Toxoplasmic retinochoroiditis is the most common cause of posterior segment infection worldwide. The causative organism, Toxoplasma gondii, is an obligate, intracellular parasitic protozoan. Because seropositivity for T gondii is very common, seropositivity alone does not confirm that uveitis is related to toxoplasmosis. Congenital disease occurs via acquisition of the organism by a pregnant woman exposed to tissue cysts or oocytes in uncooked meat or substances contaminated with cat feces (see also BCSC Section 6, Pediatric Ophthalmology and Strabismus, Chapter 28). The typical ocular finding in congenital toxoplasmosis is a chorioretinal scar, usually in the macula and often bilateral. Most cases of toxoplasmosis are currently assumed to be acquired postnatally, although proving this assumption can be difficult. A positive serologic test result for immunoglobulin M (IgM) anti–T gondii antibodies supports the diagnosis of an acquired disease.
Decreased vision and floaters are the most common presenting symptoms of toxoplasmic retinochoroiditis. Clinically, the disorder consists of a focal area of intense, necrotizing retinochoroiditis, typically with moderate to severe overlying vitreous inflammation (Fig 11-22). Recurring disease is indicated by an adjacent or nearby retinochoroidal scar. Multiple active lesions are rare and should prompt HIV testing. HIV-seropositive patients with ocular toxoplasmosis have a high risk of CNS involvement and therefore should undergo magnetic resonance imaging with contrast. Elderly patients may present with more aggressive disease due to their relative immunosuppression.
Active ocular toxoplasmosis is commonly treated with antibiotics, despite the lack of well-designed randomized controlled trials. The simplest approach is treatment with trimethoprim-sulfamethoxazole. Classic therapy uses sulfadiazine with pyrimethamine and prednisone (prescribed with folinic acid and accompanied by regular monitoring of blood cell counts); the addition of clindamycin results in so-called quadruple therapy. None of these approaches has been shown to be superior to another with regard to final vision outcome, lesion size, or recurrence rate. Treatment typically lasts 4–6 weeks, and complete healing of active lesions occurs over 4–6 months. When used, systemic corticosteroids should be given under antibiotic cover. Use of long-acting, depot periocular or intraocular corticosteroid injections should be avoided. Long-term, maintenance treatment with trimethoprim-sulfamethoxazole has been used to decrease the attack rate in patients experiencing frequent recurrences or in severely immunosuppressed patients. Intravitreal clindamycin with or without dexamethasone has been used to treat vision-threatening lesions or for patients who are intolerant of or fail to respond to systemic therapy.
Figure 11-22 Toxoplasmic retinochoroiditis. A, Color fundus photograph montage of a patient with recurring toxoplasmic retinochoroiditis. B, Color fundus photograph shows white focal retinitis (white arrow) with overlying vitreous inflammation, which creates a “headlight in the fog” appearance, with an adjacent pigmented retinochoroidal scar. There is accompanying perivasculitis and nonspecific exudates, in addition to distinct lobular periarteriolar collections of cells (black arrow) called Kyrieleis plaques.
(Courtesy of Stephen J. Kim, MD.)
Holland GN. Ocular toxoplasmosis: a global reassessment. Part I: epidemiology and course of disease. Am J Ophthalmol. 2003;136(6):973–988.
Holland GN. Ocular toxoplasmosis: a global reassessment. Part II: disease manifestations and management. Am J Ophthalmol. 2004;137(1):1–17.
Kim SJ, Scott IU, Brown GC, Brown MM, Ho AC, Ip MS, Recchia FM. Interventions for toxoplasma retinochoroiditis: a report by the American Academy of Ophthalmology. Ophthalmology. 2013;120(2):371–378.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.