Pseudomembranous Enterocolitis: Causes

Pathogenesis (disease development)

Clostridium difficile is an obligate anaerobic gram-positive rod bacterium. By forming spores, it has a high tolerance to many chemical and mechanical stimuli.

Ribotypes 014 and 020 usually result in a milder infection. Ribotypes 027, 017 (toxin-producing), and 078 (toxin-producing) can lead to severe disease.

Clostridium difficile can produce the following two toxins, toxin A (enterotoxin) and toxin B (cytotoxin). However, whether toxin release occurs depends largely on the state of the intestinal microbiome (gut flora) of the individual patient. The enterotoxin leads to increased fluid and electrolyte secretion. The cytotoxin damages the intestinal mucosa.

The genesis (cause) of Clostridium difficile infection (CDI) is multifactorial.

Etiology (causes)

Disease-related causes.

Blood, hematopoietic organs-immune system (D50-D90).

• Immunosuppression, unspecified

Mouth, esophagus (food pipe), stomach, and intestines (K00-K67; K90-K93).

• Intestinal flora disorder, unspecified

Further

• Visit to an emergency room
• Severe underlying illness, unspecified
• ≥ 2 comorbidities (concomitant diseases).
• Hospitalization or hospitalization that has taken place within the last 3 months or placement in community health care facilities/long-term care facilities.
• Abdominal surgery (abdominal surgery) procedures.
• Outpatient interventions
• Dental procedures
• Instead of C. difficile infection
• Condition after antibiotic therapy within the last 3 months.

Medication

• Antibiotics* (agents that act against bacterial infections); main risk for Clostridium difficile-associated diarrhea is current or occurred antibiotic therapy within the last 3 months; four weeks after antibiotic therapy; 40-60% of cases; especially:
  • High risk
    • Ampicillin
    • Aminopenicillins (amoxicillin)
    • Cephalosporins (cefoxitin, ceftazidime, ceftriaxone, cefuroxime).
    • Quinolones/fluoroquinolones/gyrase inhibitors (ciprofloxacin, moxifloxacin, nalidixic acid, norfloxacin, lomefloxacin, levofloxacin, ofloxacin).
    • Lincosamide (clindamycin)
  • Medium risk
    • Imipenem
    • Carbapenems (imipenem)
    • Tetracyclines (doxycycline, minocycline, tetracycline).
    • Trimethoprim
  • Low risk
    • Aminoglycosides (amikacin, apramycin, geneticin (G418), gentamicin, kanamycin, netilmicin, neomycin, paromomycin, spectinomycin, streptomycin, tobramycin).
    • Β-lactam antibiotic (piperacillin).
    • Broad-spectrum penicillins (mezlocillin, ticarcillin).
    • Glycopeptide antibiotics (vancomycin).
    • Macrolides (azithromycin, erythromycin, clarithromycin, especially clarithromycin and azithromacin).
• H2 antihistamines (H2 receptor antagonists, H2 antagonists, histamine H2 receptor anatgonists; agents that inhibit the production of gastric acid, among other things) – cimetidine, famotidine, lafutidine, nizatidine, ranitidine, roxatidine.
• Non-steroidal anti-inflammatory drugs (NSAID, NSAID; are painkillers with analgesic, antipyretic and anti-inflammatory properties) such as ibuprofen, diclofenac.
• Proton pump inhibitors (PPI; acid blockers) – esomeprazole, lansoprazole, omeprazole, pantoprazole, rabeprazoleCave! Do not use continuous therapy with PPI; these lead to a 3-fold risk of severe intestinal infection with C. difficile.

* Because Clostridium difficile is resistant to almost all broad-spectrum antibiotics, antibiotic therapy may cause this germ to multiply.