IgA : Measurement of IgA antibody titers may also be useful in a diagnosis of congenital toxoplasmosis in a fetus or newborn because IgM production is often weak during this period and the presence of IgG antibodies may indicate passive transfer of maternal antibodies in utero. IgA antibodies however usually disappear by 7 months.In atypical cases, ocular fluid testing to detect parasite DNA by polymerase chain reaction or to determine intraocular production of specific antibody may be helpful for establishing etiology. Neuroimaging is warranted in AIDS patients presenting with these findings because intracranial toxoplasmic lesions have been reported in up to 29% of these patients who have toxoplasmic chorioretinitis. Prevention
Toxoplasma infection can be prevented in large part by:

cooking meat to a safe temperature (i.e., one sufficient to kill Toxoplasma)
peeling or thoroughly washing fruits and vegetables before eating
cleaning cooking surfaces and utensils after they have contacted raw meat, poultry, seafood, or unwashed fruits or vegetables
pregnant women avoiding changing cat litter or, if no one else is available to change the cat litter, using gloves, then washing hands thoroughly
not feeding raw or undercooked meat to cats to prevent acquisition of ToxoplasmaProlonged and intense rainfall periods are significantly associated with the reactivation of toxoplasmic retinochoroiditis. Changes promoted by this climatic condition concern both the parasite survival in the soil as well as a putative effect on the host immune response due to other comorbidities. Treatment
Small extramacular lesions (lesions not threatening vision) may be observed without treatment.
Toxoplasma chorioretinitis, more simply known as ocular toxoplasmosis, is possibly the most common cause of infections in the back of the eye (posterior segment) worldwide. The causitive agent is Toxoplasma gondii, and in the United States, most cases are acquired congenitally. The most common symptom is decreased visual acuity in one eye. The diagnosis is made by examination of the eye, using ophthalmoscopy. Sometimes serologic testing is used to rule out the disease, but due to high rates of false positives, serologies are not diagnostic of toxoplasmic retinitis. If vision is not compromised, treatment may not be necessary. When vision is affected or threatened, treatment consists of pyrimethamine, sulfadiazine, and folinic acid for 4–6 weeks. Prednisone is sometimes used to decrease inflammation. Signs and symptoms
A unilateral decrease in visual acuity is the most common symptom of toxoplasmic retinitis. Under ophthalmic examination, toxoplasmic chorioretinitis classically appears as a focal, white retinitis with overlying moderate inflammation of the vitreous humour. A unifocal area of acute-onset inflammation adjacent to an old chorioretinal scar is virtually pathognomonic for toxoplasmic chorioretinitis. Focal condensation of vitreous and inflammatory cells may be seen overlying the pale yellow or gray-white raised lesion in the posterior pole. Pathophysiology
Toxoplasma gondii is an intracellular parasite that causes a necrotizing chorioretinitis. Congenital disease
Congenital disease occurs due to the acquisition of the organism by a pregnant woman exposed to tissue cysts or oocytes in uncooked meat or substances contaminated with cat feces. Spontaneous abortion may result if the disease is acquired during the first trimester.