Generated by DeepSeek V3.2| Pseudomembranous colitis | |
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| Name | Pseudomembranous colitis |
| Caption | Gross pathology of the colon showing characteristic pseudomembranes. |
| Field | Gastroenterology, Infectious disease (medical specialty) |
| Symptoms | Watery diarrhea, fever, abdominal pain, leukocytosis |
| Complications | Toxic megacolon, sepsis, perforation (medical) |
| Causes | Clostridioides difficile infection, often following antibiotic use |
| Risks | Hospital-acquired infection, advanced age, proton-pump inhibitor use |
| Diagnostic | Stool test for C. difficile toxin, colonoscopy |
| Treatment | Metronidazole, Vancomycin, Fidaxomicin, Fecal microbiota transplant |
| Prevention | Antibiotic stewardship, contact precautions, hand hygiene |
Pseudomembranous colitis. It is a severe inflammatory condition of the colon primarily caused by an overgrowth of the bacterium Clostridioides difficile, typically following disruption of the normal gut flora by antibiotic therapy. The disease is characterized by the formation of adherent yellowish plaques, or pseudomembranes, on the colonic mucosa. It represents a major cause of hospital-acquired infection and can lead to life-threatening complications such as toxic megacolon.
The cardinal symptom is profuse, foul-smelling watery diarrhea, which may be accompanied by abdominal cramping and tenderness. Systemic signs often include fever, malaise, and leukocytosis, which can be profound. In severe cases, patients may develop signs of hypovolemia due to fluid loss or exhibit symptoms of sepsis. Complications like toxic megacolon may present with abdominal distension, severe pain, and hypotension. The presentation can range from mild diarrhea to fulminant colitis, sometimes mimicking an acute abdomen requiring surgical evaluation.
The primary causative agent is Clostridioides difficile, a spore-forming, Gram-positive bacterium. Disease typically occurs after antibiotic use, such as clindamycin, fluoroquinolones, or broad-spectrum cephalosporins, which disrupt the normal colonic microbiota. This allows for the proliferation of C. difficile and the production of its exotoxins, TcdA and TcdB. These toxins inactivate Rho family GTPases within colonic epithelial cells, leading to cytoskeletal disruption, cell death, and a robust inflammatory response. The resulting necrotic debris, fibrin, and mucous coalesce to form the characteristic pseudomembranes. Risk factors include hospitalization, advanced age, use of proton-pump inhibitors, and underlying inflammatory bowel disease.
Diagnosis is confirmed by detecting C. difficile or its toxins in a stool sample. Common laboratory methods include nucleic acid amplification tests like PCR, which detect toxin genes, and enzyme immunoassays for toxins A and B. In cases of ileus or high clinical suspicion with negative stool tests, flexible sigmoidoscopy or colonoscopy may reveal the pathognomonic pseudomembranes. Imaging studies such as abdominal CT may show colonic wall thickening, ascites, or the accordion sign. Differential diagnosis includes other causes of infectious colitis like Salmonella or Campylobacter, as well as ischemic colitis and severe ulcerative colitis.
First-line treatment involves discontinuing the inciting antibiotic if possible. Specific antibiotic therapy targets C. difficile and includes metronidazole, oral vancomycin, or fidaxomicin. The choice depends on disease severity, with vancomycin or fidaxomicin preferred for initial episodes of non-fulminant disease. For recurrent infections, options include a prolonged, tapered course of vancomycin, the use of fidaxomicin, or fecal microbiota transplantation. FMT, which involves instilling processed stool from a healthy donor, is highly effective for recurrent disease by restoring the normal gut microbiome. Severe, complicated cases with toxic megacolon or perforation may require surgical consultation, potentially for a colectomy.
Prevention strategies in healthcare settings are paramount and center on infection control. Strict contact precautions, including the use of gowns and gloves and placement in a private room, are essential. Meticulous hand hygiene with soap and water is required, as alcohol-based hand sanitizers are ineffective against C. difficile spores. Environmental cleaning with sporicidal agents like bleach is necessary to eradicate spores. Antibiotic stewardship programs aimed at reducing unnecessary antibiotic prescriptions are a critical public health measure to lower incidence. Probiotic use with Saccharomyces boulardii or Lactobacillus species may be considered in high-risk patients starting antibiotics.
With appropriate treatment, the prognosis for an initial episode is generally good, though recurrence occurs in approximately 20-30% of cases. Risk factors for recurrence include advanced age, ongoing use of non-C. difficile antibiotics, and severe underlying comorbidity. Fulminant colitis carries a high mortality rate, especially if it progresses to toxic megacolon, septic shock, or requires colectomy. The success rate of fecal microbiota transplantation for recurrent disease exceeds 90%. Long-term complications can include chronic diarrhea and, rarely, the development of irritable bowel syndrome-type symptoms following infection.
Category:Infectious diseases Category:Gastroenterology Category:Medical conditions related to antibiotics