Send to

Choose Destination
Nat Rev Dis Primers. 2016 Apr 7;2:16020. doi: 10.1038/nrdp.2016.20.

Clostridium difficile infection.

Author information

Section Experimental Bacteriology, Department of Medical Microbiology, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.
Infection and Immunity Program, Monash Biomedicine Discovery Institute, and Department of Microbiology, Monash University, Victoria, Australia.
Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, and The Veterans Affairs Tennessee Valley Healthcare System, Nashville Tennessee, USA.
Institute of Biomedical and Clinical Sciences, University of Leeds, Leeds, UK.


Infection of the colon with the Gram-positive bacterium Clostridium difficile is potentially life threatening, especially in elderly people and in patients who have dysbiosis of the gut microbiota following antimicrobial drug exposure. C. difficile is the leading cause of health-care-associated infective diarrhoea. The life cycle of C. difficile is influenced by antimicrobial agents, the host immune system, and the host microbiota and its associated metabolites. The primary mediators of inflammation in C. difficile infection (CDI) are large clostridial toxins, toxin A (TcdA) and toxin B (TcdB), and, in some bacterial strains, the binary toxin CDT. The toxins trigger a complex cascade of host cellular responses to cause diarrhoea, inflammation and tissue necrosis - the major symptoms of CDI. The factors responsible for the epidemic of some C. difficile strains are poorly understood. Recurrent infections are common and can be debilitating. Toxin detection for diagnosis is important for accurate epidemiological study, and for optimal management and prevention strategies. Infections are commonly treated with specific antimicrobial agents, but faecal microbiota transplants have shown promise for recurrent infections. Future biotherapies for C. difficile infections are likely to involve defined combinations of key gut microbiota.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center