Write a short note on amoebiasis — intestinal and hepatic.

Aetiology

Amoebiasis is infection with *Entamoeba histolytica*, a protozoan parasite transmitted by the faeco-oral route through ingestion of cysts in contaminated water, food or by contaminated hands. It is endemic throughout India and is a major cause of morbidity where sanitation is poor.

Life cycle: ingested quadrinucleate cysts (the infective and resistant form) excyst in the small intestine, releasing trophozoites (the invasive form), which colonise the colon — particularly the caecum and ascending colon. Trophozoites either encyst and are passed in the stool (continuing transmission) or invade the colonic mucosa.

Crucially, *E. histolytica* must be distinguished from the morphologically identical but non-pathogenic *E. dispar* and *E. moshkovskii*, which are far more common and require no treatment — a distinction that can only be made by antigen detection or PCR, not by microscopy.

About 90% of infections are asymptomatic carriage; these individuals are nevertheless the reservoir for transmission.

Intestinal Amoebiasis

Pathology: trophozoites secrete proteinases and adhere via a galactose-binding lectin, invading the mucosa and producing the characteristic "flask-shaped" ulcers — a narrow neck through the mucosa opening into a broad base in the submucosa, with relatively normal intervening mucosa.

Clinical spectrum:

• Asymptomatic cyst passer — the majority.
• Amoebic dysentery — gradual onset (over 1–3 weeks) of abdominal cramps and loose stools containing blood and mucus, with tenesmus. Fever is present in under a third, and systemic toxicity is usually mild — an important contrast with bacillary dysentery.
• Non-dysenteric colitis — intermittent diarrhoea, abdominal pain and weight loss, often mistaken for irritable bowel syndrome or inflammatory bowel disease.
• Fulminant necrotising colitis — severe, with toxic megacolon and perforation; carries very high mortality; associated with malnutrition, pregnancy and corticosteroid use.
• Amoeboma — an inflammatory mass, usually in the caecum, mimicking carcinoma or tuberculosis; responds to medical treatment, so recognising it prevents unnecessary surgery.
• Complications: perforation and peritonitis, stricture, massive haemorrhage, rectovaginal fistula, and perianal ulceration.

Amoebic Liver Abscess

Pathogenesis: trophozoites invade colonic venules and travel via the portal vein to the liver, causing focal hepatocyte necrosis that coalesces into an abscess. It is the commonest extraintestinal manifestation.

Clinical features:

• Fever with rigors, and constant right upper quadrant or epigastric pain — often severe and sometimes referred to the right shoulder tip (diaphragmatic irritation).
• Tender hepatomegaly with point tenderness over an intercostal space — an important bedside sign.
• Anorexia, weight loss, sweating.
• Jaundice is uncommon and mild — marked jaundice suggests an alternative diagnosis or a large abscess compressing biliary structures.
• Only a minority (< 30%) have concurrent diarrhoea, and a history of dysentery is often absent altogether — its absence must not exclude the diagnosis.
• Typically a SINGLE abscess in the RIGHT lobe (which receives most of the superior mesenteric venous drainage), commonly in the posterosuperior segment.
• Male predominance is striking (about 10:1), and alcohol use is a recognised risk factor.

Complications:

• rupture — into the pleural space and lung (with an "anchovy sauce" empyema or hepatobronchial fistula and expectoration of the abscess contents), into the peritoneum (causing peritonitis with high mortality), or into the pericardium (from left lobe abscesses — the most dangerous, causing tamponade)
• secondary bacterial infection
• inferior vena cava or portal vein thrombosis.

Investigations:

• Ultrasound abdomen — the first-line test: a round or oval hypoechoic lesion with ill-defined walls and no significant wall echoes, usually in the right lobe. CT/MRI for equivocal or complex cases.
• Serology (amoebic antibody, IgG ELISA) — highly sensitive (> 90%) in liver abscess and the most useful confirmatory test; note that it remains positive for years after infection, limiting its value in endemic populations.
• Stool microscopy is negative in the majority of liver abscess patients — a negative stool does not exclude it.
• Antigen detection and PCR on stool, aspirate or serum — for species confirmation.
• CBC: leucocytosis with neutrophilia, and characteristically NO eosinophilia (a useful negative — this is a tissue-invasive protozoan, not a helminth); anaemia; raised ESR and CRP; raised alkaline phosphatase with mildly deranged transaminases.
• Chest X-ray — raised right hemidiaphragm, basal atelectasis, pleural effusion.
• Aspiration — the classic "anchovy sauce" or "chocolate-brown" odourless pus, which is sterile on bacterial culture and in which trophozoites are found only at the abscess wall, rarely in the aspirate.

Management

1. Tissue amoebicide — metronidazole (or tinidazole) is the drug of choice for both invasive intestinal disease and liver abscess. Response in liver abscess is usually dramatic, with defervescence within 72 hours — failure to respond should prompt reconsideration of the diagnosis or drainage.

2. Luminal amoebicide — ESSENTIAL and frequently omitted

Metronidazole does not reliably eradicate luminal cysts. A luminal agent — diloxanide furoate, paromomycin or iodoquinol — must be given after the tissue amoebicide in every patient, including those treated for liver abscess, to eliminate the intestinal reservoir and prevent relapse and continued transmission. Failure to give a luminal agent is the commonest cause of recurrence.

3. Asymptomatic cyst passers — treat with a luminal agent alone (in endemic areas, treatment is targeted where confirmed as *E. histolytica*).

4. Drainage of liver abscess — indications (most abscesses do NOT need drainage):

• No clinical response after 3–5 days of metronidazole
• Large abscess (particularly > 10 cm) or thin rim of liver tissue at risk of rupture
• LEFT LOBE abscess — because of the risk of rupture into the pericardium
• Suspected secondary bacterial infection or diagnostic uncertainty (to exclude pyogenic abscess)
• Impending or actual rupture

Percutaneous needle aspiration or catheter drainage under image guidance is preferred; surgery is rarely required.

5. Supportive care and prevention — hydration, nutrition, analgesia; safe water and sanitation, hand hygiene, washing of vegetables, avoidance of night soil as fertiliser, and treatment of carriers, particularly food handlers.