Pathogenesis of Clostridium Difficile (Essay Sample)

CLOSTRIDIUM DIFFICILE
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Clostridium difficile infection (CDI)
Due to rising incidences of diarrhea in patients at hospitals, I began to research about causes of diarrhea. While performing this task, I found out that Clostridium difficile has been one of the major causes of diarrhea and therefore was of a concern for research in order to find out appropriate therapy for preventing, controlling or treating the infection. Poor administration of antibiotics and spread of highly virulent strains have contributed to the rise in the number of cases of Clostridium difficile. This infection is mostly asymptomatic but when symptoms such as diarrhea of more than 20 episodes per day may occur. Other associated symptoms include abdominal pain and fever. Leukocytosis of more than 25000/mm3 is also common (1).
C. difficile is an anaerobic gram-positive bacillus bacterium that forms spores. It was first well documented to cause pseudomembranous colitis in 1978. These bacteria are found mostly in soil, water, vegetables, and meat. Patients who acquire these bacteria come in contact with contaminated food or water. During a period of harsh conditions, this pathogen starts the process of sporulation which leads to the production of spores. The pathogen gets ingested through the mouth to the gut. If the patients take antibiotics or have taken antibiotics recently, the microbiota will be disrupted. This normal microbiota plays a protective role in the host by competing with pathogens for nutrients and signaling immune system to act against microorganisms (2). Antibiotics, therefore, disrupt microbiota in the gut. It is in this disrupted microbiota where spores germinate so as to resist the acidity in the stomach. Bile acids trigger this process of sporulation which results in vegetative overgrowth. The spores proliferate in the colon and produce two main toxins: toxin A and toxin B. These two toxins are taken to cell mucosal epithelia where they colonize. They then stimulate an acute inflammatory response where neutrophils play a key role (3). This leads to diarrhea and formation of a pseudo-membrane which has inflammatory cells, epithelial cell, and an exudate. Ultimately the mucosa is eroded and colon gets damaged (4).
About 25% of patients experience recurrent diarrhea after treatment. This requires another treatment. Pathogen features contribute to this recurrence. Drugs like quinolones are resisted by certain strains of C. difficile that have binary toxins (5). In most patients with recurrent infection, it is examined that the gut microbiota does not return to its original state and therefore this is a predisposing factor to reoccurrence after treatment. Since 1979, the hospital vicinity is contaminated with the spores of C. difficile (6). The hands of hospital staffs and patients get contaminated with these spores and this accounts for repeated episodes of diarrhea and colitis in hospitalized patients (healthcare-associated C. difficile infection). Some asymptomatic patients with this infection transmit it via stool to other patients in the same ward. There are risk factors for developing CDI. These include antibiotic therapy, surgery on the abdomen, proton pump inhibitors, prior hospitalization and old age. Risk factors for developing recurrent infection also include old age and antibiotic use.
Complications of this infection when left untreated include risk of developing megacolon, shock, and hypotension. CDI is diagnosed by considering symptoms (unformed loose stool for more than 24 hours) plus a stool test to identify C. difficile organism or enzyme immunoassay to find C. difficile toxin in stool. Treatment is to first stop the offending antibiotic. For a mild infection, metronidazole is used while complicated one is treated with oral vancomycin. Those with recurrent CDI are treated with