T. gondii is one of the most common causes of infectious posterior uveitis.
Ocular toxoplasmosis results from chorioretinal infection by Toxoplasma gondii (T. gondii). It is the most common cause of infectious posterior uveitis in areas of the United States where the parasite is endemic and typically appears as a unilateral chorioretinal lesion paired with vitritis.
Diagnosis of the infection can occasionally be challenging due to uncommon findings, particularly in immunocompromised patients. Confirmation of the diagnosis often depends on the detection of antibodies in serum or samples of intraocular fluid. However, as the polymerase chain reaction (PCR) technique becomes more sensitive and widely available, diagnosis is increasingly being confirmed by directly identifying parasite DNA in samples of aqueous humor or vitreous fluid.
These and other developments in the diagnosis of ocular toxoplasmosis were covered in a recent literature review by Cem Ozgonul, MD, and Cagri Giray Besirli, MD, PhD, of the Department of Ophthalmology and Visual Sciences at the University of Michigan Medical School.
In their article, the reviewers noted that ocular toxoplasmosis was long assumed to be acquired congenitally. However, recent research indicates that the infection is acquired most frequently in adulthood through contact with cat feces or contaminated food or water.
The parasite produces its eggs only in the intestines of cats through sexual reproduction. After an infected cat defecates, these eggs form spores that spread, sporulate, and become infectious within 5 days. They then assume a crescent form that can enter a cell and multiply until the cell is filled with so many parasites that it bursts. The parasite then enters a new host cell and the cycle repeats.
As the host mounts a defense, the parasite enters a dormant phase during which it concentrates in cysts, which are responsible for chronic infection.
Most patients who first seek treatment of uveitis owing to ocular toxoplasmosis do so between the ages of 20 and 40 years, and the disease is usually more severe in older patients. In most cases, the disease recurs, and the time between recurrences shortens as the disease progresses.
The classical sign of ocular toxoplasmosis is a nidus of fluffy, white, focal necrotizing retinitis or retinochoroiditis next to a variably pigmented chorioretinal scar. Moreover, the active lesion is often surrounded by severe vitritis, which results in the classic “headlight in the fog” sign.
In addition, inflammation in the anterior segment may be granulomatous or nongranulomatous and minimal or severe enough to mask inflammation of the posterior segment.
Other common clinical features of ocular toxoplasmosis include:
Chronic eye infection with T. gondii may produce permanent vision loss from macular scarring or optic atrophy. Toxoplasmosis-related scarring close to the optic disk may even result in severe visual field loss and loss of color vision. Lesions near the peripheral retina often cause vision loss from severe vitreous inflammation.
Less severe vision loss (ie, 20/200 vision or less) may develop in at least one eye in as many as one-quarter of chronically infected patients. Active lesions often lead to symptoms of vitreous inflammation and blurry vision, and during the parasite’s inactive stage, retinochoroidal scars may result in scotomas.
In most immunocompetent patients, chorioretinitis related to T. gondii infection resolves spontaneously in a month or two. However, treatment to decrease the risk of vision loss is recommended when lesions appear in the vascular arcades or next to the optic disk, or when lesions are larger than two optic disk diameters. In immunocompromised patients, immediate treatment is recommended regardless of lesion size or location.
Effective treatment includes oral pyrimethamine and sulfadiazine. Each drug acts at different stages in T. gondii’s life cycle to impede its nucleic acid synthesis. Systemic corticosteroids are typically added, so this combination is known as triple drug therapy.
In a key clinical trial, triple drug therapy reduced the size of retinal lesions more than other treatments. Azithromycin may be substituted for sulfadiazine to reduce the frequency and severity of adverse effects while maintaining efficacy.
Trimethoprim-sulfamethoxazole is also effective and results in better compliance, quicker resolution of chorioretinitis, and better visual acuity. Moreover, it may be used to prevent recurrences, particularly in patients with scars next to the fovea.
In another key trial, intravitreal clindamycin plus dexamethasone produced equivalent results to triple drug therapy plus folinic acid but with fewer follow-up visits. Intravitreal therapy also has a better side effect profile and is particularly useful for treating pregnant women. Nevertheless, systemic treatment is recommended for immunocompromised patients to prevent complications in the fellow eye or central nervous system.
Corticosteroid treatment is contraindicated in immunocompromised patients without the normal inflammatory response to T. gondii. However, most clinicians begin giving corticosteroids to immunocompetent patients within one to three days after starting antiparasitics.
The systemic corticosteroid of choice is prednisone, given at a dosage of 0.5—1.0 mg/kg/day. Nevertheless, most ophthalmologists would rather use topical steroids, whose main indications are ocular pain, redness, photophobia, moderate or worse anterior chamber inflammation, and elevated intraocular pressure.
The review, “Recent developments in the diagnosis and treatment of ocular toxoplasmosis,” appears in the January 2017 issue of Ophthalmic Research.