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KEY POINTS
■ Incidence and prevalence rates of Clostridium difficile infection (CDI) are increasing, along with reports of community-acquired CDI. Hypervirulent C difficile strains are causing worldwide epidemics.
■ Diagnosis is confirmed by culture or the presence of C difficile toxins or toxin strains in the stool.
■ The first step in treatment is to discontinue the offending antibiotic, unless there are convincing contraindications to doing so.
■ Metronidazole is not as effective as vancomycin for severe disease or recurrent infection. FDA-approved medications to treat severe or recurrent CDI are lacking.
■ To control CDI, antibiotic stewardship and environmental infection controls are a must.
Clostridium difficile, a spore-forming, gram-positive, anaerobic bacillus, has reemerged to become the leading cause of nosocomial infectious diarrhea and a worldwide public health threat.1 Over the past decade, the changing epidemiology of C difficile infection (CDI) has been demonstrated by epidemic outbreaks of drug-resistant, toxin-producing, hypervirulent strains causing severe disease, disease recurrence, and death.2 CDI has placed a huge financial burden on the US health care system, with cost estimates of $3.2 billion annually.3
Antibiotic use continues to be the leading risk factor for CDI. However, other factors implicated in this changing infection include host immunity, comorbid diseases, the use of gastric acid-altering medications, and the use of specific antibiotics, such as fluoroquinolones and clindamycin (Cleocin, generics).1,4 Increased incidences of CDI are being reported in the community and in persons without traditional risk factors.4,5
Efficient and effective diagnosis remains a challenge; treatment options are limited; and currently, a vaccine does not exist. Preventing and controlling this disease through antibiotic stewardship, good hand hygiene, and environmental disinfection is imperative. This article provides current evidence about CDI that will enable physician assistants to serve as leaders in the prevention and intervention efforts required to curb the resurgence of this old infection.
CHANGING EPIDEMIOLOGY AND RISK FACTORS
In the United States, an estimated 500,000 cases of CDI occur annually.6 Over the 7-year period of 1996 to 2003, the discharge diagnosis rate of CDI increased almost 100% from 31 per 100,000 to 61 per 100,000.7 Similar increases in incidence rates were seen in Europe and Canada, with epidemic proportions impacting the infirm and the elderly.1,8 As the rates of CDI increased, the severity and complications of the disease also increased, with more cases of prolonged hospitalization, disease recurrence, colectomy, toxic megacolon, and death.2,4
The risk of developing CDI is directly related to the number of antibiotics to which a person is exposed, as well as the length of exposure and the spectrum of antibiotic coverage.4 Any antibiotic that disturbs colonic flora, including a single dose for surgical prophylaxis, is a risk factor for CDI.9 Several medications have been linked to CDI, including penicillins, cephalosporins, and lincosamides. In 1978, clindamycin phosphate, a lincosamide, was the first antibiotic associated with C difficile and pseudomembranous colitis (PMC)(Figure 1).10 More recently, widespread use of fluoroquinolones has been associated with a 3-fold increased risk of CDI.11 Fluoroquinolones are known to significantly decrease colonic flora, and this may be a factor in their high association with CDI.
The use of gastric acid-altering medications, such as proton pump inhibitors (PPIs), has also increased in recent years; and although the evidence is not clear-cut, some patients taking PPIs have experienced increased rates of CDI.12 The decrease in gastric acid resulting from these medications is thought to facilitate colonization and transit of C difficile through the stomach to the bile-laden small bowel, promoting growth of the organism.
Advanced age, antibiotic use, current or previous hospitalization, and comorbid disease remain traditional risk factors for CDI (Table 1). Host immunity and low production of antibody against C difficile toxins are associated with developing active disease versus asymptomatic colonization. Transplant recipients and others on immunosuppressant therapy or chemotherapeutic agents face an increased risk of CDI.4 Inflammatory bowel disease (IBD) has recently been identified as a risk factor for CDI, as rates of CDI infection are higher in patients with IBD and these patients may have a worse outcome.1,4C difficile-associated diarrhea (CDAD) and IBD may manifest very similarly. Clinicians should be judicious in their management of patients with IBD, so that they do not overlook a complicating CDI.
GI surgery and procedures that manipulate the GI tract disrupt colonic function and are risk factors for CDI.9 Community-acquired C difficile infection (CA-CDI) rates are on the rise in the pediatric and young adult population and in pregnant women.4,5 Community sources of CDI include exposure to recently hospitalized patients, soil, pets, water, animals used for food, meats, and vegetables.2,6