Ocular toxoplasmosis


Ocular toxoplasmosis is the commonest identifiable cause of posterior uveitis. It predominantly affects children and young people (25-45 years) and is characterised by recurrences that can ultimately lead to significant visual loss. Toxoplasma gondii is an obligate intracellular parasite with the cat as the definitive host. It is transmitted to humans by accidental ingestion of the egg form (oocysts) in cat faecal matter which may contaminate fruit and vegetables, ingestion of the cyst form (bradyzoites) in undercooked or raw meat, and vertical transmission to the fetus during maternal primary infection by the replicating form (tachyzoites). Most clinical episodes of ocular toxoplasmosis represent reactivation of an infection that was acquired in utero. It is likely however, that more patients with ocular disease acquire toxoplasmosis after birth than was previously recognised.


Only a small proportion of infected people develop significant ocular disease. The commonest symptoms are floaters and reduced vision. The hallmark clinical signs are a vitreous cellular infiltrate associated with a creamy white retinal lesion that is typically adjacent to a pigmented chorioretinal scar. The eye may be painful and red with anterior uveitis and high intraocular pressure.


Ensure that fruits and vegetables are cleaned and washed. Cook all meats adequately to destroy any harboured cysts. Pregnant women should avoid cat litter pans. Adequate contraceptive precautions are needed for six months in women of childbearing age following primary toxoplasmosis infection.


Ocular toxoplasmosis can be confused with a large number of other causes of posterior and pan uveitis. The differential diagnosis depends largely on the clinical setting and the clinical signs. For example disease processes such as herpetic retinitis, metastatic endophthalmitis, lymphoma, metastatic carcinomas and sarcoidosis may closely mimic the signs of ocular toxoplasmosis. The diagnosis is predominantly clinical. Using the polymerase chain reaction to test the vitreous and aqueous humours for toxoplasma DNA can be useful when the diagnosis is uncertain but is limited by low sensitivity.


The need for therapy, type of drug treatment and duration of therapy needs to be individualised. It is determined by factors such as the location of the lesion, severity of the inflammatory response, threat to vision, status of the other eye and the immune status of the patient. An episode of ocular infection is ultimately self-limiting in immunocompetent patients. If the infection involves the peripheral retina, has only mild associated inflammation and there is no involvement of the optic disc or macular region of the retina, then treatment is not necessary. Therapy is usually needed for 6 to 12 weeks in immunocompetent patients and a response is determined clinically when the retinal lesions lose their fluffy white appearance, the vitreous clears and an atrophic chorioretinal scar with sharp margins develops