Causes and Symptoms
The bacteria
Clostridium difficile that cause C. difficile
infection are transmitted through the fecal-oral route. These bacteria are shed from feces of a colonized or infected person. When shed, they form spores as a protective mechanism when they enter the environment. They are able to survive in this form for many months on environmental surfaces. C. difficile infection is spread through contact with an infected or colonized patient, the environment, or the contaminated hands of a health care worker. The incubation period of C. difficile is unknown; however, one study suggests that it might be less than seven days.
The major risk factors for C. difficile infection include advanced age, hospitalization, and antibiotic use. Nearly every antibiotic has been implicated in C. difficile infection but clindamycin, cephalosporins, and floroquinolones are associated with a higher risk. When a patient receiving antibiotics ingests C. difficile spores, they germinate in the small intestine, where the normal flora has been altered. The spores multiply, flourish, and produce toxins. The toxins, toxin A and B, cause inflammation and mucosal damage leading to colitis. In severe infection, C. difficile can cause toxic megacolon, septic shock, and death.
When a patient becomes infected with C. difficile, fever, abdominal pain or tenderness, anorexia, nausea, and watery diarrhea commonly occur. In severe infection, the patient may develop pseudomembranous colitis, which may progress to toxic megacolon, a toxic dilation of the colon. If the patient develops toxic megacolon, then sepsis and death may quickly follow.
Treatment and Therapy
Some cases may resolve in two to three days after discontinuing current antibiotic use. However in most cases a ten-day course of metronidazole or vancomycin orally is effective. Surgical intervention may be necessary in severe C. difficile infection if pseudomembranous colitis or perforation develop.
Perspective and Prospects
Before the mid 1970s, pseudomembranous colitis, an inflammatory process in the colon caused by bacterial toxins, was associated with the use of certain antibiotics; mainly lincomycin and clindamycin. It was not until 1978 that C. difficile was identified as the causative agent of antibiotic-associated pseudomembranous colitis. Since that time, C. difficile has become the leading cause of antibiotic-associated diarrhea. Between 2000 and 2007, the rate of C. difficile-related deaths rose 400 percent, and currently about 14,000 people in the United States die each year from such infections. Moreover, a hypervirulent strain called BI/NAP1/027 has emerged. This strain produces a type of toxin not previously seen in other strains; it is also highly resistant to the fluoroquinolone antibiotics. Many health care facilities have adopted infection prevention measures since 2010, but it is not yet clear how effective these measures have been in reducing infection rates. The American College of Gastroenterology reported in 2012 that while studies have shown that fecal microbiota transplants were effective in 91 percent of C. diffpatients who had them, controlled trials of the treatment have not yet been performed.
Bibliography:
Carrico, Ruth, et al. Guide to the Elimination of Clostridium difficile in Healthcare Settings. Washington, D.C.: APIC, 2008.
Centers for Disease Control and Prevention. "Healthcare-associated Infections (HAIs): Clostridium difficile Infection." CDC, Mar. 1, 2013.
Priedt, Robert. "HealthDay: Efforts to Prevent Hospital-Based Infection Falling Short, Survey Finds." MedlinePlus, Mar. 14, 2013.
Professional Guide to Diseases. 9th ed. Ambler, Pa.: Lippincott, 2008.
Surawicz, Christina M. "C. difficile Infection." American College of Gastroenterology Patient Education & Resource Center, Dec. 2012.
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