On this page
- Key messages
- Notification requirement for Clostridium difficile–associated diarrhoea
- Infectious agent of Clostridium difficile–associated diarrhoea
- Identification of Clostridium difficile–associated diarrhoea
- Incubation period of Clostridium difficile
- Public health significance and occurrence of Clostridium difficile–associated diarrhoea
- Reservoir of Clostridium difficile
- Mode of transmission of Clostridium difficile
- Period of communicability of Clostridium difficile–associated diarrhoea
- Susceptibility and resistance to Clostridium difficile–associated diarrhoea
- Control measures for Clostridium difficile–associated diarrhoea
- Outbreak measures for Clostridium difficile–associated diarrhoea
Key messages
- C. difficile–associated diarrhoea (CDAD) generally presents as antibiotic-associated colitis, with diarrhoea, abdominal cramping, fever and elevated white cell count, during or following antibiotic use.
- Not all people who acquire C. difficile will develop symptoms.
- Risk factors for acquiring CDAD include advanced age, medical comorbidities, hospital admission, antacid therapy and broad-spectrum antibiotics.
- The mode of transmission is by ingestion of viable bacteria or spores from the environment.
Notification requirement for Clostridium difficile–associated diarrhoea
Notification is not required.
Infectious agent of Clostridium difficile–associated diarrhoea
Clostridium difficile is the causative agent. It is an anaerobic, spore-forming, Gram-positive rod.
Identification of Clostridium difficile–associated diarrhoea
Clinical features
C. difficile–associated diarrhoea (CDAD) generally presents as antibiotic-associated colitis, with diarrhoea, abdominal cramping, fever and elevated white cell count, during or following antibiotic use. Severe disease may manifest as pseudomembranous colitis or toxic megacolon, in which diarrhoea may not occur but the patient presents profoundly unwell with an acute abdomen distension and pain.
Diagnosis
Diagnosis relies on analysis of fresh unformed stool for C. difficile toxin. Clostridium-specific glutamate dehydrogenase (GDH) in stool is an indicative screening test, but will also be present in the context of colonisation with a non-pathogenic strain. The organism may also be cultured from stool.
Incubation period of Clostridium difficile
Susceptible individuals are at increased risk of acquisition for months following antibiotic use. The median time from acquisition to onset of symptoms is 3 days.
Public health significance and occurrence of Clostridium difficile–associated diarrhoea
Outbreaks have occurred within hospitals, residential care facilities and childcare centres, and CDAD is the leading cause of hospital-acquired diarrhoea. ‘Hypervirulent’ strains have emerged overseas and caused epidemics in the United States and Europe. Cases have been reported in Australia.
Reservoir of Clostridium difficile
Asymptomatic carriage occurs in 15–70 per cent of neonates; the rate drops to less than 3 per cent in healthy adults.
Mode of transmission of Clostridium difficile
Acquisition occurs by the ingestion of viable bacteria or spores from the environment, including via cross-transmission from other carriers in the healthcare setting. Predisposing patient factors, including age, immune status and antibiotic use, determine whether clinical disease will develop.
Period of communicability of Clostridium difficile–associated diarrhoea
Symptomatic cases are considered infectious until 48 hours after the last episode of diarrhoea. The duration of asymptomatic carriage and presumed ongoing shedding is unclear.
Susceptibility and resistance to Clostridium difficile–associated diarrhoea
Not all people who acquire C. difficile will develop symptoms. Risk factors include advanced age, medical comorbidities, hospital admission, antacid therapy and broad-spectrum antibiotics.
Resistance to both first- and second-line therapies occurs infrequently.
Control measures for Clostridium difficile–associated diarrhoea
Preventive measures
As the disease is most frequently associated with antibiotic use, the avoidance of unnecessary antibiotics or the use of the narrowest spectrum agent for the shortest period will help to minimise the risk of CDAD. Clindamycin, extended-spectrum penicillins, third-generation cephalosporins and quinolones are frequently implicated.
Control of case
Cessation of the precipitating antibiotic where possible and administration of oral metronidazole is first-line therapy (see Therapeutic guidelines: antibiotics). Admission to an acute care facility with surgical availability is advised in the case of severe disease, particularly suspected toxic megacolon. Recurrent disease occurs in a significant percentage of patients, and specialist advice may be necessary.
Hospitalised cases should be isolated in a single room with separate bathroom until 48 hours after the resolution of diarrhoea. Routine retesting of asymptomatic patients is not encouraged, as toxin may be detected in stool for over a month after clinical cure.
Control of contacts
Contacts do not require isolation but are encouraged to practise scrupulous hand hygiene with soap and water rather than alcohol-based handrubs, due to the resistant nature of clostridial spores. Healthcare professionals in contact with the case should wear gown and gloves.
Control of environment
Rigorous clean-up procedures, including the use of bleach, are recommended to eradicate environmental spores.
Outbreak measures for Clostridium difficile–associated diarrhoea
Culture, rather than rapid detection tests, may be useful for strain typing in large outbreaks. Hospital outbreaks should trigger reviews of cleaning and isolation measures and antimicrobial stewardship programs.
Reviewed 06 September 2024