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Amoeba and Amoebiasis

The Parasite: Entamoeba histolytica

• E. dispar - a harmless commensal (most common in stool-positive individuals)
• E. moshkovskii - nonpathogenic but recently associated with diarrhoea in some studies

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Life Cycle

1. Cysts shed in faeces by infected humans (up to 1.5 × 10⁷ cysts/day from a carrier)
2. Ingestion of cysts in contaminated food/water
3. Excystation in small intestine - each cyst produces 8 trophozoites
4. Trophozoites colonize the large intestine
5. May invade colonic mucosa → disseminate via portal blood → liver/other organs
6. Trophozoites re-encyst → passed in stool → continue cycle

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Epidemiology

• 90% of infections are caused by E. dispar (non-invasive) - symptomatic disease occurs in <10% of E. histolytica infections
• Amebic liver abscess (ALA) is 3-10 times more common in men, though colonic disease is equal between sexes
• Children (especially neonates), pregnant and postpartum women have increased risk of severe disease
• Risk factors for severity: malignancy, malnutrition, corticosteroids

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Agent Factors: Zymodemes

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Mode of Transmission

1. Faecal-oral route (main):

• Contaminated water (cysts survive for days-weeks; NOT killed by chlorination at routine doses)
• Raw/uncooked vegetables irrigated with sewage water
• Food handlers (cysts found on hands and under fingernails)
• Direct hand-to-mouth

1. Sexual transmission: Oral-rectal contact (especially among MSM)
2. Vectors: Flies, cockroaches, and rodents can mechanically carry cysts to food

• Survive days-weeks in water, faeces, sewage, and soil with moisture and low temperature
• Resistant to chlorine at routine water purification concentrations
• Killed by: drying, heating to ~55°C, or freezing

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Pathogenesis

• Contact-dependent killing of host cells via galactose/N-acetyl-D-galactosamine (Gal/GalNAc) lectin attachment to colonic epithelium
• Release of amebapores (pore-forming proteins that lyse cell membranes)
• Cysteine proteases that degrade extracellular matrix
• Trophozoites cause flask-shaped ulcers in the submucosa - narrow neck at mucosa with wide base below - most commonly in cecum, rectosigmoid, and ascending colon
• Portal bloodstream invasion → liver (most common extraintestinal site)

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Clinical Features

A. Intestinal Amoebiasis

• Bloody diarrhoea with mucus
• Abdominal pain and cramping
• Trophozoite invasion of mucosa → ulceration → risk of perforation and peritonitis
• Classically: mucus- and blood-stained stools (no pus - helps distinguish from shigellosis, where pus cells are prominent)

• Milder than dysentery; may mimic inflammatory bowel disease (ulcerative colitis, Crohn's)
• Non-bloody diarrhoea, constipation, abdominal cramping, weight loss
• Flask-shaped submucosal ulcers that expand
• Segments affected: cecum > rectosigmoid > ascending colon

• Granulomatous mass in the intestine from chronic amoebic infection
• Produces a "napkin ring" lesion - may be misdiagnosed as carcinoma

B. Extraintestinal Amoebiasis

• Right upper quadrant pain + fever (most consistent finding)
• Usually a single, large abscess in the right lobe
• Anchovy sauce/chocolate paste pus (liquefied hepatic tissue)
• Stool O&P negative in >50% of ALA cases at time of presentation
• Men affected 3-10x more often than women
• Onset ~12 weeks after exposure
• ALP and aminotransferases elevated
• Can rupture into pleura, pericardium, or peritoneum

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Diagnosis

Stool Examination

• Microscopy (fresh stool) - demonstration of trophozoites containing RBCs is diagnostic
• Must examine immediately (cooling destroys trophozoites)
• Look in fresh mucus passed per rectum
• Absence of pus cells in stool: helpful differential from shigellosis
• Note: cannot distinguish E. histolytica from E. dispar by morphology alone

Serology

• Often negative in intestinal amoebiasis but positive in extraintestinal disease
• Positive serology provides a clue to extraintestinal amoebiasis
• Indirect Haemagglutination (IHA) - regarded as the most sensitive serological test
• Counter Immunoelectrophoresis (CIE) and ELISA - newer techniques
• TechLab E. histolytica II antigen detection - can specifically identify E. histolytica (vs E. dispar)

Imaging (for ALA)

• Ultrasound: peripherally located, ovoid abscess; well-circumscribed border; homogeneous hypoechoic centre
• CT scan or MRI for complex cases

Stool Antigen Tests

• Species-specific monoclonal antibody-based antigen tests can differentiate E. histolytica from E. dispar

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Treatment

Symptomatic Intestinal Amoebiasis / Amebic Colitis

Luminal Agent (always add after nitroimidazole)

• Paromomycin (aminoglycoside) - acts on organisms in the intestinal lumen; eliminates cysts; first-line for asymptomatic carriers
• Also used to prevent further transmission after metronidazole course

Amebic Liver Abscess

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Prevention and Control

Primary Prevention

1. Sanitation - safe disposal of human excreta; handwashing after defecation and before eating
2. Water supply - sand filtration and boiling are more effective than chlorination (cysts are chlorine-resistant); protect from faecal contamination
3. Food hygiene:

• Disinfect raw vegetables/fruits with 5-10% acetic acid solution or full-strength vinegar
• Thorough washing with detergents in running water removes cysts
• Periodic examination, treatment and education of food handlers

1. Health education

Secondary Prevention

1. Early diagnosis via stool microscopy and serology
2. Prompt treatment of cases
3. Trace and treat contacts

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Key Differentiating Facts (High-Yield)

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Recent Literature

• A 2025 meta-analysis from India (PMID 39979548) provides updated data on epidemiology, risk factors, and clinical characteristics of ALA specifically in the Indian subcontinent.
• A 2026 systematic review and meta-analysis on E. histolytica intestinal infection in Malaysia (PMID 42126905) highlights ongoing high burden in SE Asia.

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