Parasitic Uveitis

Ocular Toxocariasis

Ocular toxocariasis is a classic cause of unilateral granulomatous uveitis in children. It results from ingestion of Toxocara canis (or, less often, T. cati) eggs shed in the feces of infected dogs — especially puppies — that contaminate soil or sandboxes children play in. Larvae hatch after ingestion and can migrate through the body, including into the eye, where they provoke an intense granulomatous inflammatory response.

Clinically, ocular toxocariasis presents as one of three overlapping patterns: a posterior pole granuloma (roughly a quarter to nearly half of cases) — acutely a hazy, ill-defined white lesion with overlying vitritis that resolves into a distinct, well-demarcated elevated white mass; a peripheral granuloma (a similar proportion of cases), often with vitreoretinal traction strands pulling toward the optic disc; or a more severe, diffuse chronic endophthalmitis picture that can mimic true infectious endophthalmitis. Vitritis is the single most common associated finding, present in the great majority of cases, often alongside cystoid macular edema. Visual outcome tracks with presentation type — eyes with a posterior pole granuloma tend to retain the best acuity, while the diffuse endophthalmitis form carries the worst prognosis.

Onchocerciasis (River Blindness)

Onchocerciasis is caused by the filarial nematode Onchocerca volvulus and is transmitted by the bite of infected Simulium blackflies, which breed near fast-flowing rivers in endemic regions of Africa and parts of Latin America — the source of the disease's common name, "river blindness." Adult worms live in subcutaneous nodules and release microfilariae that migrate through the skin and eye over years of ongoing infection.

Ocular disease evolves in stages tied to the inflammatory response against dying microfilariae. Early corneal involvement appears as "snowflake" or punctate keratitis — fluffy opacities reacting to dead microfilariae in the anterior stroma — that typically resolves as the organisms are cleared. With prolonged, repeated infection, inflammation can progress posteriorly to sclerosing keratitis, in which the peripheral cornea becomes progressively opacified and, without treatment, the entire cornea can scar permanently. Anterior uveitis/iridocyclitis, secondary glaucoma, chorioretinitis, and optic atrophy can all occur with chronic disease.

Ivermectin is the mainstay of treatment — it reduces microfilarial burden in the skin and eye and suppresses further microfilarial production for months at a time, though it does not kill the adult worms themselves. A notable clinical wrinkle: the drug's rapid microfilaricidal effect can transiently worsen punctate keratitis and precipitate or aggravate anterior uveitis shortly after dosing, a reaction to the sudden die-off of microfilariae in ocular tissue. With regular annual dosing, however, this pattern reverses — migration of new microfilariae into the anterior chamber and cornea is prevented, punctate keratitis resolves, and early sclerosing keratitis and iridocyclitis regress.

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