Clostridium difficile colitis (pseudomembranous colitis)

Clostridium difficile colitis (pseudomembranous colitis)

    * Introduction
    * Causes
    * Signs and symptoms
    * Diagnosis
    * Treatment
Clostridium difficile colitis is an intestinal bacterial infection which occurs in people who have suffered abuse of antibiotics or prolonged antibiotic therapy, the bacterium is a commensal of the digestive tract that becomes pathogenic under certain favorable conditions.
It is most commonly found infections acquired by hospitalized patients. After a period of two days of hospitalization, 10% of patients hospitalized for another illness will develop Clostridium difficile infection. Clostidium Sprie the colon are able dormanda until the person carrying the antibiotic. Antibiotic therapy alters the existing bacterial flora in the colon and prevents excessive proliferation of clostridiilor. As a result growth factor inhibitor clostidiilor disappears, they go to form dormant spores that produce toxins in the infection and inflammation of the colon.
Colitis severity varies. In most severe cases are fatal toxins released for lining of the colon, determining ulcers, necrosis with leukocyte-white membrane covering the lining of the colon. This severe form of colitis with Clostridium difficile pseudomembranous form is called, because on the surface colonic mucosa is necrotic debris deposited by white blood cells that have the appearance of false membranes.
Not all people who are carriers of colonic clostridiilor develop colitis. Some people are carriers of dormant or passive forms antibodies that protect them.
Patients with moderate colitis shaped fever, mild diarrhea, mild abdominal cramps and tenderness feeler. Those with severe colitis will present high fever, severe diarrhea, watery stools per day over 10 with blood, severe pain and tenderness feeler painful. Diarrhea can lead to dehydration and electrolyte balance alterations. Less severe colitis can cause megacolon, colonic perforation and peritonitis.
Therapeutic decision depends on the severity of the disease. For asymptomatic carriers do not need treatment. Cessation of antibiotic is important triggers when possible. Patients with severe symptoms require specific antibiotic therapy. 95% of patients will respond to therapy for 10 days. Surgery is indicated for fulminant colitis and toxic megacolon.
In general, relapses are frequent and occur in 5-50% of cases. Reinfection typically occurs at 3 days after treatment was discontinued. While most patients recover without specific therapy, symptoms can be prolonged and debilitating. Clostridium difficile associated diarrhea has a mortality rate of 25% in older patients.
Pathogenesis
Clostridium difficile colitis begins with impaired through a normal colonic bacterial flora, colonization clostridii and release toxins that cause inflammation and necrosis of colonic mucosa. Antibiotic therapy is the main factor involved in colonic bacterial equilibrium. Are the main targets for hospitalized patients with Clostridium difficile infection. Bacteria present in 2-3% of estrous healthy adults and in 70% of healthy children. Treatment of asymptomatic carriers is not recommended.
Colonization occurs by the fecal-oral route. The bacteria form heat resistant spores that persist in the environment from several months up to several years. Clostridii epidemic diarrhea may occur in hospitals and other institutions where spore contamination is prevalent. Normal intestinal flora and colonization with Clostridium resist contamination. Consumption of antibiotics that suppress the normal flora allows clostridiilor proliferation.
Pathogenic mechanisms of Clostridium difficile produce two toxins include. Toxin A is an enterotoxin, while toxin B is a citotoxin. Both are large proteins with molecular Gruta binds to specific receptors on cells lining the colon. Receptor-toxin complex is internalized into the cell lining which catalyze reactions that alter citoskeletul specific, cellular architecture, cellular mobility and polymerization. Both toxin A and B play a role in the pathogenesis of Clostridium difficile colitis with humans.