Clostridium difficile-associated disease

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Etiology/Bacteriology

Domain: Bacteria Phylum: Firmicutes Class: Clostridia Order: Clostridiales Family: Clostridiaceae Genus: Clostridium Species: Clostridium difficile

NCBI Taxonomy link: http://www.ncbi.nlm.nih.gov/genome/?term=clostridium+difficile

Clostridium difficile causes pseudomembranous colitis, toxic megacolon, perforations of the colon, sepsis, and (rarely) death. It is a Gram positive, spore-forming rod that is an obligate anaerobe. It can be found in soil, water, feces, and the human gut. "C. difficile" is a normal inhabitant of the gut microbial community of about 1-3% of adults. The pathogenic form of "C. difficile" is transferred via the fecal-oral route as well as through spore dispersal. "Clostridium difficile"-associated disease (CDAD) was initially reported about 30 years ago and the CDC first recorded infections from a hyper-virulent strain in 2000 along with a marked increase in the number of CDAD infections. "C. difficile" causes disease by producing the toxins TcdA and TcdB that function to disrupt protein synthesis within the host cell. The toxins are responsible for producing symptoms such as watery diarrhea, fever, loss of appetite, nausea, and severe abdominal pain (1). Although "C. difficile" only causes about 20% of antibiotic associated colitis, standard treatments fail in about 25% of CDAD cases. Patients treated promptly typically recover. However, CDAD is notorious for recurrence after initial antibiotic treatment. 33% of patients with an infection will have a recurrence with 64% of those being within 30 days of the initial infection (2). Complications typically develop in about 11% of patients in the first recurrence. This likely promotes the growth of antibiotic resistant strains that are able to perform horizontal gene transfer between recurrences. In about 20% of patients the infection will resolve itself in 2-3 of discontinuing the inciting antibiotic. Most infections that persist are treated with a 10-14 day course of antibiotics like metronidazole, vancomycin, and rehydration therapy. In more serious cases fecal transplants and surgery can be performed (3). Patients at risk for developing CDAD include those taking antibiotics (especially broad spectrum), those taking proton pump inhibitors, GI manipulation or surgery, long term stays in hospital or clinical settings, immunocompromising conditions, and old age. The best practices for preventing infection include judicious administration of antibiotics, quarantine, hand hygiene, the use if EPA-registered disinfectants with a sporicide (especially hypochlorite based disinfectants).

References

Created by Laura Boucher, Marrett Hild, and Lillian Flannigan, students of Tyrrell Conway at the University of Oklahoma