Amebiasis

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Amebiasis

Definition

Amebiasis is infection caused by the enteric protozoan parasite Entamoeba histolytica. It can manifest as asymptomatic colonization, diarrhea, dysentery, colitis, or spread extraintestinally to cause liver abscess and, rarely, brain abscess. - Goldman-Cecil Medicine

The Pathogen

E. histolytica has a low infectious dose (<100 organisms), is resistant to chlorine, and is environmentally stable. It has two morphologic forms:

Feature	Trophozoite	Cyst
Role	Tissue invasion (pathogenic form)	Transmission (infective form)
Survival	Degenerates rapidly outside the body; destroyed by gastric acid	Environmentally stable; resistant to chlorination
Nuclei	1	1-4 (mature = 4)
Size	12-50 µm	10-20 µm
Chromatoidal bars	N/A	Rounded ends (vs. E. coli's splintered ends)
Karyosome	Central, sharp	Central, sharp
Ingested RBCs	Present (pathognomonic)	Absent

The tissue-destructive properties give the organism its name "histolytica." Certain genotypes are linked to colonization, while others drive invasion. - Medical Microbiology 9e

Related species (morphologically identical but non-pathogenic): E. dispar, E. moshkovskii, E. bangladeshi - these cannot be distinguished by microscopy alone but do not cause invasive disease.

Trichrome-stained stool showing E. histolytica cyst (CDC/Dr. Mae Melvin):

Trichrome-stained stool with E. histolytica cyst - mature quadrinucleate cyst visible centrally

The mature cyst in the center displays an oblong chromatoid body and four nuclei (9-25 µm diameter) each with a centrally situated karyosome. - Yamada's Textbook of Gastroenterology

Life Cycle

Ingestion of cysts from fecally contaminated food/water
Excystation in the duodenum (stimulated by gastric acid) - each quadrinucleate cyst yields 8 trophozoites
Trophozoites colonize the large intestine; multiply by binary fission
In the colon, trophozoites can encyst - cysts are shed in feces
Invasive trophozoites penetrate the mucosa, enter the portal circulation, and reach the liver (most common extraintestinal site)

Humans are the only host; natural infection of primates also documented. - Yamada's Textbook of Gastroenterology

Epidemiology

WHO estimate: ~50 million symptomatic cases and ~100,000 deaths annually worldwide
Endemic in the Indian subcontinent, Southeast Asia, sub-Saharan Africa, Central and South America
In the US: 3rd most common parasitic infection (after giardiasis and cryptosporidiosis); rate 1.2/100,000
2nd most common cause of diarrhea in returning travelers
High-risk groups: young children, elderly, malnourished, pregnant women, corticosteroid users
Typical amebic liver abscess patient in the US: 20- to 40-year-old Hispanic male immigrant
Transmitted by fecal-oral route; flies and cockroaches can serve as mechanical vectors - Goldman-Cecil Medicine

Pathogenesis

Host cell killing occurs via a sequential process:

Adherence - via the Gal/GalNAc lectin (galactose- and N-acetyl-D-galactosamine-specific), which binds host intestinal epithelium
Amebic trogytosis - a nibbling-like process
Contact-dependent cytotoxicity - trophozoites induce apoptosis in host cells by activating caspase-3; caspase-3-deficient mice are resistant
Phagocytosis of host cell corpse - requires recognition via multiple ligands (Gal/GalNAc lectin, phosphatidylserine receptor, SREHP, collectins)
Cysteine proteinases (>44 genes) - degrade colonic mucin, extracellular matrix, hemoglobin, and inactivate IL-18
Flask-shaped ulcerations form in the intestinal mucosa with hemorrhage and potential secondary bacterial infection

Immune response:

Innate: lymphoid type-2 cells, neutrophils (within 1-2 days), macrophages/T cells (by day 3)
Acquired: protective IFN-γ response; mucosal IgA against Gal/GalNAc lectin - children with anti-lectin IgA have 86% fewer new infections
TH2 response (IL-4) is deleterious; TH1 (IFN-γ) is protective
The IL-33/ILC2 pathway is an important host defense mechanism

Clinical Syndromes

1. Asymptomatic Carriage

Most infections (especially with E. dispar/moshkovskii) are asymptomatic. Carriers pass infectious cysts and are the main reservoir.

2. Amebic Colitis (Intestinal Amebiasis)

Gradual onset over 1-3 weeks
Bloody diarrhea, mucus in stool, crampy abdominal pain
Fever is present in <40% of cases (distinguishes it from bacillary dysentery, which more often has high fever)
Severe disease: fulminant colitis (1-4%) with toxic megacolon - high mortality; corticosteroids dramatically worsen this
Ameboma: inflammatory mass (usually cecum or ascending colon) that can mimic carcinoma

3. Amebic Liver Abscess (ALA) - Most Common Extraintestinal Form

Right lobe involved in >80% of cases
Presents with fever, right upper quadrant pain, and hepatomegaly with elevation of the right hemidiaphragm
"Chocolate sauce" (anchovy paste) pus on aspiration - odorless, acellular necrotic debris
Only ~30% have concurrent intestinal symptoms; stool examination is often negative
Serology is positive in virtually all patients with ALA
Rarely: rupture into pleural space, pericardium, or peritoneum

4. Other Extraintestinal Sites

Pleuropulmonary (via diaphragm from liver abscess): most common after ALA
Brain abscess: rare but high mortality
Cutaneous/genital amebiasis: direct contact with infected material

Diagnosis

Stool Microscopy

Detection of trophozoites or cysts in stool
Trophozoites with ingested RBCs are pathognomonic
Must be distinguished from commensal amebae (see table above) and from PMNs
Sensitivity is low: parasites are not homogeneously distributed; multiple specimens (3) increase yield
Cannot distinguish E. histolytica from E. dispar/moshkovskii by morphology alone

Antigen Detection (Fecal ELISA)

Detects E. histolytica-specific antigen (Gal/GalNAc lectin)
Differentiates pathogenic from non-pathogenic species
More sensitive and specific than microscopy

PCR / DNA Probes

Most specific method for distinguishing E. histolytica from look-alike species
Increasingly available commercially

Serology (Anti-amebic antibodies)

Positive in >80% of intestinal amebiasis and virtually all ALA cases
Less useful in endemic areas (background seropositivity)
IgG remains positive for years - cannot distinguish active from past infection

Imaging (for ALA)

Ultrasound: first-line - shows hypoechoic lesion, usually right lobe
CT/MRI: better characterization; single round lesion with peripheral enhancement
Aspiration: "chocolate pus" without organisms (amebae are at abscess margin, not center)

Treatment

Treatment depends on clinical form. - Katzung's Basic and Clinical Pharmacology

Clinical Setting	Drug of Choice	Alternative
Asymptomatic intestinal infection	Luminal agent only: Paromomycin 10 mg/kg TID × 7 days OR Diloxanide furoate 500 mg TID × 10 days OR Iodoquinol 650 mg TID × 21 days	-
Mild-to-moderate colitis	Metronidazole 750 mg TID (or 500 mg IV q6h) × 10 days PLUS luminal agent OR Tinidazole 2 g/day × 3 days + luminal agent	Luminal agent + Tetracycline 250 mg TID × 10 days OR Erythromycin 500 mg QID × 10 days
Severe colitis/dysentery	Metronidazole 750 mg TID × 10 days OR Tinidazole 2 g/day × 3 days PLUS luminal agent	Luminal agent + Tetracycline 250 mg TID × 10 days
Liver abscess / ameboma / extraintestinal	Metronidazole 750 mg TID × 10 days OR Tinidazole 2 g/day × 5 days PLUS luminal agent	Chloroquine 500 mg BID × 2 days then 500 mg/day × 21 days + luminal agent

Key principles:

A luminal agent is always required after tissue amebicide therapy (to eradicate residual intestinal cysts and prevent relapse)
Luminal agents alone (paromomycin, diloxanide, iodoquinol) are NOT effective against extraintestinal disease
Asymptomatic carriers in non-endemic areas should be treated with a luminal amebicide
Percutaneous aspiration of ALA is reserved for: large or left-lobe abscesses (risk of rupture into pericardium), failure to respond to metronidazole in 3-5 days, or bacterially superinfected abscess

Prevention and Control

Safe water supply (boiling, iodination - NOT chlorination alone, since cysts are chlorine-resistant)
Improved sanitation and fecal disposal
Hand hygiene and food safety
Avoid raw produce washed with contaminated water when traveling to endemic areas
Screening and treatment of cyst-passers in food-handling or institutional settings

Sources: Goldman-Cecil Medicine | Medical Microbiology 9e | Yamada's Textbook of Gastroenterology | Katzung's Basic and Clinical Pharmacology, 16th ed.

Recent literature note: A 2025 systematic review on cerebral amebiasis (PMID 40602053) highlights that rapid PCR-based diagnostics significantly improve outcomes in the rare but lethal CNS form of this disease. No recent meta-analyses challenge current first-line metronidazole-based management.

Tb ulcer

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I have rich content now. Let me compile the comprehensive answer covering both the surgical (cutaneous/external) TB ulcer and the intestinal TB ulcer.

Tuberculous (TB) Ulcer

TB ulcers arise in two main clinical contexts: (1) external/cutaneous TB ulcer - from rupture of a caseous lymph node or cold abscess, and (2) intestinal TB ulcer - from direct mucosal invasion by Mycobacterium tuberculosis. Both are discussed below.

PART 1 - External (Cutaneous) Tuberculous Ulcer

Pathogenesis

The external TB ulcer most commonly results from the bursting of a caseous lymph node onto the skin surface, or from a cold abscess (from bone/joint TB) tracking to and breaking through the skin. The sites of predilection follow the regional lymph node groups: neck > axilla > groin. - S Das, Manual on Clinical Surgery

Classic Features of a TB Ulcer

Characteristic ulcer edge diagram from Bailey & Love's Surgery:

Ulcer edge shapes: (a) non-specific - shelving, (b) TB ulcer - undermined, (c) BCC - rolled, (d) epithelioma - everted/heaped-up, (e) syphilis - punched-out

(b) in the diagram shows the pathognomonic undermined edge of a tuberculous ulcer.

Feature	Description
Site	Neck, axilla, groin (lymph node areas); also scrotum (from tuberculous epididymitis)
Edge	Thin, bluish-red, and undermined - the hallmark feature
Floor	Pale granulation tissue ("wash-leather" granulations)
Discharge	Scanty, serosanguineous; thin and watery
Base	Slight induration (indicates chronicity)
Pain	Slightly painful (less painful than acute septic ulcer)
Regional lymph nodes	Enlarged, non-tender, matted (due to underlying TB lymphadenitis)

Clinical photo of a cervical tuberculous ulcer (Bailey & Love's Surgery):

Cervical tuberculous ulcer with overhanging/undermined edges

Tongue TB Ulcer

On the tongue, the TB ulcer is shallow, often multiple, greyish-yellow with a slightly red undermining margin. These typically result from contamination with infected sputum. - S Das

Key Differential: TB Ulcer vs. Other Ulcer Types

Type	Edge	Floor	Base	Discharge
TB ulcer	Thin, bluish, undermined	Pale granulations	Slightly indurated	Serosanguineous
Non-specific (pyogenic)	Shelving/sloping	Granulation tissue	Soft	Purulent
Syphilitic (chancre)	Punched-out	Wash-leather slough	Hard, indurated ("button")	Serous
Basal cell carcinoma	Rolled, pearly	-	-	Minimal
Squamous cell carcinoma	Everted/heaped-up	Irregular	Hard	Variable

Lupus Vulgaris (Cutaneous TB)

A special form - occurs commonly on the face and hands in children and young adults. Starts as single/multiple cutaneous nodules that ulcerate superficially. Active at the periphery (spreads outward) while healing centrally. The name "lupus" (wolf) refers to its peripheral destructive nature. Squamous cell carcinoma can develop from the scar of lupus vulgaris (Marjolin's ulcer). - S Das

Investigations

Discharge microscopy: Acid-fast bacilli (ZN stain); guinea pig inoculation test
Mantoux test (TST) or IGRA (Interferon-gamma release assay) - supersedes Mantoux in endemic areas
Raised ESR and CRP, low haemoglobin
Excision biopsy of lymph node (if in adenitis stage) - sent fresh to lab
Aspiration of cold abscess for culture and sensitivity (ZN stain)
Chest X-ray - to identify pulmonary focus
Sputum for culture and ZN staining - Bailey & Love's Surgery

PART 2 - Intestinal Tuberculous Ulcer

Pathogenesis & Location

Organism: usually Mycobacterium tuberculosis; occasionally M. bovis (from contaminated dairy)
Route: direct penetration of intestinal mucosa by swallowed organisms in sputum or contaminated food
Ileum and cecum are most commonly involved (75% of cases)
Both sides of the ileocecal valve are typically affected - causing valve incompetence (a key feature distinguishing TB from Crohn's disease, which does not usually involve the valve)

Gross Morphology - Three Types

Type	Frequency	Description
Ulcerative	60%	Multiple superficial lesions confined to the epithelial surface
Hypertrophic	10%	Scarring, fibrosis, heaped-up mass lesions - can mimic carcinoma
Ulcero-hypertrophic	30%	Mucosal ulcerations combined with healing and scar formation

Key morphologic feature of intestinal TB ulcer: The ulcers are oriented transversely (circumferentially) along the bowel, perpendicular to the long axis - because TB spreads along the lymphatics which run in the transverse folds (Peyer's patches and lymphoid tissue). This contrasts with Crohn's disease, which produces longitudinal/linear ulcers along the bowel axis. - Sleisenger & Fordtran

Healing of ulcers leads to fibrosis and stricture formation, the most common complication.

Histology

Colon biopsy from intestinal TB - granulomas in mucosa and submucosa (H&E stain)

The distinguishing histological lesion is the caseating granuloma, seen in 50-80% of cases. Caseation is common but not always present. AFB are detected by acid-fast stain in ~20% of mucosal samples; PCR is more sensitive (~65%). - Sleisenger & Fordtran

Clinical Features

Chronic non-specific abdominal pain (80-90% of patients)
Weight loss, malaise, evening fever (constitutional TB symptoms)
Alternating diarrhea and constipation
Blood in stool
Palpable RLQ mass in 25-50% of patients (ileocecal involvement)
Doughy feel of abdomen on palpation
Perianal disease and fistula formation may occur

Emergency presentations:

Features of small bowel obstruction (the most common complication) - pain, distension, bilious vomiting
Peritonitis from perforation of a tuberculous ulcer (rare) - Bailey & Love's Surgery

Differentiating from Crohn's Disease

Feature	Intestinal TB	Crohn's Disease
Ulcer orientation	Transverse/circumferential	Longitudinal/linear
Ileocecal valve	Incompetent (both sides involved)	Usually spared
Stierlin sign	Present (conification of cecum)	Absent
Lymph nodes on CT	Large (>1 cm), hypodense/caseous	Smaller, reactive
Granulomas	Caseating	Non-caseating
Perianal disease	Less common	Very common
AFB stain/PCR	Positive (if present)	Negative

Investigations

Colonoscopy with biopsy - most useful; sends for histopathology, ZN stain, PCR, and culture with drug sensitivities
Barium meal follow-through / CT enterography - shows strictures, ulcers, bowel wall thickening, calcified mesenteric lymph nodes
CT abdomen - ileocecal wall thickening, large hypodense mesenteric nodes, asymmetric bowel thickening; Stierlin sign (cecal conification with incompetent ileocecal valve) is characteristic
Sputum AFB + culture (may not show active pulmonary disease at diagnosis)
IGRA / Mantoux - positive does not equal active disease; negative in HIV or elderly
PCR on tissue or stool - most sensitive (~65%) for identifying M. tuberculosis

Treatment of Intestinal TB

Standard anti-TB chemotherapy:

2 months of HRZE (isoniazid + rifampicin + pyrazinamide + ethambutol) - intensive phase
4 months of HR (isoniazid + rifampicin) - continuation phase = total 6 months
Surgical intervention may be required for obstruction (even during drug therapy), perforation, or fistula - Sleisenger & Fordtran, Bailey & Love's Surgery

TB is a reportable disease; public health authorities should be notified when suspected. Isolation precautions (masks) are required in the endoscopy suite.

Sources: S Das - A Manual on Clinical Surgery, 13th ed. | Bailey & Love's Short Practice of Surgery, 28th ed. | Sleisenger & Fordtran's Gastrointestinal and Liver Disease | Goldman-Cecil Medicine

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