Reply #31: Treatment of C. difficile [View All]

[du_grad]

http://www.emedicine.com/med/TOPIC3412.HTM

Good article here. Metronidazole (trade name Flagyl) is also used in addition to Vancomycin. The organism was discovered, according to the article, in 1935. I am a microbiology technologist. We do a LOT of tests for C. difficile at our lab. Please note that symptoms of C. diff. can present up to two months AFTER your round of antibiotics. Do not ignore this if you have recently been hospitalized. It is the toxin that is produced that is the problem with this bug. The problem is that Clostridia, in general, are spore-formers. The spores protect the bacteria from destruction. It takes a lot of bleach to kill the spores on surfaces. I think the fact that they have found this bug in meat is interesting. I would wonder also how long this has been present in meat. Decades?? Just because the bug is there doesn't mean it causes an infection. The antibiotics are what disturbs the normal bacterial flora. See quote below (and read the entire article - lots of good information):

"C difficile colitis results from a disturbance of the normal bacterial flora of the colon, colonization with C difficile, and release of toxins that cause mucosal inflammation and damage. Antibiotic therapy is the key factor that alters the colonic flora. Hospitalized patients are the primary targets of C difficile infection. C difficile is present in 2-3% of healthy adults and in as many as 70% of healthy infants. Treatment of asymptomatic carriers is not recommended. Colonization occurs by the fecal-oral route. C difficile forms heat-resistant spores that can persist in the environment for several months to years. Outbreaks of C difficile diarrhea may occur in hospitals and other outpatient facilities where contamination with spores is prevalent. Normal gut flora resists colonization and overgrowth with C difficile. Antibiotic use, which suppresses the normal flora, allows proliferation of C difficile.

Pathogenic strains of C difficile produce 2 distinct toxins. Toxin A is an enterotoxin, and toxin B is a cytotoxin. Both are high–molecular weight proteins capable of binding to specific receptors on the intestinal mucosal cells. Receptor-bound toxins gain intracellular entry where they catalyze a specific alteration of Rho proteins, small glutamyl transpeptidase (GTP)–binding proteins that assist in actin polymerization, cytoskeletal architecture, and cell movement. Both toxin A and toxin B appear to play a role in the pathogenesis of C difficile colitis in humans..."