Ocular toxoplasmosis is a disease that affects the eye, caused by the microscopic parasite Toxoplasma gondii. This condition represents the most common infectious cause of posterior uveitis, which is inflammation affecting the back segment of the eye. The infection leads to inflammation and destruction of retinal tissue, which can result in scarring and permanent vision changes. While the initial infection with the parasite is often unnoticed, the eye disease typically manifests years later due to the parasite reactivating within the eye.
Understanding the Cause and Transmission
Ocular toxoplasmosis is caused by the parasite Toxoplasma gondii, which infects most warm-blooded animals, including humans. Cats are the definitive hosts for this parasite, meaning it reproduces in their intestines and is shed in their feces as oocysts. Humans primarily become infected through three main routes: consuming undercooked meat containing tissue cysts, ingesting oocysts from contaminated sources like soil or unwashed produce, or through congenital transmission.
Once ingested, the parasite travels through the body and forms dormant tissue cysts, particularly in muscle and neural tissue. Ocular disease usually results from the reactivation of these cysts years after initial infection, though it can also follow a recently acquired infection. In the eye, the parasite enters the posterior segment, typically through the retinal circulation, where it begins to proliferate in the retinal cells.
Congenital transmission occurs when a pregnant mother becomes newly infected, passing the active parasite form to the fetus across the placenta. This route carries a high risk of developing severe complications, with retinochoroiditis being the most frequent manifestation in children. While historically thought to be primarily a congenital disease, many cases are now recognized as resulting from acquired infection later in life.
Identifying Ocular Toxoplasmosis
The symptoms of an active ocular toxoplasmosis infection are directly related to the inflammation and damage occurring in the retina. Patients commonly report a sudden decrease or blurring of vision, along with increased floaters. Other frequent complaints include eye pain, redness, and increased sensitivity to light.
An eye examination by an ophthalmologist, using fundoscopy, is typically sufficient for diagnosis. The defining sign is a focal, whitish, elevated lesion on the retina, which represents active inflammation and necrosis of the tissue. This active lesion is often seen next to an old, pigmented, inactive scar, a finding considered characteristic for the disease. Intense inflammation in the vitreous humor can obscure the view of the retina, creating an appearance described as a “headlight in the fog.”
While the clinical appearance is often diagnostic, blood tests (serology) may be used to confirm prior exposure to Toxoplasma gondii. The presence of antibodies confirms prior infection, but does not confirm active eye disease. A negative antibody test generally helps rule out the diagnosis. In atypical or complicated cases, specialized laboratory tests on fluid samples from the eye may be performed to detect the parasite’s DNA.
Medical Management of Eye Infection
Treatment is generally reserved for active lesions that threaten the macula or the optic nerve. For most immunocompetent individuals, the infection is often self-limiting and may resolve spontaneously within two months, but treatment is given to minimize the risk of permanent vision loss. The standard duration of therapy is typically four to six weeks, requiring close monitoring by a specialist.
The classic approach involves a combination of antiparasitic and anti-inflammatory medications, often termed “triple therapy.” This regimen combines pyrimethamine and sulfadiazine, which work together to target the active form of the parasite. Pyrimethamine is a folic acid antagonist and must be given alongside folinic acid to mitigate potential hematologic side effects.
Systemic corticosteroids are added to manage the destructive inflammation caused by the immune response in the retina. Corticosteroids are started one to three days after the antiparasitic drugs to prevent a temporary worsening of the infection. An alternative and widely used regimen is the combination antibiotic trimethoprim/sulfamethoxazole, which is often favored due to its convenience and lower risk of certain side effects.
For patients who cannot tolerate systemic medication, or in cases of severe localized infection, treatment may involve an intravitreal injection of drugs directly into the eye. This local therapy often combines the antiparasitic drug clindamycin with a corticosteroid like dexamethasone, offering high concentrations at the infection site while avoiding systemic side effects. Healing lesions are not typically treated with medication, as the goal is to manage the active inflammation and parasite proliferation.
Reducing Risk and Preventing Recurrence
Preventing initial infection centers on practicing good food and environmental hygiene. Thoroughly cooking meat and washing fruits and vegetables before consumption removes potential oocyst contamination. Since the parasite is shed in cat feces, avoiding contact with a cat’s litter box, or wearing gloves and disposing of the waste daily, is a key preventive measure.
For patients with a history of ocular toxoplasmosis, the focus shifts to preventing recurrence, which is common and can lead to progressive vision loss. Reactivation often occurs years later, especially in individuals with weakened immune systems. Long-term prophylactic treatment with an antibiotic like trimethoprim/sulfamethoxazole may be recommended for patients with frequent flares or lesions near the central vision.
This preventive regimen is often administered intermittently, such as three times a week, and may continue for a year or longer. Patients with a history of the disease should maintain regular follow-up appointments with their eye care specialist to monitor for any signs of reactivation. Early detection and treatment of a recurrent lesion significantly improves the visual outcome and limits further retinal scarring.