How to Prevent C difficile Infection: A New Guide

Laura A. Stokowski, RN, MS

Disclosures

May 24, 2013

In This Article

CDI Today: Changing Epidemiology

Years ago, many clinicians were taught that CDI was essentially a nuisance infection -- an inevitable consequence of old age, antibiotics, and a stint in the hospital. The past few decades have seen a steady increase in the incidence and severity of CDI,along with an increase in mortality. More cases of CDI are being reported in patients who were previously considered to be at low risk for the infection. The rate of hospital discharges in the United States with CDI listed as any diagnosis increased from 3.82 per 1000 in 2000 to 8.75 per 1000 in 2008.[3]

Another phenomenon driving the changing epidemiology of CDI is community-onset disease. "Years ago, we weren't even aware of the community factor in CDI, but that is changing. Community-associated disease is real, accounting for 32% of cases.[4] Furthermore, community-associated CDI is being diagnosed in younger and healthier individuals. Now that we have the ability to separate hospital-associated from community-associated disease, we are definitely seeing a rise in the latter," explained Dr. Limbago.

The pivotal event in the development of CDI is exposure to antibiotics, which destroys the normal gut microbiota and allows intestinal organisms that are not killed by the antibiotic to proliferate.[2] When this disruption is followed by acquisition of spores or vegetative C difficile from the environment, C difficile attaches to the mucosa of the colon and produces toxins, resulting in pseudomembranous colitis and, in some cases, toxic megacolon and death. Normal intestinal flora are able to suppress C difficile and toxin production, preventing the diarrhea and inflammation characteristic of C difficile-associated disease.

The main risk factors for CDI haven't changed: exposure to antibiotics, hospitalization, and advanced age. Most antibiotic classes have been implicated in CDI, but certain antibiotic classes, such as cephalosporins, clindamycin, and fluoroquinolones, are more likely to facilitate development of disease. This may be related to the ability of those antibiotics to disrupt normal lower intestinal microbiota. Fluoroquinolones are implicated in outbreaks of a hypervirulent strain of C difficile known as restriction endonuclease analysis type BI, North American pulsed field type 1, PCR ribotype 027 (BI/NAP1/027).[5] The virulence of this epidemic strain is related to increased production of toxin A; toxin B; and a binary toxin, the function of which is not entirely understood but might be synergistic with toxins A and B.[5]

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