Toxoplasmosis in patients with AIDS differs from toxoplasmosis in immunocompetent patients. In general, the lesions are larger in people with AIDS, and up to 40% of cases have bilateral disease. Solitary or multifocal patterns of retinitis have been observed (Fig 15-3). A vitreous inflammatory reaction usually appears overlying the area of active retinochoroiditis, but the degree of vitreous reaction may be less than that observed in immunocompetent patients (see also Chapter 11).
Figure 15-3 Toxoplasmic retinochoroditis. A, Fundus photograph showing a large area of macular toxoplasmic retinochoroiditis in a patient infected with human immunodeficiency virus (HIV). B, Fundus photograph of multifocal toxoplasmic retinochoroiditis in another HIV-infected patient.
(Courtesy of Emmett T. Cunningham Jr, MD.)
The diagnosis of ocular toxoplasmosis may also be more difficult in patients with AIDS. Ocular toxoplasmosis may result from newly acquired T gondii infection or from reactivation of chronic infection within the retina and even in nonocular sites. Preexisting retinochoroidal scars may be absent. Newly acquired T gondii infections or dissemination from nonocular sites are the most likely causes among patients with AIDS, although reactivation of quiescent toxoplasmosis also occurs. Ocular toxoplasmosis in patients with AIDS may be difficult to distinguish from acute retinal necrosis, necrotizing herpetic retinitis, or syphilitic retinitis. Definitive diagnosis may require aqueous and vitreous samples for culture and polymerase chain reaction techniques.
In general, the inflammatory reaction in the choroid, retina, and vitreous is less prominent than in patients with an intact immune system. Trophozoites and cysts can be observed in greater numbers within areas of retinitis, and T gondii organisms can occasionally be noted invading the choroid, a finding not present in immunocompetent patients.
The prompt diagnosis of ocular toxoplasmosis is especially important in patients who are immunocompromised because the condition inevitably progresses if left untreated, in contrast to the self-limiting disease in immunocompetent patients. In addition, ocular toxoplasmosis in immunocompromised patients may be associated with cerebral or disseminated toxoplasmosis, an important cause of morbidity and mortality in patients with AIDS. For HIV-infected patients with active ocular toxoplasmosis, computer-assisted tomography (CT) and/or magnetic resonance imaging (MRI) of the head and consultation with specialists in infectious diseases should be pursued to rule out central nervous system (CNS) involvement.
Antitoxoplasmic therapy with synergic combination of pyrimethamine, sulfadiazine, sulfamethoxazole and trimethoprim, azithromycin, atovaquone, and/or clindamycin is required. Corticosteroids should be used with caution and only in the presence of appropriate antimicrobial cover because of the risk of further immunosuppression in this population. In selecting the therapeutic regimen, the physician should consider the possibility of coexisting cerebral or disseminated toxoplasmosis as well as the toxic effects of pyrimethamine and sulfadiazine on bone marrow. Continued maintenance therapy may be necessary for patients with poor immune status that is not improving.
Moshfeghi DM, Dodds EM, Couto CA, et al. Diagnostic approaches to severe, atypical toxoplasmosis mimicking acute retinal necrosis. Ophthalmology. 2004;111(4):716–725.
Excerpted from BCSC 2020-2021 series: Section 9 - Uveitis and Ocular Inflammation. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.