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 textbook reference chapters (Sabiston Ch52 - Infectious & Ischemic Colitis, ASCRS Ch51 - Infectious Colitis), not primary literature. See Enteritis in the Immunocompromised Host for the parallel Sabiston-sourced chapter on how these and other pathogens present differently (more frequent, more virulent, and with a wider range of causative organisms) in AIDS/transplant patients specifically — ASCRS Ch51 - Infectious Colitis substantially deepens that immunocompromised-host picture too; see the new "Infectious colitis in immunocompromised patients" section below.

Clostridioides difficile infection (CDI)

Content in this section now draws on both Sabiston Ch52 - Infectious & Ischemic Colitis and the much more granular ASCRS Ch52 - Clostridium difficile Infection — the two are consistent throughout; Ch52 adds substantial epidemiology/mechanism/trial-level depth to nearly every subsection below and two entirely new ones (Nomenclature and genetics; Ribotype and severity).

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. (ASCRS Ch52 adds): in many hospital settings CDI has become the most common cause of hospital-acquired infection overall, surpassing MRSA; CDC data show a fourfold increase in CDI from 1993–2009, with a >200% increase specifically among patients

65. Economic burden: $8,911–$30,049 attributable direct cost per hospitalization (Nanwa meta-analysis), extrapolating to a total US healthcare-system cost estimated at $3 billion.

Microbiology, nomenclature, and genetics

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.

(New — ASCRS Ch52): the proper genus designation is Clostridioides, not Clostridium (reassigned 2016 based on phylogenetic studies), though the common name "C. difficile" has persisted clinically. CDI pathogenesis centers on the pathogenicity locus (PaLoc), a 19.6 kb region of bacteriophage origin containing the toxin A (tcdA) and B (tcdB) genes; both toxins cause monoglucosylation of intracellular Rho GTPases, depolymerizing the colonocyte cytoskeleton. Some strains also carry binary toxin (CDT), encoded outside PaLoc — present in up to 6% of isolates, and thought to increase colonocyte membrane surface area (up to fivefold) to promote adherence of the organism and its toxins. Toxins A and B are present in virtually all symptomatic infections.

Ribotype and clinical severity (new — ASCRS Ch52): ribotyping (restriction-enzyme characterization of the ribosomal intergenic spacer region) is the standard way to characterize dominant strains. Ribotype 027 produces >15× the toxin A/B of other strains plus binary toxin, and is the strain most frequently identified in severe CDI and in patients from long-term healthcare facilities (adjusted OR 4.87 vs. patients from a private residence) — comparative genomics show it carries >200 genes not found in other strains. Ribotype 078 is a further virulent strain with a zoonotic (human-animal) link.

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 — (ASCRS Ch52 quantifies this): a review of 13 studies found ORs of 3.2 (cephalosporins), 2.8 (clindamycin), and 1.6 (fluoroquinolones). Other risk factors: immunodeficiency (including HIV — CD4 ≤50/mm³ carries an adjusted OR of 5.2–27.6 for CDI specifically, per Ch52), chemotherapy, acid-suppressing medications (PPIs — Ch52 cites a plausible mechanism: an in vitro study found omeprazole stimulates C. diff toxin production in both acidic and basic environments, and four meta-analyses of >300,000 patients suggest an OR of 1.6–1.7, though randomized/confounder-controlled data is lacking and global PPI discontinuation isn't supported), 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). (ASCRS Ch52 adds a genetic risk factor): the TNFRSF14 locus has been associated with a sixfold increase in CDI risk in IBD patients in one study; other IBD-specific CDI risk factors include low albumin, hemoglobin <9 g/dL, active colitis, biologic use, and antibiotic use, and at least one study estimated a sixfold increase in colectomy need when CDI complicates IBD. Risk factors for death from CDI: advanced age, multiple comorbidities, hypoalbuminemia, leukocytosis, acute renal failure, and Ribotype 027 infection. General Postoperative Complications (ASCRS Ch8) puts a number on the postoperative incidence specifically (0.2–8.4% after major surgery, using largely the same risk-factor list already above) — cited there as a colorectal-surgery-specific data point rather than duplicating this page's fuller epidemiology/microbiology/treatment content. (ASCRS Ch52 adds a perioperative-specific nuance): patients receiving perioperative antibiotics for >24 hours had a 6.7-fold increase in CDI incidence vs. those receiving ≤24 hours (Balch) — the most important modifiable factor in reducing perioperative CDI risk is likely prompt cessation of prophylactic antibiotics per guideline, more so than the choice of bowel preparation itself (data does not support the theoretical concern that mechanical-bowel-prep-plus-oral-antibiotic microbiome changes increase CDI susceptibility — one comparative dataset actually found lower postoperative CDI incidence with combined mechanical prep plus oral antibiotics). Hospital-level factors matter too: a New York statewide study of 150,878 segmental-colectomy/proctectomy patients found CDI incidence ranging 0–11.3% by surgeon and 0–6.8% by hospital, with patient factors explaining only 24% of this variation and ~70% coming from unexplained hospital-level factors (antibiotic stewardship, hand hygiene practice, disinfection protocols, etc.).

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. The ATLAS criteria is a simple bedside score (age, temperature, leukocytosis, albumin, systemic antibiotic treatment) used to assess response to treatment. Two severity schemas are in clinical use (ASCRS Ch52 adds the second, ACG, schema alongside the wiki's existing IDSA one):

Schema	Non-severe	Severe	Fulminant
IDSA (2017)	WBC <15,000/µL and creatinine <1.5 mg/dL	WBC ≥15,000/µL and/or creatinine ≥1.5 mg/dL	Cardiovascular shock, ileus, or megacolon
ACG	—	WBC ≥15,000/µL and albumin <3 g/dL	Any ICU admission requirement, or temp ≥38.5°C, ileus, significant distention, altered mental status, WBC >35,000 or <2,000/µL, lactate >2.2 mmol/L, or organ dysfunction

(ASCRS Ch52 adds a diagnostic distinction): CDI should be kept conceptually distinct from carrier states (positive stool test, no symptoms) — not rare (one study: 16.4% of geriatric patients without diarrhea were toxin-B-PCR-positive, of whom 16.3% went on to develop symptomatic CDI), and more common with frequent healthcare contact.

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).

(ASCRS Ch52 adds the testing-method evolution and current algorithm): bacterial culture → cell-culture cytotoxicity neutralization assay (CCCNA, the historical "gold standard," now largely replaced — sensitivity as low as 65%, 24–48h turnaround) → toxigenic culture (also now outdated). Current standard: a GDH (glutamate dehydrogenase) immunoassay as a high-sensitivity (80–100%) screen — GDH alone lacks specificity, so a positive result requires a confirmatory toxin EIA; a GDH-positive/EIA-negative result is resolved with a NAAT (PCR-based, most sensitive but 2–3× the cost of GDH-EIA and possibly slower). Routine re-testing with NAATs to confirm resolution is not recommended — bacterial DNA can persist up to 30 days after a patient is no longer infected.

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	—

(ASCRS Ch52 supplies the trial evidence behind this table): Zar's 2007 RCT (150 patients, mild or severe CDI) found vancomycin non-superior to metronidazole in mild disease, but significantly higher cure rates in severe disease (97% vs. 76%, p=0.02) — current IDSA guidance now restricts metronidazole to non-severe first episodes when other agents are unavailable/contraindicated, given this evidence plus case reports of neurotoxicity with prolonged/repeated metronidazole courses. Fidaxomicin's first Phase III trial (629 patients) showed non-inferiority to vancomycin with lower recurrence — but only for non-ribotype-027 strains. The EXTEND trial (364 patients, vancomycin vs. extended-pulse fidaxomicin) found an 11% improvement in 30-day clinical cure with fidaxomicin, no difference in adverse events. A 22-study/3,215-patient Cochrane review concluded vancomycin > metronidazole and fidaxomicin > vancomycin, though the effectiveness differences "were not too large," and metronidazole's far lower cost remains a genuine practical advantage. For fulminant disease specifically, vancomycin can be given as a retention enema (500 mg/100cc NS q6h) if ileus limits oral/enteral delivery, though the supporting data for this route is weak.

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. (ASCRS Ch52 adds): FMT is no longer experimental for in/outpatient recurrent CDI, with cure rates >80% routinely described — some now question whether FMT should be first-line for recurrence given its superiority to conventional antibiotics in that setting (though it remains not first-line for a primary CDI episode). FMT for fulminant CDI has the least evidence of any FMT application; the few available studies are promising, but recurrence (with associated mortality) is a specific challenge in this setting, and incorporating vancomycin alongside FMT appears important for reliable cure.

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. (ASCRS Ch52 substantially deepens this with trial-level detail): surgery is needed in up to 10% of CDI patients; multidisciplinary management and early surgical consultation are recommended once severe/fulminant disease is recognized, with attention to trending organ function (CDI often causes an exaggerated leukocytosis, sometimes >30,000/mm³) rather than absolute lab cutoffs, and de-escalation of non-CDI-targeted antibiotics. Total abdominal colectomy with end ileostomy has the largest evidence base; partial colectomy has a much higher reoperation rate and limited utility. Evidence for diverting loop ileostomy: Neal 2011 (the landmark first description, 42 fulminant-CDI patients vs. historical colectomy controls) found significantly lower postoperative mortality with diversion (19% vs. 50%) and shorter operative time, 83% completed laparoscopically; the EAST multicenter study (2017, 10 centers) found no significant differences in most perioperative/postoperative measures between colectomy and diversion, but after propensity-score weighting, mortality was significantly lower with diversion (17.7% vs. 39.7%, p=0.002) — albeit with a real limitation (the study couldn't identify the actual per-center selection criteria driving which patients got which operation); a 2019 Nationwide Inpatient Sample study (2,408 patients) found diversion use increasing from 11% (2011) to 25% (2015) of CDI surgical patients, with no significant in-hospital mortality difference between approaches in that dataset. An open question raised in response to the EAST study: the infecting C. difficile strain (frequently unreported in the surgical literature) may itself influence outcomes, particularly when a diverting stoma leaves an infected colon in situ. Bottom line: total colectomy with end ileostomy remains the best-evidenced approach; loop ileostomy is now an acceptable alternative with a growing but still incomplete evidence base.

Other enteric bacterial 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). The original table below (from Sabiston Ch52 - Infectious & Ischemic Colitis) is retained, followed by substantially fuller per-organism detail from ASCRS Ch51 - Infectious Colitis — the two are consistent, with Ch51 providing the epidemiology, treatment specifics, and complication data the table alone lacks.

Pathogen	Microbiology	Exposure	Presentation
Campylobacter jejuni	Spiral, microaerophilic gram-negative rod (Sabiston'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

Campylobacter (ASCRS Ch51): the most common cause of bacterial colitis worldwide (US incidence 19.6/100,000; 25–30/100,000 worldwide) — poultry is the most common but not exclusive source. Usually self-limited (median incubation 2–4 days, resolves ~7 days), though up to 16% have persistent colonization for up to 10 weeks. Severe complications: lower GI bleeding, toxic colitis, pancreatitis, Reiter's syndrome, Guillain-Barré syndrome. Antibiotics not usually required but may help in severe disease; fluoroquinolone resistance is common (>25% in the USA, up to 80% in some regions worldwide) — azithromycin is nearly as effective with lower resistance rates. Most advise ≤3 days of antibiotic therapy; severely compromised patients may need longer/parenteral/multi-drug treatment. No specific isolation precautions required.

Salmonella (ASCRS Ch51): non-typhoid disease (self-limited, incubation 8–48h) vs. typhoid fever (bacteremic, fever/delirium/rash, S. typhi/S. paratyphi); S. enteritidis and S. typhimurium most common in the US. Transmission via "the 5 F's" — food, feces, fingers, fomites, flies. Most infections self-limited; antibiotics reasonable for bacteremic, immunocompromised, or frail patients — fluoroquinolones first-line, azithromycin a reasonable alternative (particularly in developing nations or with endemic-area travel exposure).

Shigella (ASCRS Ch51): more common in young children; S. sonnei most common in the USA. Diarrhea progresses to bloody stools/tenesmus over 3–5 days; children recover in 3–4 days, adults may need 3–4 weeks. Complications: perforation, toxic colitis, HUS, dehydration/electrolyte abnormalities. Antibiotic resistance is increasing, and empiric/universal antibiotic treatment is not advisable — most patients recover without therapy (though shedding can persist up to 6 weeks asymptomatically). Treatment reserved for systemic disease, complications, immunosuppression, or public-health-relevant shedders (food handlers, child-care workers, nursing-home residents): fluoroquinolones, azithromycin, or a third-generation cephalosporin, limited to 3–5 days.

Escherichia coli (ASCRS Ch51, new to this page): five pathotypes conclusively linked to diarrhea — STEC (shiga toxin-producing, aka VTEC/EHEC), ETEC (enterotoxigenic, traveler's diarrhea), EPEC (enteropathogenic, infants), EAEC (enteroaggregative, persistent childhood diarrhea/traveler's diarrhea), EIEC (enteroinvasive, endemic in South America/parts of Europe, causes dysentery). STEC (incl. E. coli O157:H7, reservoir cows, transmission via undercooked beef/milk) causes hemorrhagic colitis and can progress to hemolytic uremic syndrome (HUS) — non-O157 strains account for up to 75% of STEC infections in some series and are an important, easily-overlooked cause. Diagnosis: stool culture/multiplex PCR should be considered for all patients with bloody diarrhea. No antibiotic regimens exist for E. coli infection and antibiotics are not recommended in most cases — several antibiotics have actually been found to increase HUS risk in STEC specifically, and antimotility agents should also be avoided in suspected STEC. EAEC in children may be treated with rifaximin for protracted cases.

Yersinia (ASCRS Ch51 deepens the existing table row): transmission via contaminated animals or undercooked pork/milk; diarrhea with fever/abdominal pain lasting up to 21 days. Beyond mimicking Crohn's disease clinically and endoscopically (right-colon erosions), can cause migratory arthritis, Reiter's syndrome, and erythema nodosum, further complicating the diagnostic picture. Diagnosis: stool culture (may miss the organism), hemagglutinin titers ≥1:128, or newer PCR-based virulence-gene assays. Most cases resolve without treatment; for systemic manifestations, aminoglycosides, TMP-SMX, doxycycline, and fluoroquinolones are all effective.

Vibrio (ASCRS Ch51, new to this page): shellfish-associated; V. parahaemolyticus causes self-limited diarrhea/cramping, while V. cholerae (O1/O319 strains most associated with outbreaks) causes severe, voluminous (up to 1 L/hour) diarrhea leading to hypovolemic shock and death within hours if untreated. Routine stool cultures don't reliably include vibrio — a special request based on exposure history is needed. Treatment: tetracycline/fluoroquinolones/aminoglycosides/third-generation cephalosporins for severe non-cholerae infection; cholera requires high-volume crystalloid resuscitation plus a single dose of ciprofloxacin or doxycycline.

Other bacterial colitidities (ASCRS Ch51, new to this page): Mycobacterium tuberculosis colitis can mimic new-onset Crohn's disease or complicated appendicitis (ileocecal inflammation from swallowed sputum); surgery reserved for diagnostic purposes in undiagnosed cases or for perforation/obstruction in an established diagnosis. Aeromonas colitis presents with diarrhea persisting ≥2 weeks, usually travel-associated and self-limited; treatment (fluoroquinolones or azithromycin) reserved for immunocompromised patients. Bacteroides fragilis colitis (a toxin-secreting subclass) and Listeria monocytogenes colitis (immunocompromised hosts, TMP-SMX) round out the less-common bacterial causes.

Parasitic colitidities (new section — ASCRS Ch51)

Not previously covered on this page. The chapter surveys twelve organisms; amebic colitis gets by far the most depth (including a large surgical-outcomes series) and is the one most relevant to a colorectal surgeon.

Amebic colitis — caused by Entamoeba histolytica, prevalent in tropical central/southern America, Africa, and Asia; travel exposure is the most common finding in US-diagnosed patients. Fecal-oral transmission, cysts persist in soil up to a month, incubation 2–4 weeks. Spectrum from asymptomatic/mild to poor appetite, weight loss, fever, bloody diarrhea, and anemia. Can cause deep colonic ulcerations leading to full-thickness perforation; extraintestinal spread (liver, brain, lung) via bloodstream — hepatic abscess can occur without colonic symptoms and can rupture into the abdomen or chest. Reported mortality up to 50% with perforation/systemic disease; ~55,000 amebiasis-related deaths reported globally in 2010. Diagnosis: stool PCR antigen testing (highly sensitive/specific, may need >1 sample on different days) or microscopy; serologic antibody testing becomes positive after ~2 weeks and can remain positive long after treatment, so a positive serology doesn't necessarily mean active disease. Endoscopy: ulcerations of varying depth/width, most often right colon. Histopathology: classic flask-shaped ulcers. An uncommon presentation is ameboma (granulomatous colonic-wall mass that can be confused with malignancy).

Treatment: asymptomatic patients get a luminal agent alone (paromomycin, diloxanide furoate, or iodoquinoline) to prevent transmission; active colitis needs combination therapy — a 10-day metronidazole course (first-line amebicidal agent; tinidazole, nitazoxanide, dehydroemetine, or chloroquine are alternatives) followed by a luminal medication. Amebic hepatic abscess: medical therapy first-line, with imaging-guided aspiration/drainage for large abscesses or medical failures. Surgery reserved for perforation or toxic colitis. A 30-year, 112-case Mexico City series of amebic colonic perforation (0.6% of all emergency abdominal operations there) found the right colon most commonly affected (90.5%), multiple perforations in 74% of patients, segmental colectomy performed in 53.3%, subtotal colectomy with end ileostomy in 35.3%, exteriorization in 10.7%, and primary repair in just 0.8% — with an overall 40% mortality.

Other parasitic colitidities, more briefly: Anisakidosis (Anisakis simplex, raw fish, mostly Japan — can mimic appendicitis/diverticulitis/acute abdomen; albendazole). Ascaris lumbricoides (up to 1.2 billion infected worldwide; high worm burden causes obstruction, sometimes requiring resection even without bowel compromise; mebendazole/albendazole). Strongyloides stercoralis (Appalachian USA has a notable incidence; chronic infection can mimic pancolitis/ulcerative colitis endoscopically; auto-infection is a distinguishing feature; ivermectin first-line). Trichuris trichiura/whipworm (~800 million affected; can cause symptomatic rectal prolapse with visible worms; mebendazole/albendazole). Enterobius vermicularis/pinworm (tape test for diagnosis; treat the whole family). Cryptosporidium (oocysts resist chlorination and filtration; four clinical patterns incl. protracted disease with biliary involvement in immunocompromised patients; HAART shortens course in HIV, nitazoxanide in immunocompetent patients — see also the immunocompromised-host section below). Balantidium coli (the only ciliated protozoan infecting humans; pigs are the reservoir; tetracycline). Giardia lamblia (foul-smelling greasy stool; metronidazole). Schistosoma haematobium/mansoni/japonicum (~250 million affected, mostly Africa; snail-borne; praziquantel). Tapeworms (Taenia solium/saginata, Diphyllobothrium latum, Hymenolepis nana, Dipylidium caninum — praziquantel; T. solium can cause cysticercosis). Trypanosoma cruzi/Chagas disease (Central/South America; chronic GI neuron damage causes megacolon/megaesophagus in up to 30% of infections; benznidazole/nifurtimox).

Fungal colitidities (new section — ASCRS Ch51)

Not previously covered on this page in depth (see Enteritis in the Immunocompromised Host for a brief pre-existing Histoplasma/coccidioidomycosis mention in the AIDS-specific context, which this section now substantially deepens for Histoplasma and extends to three further organisms).

Histoplasma — Histoplasma capsulatum, endemic in the Ohio/Mississippi river valley (USA). Progressive disseminated histoplasmosis (PDH) can cause GI ulcerations and pseudopolyps confusable with IBD or malignancy. Diagnosis by tissue culture; treatment is IV amphotericin B (itraconazole an alternative, not first-line); surgery may be needed for perforation/obstruction.

Candida — colitis is rare given how common the organism is in humans; associated with severe systemic illness/immune compromise. Endoscopy shows white plaque-like lesions. Treatment: fluconazole; mortality is high in immunocompromised patients, and colectomy for perforation/ peritonitis carries a very high mortality risk.

Other fungal colitidities: disseminated Aspergillus (fever, pain, GI bleeding; voriconazole, amphotericin B second-line; surgery for perforation/ischemia). Cryptococcus neoformans/C. gattii (usually immunocompromised hosts; can cause spontaneous perforation; GI nodules can mimic IBD; IV amphotericin B).

Viral colitidities

CMV colitis — an important cause of viral colitis in immunocompromised hosts (advanced HIV, transplant patients, IBD patients, chemotherapy). ASCRS Ch51 substantially deepens the epidemiology and diagnostic/treatment detail beyond the original brief paragraph here: CMV is an extremely common virus (US pediatric seroprevalence 31–70% depending on ethnicity; global seroprevalence up to 83%), transmitted perinatally, via breast milk, close contact, sexual contact, or blood products/ transplantation. Primary infection in immunocompetent hosts is usually asymptomatic; symptomatic disease is concentrated in immunocompromised patients, though it has also been reported in immunocompetent elderly or critically ill individuals. CMV colitis is believed most often to represent reactivation of latent infection following a change in T-lymphocyte immune competence (rather than new/primary infection, though that can also occur in previously-unexposed immunocompromised patients). Presents with fever, malaise, abdominal pain, diarrhea, rectal bleeding, weight loss; can present as an ischemic-like colitis or a polypoid mass suspicious for colon cancer.

Diagnosis: endoscopic biopsy is critical, since population seropositivity is too common to answer the "is this active infection?" question by itself — representative biopsies from multiple parts of the lesion, including its edges, are important. H&E staining showing the classic "owl's eye" intranuclear inclusion body (surrounded by a clear halo) within inflamed cells indicates active colitis; inclusion bodies surrounded by normal-appearing cells may represent colonization only. Because H&E has low sensitivity, PCR or CMV-specific immunohistochemistry is advisable if the diagnosis isn't confirmed initially by H&E. Treatment: IV therapy initially in severely ill patients, followed by oral therapy — ganciclovir and foscarnet are the antivirals of choice. Surgery for patients who fail medical management or develop persistent bleeding/perforation (most often between the ileum and splenic flexure, with multiple perforation sites possible especially in immunocompromised patients) — resection without primary anastomosis plus fecal diversion is advisable when surgery is needed. Mortality with perforation is significant: one series (Galiatsatos) reported 31% mortality even in immunocompetent patients, with significantly higher mortality in immunosuppressed/immunocompromised patients.

Other viral colitidities (ASCRS Ch51, new to this page): rotavirus, Norwalk virus, astrovirus, picobirnavirus, calicivirus, HSV, norovirus, sapovirus, adenovirus — most cause gastroenteritis with predominantly upper-GI symptoms, but some cause colitis specifically; HSV-2 is associated with sexually-transmitted proctitis. Symptom overlap with gastroenteritis requires careful assessment for the correct diagnosis; these viruses can also affect immunosuppressed patients including those with IBD.

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.

Infectious colitis in immunocompromised patients (new section — ASCRS Ch51)

See Enteritis in the Immunocompromised Host for the pre-existing, more granular Sabiston-Ch50-sourced page on this topic (protozoa, bacteria, mycobacteria, viruses, fungi in AIDS/transplant patients specifically). ASCRS Ch51 adds a genuinely new clinical-reasoning layer that page doesn't cover, organized around three patient populations:

IBD — the key point, not previously stated anywhere in this wiki this explicitly: IBD patients with infectious colitis are, unless promptly diagnosed with a superimposed infection, often instead treated for an IBD exacerbation by escalating immunosuppression — which can lead to disastrous complications with sepsis and perforation. Diagnosis is genuinely difficult because clinical/ endoscopic findings of IBD and infectious colitis can be indistinguishable, and initial stool analysis/endoscopic biopsies may not demonstrate the superimposed infection. Progressive symptoms in an IBD patient should prompt a multidisciplinary evaluation with repeat testing, with suspicion held specifically for an infectious element. All organism classes above have been reported in IBD patients (with parasitic-infection incidence varying by endemic area). C. difficile-superimposed infection is well described and now routinely tested for in worsening IBD (see also Inflammatory Bowel Disease); IBD is associated with higher CDI treatment failure/recurrence rates. CMV is prevalent in IBD (reported incidence 10–33%, more common in UC than Crohn's though seen in both); treatment should be strongly considered for severe or steroid-resistant symptoms, and antiviral therapy may have a beneficial long-term effect on IBD management. Illustrative case (Abbas): a patient presumed to have a UC exacerbation, treated with prolonged steroids, underwent surgical resection that instead revealed severe amebic colitis with no evidence of IBD — the cautionary example behind the chapter's warning above.

HIV — susceptible to all organism classes above; CD4+ <200/mm³ marks significant opportunistic- infection risk. CMV is the most common opportunistic colitis in HIV, especially with low CD4+ counts or non-response to conservative management. Multiplex PCR stool assays can screen for many pathogens at once; HAART improves CD4+ count and immune function.

Transplant patients — genuinely new data point for this wiki: diarrhea is common after solid-organ transplant (some series report 22–52% incidence), and distinguishing infectious diarrhea from a side effect of the immunosuppressive medications themselves is an important diagnostic step. A retrospective review of 422 transplant-patient admissions with diarrhea over 18 months found most had no identifiable etiology and were self-limited; the most common identifiable infectious causes were C. difficile, norovirus, and CMV.

Open items / gaps

• No primary trial data yet independently ingested on FMT efficacy, monoclonal antibody outcomes, or the diverting-ileostomy-vs-colectomy comparison for fulminant CDI — ASCRS Ch52 - Clostridium difficile Infection names the specific load-bearing studies (Zar 2007 vancomycin-vs-metronidazole RCT; Neal 2011 diverting-ileostomy landmark study; the EAST 2017 multicenter colectomy-vs-diversion study; the EXTEND fidaxomicin trial; a 22-study/3,215-patient Cochrane review) — all now flagged in Research Priorities.md as worth independently ingesting.
• 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.
• All of ASCRS Ch51 - Infectious Colitis's content (bacterial/parasitic/fungal/viral detail, and the immunocompromised-host section) is textbook-level/secondary, same caveat as the pre-existing Sabiston-sourced content on this page — no primary literature independently ingested for any of the named organisms, studies, or case reports above (including the Mexico City amebic-perforation series, the Galiatsatos CMV-mortality series, and the 422-patient transplant-diarrhea review).