By Kesa Wilson
Clostridium difficile (C. diff); Etiological agent- Clostridium difficile.
The bacteria are found in the feces. Patients develop Clostridium difficile infection as a results of long term antibiotic use and through fecal-oral transmission (1). People can become infected if they touch items or surfaces that are contaminated with feces and then touch their mouth or mucous membranes. Healthcare workers can spread the bacteria to patients or contaminate surfaces through hand contact (5).
C difficile is a component of the normal intestinal flora of a small percentage of healthy adults and of a relatively large percentage of healthy neonates. It also may be found in the environment, especially in hospitals (2). The majority of Clostridium difficile infections are aquired nosocomially (3).
Clostridium difficile is a spore-forming gram-positive anaerobic bacillus that produces at least two exotoxins: toxin A, primarily an enterotoxin, and toxin B, a cytotoxin (3). C. difficile moves via peritrichous flagella. These flagella are evenly spread around the surface of each cell and allow the bacteria to be highly motile. The bacteria are able to move by a tumbling motion and by movement in a forward direction (8).
Test for Identification:
The cytotoxin assay is the standard test for identification (1). A fresh stool sample is needed and no prep is required. Other tests include endoscopy and anaerobic cultures.
Signs and Symptoms:
Watery diarrhea (at least three bowel movements per day for two or more days), fever, loss of appetite, nausea, abdominal pain/tenderness (5). There is also a disctinct odor when the feces contains Clostridium difficile. More severe cases of Clostiridium difficile infection present with ulcerative colitis which can be severe enough to result in the need for a bowel resection. Signs and symptoms of colitis can include the above list as well as dehydration and bloody stool.
Clostridium difficile was first discovered in 1935 and first associated with disease in 1978 (9).
In addition to the two major toxins of Clostridium difficile--toxins A and B, which represent the major virulence factors--a number of other putative virulence factors have been described. These factors include fimbriae and the ability to associate with gut cells/mucus, the production of a capsule, the secretion of a range of hydrolytic enzymes, the production of other toxins (such as an actin-specific ADP-ribosyltransferase by some strains), and the controversial possibility of the production of a second enterotoxin (10).
The first step that should be taken once a diagnosis is made is to stop administering currently prescribed antibiotics to the patient. In mild cases of Clostridium difficile infection, Metronidazole is administered. In sever cases, treatment can begin with the administration of Vancomycin but can also require surgical intervention.
Hand washing is the primary, most effective preventive of the spread of Clostridium difficile. Any infected patient should be placed in isolation and all staff and visitors should follow isolation precautions that include wearing personal protective equipment. PPE for C. diff includes gloves and isolation gowns. If coming in direct contact with stool, one should wear mask and face shield. All inanimate objects must be disinfected with a chlorine-based germicide (1).
An increase in the number and severity of C diff associated colitis cases has been reported. In July 2007, data obtained from 1993 to 2003 from the Nationwide Inpatient Sample (NIS) was analyzed. They reported that the prevalence, case fatality, total mortality and colectomy rates had significantly increased (1). A case study was performed from January 2003 through January 2005 including 165 C diff patients requiring prolonged ICU stays. They found that 87 of the patients (53%) with fulminate C diff associated colitis dies within 30 days of diagnosis (1).
1. Vasaly, F. et al (August 2009) “A Quality Committee’s Evaluation of Surgical Intervention for Clostridium difficile Infection.” AORN: The Official Voice of Perioperative Nursing. 90(2), 192-200.
2. Carol L. Wells and Tracy D. Wilkins. “Clostridia: Sporeforming Anaerobic Bacilli.” Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. May 3, 2011. http://www.ncbi.nlm.nih.gov/books/NBK8219/#A1078
3. D. Gerding et. al, “Clostridium Difficile-Associated Diarrhea and Colitis” in Infection Control and Hospital Epidemiology. August 1995, vol 16(8); 459-77. May 3, 2011. http://www.shea-online.org/assets/files/position_papers/Cldiff95.PDF
4. “Clostridium difficile Infection” Centers for Disease Control and Prevention. May 3, 2011. http://www.cdc.gov/HAI/organisms/cdiff/Cdiff_infect.html
5. “Clostridium difficile (C. diff) in Healthcare Settings” Centers for Disease Control and Prevention. May 5, 2011. http://www.cdc.gov/HAI/organisms/cdiff/Cdiff.html
6. C. Deneve et. al, “New trends in Clostridium difficile virulence and pathogenicity” International Journal of Antimicrobial Agents. 2009. Vol 33(S1); S24-S28. May 6, 2011.
7. “Information about the Current Strain of Clostridium difficile” Centers for Disease Control and Prevention. May 6, 2011. http://www.cdc.gov/HAI/organisms/cdiff/Cdiff-current-strain.html
8. J. Kumm. “Clostridium difficile: A ‘difficult’ human pathogenic bacterium.” University of Wisconsin. April 2009. May 5, 2011. http://bioweb.uwlax.edu/bio203/s2009/kumm_jakl/growth&adapt.htm
9. “Frequently Asked Questions.” The Department of Microbiology, Mount Sinai Hospital. http://microbiology.mtsinai.on.ca/faq/cdifffaq.shtml
10. S. Borriello et. al, “Virulence factors of Clostridium difficile” Reviews of Infectious Diseases. January/February 1990, Vol 12(2); 185-91. May 5, 2011.