Clostridium difficile (C. difficile) is a bacterium that is the most common pathogen causing diarrhoea in hospitalised patients and residents of aged care facilities (1). This bacterium causes the gastrointestinal infection commonly known as ‘C. difficile infection’ (CDI), sometimes abbreviated to ‘C. diff’. CDI can result in a spectrum of conditions from uncomplicated diarrhoea right through to pseudomembranous colitis, fulminate colitis, toxic megacolon, colon perforation, septic shock and even death.

In healthcare facilities, CDI can spread rapidly amongst vulnerable patients, yet whilst we recognise and manage other healthcare-associated infections such as methicillin-resistant staphylococcus aureus (MRSA) and vancomycin-resistant enterococcus (VRE), the question to be considered is: are we as knowledgeable and alert in relation to CDI and its transmission?

A gram-positive spore-forming, anaerobic bacillus, the primary mode of transmission of C. difficile is person to person via the faecal–oral route. However C. difficile has been isolated on environmental surfaces such as clothes, eating utensils and furniture, where it can exist in its spore form for several months, surviving well under a range of conditions. C. difficile has also been cultured from the hands of healthcare workers.

Hand hygiene, high standards of environmental cleanliness, prompt isolation of infected patients, preventative strategies and appropriate antimicrobial stewardship are critical to the control of CDI and protection of those people in our healthcare facilities.

CDI is thought to occur when C. difficile spores are ingested and germinate in the gut, releasing toxins and overwhelming normal gut flora that has been compromised in some way, usually by one or more risk factors. These risk factors include recent exposure to antibiotic drugs (for unrelated infections); gastric acid-suppression treatment; advanced age; prolonged hospitalisation; chemotherapy; weakened or suppressed immune systems; abdominal surgery; nasogastric tubes; and multiple co-morbidities. It is understandable then that CDI occurs most frequently in healthcare settings where patients and/or elderly residents are vulnerable and the risk of transmission is high.

The incidence and severity of CDI are increasing around the world. In the United States, C. difficile now rivals MRSA as the most common healthcare-associated infection. The C. difficile bacterium was first identified clinically in the United States in the late 1970s and since then, new and more virulent strains have continued to emerge globally. Patterns of increased antibiotic usage and environmental factors such as travel, migration and transmission patterns are also contributors to the escalation in occurrence and severity of CDI.

In the last decade, the global rates of hospital-acquired CDI have increased dramatically (2). In the early 2000’s, hospitals and nursing homes in North America, the United Kingdom and Europe experienced regional outbreaks of CDI. In 2005, a hyper-virulent strain of CDI (PCR ribotype 027) was identified in Quebec. This strain causes significant increases in morbidity and mortality and has high resistance, leading to potentially epidemic outbreaks. The USA, UK, Asia, Central America and Europe have experienced outbreaks of CDI (PCR ribotype 027). In 2011, approximately 29,000 people in the United States died as a result of CDI.

In an editorial in the Medical Journal of Australia 2014, Johnson and Stuart discussed the prevalence of CDI in Australia, posing the question, “Have distance and preparedness helped our hospitals dodge the C. difficile bullet?” (3). Johnson and Stuart write that the experiences of the US, UK and Europe, along with international collaboration, allowed Australia to prepare. “In Australia, we made ready, we wrote guidelines, we kept watch…” say Johnson and Stuart. “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, however, been smaller outbreaks of other strains, emphasising the need for ongoing vigilance and surveillance.

In Australia, the first documented case of C. difficile (PCR ribotype 027) occurred in Perth in 2009. The patient had a complex medical history and was believed to have acquired the infection whilst travelling in North America (4). In 2010 the first ‘locally acquired’ case (that is, where the patient had no history of travel) was reported in Melbourne. It is likely that CDI simply came into Australia in the gastrointestinal tracts of healthy travellers and that many instances of CDI occurred in travellers and in local settings without actually being identified as CDI.

The clinical symptoms of CDI can range from mild diarrhoea with or without bloating, cramping and abdominal pain, right through to devastating and sometimes life-threatening pseudomembranous colitis. Dehydration and electrolyte disorders are common. Late-stage disease can include toxic megacolon, high fevers, renal failure, hypotension, lactic acidosis and overwhelming sepsis. CDI is rare in children and young adults; the risks and severity increase with age.

Diagnosis can only be confirmed by laboratory testing for C. difficile’s specific toxins in stool cultures; in many cases, examination and testing are performed via colonoscopy procedures. Healthcare providers should be alert to the early symptoms of CDI in ‘at risk’ patients, and take precautionary measures even while waiting for the results of laboratory tests.

Treatment of CDI depends on the severity of the disease. In mild cases, treatment may be as simple as discontinuing the implicated antibiotic along with symptomatic relief. In more severe cases, treatment with metronidazole, vancomycin and other antibiotic agents may be employed. Symptomatic and supportive care is also necessary for pain, fluid and electrolyte management, and other associated complications. Surgery may be necessary in fulminant disease; total colectomy may be required as a lifesaving procedure.

Preventing the spread of the infection is crucial to the management of C. difficile and CDI. There are several strategies that work together in this process. These include: isolation of symptomatic patients, contact precautions, appropriate antibiotic management, high standards of environmental cleanliness and, of course, diligent hand hygiene practices. Prevention and control strategies include antimicrobial stewardship policies and protocols, surveillance practices for the early recognition of infected patients, prompt testing of patients with suspected disease and education of healthcare workers, patients and their families.

CDI poses a significant risk for hospitalised patients and residents of aged care facilities. It is a potentially debilitating disease, which is known to increase morbidity and cause severe illness and which can be fatal. In many countries, including Australia, research is being conducted to develop prevention and treatment options to combat and manage CDI. In the meantime, we can protect our most vulnerable patients from CDI with vigilant adherence to infection control practices, most particularly hand washing, improving our knowledge and remaining alert to the possible presence of C. difficile.


References

1. A. L. Bull, L. J. Worth and M. J. Richards, Implementation of standardised surveillance for Clostridium difficile infections in Australia: initial report from the Victorian Healthcare Associated Infection Surveillance System. Internal Medicine Journal 2012 pp715-718
2. C. Slimings, P Armstrong and W. Beckingham, Increasing incidence of Clostridium difficile infection, Australia, 2011–2012. MJA 2014 200(5) pp272 -276
3. P. D. Johnson and R.L. Stuart, Clostridium difficile — What is the Australian story? Have distance and preparedness helped our hospitals dodge the C. difficile bullet? MJA 2014 200(5) p242
4. R. L. Stuart and C. Marshall, Clostridium difficile infection: a new threat on our doorstep. MJA 2011 194(7) p331-2