Definition/General
Introduction:
Amebic colitis is parasitic infection of the colon caused by Entamoeba histolytica
Shows characteristic flask-shaped ulcers
Endemic in tropical countries including India
May progress to fulminant colitis or liver abscess
Important differential for inflammatory bowel disease.
Origin:
Caused by Entamoeba histolytica trophozoites
Results from ingestion of cysts in contaminated food/water
Shows invasion of colonic mucosa
Demonstrates cytolytic enzymes and tissue destruction
Associated with poor sanitation.
Classification:
Acute amebic dysentery (bloody diarrhea)
Chronic amebic colitis (recurrent symptoms)
Fulminant amebic colitis (severe form)
Ameboma (mass-like lesion)
Extraintestinal amebiasis (liver abscess).
Epidemiology:
Endemic in tropical regions
High prevalence in India
Young to middle-aged adults commonly affected
Male predominance (2:1 ratio)
Associated with poverty and poor sanitation
Travel-associated infections.
Clinical Features
Presentation:
Bloody diarrhea (classical dysentery)
Lower abdominal pain
Tenesmus
Low-grade fever
Mucus passage
Constitutional symptoms.
Symptoms:
Bloody mucoid stools (10-20 per day)
Crampy abdominal pain
Urgency
Rectal bleeding
Weight loss
Anemia (chronic cases).
Risk Factors:
Travel to endemic areas
Poor sanitation
Contaminated food/water
Overcrowding
Male gender
Homosexual practices
Immunocompromised state.
Screening:
Stool microscopy (trophozoites, cysts)
Antigen detection (ELISA)
PCR (E
histolytica specific)
Serology (antibody detection)
Colonoscopy (mucosal visualization).
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Gross Description
Appearance:
Flask-shaped ulcers (pathognomonic)
Undermined edges
Yellow necrotic base
Surrounding normal mucosa
Punched-out appearance
Variable size (0.5-3 cm).
Characteristics:
Deep mucosal ulceration
Narrow neck, wider base
Minimal surrounding inflammation
Sharp borders
Necrotic debris in ulcer base
Skip lesions between ulcers.
Size Location:
Right-sided colon (cecum, ascending)
Rectosigmoid involvement common
Pan-colonic in severe cases
Terminal ileum may be involved
Skip pattern distribution.
Multifocality:
Multiple discrete ulcers
Varying stages of development
Skip areas of normal mucosa
Asymmetric distribution
Rectal involvement frequent.
Microscopic Description
Histological Features:
Flask-shaped ulcers extending into submucosa
E
histolytica trophozoites at ulcer edges
Minimal inflammatory response
Necrotic tissue in ulcer base
Normal intervening mucosa.
Cellular Characteristics:
Trophozoites (12-50 μm diameter)
Large karyosome in nucleus
Engulfed red blood cells
Minimal host inflammatory response
Neutrophils (limited)
Tissue necrosis.
Architectural Patterns:
Mucosal destruction with submucosal extension
Undermined edges
Normal crypt architecture in uninvolved areas
Focal distribution
Sharp demarcation between involved and normal areas.
Grading Criteria:
Mild: superficial mucosal ulcers, few organisms
Moderate: deep ulcers, moderate organism load
Severe: extensive ulceration, numerous organisms
Fulminant: transmural necrosis, perforation risk.
Immunohistochemistry
Positive Markers:
E
histolytica antigen (specific antibodies)
PAS stain (highlights organisms)
Iron hematoxylin (nuclear morphology)
Calcofluor white (cyst walls)
CD68 (macrophages).
Negative Markers:
Other parasitic antigens
Bacterial antigens
Viral markers
Malignancy markers
IBD-associated markers.
Diagnostic Utility:
E
histolytica antigen confirms diagnosis
PAS staining highlights trophozoites
Distinguishes from other parasites
Tissue-based diagnosis
Morphology usually sufficient.
Molecular Subtypes:
E
histolytica (pathogenic strain)
E
dispar (non-pathogenic, morphologically similar)
E
moshkovskii (rare pathogen)
Mixed infections possible.
Molecular/Genetic
Genetic Mutations:
E
histolytica virulence genes
Cysteine protease genes
Lectin genes
Host susceptibility factors
HLA associations.
Molecular Markers:
E
histolytica antigens (Gal/GalNAc lectin)
Cysteine proteases
Amoebapores
Host inflammatory mediators
Cytolytic factors.
Prognostic Significance:
Early diagnosis improves outcome
Organism load correlates with severity
Extraintestinal spread (liver abscess)
Perforation risk (fulminant cases)
Response to treatment.
Therapeutic Targets:
Metronidazole (tissue-invasive forms)
Paromomycin (luminal forms)
Combination therapy
Supportive care
Prevention measures.
Differential Diagnosis
Similar Entities:
Ulcerative colitis (inflammatory bowel disease)
Bacterial dysentery (Shigella)
Ischemic colitis
Crohn disease
Balantidium coli
Malignancy.
Distinguishing Features:
Amebic colitis: Flask-shaped ulcers, trophozoites, skip lesions
Ulcerative colitis: Continuous involvement, chronic changes
Bacterial dysentery: Bacteria identified, acute onset
Ischemic: Watershed zones
Crohn: Transmural, granulomas.
Diagnostic Challenges:
Distinguishing from IBD (clinical correlation important)
Identifying trophozoites in tissue
Differentiating from other parasites
Recognizing chronic forms
Serology correlation.
Rare Variants:
Ameboma (mass-like lesion)
Fulminant amebic colitis
Chronic amebic colitis
Cutaneous amebiasis
Perianal amebic ulcers.
Sample Pathology Report
Template Format
Sample Pathology Report
Complete Report: This is an example of how the final pathology report should be structured for this condition.
Specimen Information
[specimen type] from [anatomical location]
Clinical Information
Bloody diarrhea/dysentery. Travel history: [endemic area]. Duration: [acute/chronic]
Ulcer Morphology
Flask-shaped ulcers: [present/absent]. Undermined edges: [present/absent]. Skip lesions: [present/absent]
Organism Identification
E. histolytica trophozoites: [identified/not identified]. Size: [X] micrometers. Nuclear features: [large central karyosome]
Inflammatory Response
Host inflammatory response: [minimal/moderate/marked]. Neutrophilic infiltrate: [limited/moderate]
Special Features
Erythrophagocytosis: [present/absent]. Tissue necrosis: [present/absent]
Recommendations
Stool microscopy for trophozoites/cysts. E. histolytica antigen testing. Serology may be helpful.
Final Diagnosis
Amebic Colitis - Entamoeba histolytica infection