ASCRS Ch51 - Infectious Colitis

Fifty-first chapter of the ASCRS Textbook of Colon and Rectal Surgery, 4th edition (Reickert CA, Abbas MA). Book pages 865–877 (PDF pages 858–870 of raw/ASCRS Textbook 4th Ed.pdf, offset +7 — confirmed by printed folio). A broad survey chapter covering bacterial, parasitic, fungal, and viral causes of infectious colitis, plus a dedicated section on infectious colitis in immunocompromised hosts (IBD, HIV, and solid-organ/stem-cell transplant patients). C. difficile infection is explicitly deferred to the next chapter ("covered in a separate chapter of this textbook") and is not covered in depth here — only mentioned in the context of IBD-superimposed infection and the differential for infectious colitidities generally.

Key concepts (chapter's own summary box)

• Campylobacter is the most common cause of bacterial colitis worldwide.
• Yersinia may cause a mesenteric adenitis and ileitis resembling Crohn's disease.
• Amebic colitis causes flask-like ulcers.
• The diagnosis of CMV may be made by identification of viral inclusion bodies on mucosal biopsies.

Bacterial colitidities

Campylobacter — 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. Diagnosis: stool culture or PCR. Usually self-limited (median incubation 2–4 days, resolves in ~7 days), though up to 16% have persistent colonization for up to 10 weeks. Can inflame the terminal ileum/cecum, mimicking appendicitis. Severe complications: lower GI bleeding, toxic colitis, pancreatitis, Reiter's syndrome, Guillain-Barré syndrome. Treatment with antibiotics not usually required but may be indicated for severe disease; drug resistance is common in high-incidence areas (fluoroquinolone resistance >25% in the USA, up to 80% in some regions); azithromycin 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 — two clinical presentations: (1) non-typhoid (self-limited GI illness, incubation 8–48h after contaminated food); (2) typhoid fever (bacteremic illness with fever, delirium, rash, associated with S. typhi/S. paratyphi). S. enteritidis and S. typhimurium most common in the US. Transmission: food, feces, fingers, fomites, flies ("the 5 F's"), often contaminated meat/poultry. Diagnosis: stool culture or PCR, or positive blood culture (confirmatory of bacteremia). Most infections self-limited and don't require treatment; antibiotics reasonable for bacteremic, immunocompromised, or frail patients. Fluoroquinolones are first-line; azithromycin is a reasonable alternative, particularly in developing nations or with travel exposure to endemic areas.

Shigella — more common in young children; Shigella sonnei most common in the USA. Transmission via contaminated water or infected individuals. Diarrhea (usually non-bloody at first), colitis, tenesmus, bloody stools developing 3–5 days after symptom onset. Children recover in 3–4 days; adults may need 3–4 weeks. Complications: perforation, toxic colitis, hemolytic-uremic syndrome (HUS), dehydration/electrolyte abnormalities. Diagnosis: stool culture or PCR. Antibiotic resistance increasing; empiric/universal antibiotic treatment not advisable — symptoms usually resolve without therapy, though shedding can persist up to 6 weeks without symptoms. Treatment reserved for more systemic disease, complications, immunosuppression, or public-health-relevant shedders (food handlers, child-care providers, nursing-home residents): fluoroquinolones, azithromycin, or a third-generation cephalosporin, limited to 3–5 days for most patients.

Escherichia coli — five pathotypes conclusively associated with diarrhea: STEC (shiga toxin-producing, aka VTEC/EHEC), ETEC (enterotoxigenic), EPEC (enteropathogenic), EAEC (enteroaggregative), EIEC (enteroinvasive). EPEC and EIEC are non-toxin producers. A sixth pathotype, DAEC (diffusely adherent), has been described but not conclusively linked to disease. EPEC frequently affects infants; ETEC/EAEC are associated with traveler's diarrhea (EAEC causing more persistent diarrhea in children); EIEC is endemic in South America/parts of Europe and causes dysentery. Non-STEC infections collectively have lower incidence in the USA/Canada/Australia/Japan/ Northern & Western Europe, and highest incidence across most of Asia, the Middle East, Africa, Mexico, and Central/South America.

STEC (incl. VTEC/EHEC) causes hemorrhagic colitis with diarrhea that may be bloody; more common in industrialized nations, often food-borne outbreaks. E. coli O157:H7 (first identified 1982) is a well-described strain; reservoir is cows, transmission via undercooked beef or milk. Outbreaks associated more often with O157:H7, but non-O157 strains are important too — accounting for 75% of STEC infections in some series. Some patients progress to bloody diarrhea and a subgroup develops HUS with life-threatening complications. Diagnosis: stool culture/multiplex GI panel PCR for STEC should be considered for all patients with bloody diarrhea; endoscopic colitis/focal ulcers may be seen but are non-diagnostic. Treatment: supportive (hydration, electrolyte correction); avoid antimotility agents (may increase toxin production/HUS risk in STEC). 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. EAEC in children may be treated with rifaximin for protracted cases. No current vaccines or prophylactic regimens for traveler's-diarrhea- associated E. coli.

Yersinia — transmission via handling contaminated animals or ingesting undercooked pork/milk products. Diarrhea with fever and abdominal pain lasting up to 21 days. Mesenteric adenitis or ileitis can mimic Crohn's disease; migratory arthritis, Reiter's syndrome, and erythema nodosum can further complicate the diagnostic picture. Colonoscopy findings (right-colon erosions) can also mimic Crohn's disease. Diagnosis: stool culture (may miss the organism by isolation method), hemagglutinin titers ≥1:128 (indirect confirmation), or newer PCR-based virulence-gene assays. Most cases resolve without treatment. For systemic manifestations, effective antibiotics include aminoglycosides, TMP-SMX, doxycycline, and fluoroquinolones.

Vibrio — non-cholerae and cholerae presentations. Contaminates shellfish; consumption of raw/ undercooked shellfish is the main transmission route, with diarrhea/cramping within 48h. Routine stool cultures don't often include vibrio — a special request is needed based on exposure history; PCR stool testing can help. V. parahaemolyticus causes self-limited diarrhea/cramping (not massive). Vibrio cholerae species cause invasive infection with severe, voluminous (up to 1 L/hour) diarrhea leading to dehydration, hypovolemic shock, and death within hours; O1 and O319 strains most associated with outbreaks. Treatment: tetracycline, fluoroquinolones, aminoglycosides, or third-generation cephalosporins for severe non-cholerae infection; cholerae symptoms require high-volume crystalloid resuscitation plus ciprofloxacin or doxycycline (single dose) to control the active bacteria.

Other bacterial colitidities — Mycobacterium tuberculosis, Aeromonas, Bacteroides fragilis, Listeria monocytogenes, and (covered in separate chapters) C. difficile and bacterial STDs (gonorrhea, chlamydia, syphilis affecting the anorectum). TB colitis: carried from the primary pulmonary site via swallowed sputum; associated with abdominal pain, fever, weight loss; inflammation of the ileocecal region can be mistaken for new-onset Crohn's disease or complicated appendicitis; endoscopic/biopsy findings non-pathognomonic; CT findings non-specific; surgery reserved for diagnostic purposes in undiagnosed cases, or for perforation/obstruction in an established diagnosis. Aeromonas colitis: most often diarrhea persisting ≥2 weeks; suspected with travel to endemic areas; stool cultures diagnostic but need specific request in non-endemic areas; often self-limited; treatment in immunocompromised patients with fluoroquinolones or azithromycin. Bacteroides fragilis colitis: associated with infection by a toxin-secreting subclass; usually self-limited. Listeria monocytogenes: associated with acute colitis in immunocompromised individuals; TMP-SMX treatment in immunocompromised patients, not required in most otherwise-healthy patients.

Parasitic colitidities

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. Transmission fecal-oral; cysts persist in soil up to a month; incubation 2–4 weeks. Spectrum from asymptomatic/mild to poor appetite, weight loss, fever, nausea, vomiting, lower abdominal pain, diarrhea (including bloody), and anemia. Can cause deep colonic ulcerations leading to full-thickness perforation. Extraintestinal complications via bloodstream infection can involve liver, brain, and lung; hepatic abscess can develop without colonic symptoms and can rupture into the abdomen or chest cavity (lung abscess/empyema). Amebiasis can be fatal with colonic perforation or systemic extraintestinal disease — reported mortality up to 50%; ~55,000 amebiasis-related deaths reported globally in 2010. Diagnosis: stool tests (microscopy, elevated WBC — non-specific, PCR antigen testing — highly sensitive/specific, may need >1 sample on different days); serologic antibody testing becomes positive after ~2 weeks and can remain positive long after treatment (so a positive test doesn't necessarily mean active disease — higher antibody levels seen with extraintestinal disease e.g. hepatic abscess). Endoscopic findings: ulcerations of varying depth/width, most often right colon but can occur left-sided too. Histopathology: flask-shaped ulcers, sometimes with trophozoites at the ulcer periphery (IHC stains available). CT can help delineate inflammation but is not specific for hepatic abscess vs. other causes; abscess further assessed by ultrasound, CT, or MRI. An uncommon presentation is ameboma (granulomatous colonic-wall mass, obstructive symptoms, can be confused with malignancy).

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

Anisakidosis — Anisakis simplex / Pseudoterranova decipiens, associated with gastritis;

90% of infections reported from Japan; consumption of contaminated raw fish (4% involving colon). Larvae burrow into the muscular wall causing hypersensitivity reaction with granulomas/eosinophils; can mimic appendicitis, ileitis, diverticulitis, acute abdomen. Surgery for perforation/obstruction complications; often the means of diagnosis. Albendazole 7–21 days can be effective.

Ascaris — Ascaris lumbricoides, prevalent in tropical/subtropical climates, up to 1.2 billion infected persons worldwide. Life cycle: ingested eggs hatch in small intestine, larvae migrate via venous return to lungs, can be swallowed back into GI tract, grow into adults producing thousands of eggs/day for up to 2 years. Most infections asymptomatic; high worm burden causes abdominal pain or bowel obstruction (obstructing worm masses can be milked distally; resection may be required even without bowel compromise). Diagnosis: stool microscopy (eggs/larvae well described, easy to identify); retrograde GI contrast studies can identify curvilinear densities/obstruction. Treatment: mebendazole or albendazole, highly effective. Ascaris suum (a pig infection) is an important alternate human infection source where pig manure is used as fertilizer.

Strongyloides — Strongyloides stercoralis, prevalent in tropics, notable incidence in Appalachian USA. Larvae penetrate skin, travel to lungs, swallowed to mature in GI tract; can auto-infect the host. Acute infection: skin changes from burrowing larvae (larva currens). Chronic states: diarrhea, pain, wasting; can mimic pancolitis and potentially ulcerative colitis endoscopically. Diagnosis: stool detection of larvae; repeated testing, duodenal biopsy, ELISA, or bronchial washings may be needed. Treatment: ivermectin ×2 days first-line; albendazole/mebendazole alternatives.

Trichuris — Trichuris trichiura (whipworm), affects ~800 million people, mostly tropical/ subtropical. Ingestion of contaminated soil/food allows larvae to grow in the colon; adult worms secrete thousands of eggs/day. Most infected humans minimally/asymptomatic; advanced infection creates diarrhea, bleeding, tenesmus with characteristic-odor stool. Symptomatic rectal prolapse can occur with visible worms on the mucosa; anemia and growth retardation noted in children. Diagnosis: stool microscopy (barrel-shaped eggs and worms easily identified); colonoscopy can visually identify worms. Treatment: mebendazole or albendazole. Surgical repair of prolapse can be required but otherwise surgery isn't typically part of treatment.

Enterobius — Enterobius vermicularis (pinworm), common worldwide, mostly children. Spread by egg ingestion; adult worms migrate to cecum for 10–12 weeks; females deposit up to 10,000 eggs in perianal skin folds causing intense pruritus; scratching allows auto-infection/transmission via fingers. Diagnosis: tape test (adhesive tape against perianal skin, microscopic detection). Treatment: mebendazole or albendazole; treat all family members; environmental cleaning to prevent reinfection.

Cryptosporidium — intracellular protozoan parasite, first described in humans 1976. Oocysts (small, filtration-resistant, chlorination-resistant, but destroyed by heating/freezing/ozonation) from contaminated food/water are ingested and shed in stool. Four clinical scenarios: pediatric diarrhea in developing areas, traveler's diarrhea, diarrhea in immunocompromised patients, water-borne outbreaks in developed areas. Immunocompetent patients: usually self-limited explosive diarrhea ± fever/abdominal pain/nausea. Immunocompromised patients: protracted symptoms, biliary involvement (acalculous cholecystitis, cholangitis) — cholecystectomy can help in severe cases. Diagnosis: PCR or ELISA detection of oocysts in stool. No medication effective to control infection generally; in HIV patients, HAART can shorten the disease course; nitazoxanide shown to help shorten disease in immunocompetent patients (cure rates 60–75%). Avoid swimming for 2 weeks after symptom resolution.

Balantidium — Balantidium coli, the only ciliated protozoan infecting humans; major source is pigs. Ingested cysts lodge in the colon causing ulceration/inflammation with bloody and non-bloody diarrhea. Diagnosis: stool study for trophozoites. Treatment: tetracycline first-line; metronidazole or doxycycline alternatives.

Giardia — Giardia lamblia, common in the USA and worldwide. Transmission: water, fecal contamination, fecal-oral spread; untreated rural water or contaminated swimming pools. Diarrhea usually develops 1–2 weeks after infection; foul-smelling, greasy stool. Diagnosis: stool exam, ELISA or immunofluorescence antigen detection, PCR. Treatment: metronidazole first-line.

Schistosomiasis — Schistosoma haematobium, S. mansoni, S. japonicum, affecting ~250 million people/year, mostly in Africa. Snails are intermediate hosts; cercariae released into water attach and invade skin, migrate to heart/lungs then liver while maturing. S. haematobium affects the urinary bladder; S. mansoni/S. japonicum affect the mesentery of the small bowel and colon; eggs deposited in tissues, immune response causes significant local organ damage. Symptoms: pain, diarrhea, additional organ damage (urinary obstruction, mass, enteric fistulas, hepatic/pulmonary/neurologic impairment). Diagnosis: stool evaluation identifies eggs. Treatment: praziquantel is effective. Surgical intervention for perforation/obstruction complications uncommon.

Tapeworms — Taenia solium, T. saginata, Diphyllobothrium latum, Hymenolepis nana, Dipylidium caninum. Most infections asymptomatic. T. solium spread by contaminated pork; can be associated with cysticercosis (progressive neurologic symptoms). T. saginata associated with contaminated beef. D. latum associated with raw fish consumption; adult worm attaches to terminal ileum, may cause megaloblastic anemia. Diagnosis: worm identification in feces; ELISA/PCR stool testing. Treatment: praziquantel for all; a bowel prep to clear the GI tract shortly after treatment can help in some cases.

Trypanosoma (Chagas disease) — Trypanosoma cruzi, endemic in Central/South America. Acute phase: fever, malaise, edema, lymphadenopathy, hepatosplenomegaly, resolving into a latent period. Up to 30% develop chronic symptoms (remainder stay asymptomatic for life); chronic symptoms relate to end-organ damage — cardiomyopathy, megaesophagus, megacolon — via GI neuron damage causing dilation/ impaired function (constipation, abdominal pain, dysphagia, volvulus). Surgical intervention for complications may be required but is not curative. Benznidazole and nifurtimox are indicated but can have significant GI/neurological side effects.

Fungal colitidities

Histoplasma — Histoplasma capsulatum, endemic in the Ohio/Mississippi river valley regions (USA). Pulmonary infection is common; a subgroup develops progressive disseminated histoplasmosis (PDH), which can cause GI ulcerations (sometimes severe/deep) and pseudopolyps confusable with IBD or malignancy. Diagnosis: tissue culture. Treatment: IV amphotericin B; itraconazole is an alternative but not first-line. Surgical intervention may be required for perforation/obstruction.

Candida — common human organism; Candida colitis is rare, presenting with diarrhea/abdominal pain, associated with severe systemic illness/immune compromise. Diagnosis: microscopic confirmation of budding yeast/hyphae, or culture; endoscopy shows white plaque-like lesions. Treatment: fluconazole; mortality is high in immunocompromised patients. Colectomy may be performed for perforation/peritonitis but is associated with very high mortality risk.

Other fungal colitidities — disseminated Aspergillus presents with fever, pain, GI bleeding, tenderness; perforation/ischemia complications may require surgery; pathology confirms characteristic hyphae; treatment is voriconazole (amphotericin B second-line). Cryptococcus neoformans/C. gattii can affect the GI tract in severe cases, usually in immunocompromised/immunosuppressed patients; colitis with spontaneous perforation described; surgical intervention may be required for the abdominal emergency; GI nodules from disseminated infection can mimic IBD; biopsy/culture confirms diagnosis; treatment is IV amphotericin B.

Viral colitidities

Cytomegalovirus (CMV) — double-stranded DNA herpesvirus; extremely common (US pediatric seroprevalence 31–70% depending on ethnicity; global seroprevalence up to 83%). Transmission: perinatal, breast milk, close-contact viral shedding, sexual transmission, blood products/ transfusion/transplantation. Primary infection in immunocompetent hosts usually asymptomatic. Highest-risk for symptomatic infection: immunocompromised/immunosuppressed patients (HIV, IBD, transplant recipients); symptomatic infection has also been reported in immunocompetent elderly or critically ill patients. Can affect brain/CNS, eyes, lungs, heart, kidneys, esophagus, liver, pancreas, small bowel, colon. CMV colitis is speculated to represent reactivation of latent infection from an alteration in T-lymphocyte immune competence — believed to be the most common cause of CMV colitis; primary infection can also occur in a previously-unexposed immunocompromised patient. Symptoms: fever, malaise, abdominal pain, diarrhea, rectal bleeding, weight loss. Endoscopic findings: mucosal friability and ulcerations; CMV can present as ischemic-like colitis or a polypoid mass suspicious for colon cancer. Biopsies during colonoscopy are critical (seropositivity is too common in the general population to answer the "active infection?" question by itself) — representative biopsies from various parts of the colonic lesion including the edges are important. H&E-stained "owl's eye" intranuclear inclusion bodies surrounded by a clear halo, within inflamed cells, indicate active colitis; inclusion bodies surrounded by normal-appearing cells may represent colonization only. Due to the low sensitivity of H&E stains, PCR or CMV-specific immunohistochemistry is advisable if diagnosis isn't confirmed initially by H&E.

Treatment: active CMV colitis should be treated — IV initially in severely ill patients, followed by oral therapy; ganciclovir and foscarnet are the antiviral drugs of choice. Surgery for patients who fail medical management or have persistent bleeding/perforation; perforation most often occurs between the ileum and splenic flexure, and multiple perforation sites can occur especially in immunocompromised patients; resection without primary anastomosis and fecal diversion is advisable when surgery is needed. Morbidity/mortality of CMV colitis with perforation is significant — one series (Galiatsatos) reported 31% mortality in immunocompetent patients, with significantly higher mortality in immunosuppressed/immunocompromised patients.

Other viral colitidities — rotavirus, Norwalk virus, astrovirus, picobirnavirus, calicivirus, herpes simplex virus (HSV), norovirus, sapovirus, adenovirus. Most cause gastroenteritis with predominantly upper-GI symptoms (nausea, vomiting, diarrhea), but some can cause colitis specifically. HSV-2 is associated with sexually-transmitted proctitis. Symptom overlap between gastroenteritis and colitis (abdominal pain, cramping, diarrhea) requires careful assessment for the proper diagnosis. These viruses have been implicated in outbreaks and can also affect immunosuppressed/ immunocompromised patients such as those with IBD.

Infectious colitis in immunocompromised patients

Inflammatory bowel disease — IBD patients (UC and Crohn's) with infectious colitis pose two specific challenges: delay in diagnosis, and overall health status (malnutrition, anemia, immunosuppression). Clinical/endoscopic findings of IBD may be indistinguishable from infectious colitis; initial stool analysis and endoscopic biopsies may not demonstrate superimposed infection. Patients with IBD who are susceptible to infectious colitis, unless promptly diagnosed with a superimposed infection, are often instead treated for an exacerbation of their IBD by escalating immunosuppression — which can lead to disastrous complications with sepsis and perforation. IBD patients with progressive symptoms should therefore be evaluated carefully with suspicion for an infectious element, with a multidisciplinary evaluation including repeat testing/assessment to optimize outcome. All types of infectious colitidities (bacterial, mycobacterial, fungal, viral, parasitic) have been reported in IBD patients; the incidence of parasitic infection specifically can vary by endemic area (a Turkish study found regional variation in amebiasis incidence among UC patients within the same country). Of particular interest in IBD: C. difficile-superimposed infection is well described and now routinely tested for in patients with worsening IBD symptoms; IBD is associated with a higher rate of CDI treatment failure and recurrence (C. difficile itself covered in a separate chapter). CMV infection is prevalent in IBD patients (reported incidence 10–33%), more common in ulcerative colitis than Crohn's disease though it occurs in both; multiplex PCR of stool is one of the best test methods for CMV and other infectious-colitis causes in this setting. While CMV presence may not always be the cause of symptoms, treatment should be strongly considered in patients with severe symptoms or those who are steroid-resistant; antiviral therapy for CMV may have a beneficial long-term effect on IBD management. Immunosuppression for IBD (steroids and other immune-modulating drugs including anti-TNF biologic therapy) can hinder the immune system's ability to limit the extent/progression of infectious colitis, and can lead to progression/perforation regardless of underlying IBD status — one reported case (Abbas) of a patient presumed to have UC exacerbation, treated with prolonged steroids, whose surgical resection instead revealed severe amebic colitis without evidence of IBD.

Human immunodeficiency virus (HIV) — patients with HIV are susceptible to all types of infectious colitidities described in the chapter (bacterial, fungal, parasitic, viral). CD4+ T-cell count <200/ mm³ marks significant risk for opportunistic infections. The most common type of opportunistic colitis in HIV patients is CMV, especially in patients with low CD4+ counts and those not responding promptly to conservative medical management — stool studies and endoscopic evaluation with biopsies are helpful. Newer multiplex PCR stool assays can detect many types of viral, bacterial, and parasitic infections at once. HAART improves immune system function by increasing CD4+ count.

Transplant patients — long-term immunosuppression after solid-organ transplantation carries ongoing infectious-complication risk despite advances in less-toxic immunosuppressive regimens. GI infections and diarrhea are common in the solid-organ-transplant population, with some series reporting diarrhea incidence between 22% and 52%. Important to differentiate infectious diarrhea from diarrhea caused by immunosuppressive medications themselves. A retrospective review of 422 transplant patient admissions with diarrhea over an 18-month period found the majority had no identifiable etiology and were often self-limited; the most common identifiable infectious causes were C. difficile, norovirus, and CMV. Workup includes CBC, renal/liver function tests, blood cultures (if warranted), and stool studies including PCR-based multiplex GI pathogen testing; colonoscopy is considered for patients with persistent severe symptoms and negative preliminary workup.

Open items / gaps

• All content above is textbook-level/secondary — no primary literature independently ingested from this chapter's reference list (109 references spanning epidemiology, case reports, and a handful of larger retrospective series — none individually flagged as load-bearing enough for Research Priorities.md at this pass, given the breadth-over-depth nature of this survey chapter).
• The chapter explicitly defers C. difficile to the next chapter (Ch52, "Clostridium difficile Infection") — not covered in depth here.