Enterocolitis

Enterocolitis = inflammation of the small intestine (enteritis) and colon (colitis)

• Causes diarrhea + pain, urgency, perianal discomfort and incontinence

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A) Types of Diarrhea

Type	Key Feature
Secretory	Isotonic fluid secretion; persists during fasting
Osmotic	Excessive luminal solutes; subsides with fasting
Exudative	Purulent, bloody stools; persists on fasting
Malabsorption	Voluminous, bulky stools; ↑ osmolarity; steatorrhea; subsides with fasting
Deranged motility	Highly variable features
Dysentery	Severe bloody diarrhea + fever + abdominal pain + rectal tenesmus; can be fatal

Dysentery causes: Shigella spp., amoeba parasites, Pseudomembranous colitis (C. difficile overgrowth after broad-spectrum antibiotics destroy normal flora)

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B) Infectious Enterocolitis

• Marked by diarrhea + sometimes ulceroinflammatory changes in small/large intestine
• Common as traveler’s disease; fecal-oral or contaminated food/water transmission
• Common offenders: ETEC (enterotoxic E. coli), rotavirus, calicivirus

Viral Gastroenteritis

• Destroys intestinal epithelial cells and their absorptive function
• Repopulation with immature enterocytes + preservation of crypt secretory cells → net secretion of water + electrolytes → osmotic diarrhea (secretion OK; absorption impaired)
• Causative agents:
  • Rotavirus/Adenovirus: mainly infants and children
  • Caliciviruses: food-borne; all age groups

Bacterial Enterocolitis

3 mechanisms of bacterial diarrheal illness:

1. Ingestion of preformed toxin (S. aureus, Vibrio spp., C. perfringens) → vomiting, explosive diarrhea, acute abdominal distress
2. Infection by toxigenic organisms (ETEC) → proliferate in gut lumen + elaborate enterotoxin (traveler’s diarrhea)
3. Infection by enteroinvasive organisms (C. jejuni, Salmonella, EIEC, Shigella, Yersinia) → invade + destroy mucosal epithelial cells

3 key bacterial virulence properties:

• Ability to adhere to mucosal epithelial cells
• Ability to elaborate enterotoxins
• Capacity to invade + intracellular proliferation + cell-to-cell spread

Morphology: surface epithelial damage + ↑ mitotic rate in mucosal crypts; lamina propria = edematous, hyperemic, neutrophilic infiltration → crypt abscess → dysentery (exudative diarrhea with blood, pus, mucus, necrotic debris)

Complications: dehydration, sepsis, perforation

Protozoal Infection

• Entamoeba histolytica: amoebic dysentery; creates flask-shaped ulcer; may cause abscesses in other organs
• Giardia lamblia: waterborne; malabsorptive diarrhea
• Cryptosporidium: major cause of childhood diarrhea; fatal in AIDS patients

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C) Necrotizing Enterocolitis

• Acute necrotizing inflammation of small and large intestines
• GI emergency in neonates (especially premature / low birth weight)
• Pathogenesis: functional immaturity of neonatal gut + pathogenic organism colonization + secondary ischemic injury
• Morphology: mucosal edema, hemorrhage, necrosis + submucosal gas bubbles
• Clinical: bloody stool, abdominal distention, shock; high mortality rate

💡 High-yield: Dysentery = Shigella/amoeba/C. difficile; fever + bloody diarrhea + tenesmus. Viral = osmotic diarrhea; immature enterocytes; rotavirus (children) + calicivirus (all ages). Bacterial = preformed toxin (S. aureus) vs. toxigenic (ETEC) vs. enteroinvasive (Salmonella, Shigella, C. jejuni). Entamoeba = flask-shaped ulcer. Cryptosporidium = fatal in AIDS. Necrotizing enterocolitis = neonates; gas bubbles; high mortality.