Intestinal Protozoa — Entamoeba histolytica and Giardia lamblia

Both organisms exist as a hardy cyst and a fragile trophozoite, and both infect by the faeco-oral route. The cyst is the infective and environmentally resistant form; trophozoites are the active, disease-causing form but do not survive for long outside the body. Cysts are usually found in formed stool and trophozoites in diarrhoeal stool.

Infection follows ingestion of mature cysts in contaminated food or water; sexual transmission also occurs. The cysts excyst in the intestine and release trophozoites that colonise the colon. Roughly 90% of infections are asymptomatic and self-limiting, and only about 10% of infected people develop invasive disease. Trophozoites invade the mucosa and submucosa with secreted enzymes and the Gal/GalNAc lectin, and some enter the portal circulation and reach the liver.

At least nine Entamoeba species can live in the human gut, but only E. histolytica is a well-recognised pathogen. E. dispar is considered non-pathogenic, and the remaining species are non-pathogenic or rare causes of disease. Microscopy cannot separate E. histolytica from the non-pathogens, which led older studies to overestimate prevalence.

India is among the highest-burden countries. In tropical settings E. histolytica is the commonest cause of liver abscess, accounting for up to 87.5% of cases in countries such as India. Risk factors include poor hand hygiene, untreated drinking water, defecation into water sources and alcohol use. For other faeco-oral helminths see intestinal nematodes.

Patients typically report several weeks of cramping abdominal pain, weight loss and watery or bloody diarrhoea; the course often resembles chronic colitis, and amoebiasis can be mistaken for inflammatory bowel disease. Right-colon disease is common. Typical ulcers lie in the caecum, sigmoid colon and rectum; nodular lesions are small (0.1–0.5 cm) with necrotic centres, and irregular serpiginous ulcers of 1–5 cm are usually in the caecum and ascending colon.

• Early lesion: mucosal thickening with glandular hyperplasia and stromal oedema; surface epithelium preserved.
• Advanced lesion: the classic flask-shaped ulcer — a small mucosal defect that undermines widely into the submucosa.
• Ulcer base: fibrin-rich exudate with red cells and abundant trophozoites; inflammatory infiltrate of neutrophils, plasma cells, eosinophils, macrophages and lymphocytes.
• Complications: stricture, rectovaginal fistula, obstruction, toxic megacolon, perforation and peritonitis.
• Fulminant (necrotising) colitis: less than 0.5% of cases but mortality above 40%; risk factors include pregnancy, corticosteroids, immunosuppression, diabetes and alcohol.

About 1% of clinical amoebic infections involve the liver, but amoebic liver abscess (ALA) is the commonest extra-intestinal complication. It usually presents 2–4 weeks after exposure with fever and right upper quadrant pain; fewer than one-third have diarrhoea at diagnosis. About 10% are jaundiced and 5–14% have pulmonary symptoms. Young adult males and alcohol users are most at risk, and the right lobe is the usual site. Examination shows liver tenderness, with hepatomegaly in about half.

Ultrasound is the gold-standard imaging test: a hypoechoic cystic lesion with a thick wall, usually unilocular and close to the liver capsule in the right lobe. On a gallium scan amoebic abscesses appear cold, while pyogenic abscesses appear hot. Rupture can cause empyema, a hepato-bronchial fistula or pericardial involvement.

With prompt medical treatment mortality of ALA is about 1–3%. Pleuropulmonary amoebiasis carries mortality up to 16% and cardiac involvement up to 30%. For comparison with the bacterial type, use amoebic versus pyogenic liver abscess.

Giardia duodenalis (formerly G. lamblia or G. intestinalis) is a common treatable cause of gastroenteritis. Each cyst releases two bilaterally symmetrical, pear-shaped, binucleate trophozoites with four pairs of flagella. Excystation is triggered by gastric acid and completed in the small intestine; trophozoites multiply by binary division, and when exposed to bile some encyst and pass in stool. Cysts remain viable for weeks to months, and as few as about 10 cysts can cause infection. Only assemblages A and B infect humans.

The ventral adhesive disc attaches the trophozoite to the proximal small-bowel mucosa without invading it. Attachment is associated with villous atrophy, increased crypt depth and microvillus shortening, with brush-border disaccharidase deficiency contributing to malabsorption. Biopsy is not needed for diagnosis; if done, it may be normal or show mild to subtotal villous atrophy that reverses after treatment.

Up to 15% of infected people are asymptomatic, and acute symptoms usually begin 1–2 weeks after exposure. Giardiasis should be considered in persistent diarrhoea lasting more than 3 days, in travellers, contacts of diapered children and people who drink untreated freshwater. Compare with other malabsorptive causes in malabsorption: coeliac, Whipple and tropical sprue.

Giardiasis needs treatment when symptomatic; asymptomatic infection may be treated to protect vulnerable contacts (for example food handlers or childcare workers). Options include tinidazole as a single 2 g dose (considered most effective and best tolerated), nitazoxanide 500 mg twice daily for 3 days, or metronidazole 250 mg three times daily for 5–7 days. Albendazole, mebendazole and paromomycin are alternatives. Tinidazole is contraindicated in early pregnancy; paromomycin is generally used when treatment is needed. Nitroimidazole resistance is increasingly recognised, and refractory cases may receive a nitroimidazole plus albendazole. See the drug of choice list for wider revision.

• Differentials for amoebic dysentery: Shigella, E. coli, Salmonella, Campylobacter, C. difficile, other protozoa, inflammatory bowel disease, ischaemic colitis (see diarrhoeagenic bacteria).
• Differentials for amoebic liver abscess: pyogenic abscess, echinococcal disease and malignancy.
• Giardiasis follow-up: repeat stool testing only if symptoms persist; distinguish reinfection from true failure.