Cysticercosis_Robbins and harsh mohan.pptx

Cysticercosis is the main brain lesion.

1. Cysticercosis Parasitic infection by Taenia solium (larval stage: cysticercus cellulosae) Major cause of seizures in endemic regions

2. Etiology Causative agent: Taenia solium (pork tapeworm) Source: Ingestion of eggs from contaminated food/water Not from pork meat → that causes taeniasis, not cysticercosis

3. Pathogenesis (Flowchart) Ingestion of T. solium eggs → Oncospheres hatch in intestine → Penetrate intestinal wall → bloodstream → Disseminate to brain, eye, muscle, subcutaneous tissue → Develop into fluid-filled cysticerci → Host immune response (inflammation, fibrosis, calcification)

4. Pathology (Gross) Brain: Multiple cysts, 5–20 mm, translucent, with scolex Muscle: Firm nodules, sometimes palpable Eye: Cysts in vitreous/retina → visual loss Subcutaneous: Small mobile nodules

5. Pathology (Microscopy) Viable cyst: little/no inflammation Degenerating cyst: granulomatous inflammation, eosinophils, giant cells Late stage: fibrosis + calcification Scolex visible (hooklets & suckers)

6. Cystic cavity contains the the larval form: scolex with hooklets and 2 pairs of suckers The larval form, composed of duct-like invaginations, is lined by a double layered, eosinophilic membrane Scolex is single and invaginated; contains a rostellum, 4 suckers and 22 - 23 bifrefringent hooklets (may persist for a long time) Body wall exhibits a myxoid matrix and calcareous bodies (calcified concretions) Cysticerci may remain viable for years Colloidal stage: first stage of involution of cysticerci ; transparent vesicular fluid is replaced by a turbid, viscous fluid and the scolex shows signs of hyaline degeneration

7. Granular stage: cysticercus is no longer viable; cyst wall thickens and the scolex is transformed into coarse mineralized granules Host inflammatory reaction is usually not present if the larva is viable Finally, a granulomatous reaction develops characterized by histiocytes, epitheloid cells and foreign body giant cells, leading to fibrosis of the supporting stroma and calcification of the parasitic debris

8. Clinical Features Neurocysticercosis: - Seizures (most common) - Raised intracranial pressure, hydrocephalus - Focal neurological deficits Ocular: floaters, retinal detachment, blindness Muscle/Subcutaneous: nodules (asymptomatic)

9. Robbins High-Yield Point Disease due to both: 1. Space-occupying lesion effect of cysts 2. Host immune reaction to degenerating larvae

10. Diagnosis Imaging: CT/MRI (cysts ± calcifications) Serology: ELISA, EITB Biopsy (rare, for subcutaneous nodules)

11. Treatment Albendazole / Praziquantel Steroids (reduce inflammation) Antiepileptics (for seizures) Surgery (ocular cysts)

12. Summary (Exam Box) Etiology: T. solium eggs Pathogenesis: eggs → oncospheres → bloodstream → cysticerci Organs: brain, eye, muscle, subcutaneous tissue Pathology: viable (no inflammation) → degenerating (granuloma) → calcified (scar) Clinical: seizures, ocular defects, nodules Treatment: albendazole + steroids