Acute Gastroenteritis (AGE) — Final Year MBBS Review (Based on Harrison's Principles of Internal Medicine)

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"acute gastroenteritis" management

I now have all the content I need. Let me compile the comprehensive Final Year MBBS review on Acute Gastroenteritis based on Harrison's and supporting textbooks.

Acute Gastroenteritis (AGE) - Final Year MBBS Review

Based on Harrison's Principles of Internal Medicine 22nd Edition (2025)


1. DEFINITION

Acute Gastroenteritis (AGE) is an inflammation of the gastrointestinal tract (stomach and intestines) characterized by the acute onset of diarrhea (with or without nausea, vomiting, fever, and abdominal pain), typically lasting <14 days. Diarrhea is defined as passage of ≥3 unformed stools in 24 hours.

2. EPIDEMIOLOGY

  • One of the most common illnesses worldwide; second leading cause of death in developing countries
  • Predominantly affects children under 5 and the elderly
  • Rotavirus: leading cause in infants/toddlers globally
  • Norovirus: leading cause in adults and older children; responsible for most outbreaks in community settings (cruise ships, nursing homes, recreational camps)
  • Seasonal variation: rotavirus peaks in winter (temperate climates)
  • Fecal-oral route and contaminated food/water are primary transmission modes

3. CLASSIFICATION

By Duration

TypeDuration
Acute<14 days
Persistent14-30 days
Chronic>30 days

By Mechanism (Pathophysiology)

TypeMechanismPathogen Examples
Noninvasive / SecretoryToxin or virus impairs absorption, stimulates secretion; no mucosal destructionNorovirus, Rotavirus, ETEC, Vibrio cholerae
Invasive / InflammatoryOrganism invades mucosa; cytotoxin-mediated destruction; bloody/mucoid stoolsShigella, Salmonella, Campylobacter, EHEC, EIEC, Entamoeba
OsmoticNon-absorbable solutes draw water into lumenLactose intolerance, laxative abuse, sorbitol ingestion

4. ETIOLOGY

Viral (Most Common - ~70% of AGE)

VirusKey Features
NorovirusLeading cause in adults; outbreaks on cruise ships/nursing homes; highly contagious (low inoculum); incubation 12-48 h; watery diarrhea, vomiting, fever, myalgia; lasts 1-2 days
RotavirusLeading cause in infants/toddlers; highly contagious (survives on surfaces); incubation 1-3 days; fever, vomiting, watery diarrhea; lasts 5-7 days (longer in immunocompromised); ~50% of household children infected when one member affected
Enteric AdenovirusCommon in infants/young children; incubation 8-10 days (longest); lasts 5-12 days; most adults asymptomatic
AstrovirusMilder illness; children and elderly; similar to norovirus

Bacterial

PathogenMechanismKey ClueIncubation
ETEC (Enterotoxigenic E. coli)Heat-labile (LT) and heat-stable (ST) toxins → secretory diarrheaTraveler's diarrhea14-50 h
EPECAttaches, effaces microvilliInfantile diarrhea in developing world12-72 h
EHEC (O157:H7)Shiga toxin → hemorrhagic colitis; HUSBloody diarrhea, no fever; rare/absent WBCs in stool3-4 days
EIECInvasive; similar to ShigellaDysentery-like1-3 days
ShigellaInvasion of mucosal epithelium + Shiga toxinClassic dysentery (fever, blood, mucus in stool); highly infectious (very low inoculum - 10-100 organisms)1-7 days
Salmonella (non-typhoidal)Mucosal invasion, inflammatory diarrheaPoultry, eggs, reptile contacts; bacteremia risk6-48 h
Salmonella TyphiPenetrates Peyer patches → enteric feverRelative bradycardia, Rose spots, splenomegaly, leukopenia7-14 days
CampylobacterInvasive; ascending paralysis complicationPost-infectious Guillain-Barre syndrome risk1-7 days
V. choleraeCholera toxin → massive secretory diarrhea"Rice-water stools", severe dehydrationHours-5 days
Yersinia enterocoliticaPenetrates intact intestinal mucosa, multiplies in Peyer patchesPseudoappendicitis (RLQ pain), reactive arthritis1-11 days
C. difficileToxin A (enterotoxin) + Toxin B (cytotoxin)Post-antibiotic diarrhea, pseudomembranous colitisDuring/after antibiotics
Staph. aureusPreformed toxin (enterotoxin)Rapid onset (1-6 h), no fever, vomiting predominant1-6 h
B. cereusPreformed toxin (emetic type) or enterotoxin (diarrheal type)Fried rice syndrome (emetic: 1-6 h); diarrheal: 8-16 h1-16 h
Clostridium perfringensEnterotoxinMeat/poultry; self-limited, 24 h8-24 h

Protozoal

ParasiteKey Features
Giardia lambliaWatery/greasy, foul-smelling stools; bloating, flatulence; lasts >14 days; acquired from contaminated water; treat with metronidazole, tinidazole, or nitazoxanide
CryptosporidiumProfuse watery diarrhea; self-limited in immunocompetent (5-10 days); chronic in HIV (CD4<50 → biliary involvement/sclerosing cholangitis); treat with nitazoxanide
Entamoeba histolyticaAmebic dysentery; bloody diarrhea; liver abscess complication; treat with metronidazole + luminal agent (diloxanide)
Cyclospora cayetanensisLow-grade fever, fatigue, prolonged course (weeks-months if untreated); treat with TMP-SMX
Cystoisospora (Isospora)Indistinguishable from Cryptosporidium clinically; responds promptly to TMP-SMX (unlike Cryptosporidium)

5. PATHOPHYSIOLOGY

Host Defense Mechanisms (Harrison's)

  1. Intestinal microbiota: Colonization resistance - geographic/nutritional exclusion of pathogens; >99% of normal colonic microbiota is anaerobic bacteria; acidic pH and volatile fatty acids are critical. Disruption by antibiotics increases susceptibility.
  2. Gastric acid: Critical barrier - achlorhydria (PPI use, post-gastrectomy) increases susceptibility to Salmonella, Giardia, and helminths. Rotavirus and Shigella are notably acid-stable and can survive this barrier.
  3. Intestinal motility: Peristalsis clears bacteria from the proximal small intestine. Impaired motility (opioids, antidiarrheal drugs, anatomic abnormalities) increases bacterial overgrowth and infection risk. Note: Lomotil (diphenoxylate + atropine) in Shigella infection prolongs fever and organism shedding; opioids in Salmonella gastroenteritis increase bacteremia risk.
  4. Intestinal mucin: Complex mucus layer separates luminal microbiota from epithelium; turns over rapidly; acts as a physical and immunological barrier.
  5. Secretory IgA: Prevents microbial adhesion to epithelium.
  6. Innate immune responses: Toll-like receptors on enterocytes recognize pathogen-associated molecular patterns (PAMPs); trigger inflammatory cytokines.

Mechanisms of Diarrhea Production

Secretory (Non-inflammatory):
  • Vibrio cholerae: Cholera toxin activates adenylyl cyclase → ↑cAMP → massive Cl⁻ secretion into intestinal lumen → osmotic water loss ("rice-water stools")
  • ETEC: LT toxin (same mechanism as cholera - ↑cAMP); ST toxin (↑cGMP via guanylyl cyclase)
  • Rotavirus/Norovirus: NSP4 (rotavirus enterotoxin) acts as viroporin; direct enterocyte damage and intestinal epithelium dysfunction
  • Staphylococcal enterotoxin: Preformed; rapid onset; acts as superantigen
Invasive (Inflammatory/Dysenteric):
  • Shigella/EIEC: Invade mucosal epithelial cells → intracellular multiplication → spread to adjacent cells → mucosal destruction → bloody mucoid stools (dysentery)
  • Salmonella: Invades bowel mucosa without the full clinical dysentery syndrome; bacteremia risk
  • S. Typhi and Yersinia: Penetrate intact mucosa → multiply in Peyer patches and lymph nodes → systemic dissemination → enteric fever

6. CLINICAL FEATURES

Approach to History

Key questions:
  • Onset and duration of symptoms
  • Character of stool: watery vs. bloody/mucoid (secretory vs. inflammatory)
  • Associated symptoms: fever, vomiting, abdominal pain, tenesmus
  • Epidemiologic clues:
    • Recent travel (ETEC, Salmonella, Shigella, Giardia, Cryptosporidium)
    • Food history (last meal, suspected contaminated food)
    • Outbreak setting (multiple cases - norovirus, Staph. aureus, Salmonella)
    • Contact with animals/reptiles (Salmonella, Campylobacter)
    • HIV/immunocompromised status (Cryptosporidium, CMV, Microsporidium, Cyclospora)
    • Antibiotic use (C. difficile)
    • Hospitalization (C. difficile, nosocomial pathogens)
    • Sexual history (MSM: Shigella, Neisseria, Entamoeba)

Clinical Syndromes

SyndromeKey FeaturesCommon Causes
Watery (secretory) diarrheaLarge volume, no blood/mucus, minimal feverNorovirus, Rotavirus, ETEC, V. cholerae
DysenterySmall-volume bloody/mucoid stools, fever, tenesmus, abdominal painShigella, EIEC, Entamoeba, Campylobacter
Enteric feverFever, relative bradycardia, rose spots, splenomegaly, leukopenia, abdominal painS. Typhi, S. Paratyphi, Yersinia
Food poisoning (preformed toxin)Rapid onset (<6 h), vomiting predominant, briefStaph. aureus, B. cereus (emetic)
Traveler's diarrheaSelf-limited watery diarrhea in travelerETEC, Campylobacter, Norovirus

Dehydration Assessment (WHO Classification)

DegreeClinical Features
No dehydrationAlert, normal eyes/mouth, normal skin turgor, drinks normally
Some dehydrationRestless/irritable, sunken eyes, dry mouth, reduced skin turgor, drinks eagerly
Severe dehydrationLethargic/unconscious, very sunken eyes, dry mucous membranes, absent skin turgor, unable to drink

7. DIAGNOSIS

Approach (Harrison's)

Most AGE is self-limited and does NOT require investigations.
Indications for stool culture/workup:
  • Bloody or inflammatory diarrhea (fecal leukocytes/lactoferrin positive)
  • Severe dehydration
  • Fever >38.5°C
  • Duration >3-7 days
  • Immunocompromised host
  • Systemic manifestations
  • Community outbreak investigation
  • Recent antibiotic use (rule out C. difficile)
  • Healthcare-associated diarrhea

Investigations

TestWhat It DetectsWhen to Use
Stool cultureBacteria (Salmonella, Shigella, Campylobacter, Yersinia, E. coli O157:H7)Inflammatory diarrhea, severity, outbreak
Fecal leukocytesInflammatory diarrheaScreen for invasive etiology
Fecal calprotectin/lactoferrinIntestinal inflammation markerMore sensitive than fecal leukocytes
C. difficile toxin A/B (EIA or NAAT)C. difficile colitisPost-antibiotic diarrhea
Stool O&P (ova and parasites)Giardia, Entamoeba, CryptosporidiumPersistent diarrhea, travel history
Stool ELISA/PCRViral antigens (Rotavirus, Norovirus), Giardia/Crypto antigenOutbreak settings, immunocompromised
Multiplex PCR panelsMultiple pathogens simultaneouslyRapid, broad diagnosis
Blood cultureBacteremia (Salmonella typhi)Enteric fever, toxic patient
CBC, electrolytes, BUN/CrAssess severity, dehydration, HUS (low platelets, hemolytic anemia + renal failure)Bloody diarrhea (EHEC), severe disease
Sigmoidoscopy/colonoscopyC. difficile (pseudomembranes), CMV colitis, IBDPersistent/severe colitis
D-xylose absorption testSmall intestine malabsorptionChronic/osmotic diarrhea workup
Note on EHEC (O157:H7): Antibiotics are contraindicated in EHEC as they increase the risk of Hemolytic Uremic Syndrome (HUS) by increasing toxin release. HUS = Microangiopathic hemolytic anemia + thrombocytopenia + acute renal failure.

8. MANAGEMENT

Oral Rehydration Therapy (ORT) - CORNERSTONE

The WHO low-osmolarity ORS (2002) is the standard:
  • Na 75 mEq/L, Cl 65 mEq/L, Glucose 75 mmol/L, K 20 mEq/L, Citrate 10 mEq/L
  • Osmolarity: 245 mOsm/L (reduced from original 311 mOsm/L)
  • Mechanism: glucose-sodium co-transport (SGLT1) in enterocytes drives Na absorption, water follows
WHO ORS can be prepared at home: Dissolve in 1L of clean water: 3.5 g NaCl + 2.5 g NaHCO₃ + 1.5 g KCl + 20 g glucose.
IV Fluids: Indicated when:
  • Severely dehydrated
  • Unable to drink
  • Vomiting precludes oral therapy
  • Use Ringer's Lactate (preferred over normal saline)

Antiemetics

  • Ondansetron (0.15 mg/kg/day): Serotonin (5-HT₃) antagonist; effective in reducing vomiting from gastroenteritis during oral rehydration phase. Supported by multiple studies.

Dietary Advice

  • Continue normal feeding during treatment (do NOT fast)
  • BRAT diet (Bananas, Rice, Applesauce, Toast) has limited evidence
  • Breastfeeding should continue in infants
  • Avoid hyperosmolar fluids (fruit juices, sports drinks) as they can worsen diarrhea

Antimotility Agents

  • Loperamide: Safe in secretory (non-inflammatory) diarrhea; contraindicated in bloody diarrhea, high fever, suspected invasive infection, and children <2 years
  • Codeine/opioids: Increase bacteremia risk in Salmonella gastroenteritis; avoid in invasive infections
  • Diphenoxylate + atropine (Lomotil): Prolongs fever and organism shedding in Shigella; contraindicated

Specific Antibiotic Therapy

PathogenFirst-LineAlternativeNotes
ShigellaCiprofloxacin 500 mg BD x 3 daysAzithromycin; TMP-SMX (if sensitive)Resistance to TMP-SMX common
Salmonella (non-typhoidal)Usually NO antibioticsCiprofloxacin if at risk for bacteremiaAntibiotics NOT recommended for uncomplicated disease (prolong carrier state); treat high-risk patients (extremes of age, immunocompromised, prosthetic devices, hemoglobinopathy)
Enteric fever (S. Typhi)Ciprofloxacin / CeftriaxoneAzithromycin (oral)Increasing fluoroquinolone resistance from South Asia
CampylobacterAzithromycinCiprofloxacin (increasing resistance)Treat if severe/prolonged
C. difficile (mild-moderate)Vancomycin 125 mg QID x 10 days OR FidaxomicinMetronidazole (alternative)Stop precipitating antibiotics
C. difficile (severe/complicated)Vancomycin PO ± IV metronidazoleFecal microbiota transplant for recurrenceColectomy for fulminant colitis
GiardiaMetronidazole 250 mg TID x 5-7 daysTinidazole (single dose 2g); Nitazoxanide
Entamoeba histolyticaMetronidazole x 7-10 days THEN luminal agent (diloxanide furoate or paromomycin)Luminal agent essential to clear cysts
CryptosporidiumNitazoxanideSupportive in immunocompetentAntiretroviral therapy is cornerstone in HIV
CyclosporaTMP-SMX
CystoisosporaTMP-SMXResponds promptly (unlike Crypto)
CholeraDoxycycline 300 mg single doseAzithromycin; TMP-SMXAntibiotics adjunct to aggressive ORS
EHEC (O157:H7)NO antibioticsSupportive careAntibiotics increase HUS risk
Norovirus/RotavirusSupportive (ORS)Nitazoxanide (small trials for rotavirus)Self-limited; vaccine available for Rotavirus
Traveler's diarrheaAzithromycin OR RifaximinCiprofloxacin (increasing resistance)

Probiotics

  • A 2025 meta-analysis (PMID: 40739406) confirmed efficacy of probiotics in reducing duration and severity of AGE in children (meta-analysis of RCTs). Lactobacillus rhamnosus GG and Saccharomyces boulardii have the most supporting evidence.

9. COMPLICATIONS

ComplicationAssociation
Dehydration & electrolyte imbalanceAll causes, especially cholera and rotavirus
Hemolytic Uremic Syndrome (HUS)EHEC O157:H7 (Shiga toxin)
Guillain-Barre SyndromeCampylobacter jejuni (post-infectious)
Reactive arthritis (Reiter's syndrome)Salmonella, Shigella, Campylobacter, Yersinia
Intestinal perforationS. Typhi (3rd week), severe Shigella/Ameba
Liver abscessEntamoeba histolytica
Toxic megacolonC. difficile, severe Shigella
Chronic diarrheaPost-infectious IBS, Giardia, Cryptosporidium (in HIV)
IntussusceptionNatural rotavirus infection (especially in older children); original RotaShield vaccine (withdrawn)
Pseudomembranous colitisC. difficile
Bacteremia/sepsisSalmonella, Campylobacter (elderly, immunocompromised)

10. PREVENTION

Vaccines

VaccineTargetNotes
Rotavirus vaccine (RotaTeq, Rotarix)RotavirusOral live-attenuated; 2-3 doses in infancy; major reduction in rotavirus mortality globally; slight increased risk of intussusception (very small)
Typhoid vaccine (Vi polysaccharide / Ty21a)S. TyphiUsed in endemic areas and travelers; not 100% protective
Cholera vaccine (Dukoral, Vaxchora)V. choleraeOral; travelers to endemic areas

Non-Vaccine Prevention

  • Hand hygiene with soap and water (especially before food handling, after toilet use)
  • Safe water and sanitation (WASH)
  • Proper food handling and cooking temperatures
  • Breastfeeding (protective against infantile diarrhea)
  • Rotavirus vaccination (most significant public health intervention for childhood AGE)

11. SPECIAL CONSIDERATIONS

HIV/Immunocompromised Patients

  • Greater risk of chronic/severe AGE from usual pathogens
  • Cryptosporidium: biliary involvement when CD4 <50/μL (serum ALP elevation) → consider sclerosing cholangitis
  • Cystoisospora, Cyclospora, CMV colitis, Microsporidium are important in AIDS
  • Antiretroviral therapy to suppress viral load is the cornerstone of managing Cryptosporidiosis in HIV

Traveler's Diarrhea (TD)

  • Most common illness in travelers
  • Onset usually within first week of travel
  • Common destinations: South/Southeast Asia, Sub-Saharan Africa, Latin America
  • Etiology: ETEC (most common bacterial), Campylobacter, Shigella, Norovirus
  • Treatment: Azithromycin (preferred, due to increasing fluoroquinolone resistance); rifaximin for non-invasive TD
  • Prophylaxis: Bismuth subsalicylate; rifaximin (high-risk individuals)

Food-Borne Illness by Incubation Period (High-Yield)

OnsetOrganismMechanism
1-6 hoursStaph. aureus, B. cereus (emetic)Preformed toxin
8-16 hoursC. perfringens, B. cereus (diarrheal)Toxin produced in gut
16-48 hoursNorovirus, ETECInfection
1-3 daysSalmonella, CampylobacterInvasion
3-5 daysEHEC, YersiniaInvasion/toxin
7-14 daysGiardiaCyst to trophozoite
8-10 daysAdenovirusViral replication

12. HIGH-YIELD EXAM MNEMONICS & PEARLS

"RICE-WATER stool" = Cholera (massive secretory diarrhea; V. cholerae)
"The 3 S's of low-inoculum organisms" = Shigella, Staph. aureus, Norovirus (few organisms cause disease)
"EHEC - No Antibiotics" = Hemolytic Uremic Syndrome risk (EHEC O157:H7)
"Campylobacter - GBS connection" = Most common antecedent infection in Guillain-Barre Syndrome
"cAMP up" = Cholera + ETEC (LT) | "cGMP up" = ETEC (ST)
"Rotavirus NSP4" = First described viral enterotoxin
Acid-stable pathogens (survive gastric acid): Rotavirus, Shigella (very low inoculum needed)
Antidiarrheals contraindicated in: Bloody diarrhea, suspected EHEC, Shigella (prolonged fever/shedding with Lomotil), children <2 years
ORS works because: Glucose-Na co-transport (SGLT1) is intact even during secretory diarrhea - this is the physiologic basis of oral rehydration therapy
Rotavirus vaccine - reduced osmolarity ORS (245 mOsm/L vs original 311 mOsm/L) - the reduced osmolarity version decreased unscheduled IV use by ~33%

Sources: Harrison's Principles of Internal Medicine 22nd Edition (2025), Frameworks for Internal Medicine, Goldman-Cecil Medicine, Sleisenger and Fordtran's Gastrointestinal and Liver Disease, Yamada's Textbook of Gastroenterology
Recent evidence: A 2025 meta-analysis (PMID: 40739406) confirms probiotics significantly reduce duration and severity of AGE in children.

Make a comparison table of viral vs bacterial vs parasitic gastroenteritis

Here's a comprehensive comparison table based on the content already synthesized from Harrison's and supporting textbooks:

Viral vs Bacterial vs Parasitic Gastroenteritis — Comparison Table

FeatureViralBacterialParasitic
Common PathogensNorovirus, Rotavirus, Enteric Adenovirus, AstrovirusSalmonella, Shigella, Campylobacter, ETEC, EHEC, V. cholerae, C. difficile, Staph. aureus, C. perfringensGiardia lamblia, Entamoeba histolytica, Cryptosporidium, Cyclospora, Cystoisospora
OnsetAcute (hours to 1-3 days)Acute (hours to 5 days); preformed toxin = 1-6 hSubacute to gradual (7-14 days)
DurationShort: 1-7 days (Norovirus 1-2 days; Rotavirus 5-7 days; Adenovirus up to 12 days)Short to medium: 1-7 days; C. difficile can be prolongedProlonged: >14 days; Giardia/Cyclospora can last weeks to months if untreated
Stool CharacterWatery, large volume, no bloodWatery (toxigenic) OR bloody/mucoid (invasive)Watery, greasy, foul-smelling (Giardia); bloody (Entamoeba); bulky, watery (Crypto)
FeverLow-grade or absent (Rotavirus/Norovirus may have mild fever)Often present; high fever in invasive infections (Shigella, Salmonella, Campylobacter)Usually absent or low-grade; present in Entamoeba invasive disease
VomitingProminent (especially Norovirus and Rotavirus)Variable; prominent with preformed toxins (Staph. aureus)Mild or absent
Abdominal PainMild crampingModerate to severe; tenesmus in dysenteryCramping, bloating, flatulence (Giardia); colicky pain (Entamoeba)
TenesmusAbsentPresent in dysentery (Shigella, EIEC, Entamoeba)Present in amebic dysentery
Blood/Mucus in StoolAbsentPresent in invasive types (Shigella, EHEC, Campylobacter, Salmonella)Present in Entamoeba histolytica ("flask-shaped" ulcers)
Fecal LeukocytesAbsentPresent in invasive bacterial infectionsAbsent (most); present in Entamoeba
Inoculum RequiredVery low (Norovirus, Rotavirus - highly contagious)Variable: Shigella = 10-100 organisms; Salmonella = 10⁵-10⁸ organisms; V. cholerae = 10⁸Moderate to low: Giardia cysts = 10-25; Cryptosporidium = 10-100 oocysts
TransmissionFecal-oral; vomitus aerosols (Norovirus); contaminated surfacesContaminated food/water; fecal-oral; zoonotic (Salmonella from poultry/reptiles)Contaminated water (Giardia, Cryptosporidium); food, fecal-oral (Entamoeba)
Outbreak SettingCruise ships, nursing homes, schools (Norovirus); daycare (Rotavirus)Restaurant/food handling outbreaks (Salmonella, Staph. aureus); hospital (C. difficile)Travelers; waterborne outbreaks (Giardia, Crypto); immunocompromised clusters
SeasonalityRotavirus peaks in winter (temperate); Norovirus year-roundYear-round; Campylobacter peaks in summerGiardia peaks in late summer/fall; Cyclospora associated with produce outbreaks
Age GroupRotavirus: infants/toddlers; Norovirus: all ages, predominant in adultsAll ages; C. difficile in elderly/hospitalized; ETEC in travelersAll ages; Giardia peaks in children and late summer; Crypto severe in HIV
MechanismDirect enterocyte damage; viroporins (Rotavirus NSP4 - first viral enterotoxin described); impaired absorptionSecretory (↑cAMP/cGMP via toxins) OR invasive mucosal destructionTrophozoite attachment and mucosal invasion (Entamoeba); brush-border damage (Giardia); intracellular parasitism (Crypto)
cAMP/cGMPNot applicablecAMP ↑: Cholera toxin, ETEC (LT); cGMP ↑: ETEC (ST)Not applicable
Systemic FeaturesMyalgia, headache (Norovirus)Bacteremia (Salmonella, Campylobacter); enteric fever (S. Typhi - rose spots, relative bradycardia, splenomegaly)Liver abscess (Entamoeba); biliary involvement in Crypto + HIV
Extra-intestinal ComplicationsPost-infectious: rareGuillain-Barre (Campylobacter); HUS (EHEC); reactive arthritis (Salmonella, Shigella, Campylobacter, Yersinia); toxic megacolon (C. difficile, Shigella)Liver abscess (Entamoeba); sclerosing cholangitis (Crypto in HIV CD4 <50)
DiagnosisClinical; ELISA/PCR for rotavirus antigen, norovirus PCR; multiplex stool panelsStool culture (gold standard); C. difficile toxin EIA/NAAT; stool NAAT panelsStool O&P (microscopy); ELISA antigen detection (Giardia, Crypto); trichrome stain (Entamoeba)
Fecal Lactoferrin/CalprotectinNegativePositive in invasive infectionsNegative (usually)
Blood CultureNot indicatedIndicated in S. Typhi (enteric fever), severe Salmonella, toxic patientsNot indicated
TreatmentSupportive (ORS); Ondansetron for vomiting; self-limitedORS + specific antibiotics (pathogen-dependent); NO antibiotics for EHEC; supportive for most food poisoningPathogen-specific antiparasitic agents (see below)
Specific Antibiotic/AntiparasiticNone routinely (Nitazoxanide trialed for Rotavirus)Ciprofloxacin/Azithromycin (Shigella); Vancomycin/Fidaxomicin (C. difficile); Doxycycline (Cholera); Ceftriaxone (Typhi)Metronidazole/Tinidazole (Giardia, Entamoeba); Nitazoxanide (Crypto, Giardia); TMP-SMX (Cyclospora, Cystoisospora)
Antibiotics ContraindicatedN/AEHEC O157:H7 (↑ HUS risk); uncomplicated non-typhoidal Salmonella (prolongs carrier state)N/A
Antidiarrheal AgentsSafe in uncomplicated casesContraindicated in invasive/bloody diarrhea (Shigella, EHEC) - prolongs shedding/increases bacteremiaGenerally safe; treat underlying infection
Vaccine AvailableRotavirus (RotaTeq, Rotarix) - oral live-attenuated, 2-3 doses in infancyTyphoid (Vi polysaccharide / Ty21a); Cholera (Dukoral, Vaxchora)None routinely available
Hospitalization RateRotavirus: high in infants (IV rehydration); Norovirus: low (most manage at home)Variable: high in severe Salmonella, Shigella, Typhi; low in ETECLow in immunocompetent; high in HIV/immunocompromised
Immunocompromised RiskRotavirus prolonged sheddingSalmonella bacteremia greatly increased; C. difficile recurrence ↑Cryptosporidiosis: chronic, life-threatening; Cyclospora/Cystoisospora more severe
Key High-Yield ClueOutbreak setting + no blood + short duration + vomiting prominentFood history + incubation period + presence of blood/feverTravel + prolonged course + greasy/foul stools + immunocompromised status

Quick Memory Aid

ViralBacterialParasitic
StoolWatery, no bloodWatery or bloodyWatery, greasy, or bloody
FeverLow/absentHigh (invasive)Low/absent
VomitingProminentVariableMild
DurationDaysDays-weekWeeks-months
TreatmentORS onlyORS ± antibioticsAntiparasitic
Fecal WBCsAbsentPresent (invasive)Absent (mostly)
Sources: Harrison's Principles of Internal Medicine 22nd Edition (2025), Frameworks for Internal Medicine, Goldman-Cecil Medicine
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