Infectious Colitis
Diagnosed among patients with acute diarrhea and colonic inflammation; relevant to the surgeon because it can mimic surgical conditions like an acute abdomen or IBD, and in some cases deteriorates to the point of requiring surgery. Content below is from a textbook reference chapter (Sabiston Ch52 - Infectious & Ischemic Colitis), not primary literature. See Enteritis in the Immunocompromised Host for how these and other pathogens present differently (more frequent, more virulent, and with a wider range of causative organisms) in AIDS/transplant patients.
Clostridioides difficile infection (CDI)
Epidemiology
Most common cause of healthcare-associated diarrhea and a major source of healthcare-associated morbidity, occurring in ~2% of all hospital discharges. Asymptomatic colonization prevalence among hospitalized adults: 3–26% across studies. In the US: ~453,000 new CDI cases/year, of which 83,000 are recurrent, and ~29,300 attributed deaths. Incidence has begun to decline in some regions after a historical peak (Canadian data: 7.9/10,000 patient-days in 2011 → 4.3/10,000 in 2015), attributed to targeted prevention/treatment programs.
Microbiology and transmission
Anaerobic, spore-forming, gram-positive bacillus. Transmission is person-to-person via the fecal-oral route or through exposure to spores in a contaminated environment, including via healthcare personnel’s hands. Toxigenic strains produce A and/or B toxins, which bind colonocyte glycoprotein receptors and lead to colonocyte death and release of inflammatory mediators. The emergence of the Ribotype 027 strain in the mid-2000s drove significant outbreaks across the Western world with more severe disease and higher mortality.
Risk factors
The single most important risk factor is recent antibiotic exposure, which disrupts the natural flora’s ability to suppress C. diff growth/spread. Virtually all antibiotics have been associated with CDI, but third- and fourth-generation cephalosporins, fluoroquinolones, clindamycin, and carbapenems carry particularly elevated risk. Other risk factors: immunodeficiency (including HIV), chemotherapy, acid-suppressing medications (PPIs), GI surgery or tube feeding, and prolonged hospitalization or nursing-home/rehab stay. IBD patients have increased rates of CDI along with worse outcomes (higher rates of colectomy) — differentiating an IBD exacerbation from superimposed CDI can be genuinely difficult given overlapping symptoms, and requires a high index of suspicion (relevant cross-link: Inflammatory Bowel Disease). Risk factors for death from CDI: advanced age, multiple comorbidities, hypoalbuminemia, leukocytosis, acute renal failure, and Ribotype 027 infection.
Clinical presentation and severity
Symptoms commonly begin 4–9 days after starting antibiotics, but can start up to 10 weeks after treatment. Typical presentation: new-onset, unexplained watery diarrhea (3+ unformed stools in 24 hours) ± abdominal pain, fever, ileus. Categorized as: asymptomatic colonization, nonsevere disease, severe disease, and fulminant disease. IDSA severity predictors: leukocytosis ≥15,000/µL and/or serum creatinine ≥1.5 mg/dL. Fulminant/severe disease is diagnosed in patients with hypotension/shock, ileus, or megacolon. The ATLAS criteria is a simple bedside score (age, temperature, leukocytosis, albumin, systemic antibiotic treatment) used to assess response to treatment.
Diagnosis
Based on typical symptoms plus stool testing: enzyme-linked immunosorbent assay for toxin detection, glutamate dehydrogenase immunoassay for C. diff antigen, nucleic acid amplification/ PCR testing, and stool cultures. Flexible sigmoidoscopy can help diagnostically — classic yellowish-white plaques (pseudomembranes, 2–10 mm) seen in about half of CDI patients, with nonspecific colitis in another ~25%; endoscopy should be considered only when its benefit outweighs perforation risk, particularly in fulminant disease. Imaging is not useful for diagnosis (not specific) but helps assess severity and treatment response — CT findings include colonic wall thickening, bowel dilation, pericolonic fat stranding, the “accordion sign” (high-attenuation oral contrast alternating with low-attenuation inflamed mucosa), and ascites. Ultrasound can be a useful alternative for critically ill patients who can’t be transported for CT (wall thickening, luminal narrowing, hyperechoic lines representing pseudomembranes).
Treatment
Initial measures: stop/minimize the inciting antibiotics, parenteral fluids, correct electrolytes; avoid antiperistaltic agents.
| Clinical setting | Treatment | Duration |
|---|---|---|
| First episode | Oral vancomycin 125 mg QID, or fidaxomicin 200 mg BID. If neither available: metronidazole 500 mg TID (nonsevere disease only) | 10 days |
| First episode — fulminant (hypotension/shock, ileus, megacolon) | Vancomycin 500 mg QID (oral or NG tube); consider adding rectal vancomycin instillation if ileus present; plus IV metronidazole 500 mg q8h given together with oral/rectal vancomycin | ≥10 days, individualized |
| Recurrent episodes | Change antibiotic class (metronidazole → vancomycin, or vancomycin → fidaxomicin); tapered/pulsed regimens also used | — |
Fecal microbiota transplant (FMT) — a relatively new option for recurrent CDI. Patients with recurrent CDI lack protective colonic microbiota to resist recolonization; FMT reimplants normal gut bacteria (particularly bacteria resistant to C. diff) to restore biodiversity. Delivery routes: nasogastric, oral (frozen fecal microbial capsules), rectal enema, or colonic (via colonoscopy) — a recent comparison found lower-GI delivery routes more effective than upper-GI. Efficacy ranges 77–100%, with some patients needing multiple FMTs. Current guidelines recommend FMT for patients with multiple recurrences who have failed antibiotic therapy.
Monoclonal antibodies — bezlotoxumab (anti-toxin B) and actoxumab (anti-toxin A) limit colonic damage by neutralizing toxin and blocking host-cell binding. Used as coadjuvant therapy to help prevent recurrence, especially in Ribotype 027 infection, severe CDI, and immunocompromised patients.
Surgery — patients with fulminant CDI showing systemic toxicity, toxic megacolon, or perforation should be operated on emergently. Emergency colectomy in fulminant colitis provides a survival advantage over continued antibiotic therapy alone. Traditional approach: total or subtotal abdominal colectomy with preservation of the rectum in severely ill patients. A newer option with comparable results in patients without necrosis or perforation: exteriorization of a diverting loop ileostomy with on-table colonic lavage, followed by antegrade vancomycin flushes — a colon-sparing alternative.
Other enteric pathogens
Most infectious diarrhea/colitis does not require surgery. A careful exposure history is often diagnostic (contaminated water/food, unpasteurized milk, undercooked meat/fish/shellfish/eggs, international travel, contact with animals/feces).
| Pathogen | Microbiology | Exposure | Presentation |
|---|---|---|---|
| Campylobacter jejuni | Spiral, microaerophilic gram-negative rod (chapter’s table lists this as gram-positive — a source error; corrected here) | Improperly prepared chicken or beef | Fever, watery diarrhea, abdominal pain; commonly involves cecum/terminal ileum; may mimic appendicitis or Crohn’s disease |
| Yersinia enterocolitica | Gram-negative coccobacillus | Contaminated water or food | Abdominal pain, bloody diarrhea; may mimic appendicitis or Crohn’s disease |
| Shigella | Gram-negative facultative anaerobe | Common cause of dysentery in developing countries | Often affects rectum/sigmoid; fever, abdominal pain, watery diarrhea progressing to bloody diarrhea |
| Salmonella typhi / S. enterica serotypes (Paratyphi) | Gram-negative, facultatively anaerobic bacilli | Recent travel to an endemic area, food prepared by a traveler to an endemic area | Fever with or without diarrhea, abdominal pain, cramping, vomiting |
CMV colitis — an important cause of viral colitis in immunocompromised hosts (advanced HIV, transplant patients, IBD patients, chemotherapy). Presents with watery or bloody diarrhea, fever, abdominal pain. Diagnosis via serology and viral load; endoscopy shows patchy mucosal erythema; inclusion bodies on biopsy are pathognomonic. Can progress to sepsis, toxic megacolon, and colon perforation. Treatment usually supportive plus ganciclovir; severe/complicated disease may require surgery.
Septic patients or those with suspected enteric fever should receive empirical broad-spectrum antimicrobial therapy (fluoroquinolones such as ciprofloxacin, or macrolides such as azithromycin, depending on local susceptibility patterns). Surgical intervention is rarely needed for these pathogens except in severe fulminant disease leading to perforation or toxic megacolon.
Open items / gaps
- No primary trial data yet on FMT efficacy, monoclonal antibody outcomes, or the diverting- ileostomy-vs-colectomy comparison for fulminant CDI.
- Current IDSA/SHEA CDI guidelines not ingested directly — the antibiotic table above is the textbook’s summary of them, worth verifying against the primary guideline if making a specific treatment decision.