Amoebic Abscess

Description

Amoebic abscess refers to a parasitic liver abscess caused by Entamoeba histolytica, an invasive protozoan that most commonly affects the colon but may disseminate via the portal venous system to the liver. It represents the most frequent extraintestinal manifestation of amoebiasis, and is the leading cause of liver abscess in the developing world.

It is typically solitary, located in the right hepatic lobe, and contains a distinctive anchovy paste-like necrotic fluid that is brown, odourless, and pathognomonic. Amoebic abscesses are sterile and characteristically culture-negative.

The word amoebic is derived from Greek amoibe, meaning “change,” reflecting the organism’s morphologic variability. Abscess comes from Latin abscedere, meaning “to go away,” referencing pus-draining collections.

Pathogenesis

After ingestion of cysts in faecally contaminated food or water, E. histolytica excysts in the ileum, releasing trophozoites. These trophozoites invade the colonic mucosa, form flask-shaped ulcers, and can gain access to the portal venous system, seeding the liver.

Once in hepatic tissue, trophozoites:

• Release cytotoxins that directly lyse hepatocytes.
• Inhibit neutrophil chemotaxis, resulting in minimal peripheral inflammatory response.
• Cause liquefactive necrosis and form collections of acellular necrotic material.
• Preferentially localise to the right lobe of the liver due to portal drainage patterns from the right colon.

The host response is limited, allowing the parasite to create a large necrotic cavity surrounded by granulation tissue but without a true capsule.

Epidemiology, Risk Factors & Associations

• Endemic in developing countries (India, Bangladesh, Mexico, sub-Saharan Africa)
• Male predominance (male:female ratio ~9:1)
• Most frequent in 20–40 year-old adults
• Alcohol consumption (present in ~50% of cases)
• Poor hygiene and sanitation
• Recent travel to endemic areas
• Immunosuppression (e.g. HIV/AIDS, steroids)
• Malnutrition and low socioeconomic status

Clinical Features

• Fever and chills
• Right upper quadrant pain or tenderness
• Hepatomegaly
• Anorexia and weight loss
• Diarrhoea (in only 30–40% of cases)
• Anchovy paste aspirate is pathognomonic
• Jaundice (rare, <10%), usually from biliary compression
• Pleuritic chest pain or referred shoulder pain if diaphragmatic irritation is present

Complications

• Rupture (up to 15%)
  • Into peritoneum → generalised peritonitis
  • Into pleura → empyema
  • Into pericardium (left-sided abscesses more prone)→ cardiac tamponade (rare but highly fatal)
• Secondary bacterial infection
• Portal or hepatic vein thrombosis
• Biliary tract obstruction
• No risk of malignant transformation

Pathological Features

Histopathology

• Macroscopic:
  • Round or oval lesion, usually subcapsular, with central liquefied necrosis and a thin rim of compressed parenchyma
  • Contents are thick, brown, odourless material resembling anchovy paste
• Microscopic:
  • Central area of eosinophilic necrotic debris without neutrophils
  • Peripheral granulation tissue with ingested erythrocytes inside E. histolytica trophozoites
  • No true fibrous capsule

Serology

• High sensitivity and specificity using ELISA or indirect haemagglutination
• Positive in >90% of cases, especially useful in non-endemic areas
• Serology remains positive for months post-infection

Biochemistry

• Alkaline phosphatase elevated in >90%
• Mild elevation in transaminases (AST/ALT)
• Raised white cell count, CRP and ESR
• Bilirubin may be elevated if biliary compression occurs

Immunohistochemistry

• Not routinely performed clinically
• Trophozoites may be highlighted using PAS stain on biopsy

Molecular

• PCR testing from aspirated abscess fluid confirms E. histolytica DNA with high specificity
• Useful in difficult or atypical presentations

Genetics

• No genetic predisposition known

Radiological Features

General Features

• First-line imaging modality is ultrasound
• Gold standard is contrast-enhanced CT
• Characteristically demonstrates a solitary, round, well-defined lesion, typically in the right lobe, with non-enhancing necrotic core and rim enhancement
• Lesion often measures >5 cm, appears subcapsular, and lacks internal septations or gas
• No internal nodules or calcifications

XR

• Chest radiograph may show:
  • Elevated right hemidiaphragm
  • Right basal pleural effusion
  • Atelectasis if diaphragmatic irritation or pleural involvement occurs
• Not sensitive or specific but may help identify thoracic complications from rupture

CT

• Non-contrast:
  • Low-attenuation lesion, usually unilocular, round or oval
  • No internal gas (differentiates from pyogenic abscess)
• C+ Arterial:
  • Thin peripheral rim enhancement, sometimes with double target sign
  • Hyperaemic hepatic parenchyma may be seen surrounding the lesion
• C+ Venous:
  • Peripheral capsule enhancement persists
  • Central core remains hypoattenuating
  • Perilesional fat stranding or mild hepatomegaly may be present
• Signs of rupture:
  • Perihepatic free fluid
  • Diaphragmatic discontinuity
  • Extension into pleural or pericardial space

MRI

• T1: Hypointense central content with peripheral rim
• T2: Hyperintense liquefied centre with well-defined capsule
• DWI/ADC: Restricted diffusion in the rim; central core shows facilitated diffusion
• T1 Gad+:
  • Ring-like enhancement
  • Absence of mural nodules or internal septations helps differentiate from cystic neoplasms
• SWI/GRE/T2*: May demonstrate haemorrhagic component if present

US

• B-mode:
  • Hypoechoic, round or oval lesion with posterior acoustic enhancement
  • Usually solitary, subcapsular, and >5 cm
  • Homogeneous contents without internal septations or gas
• Colour Doppler:
  • No internal vascularity
  • Peripheral vascular ring may be seen (inflammatory hyperaemia)

NM

• PET-FDG:
  • Not routinely used
  • May show peripheral uptake due to inflammation
  • Poor specificity; unable to distinguish from necrotic tumour or pyogenic abscess

Diagnosis

• Clinical presentation in endemic/travel setting
• Imaging (US or CT) showing characteristic features
• Positive serology for E. histolytica antibodies
• Therapeutic response to metronidazole
• Aspirated material with anchovy paste appearance; sterile on culture
• PCR of aspirate if diagnostic doubt exists

Differential Diagnosis

Image-based

• Pyogenic liver abscess: More likely to be multiple. Internal gas or air-fluid levels. Positive blood or pus cultures. Septations and complex internal echogenicity
• Hydatid cyst: Calcified rim or daughter cysts. No enhancement unless secondarily infected. Positive echinococcal serology
• Cystic hepatic metastases: Known malignancy history. Irregular rim enhancement or mural nodules
• Hepatocellular carcinoma (necrotic): Occurs in background of cirrhosis. Arterial enhancement with venous washout. Elevated AFP
• Biliary cystadenoma: Internal septations, mural nodules. Slow growth

Clinically-based

• Malaria (fever, hepatosplenomegaly)
• Viral hepatitis (AST/ALT markedly elevated)
• Right lower lobe pneumonia (referred RUQ pain)
• Leptospirosis
• Acute cholecystitis

Management

• Referral to infectious diseases and hepatobiliary teams
• Medical:
  • Metronidazole 750 mg TDS orally for 7–10 days (tissue trophozoite eradication)
  • Followed by a luminal agent (paromomycin or diloxanide furoate) to clear cysts
• Aspiration:
  • Indicated if:
    • Left lobe abscess (risk of pericardial rupture)
    • Abscess >10 cm or close to rupture
    • No clinical improvement in 5–7 days
    • Diagnostic uncertainty
• Percutaneous drainage: Rarely required if aspirated material is not resolving or if secondary infection suspected
• Surgical intervention: Reserved for ruptured abscess with generalised peritonitis or failed percutaneous therapy