile infection were made a key performance indicator for National Health Service hospitals.6

In Australia, we made ready, we wrote guidelines,7 we kept watch. Sure enough, our first case of PCR ribotype 027 C. difficile infection was identified in Perth in 2009 in a patient with a complex medical history, who had acquired the infection in New York.8 The following year, a locally acquired severe case was identified in Melbourne in a patient without a travel history.9 PCR ribotype 027 had arrived, and has probably arrived hundreds of other times without us knowing about it.

Fortunately, and perhaps because we were forewarned and forearmed, we have not experienced waves of severe PCR ribotype 027 C. difficile infection spreading through our hospitals. There have been small outbreaks of other strains, as has recently occurred in Melbourne, where moxifloxacin-sensitive PCR ribotype 244 was found to be associated with increased disease severity.10 Such outbreaks emphasise the importance of ongoing surveillance.

Increasingly we are aware that C. difficile infection may also be community-acquired and that although antibiotic use is a key risk factor, some infected patients have not received antibiotics. Most interestingly, in a recent report from the UK, about half of new cases diagnosed in hospitals in Oxfordshire were caused by unrelated strains of C. difficile, likely to have been silently brought into hospital from the community and only detected when a patient developed diarrhoea after admission.11 Hence, just counting the number of C. difficile infections in our hospitals without culturing the causative isolates and testing for clonality may not be a useful key performance indicator for cross infection, although it may still provide an indirect measure of the effectiveness of antibiotic stewardship programs.

So what is the C. difficile story in Australia? In this issue of the Journal, Slimings and colleagues report on a 2-year national survey of hospital-identified cases of C. difficile infection, in which 450 public hospitals (covering 92% of patient-days in Australian acute public hospitals) participated.12 More than 12 500 cases of C. difficile infection were identified, with an overall incidence of about four per 10 000 patient-days. Clearly, C. difficile infection is not a trivial problem! About a quarter of the cases turned out to be community-acquired. Worryingly, there appeared to be a progressive increase in C. difficile cases during the first year of the study, but this largely stabilised in the second year. Seasonal variation may partly explain this observation, although it is not yet understood why this should occur.

It is heartening to see a national community of hospitals, microbiologists and clinicians working together and sharing their information to develop a snapshot of this important emerging pathogen. Changes in diagnostic methods may also partly explain the apparent increase in the first year of the study, but, despite this limitation, we now have a reasonable national estimate of the dimensions of Australia's C. difficile problem.