CESTODES – ECHINOCOCCUS GRANULOSUS

Q. What is Echinococcus granulosus?
A. – Small tapeworm (cestode) causing hydatid disease (unilocular cyst)
– Definitive hosts: dogs, wolves, other canids
– Intermediate hosts: sheep, goats, cattle, humans (accidental)

Q. Morphology of adult worm
A. – Length 3–6 mm, width 0.5–1.5 mm
– Scolex with 4 small suckers, no hooks (distinguishes from E. multilocularis)
– Long narrow neck → few proglottids (usually 2–3)
– Mature proglottid contains 300–500 embryonated eggs

Q. Life cycle (step‑wise)

1. Adult worm lives in small intestine of definitive host → produces eggs
2. Eggs passed in feces → contaminate soil, water, vegetation
3. Intermediate host ingests eggs (grazing → sheep, cattle; humans → food‑hand‑mouth)
4. Egg hatches → oncosphere released in duodenum → penetrates intestinal wall
5. Oncosphere enters portal circulation → carried to liver (first filter) or lungs (second filter)
6. Oncosphere develops into a fluid‑filled hydatid cyst → grows slowly (1–5 cm/yr)
7. Cyst becomes fertile → produces protoscolices & daughter cysts → if eaten by definitive host, cycle repeats

Memory trick: “Dog → Eggs → Human gets Infected → Cyst Develops in Liver” (D‑E‑H‑I‑C)

Q. Pathogenesis (step‑wise)

1. Ingested egg → oncosphere penetrates gut wall → reaches liver via portal vein
2. Oncosphere transforms into germinal layer → secretes laminated cyst wall (protective)
3. Cyst fluid accumulates → expands → compresses adjacent parenchyma → organ dysfunction
4. Antigenic cyst fluid leaks → hypersensitivity, eosinophilia, occasional anaphylaxis
5. Rupture (trauma, pressure) → release of protoscolices → secondary cysts in peritoneum, pleura, etc.

Memory rhyme: “Penetrate, Transform, Expand, React, Rupture – P‑T‑E‑R‑R”

Q. Clinical features of hydatid disease (organ‑wise)
– Liver (most common, 60‑70 %): right upper quadrant dull pain, hepatomegaly, palpable mass, jaundice if bile duct compression
– Lung (20‑30 %): cough, chest pain, dyspnea, hemoptysis, occasional pneumothorax
– Spleen, kidney, brain, bone: site‑specific mass effect, neurological signs if brain involved
– General: low‑grade fever, weight loss, eosinophilia, allergic reactions after cyst rupture

Q. Complications
– Cyst rupture → anaphylactic shock, secondary dissemination
– Superinfection → abscess formation
– Biliary or bronchial fistula → bilious cough, cholangitis
– Obstructive jaundice, portal hypertension (large hepatic cyst)

Q. Laboratory diagnosis

1. Imaging (first line) →
   – Ultrasound: “wheel‑spoke” or “water‑lily” sign, cyst size & number
   – CT/MRI: better for lung, brain, bone, delineates daughter cysts
2. Serology →
   – ELISA (IgG) – high sensitivity for hepatic disease
   – Indirect hemagglutination, immunoblot – confirmatory
3. Microscopy (when cyst fluid obtained) → protoscolices with hooklets, laminated membrane fragments
4. Routine labs → eosinophilia, mild anemia, raised ESR

Q. Management (exam‑oriented points)
– Surgical excision (total pericystectomy or cystectomy) – preferred for large, complicated cysts
– PAIR technique → Puncture, Aspiration, Injection of scolicidal (hypertonic saline/ethanol), Re‑aspiration – for selected hepatic cysts
– Albendazole (10–15 mg/kg/day) ± praziquantel – pre‑ and post‑operative to sterilize cyst, reduce recurrence
– Follow‑up: US/CT every 6 months for 2 years, repeat serology to monitor response

Memory cue for treatment: “Surgeon’s PAIR, Albendazole’s Care” (S‑P‑A).