Abstract
Clostridioides difficile (CDI) infection is a disease associated with a disruption of the gut microbiome with over-colonization of C. difficile, the toxins of which cause inflammation and damage to the colon. A dynamic assessment of the CDI prevalence indicates a significant increase in laboratory-confirmed cases of infection and a high mortality associated with it. C. difficile is recognized as the main causative agent of nosocomial infections in Europe, USA, Canada and Australia, which develops 48 hours after hospitalization in a medical facility and within 12 weeks after discharge. The severity of CDI is determined by the severity of infectious-toxic, diarrheal and abdominal syndromes. Severe CDI is characterized by manifestations of colitis, accompanied by severe leukocytosis, a decrease in albumin levels and an increase in serum creatinine levels. Development of fulminant forms, pseudomembranous colitis, toxic megacolon, intestinal perforation, sepsis is possible. The risk factors include in-hospital stay; recent use of antibiotics (within the previous 12 weeks, especially the use of fluoroquinolones, cephalosporins of III–IV generations, carbapenems and clindamycin), PPI and H2-histamine blockers; presence of inflammatory bowel diseases (ulcerative colitis, Crohn’s disease), immunodeficiency states, including iatrogenic; recent endoscopic examinations, surgical interventions on the gastrointestinal tract, tube feeding, enemas; possible contact with a family member who recently had a C..difficile infection. The «gold standard» for confirming the CDI diagnosis is the identification of the causative agent and/or toxins of C. difficile in the stool using specific laboratory research methods. Vancomycin or metronidazole are recommended as first-line therapy.
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