Amoebic dysentery

Etiology

• Caused by the protozoan Entamoeba histolytica.
• Transmission is fecal-oral, through ingestion of infective cysts in contaminated food or water.
• The cyst wall contains chitin and is resistant to gastric acid, allowing cysts to survive passage through the stomach.
• In the colon, cysts release trophozoites, the anaerobically reproducing amoeboid forms.
  Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 742.

Pathogenesis

1. Following ingestion, cysts reach the colon and excyst to produce trophozoites.
2. Trophozoites colonize the epithelial surface of the colon, especially the:
   • Cecum and ascending colon
   • Less commonly sigmoid colon, rectum, and appendix
3. Dysentery occurs when amoebae:
   • Adhere to colonic epithelium
   • Induce epithelial-cell apoptosis
   • Invade intestinal crypts
   • Extend laterally through the lamina propria
4. This produces neutrophilic inflammation, tissue necrosis, and the characteristic flask-shaped ulcer, with:
   • Narrow mucosal neck
   • Broad undermined base in the submucosa
5. Amoebae can enter splanchnic vessels and spread through the portal circulation to the liver, producing amoebic liver abscesses.
   Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 742.

Clinical features

• Many infections may be asymptomatic.
• Symptomatic intestinal amoebiasis commonly presents with:
  • Abdominal pain
  • Bloody diarrhea or dysentery
  • Weight loss
• Severe disease may cause:
  • Acute necrotizing colitis
  • Toxic megacolon
    Both carry significant mortality.

Extraintestinal disease

• Amoebic liver abscess is the important complication of invasive colonic disease.
• Abscesses may be large, sometimes exceeding 10 cm, with scant peripheral inflammation and a shaggy fibrinous lining.
• The hepatic abscess can persist even after the intestinal illness resolves.
• Rarely, it may extend directly into the lung or heart. Hematogenous spread may also involve the kidneys and brain.
  Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 742.

Morphology of amoebic dysentery

Site

• Mainly involves the cecum and ascending colon.
• May also involve the appendix, sigmoid colon, and rectum.

Gross morphology

• Multiple discrete ulcers occur in the colonic mucosa.
• The classic lesion is a flask-shaped ulcer:
  • Narrow neck at the mucosal surface
  • Broad, undermined base extending laterally in the submucosa/lamina propria
• Ulcers result from trophozoites invading crypts and spreading laterally beneath the mucosa.
• Intervening mucosa may be relatively normal early in disease.
• In severe cases there may be extensive ulceration, necrotizing colitis, perforation, or toxic megacolon.

Microscopy

• Mucosal ulceration with necrosis and an acute inflammatory infiltrate, predominantly neutrophils.
• Trophozoites of Entamoeba histolytica are found especially:
  • At the advancing edge of the ulcer
  • In the submucosa
  • Occasionally within blood vessels
• Trophozoites may resemble macrophages. A diagnostic clue is ingested erythrocytes within trophozoites.
• Amoebae invade through the bowel wall and may enter splanchnic vessels, leading to portal spread and liver abscess.