Description
Toxoplasma gondii is a protozoan that exists in three forms – tachyzoite (proliferative form), bradyzoite (slowly-metabolising form found in cysts), and sporozoite, produced in the intestines of cats, which are the definitive hosts. It is usually ingested following contamination of hands with cat feces, or by eating undercooked, contaminated meat. The organisms can also cross the placenta (congenital toxoplasmosis).
Toxoplasma organisms reach the eye hematogenously and form cysts within the retina. These cysts are able to survive for years without causing noticeable tissue damage, while the bradyzoites slowly multiply until the cyst bursts. Toxoplasma retinochoroiditis ensues as the bradyzoites convert into tachyzoites, which invade cells and induce granulomatous inflammation. Once established, the disease has a tendency to recur in the eye without systemic manifestations.
Symptoms
Acute acquired systemic toxoplasmosis in immunocompetent patients is usually subclinical. Some experience a nonspecific flu-like illness. Retinochoroiditis may occur simultaneously, or up to several years after the acute illness. Common symptoms are floaters and blurred vision. Spread of the inflammatory reaction to the anterior segment causes pain and photophobia in some patients.
Signs
Ocular toxoplasmosis most often appears as a cloudy, yellow-white lesion surrounded by retinal edema. A large granuloma may present as a yellowish mass. Iritis and vitritis are less common. Involvement of blood vessels in the region can lead to focal vasculitis, or retinal artery or vein occlusion. Optic nerve head swelling occurs when adjacent retinal tissue, or the nerve itself, is inflamed. Choroidal neovascular membranes and vitreous strands have been observed after prolonged disease. Signs in immunosuppressed patients tend to be more severe, bilateral and multifocal. Lesions are less likely to form adjacent to old scars; and central nervous system involvement is common.
Healed chorioretinal lesions contain scar tissue and appear as flattened, pale areas surrounded by variable amounts of pigment. Flares or recurrences are often located adjacent to these scars.
Prevalence
Toxoplasmosis is the most common infection of the retina. Serologic evidence of previous infection is very common in healthy adults (over 50 percent in many areas). Congenital infection is rare (approximately 1/10,000 births).
Significance
Acute infection in early pregnancy may prompt consideration of termination of pregnancy. Infection in immunosuppressed patients requires prolonged treatment, and is potentially fatal. Loss of vision can occur in immunocompetent patients.
Differential Diagnosis
Syphilis, Tuberculosis, Toxocariasis, Cytomegalovirus retinitis, Acquired Immunodeficiency Syndrome (AIDS) retinopathy, Sympathetic Ophthalmia, Candida retinitis, Lyme Disease, Histoplasmosis.
See Also
Retinal Detachment, Pregnancy.
Management
Blood tests
Diagnosis rests on the clinical features and serological tests: most commonly enzyme-linked immunosorbent assay (ELISA) or indirect fluorescence antibody (IFA). HIV testing is recommended in patients with atypical presentations or with a suggestive clinical history.
Medications
Several antibiotics (e.g., pyrimethamine, sulfadiazine & clindamycin) are effective against the tachyzoite, but not the bradyzoite, of T. gondii. Hence, they can help minimize ocular damage during acute episodes, but cannot eliminate the organisms. Systemic antibiotics are indicated when vision is significantly affected or threatened. Systemic corticosteroids (e.g., prednisolone, 1mg/kg/day) may be indicated to control inflammation after commencement of antibiotics.
Prognosis
Most cases of reactivation resolve spontaneously in several weeks to months. After the first attack, the mean recurrence rate is 50 percent over 3 years.
Advice
Prevention is facilitated by thorough cooking of meat, and handwashing after handling raw meat, cats and cat litter. Pregnant women are advised to minimize contact with cats and cat litter.


Figure 1
White lesion from acute toxoplasmosis. The detail is obscured by overlying vitreous inflammatory haze.
Figure 2
Same eye as figure 1 after 4 months: chorioretinal scar tissue with a small focus of residual inflammation.
