Cysticercosis

A parasitic infection caused by the larval stage of the pork tapeworm Taenia solium
Caused by ingesting food or water contaminated by the worm's eggs (frequently fecal-oral transmission) which hatch in the gut and larvae migrate to the tissues then form cysts in the tissue.
- Cysts can be viable (dormant), degenerating (non-viable) or resolved with calcification
The larvae spread hematologically and settle in tissues, especially the CNS and eye.
Neurocysticercosis is the leading cause of epilepsy in endemic areas
Endemic areas
- Latin America, sub-Saharan Africa, Indian Subcontinent, Southeast Asia and China.
- In the USA (not endemic) cases are more often seen among immigrant populations

Neuroimaging
- MRI
  - T2-hyperintesnse and T1-hypointense showing cyst morphology (scolex, cyst fluid and surrounding inflammation)
- CT
  - Complementary to MRI, more sensitive for detecting calcified lesions
Ocular imagining
- B-scan
  - Well defined cystic lesion with eccentric intracystic echogenic focus (nidus) representing the scolex, thick cyst wall, surrounding inflammation and retinal detachment
Serologic testing- enzyme linked immunoelectrotransfer blot assay (EITB)

1-3% of all cases have ocular infection but T. solium is the most common intraocular parasite worldwide
Intraocular cysts
- Free floating in vitreous (60%)
- Subretinal space (40%)
- Vitreous inflammation 84%
- Anterior segment inflammation 30%
- Retinal detachment +/- PVR 50%
- cyst rupture causes more inflammation than intact cysts
Orbital/Extraocular involvement common
- Most often superior rectus affected causing restriction, proptosis, diplopia and ptosis
- Retro-orbital cysts can affect optic nerve and cause proptosis
Vision loss from CNS disease
- papilledema, or chiasmal compression

Intraocular cysts require surgical removal
- Vitrectomy and cyst removal and repair of retinal detachment
Subconjunctival cysts are usually removed as well.
Cysticidal therapy can cause severe ocular inflammation
- Extraocular cysts are more amenable to medical treatment alone
- Albendazole + cortiosteroids >90% resolution
  - Standard regimen:
    - albendazole PO (15mg/kg/day usually about 400 mg BID, max 1200 mg/day) for 10-14 days (FDA label permits up to 30 days but some evidence supports shorter courses 3-7 days for example)
    - prednisone PO (1mg/kg/day) given for the duration and the tapered.
  - possible persistent motility restriction, proptosis or ptosis
- Treatment response monitored by vision exam, and repeat imaging.
- If cystic lesions persist beyond 6-12 months, retreatment is recommended.
  - albendazole can be repeated, praziquantel can be added or switched to.
  - a combination may be superior if ≥ 3 cysts
- Monitor: liver enzymes, CBC
  - Hepatotoxicity occurs in 16%
  - Leukopenia in 10%
  - Reversable alopecia may occur
  - More common to have above with more prolonged treatment

Diagnosis