Diarrhea is commonly associated with the use of antibiotics that are capable of killing/ arresting growth of infection causing organism but in some cases this association could be related with the proliferation and colonization of opportunistic pathogen Clostridium difficile. In…
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C. difficile is a spore forming, anaerobic bacilli, shows positive Gram reaction and is known to be associated with nosocomial diarrhea. It is an etiological representative of pseudo membranous colitis (PMC) and 15-25% of diarrhea associated with the intake of antibiotics (Bartlett, 2002).
It is known that bacteria adapt to the shifting environment and so do their response to antibiotics, making them resistant and more virulent. Severity of CDAD is also associated with similar paradigm. In severe and acute cases CDAD may cause ulceration and hemorrhage. The disease encompasses diarrhea, fever, amplified fecal leukocytes, abdominal cramping and dehydration; leading to hypoalbuminaemia, toxic megacolon, colonic perforation and PMC causing amplification in morbidity and mortality (Poutanen, 2004).
Pathogenic Clostridium difficile produces exotoxins- A and B. They have potential role in causing CDAD (Pothoulakis, 1996). Strains producing toxin either A+ B+ or A‑B+ are responsible for virulence while non-toxin producing strains are non virulent and do not cause diarrhea.
In normal individuals, enteric pathogens are prohibited from establishment due to native intestinal microflora, contributing to host’s defense mechanism. Clostridium difficile is a potent pathogen that successfully establishes infection because of its immense ability to produce toxins thereby paving the way for C. difficile colonization. Toxins generated by C. difficile are highly enterotoxic and cytotoxic. Healthy individuals possess antibodies serum IgG and intestinal secretory IgA against toxin A, and efficiently bind to the intestinal receptors of toxin A. This is a condition where humoural response to toxin A is hampered and thus C. difficile finds way for proliferation. The action of toxin A causes disruption of epithelial cells, enhanced fluid emission, damage of mucosa, irritation and tenderness due to enhanced permeability of tight junctions causing diarrhea or PMC
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