Clostridium difficile (C.diff) infection (CDI) is the most common US healthcare pathogen-associated infection with over 450,000 cases and 29,000 deaths per year. If you work in healthcare, you’ve likely heard of CDI… but where does this bug come from and what can we do about it?
30-40% of households, 20% of grocery meats, and 10-20% of hospital patients are colonized with C.diff. Consequently, some patients present with C.diff on admission to the hospital and CDI is activated from antibiotics, antacids, immunosuppressants, etc. Transmission also occurs from symptomatic and asymptomatic patients via spores carried on staff members’ hands, clothing, equipment, and the environment. One study showed that if you had the misfortune to be admitted to a room previously occupied by a patient with CDI, you have a 2.4x higher risk of contracting CDI. Additionally, if the previous occupant was NOT diagnosed with C.diff but ONLY received antibiotics as part of their care, you’re still at an increased risk likely from asymptomatic colonization.
So, how about diarrhea in the ICU? We used to be so trigger-happy about ordering C. diff in anyone who had new-onset diarrhea, but the reality is that only 5% of ICU diarrhea is related to CDI. Close to 70% is due to medications, chemotherapy, and tube feeds, and 25% is due to laxatives, enemas, and suppositories in the preceding 24 hours.
To date, the C.diff toxin enzyme immunoassay (EIA) remains the best test for CDI although it isn’t always accurate. A PCR test only tests for the gene that creates toxin, but does not shed light on whether or not that toxin is being produced. The C.diff antigen tests for glutamate dehydrogenase, an enzyme produced by all C.diff organisms. A positive toxin is concerning for CDI. A negative toxin, negative antigen or negative toxin, positive antigen are equivocal and reassuring. As a side note, Cliff the Beagle has been shown to have 100% sensitivity and specificity in identifying C.diff in stool! How cool! 🙂
What’s the best treatment for CDI? In the case of mild disease, oral vancomycin and metronidazole seem equivocal; however in our critically ill ICU patients, we always opt for oral vancomycin. More novel agents like fidaxomicin offer the advantage of decreased CDI recurrence rate but similar efficacy when compared to oral vancomycin. How about combining oral vancomycin AND IV metronidazole? There’s some retrospective evidence in favor of combining therapies to improve mortality rates in critically ill patients.
How about CDI recurrence? We should treatment by reestablishing control with oral vancomycin therapy and consider a vancomycin taper/pulse which, in theory, should target newly created C.diff spores. Other considerations include fidaxomicin, a fecal microbiota transplant (FMT), and bezlotoxumab – a $4,000/dose monoclonal antibody targeted at the toxin.
What’s your experience with CDI? Any crazy recurrences? Toxic megacolon? Drop me a comment below! 🙂
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