What the Cat Dragged In?

Strange Things Seen in Practice

Sina Rezaei, BS; Rizwan Shaikh, MD; Christina Y. Weng, MD, MBA

Disclosures

April 23, 2019

Felines: The Hosts With the Most

T gondii, the most common cause of posterior uveitis in immunocompetent individuals, is a prevalent protozoan intracellular infection that affects 25%-30% of humans.[1] In approximately two thirds of those affected, it represents a reactivation of a prior infection.[2] Felines are the definitive hosts and can contaminate drinking water and soil with the parasite through their feces. The parasite can also infect humans through the consumption of undercooked meat and can even spread between humans transplacentally or via organ transplantation.[1] These indirect means of infection may cause ocular toxoplasmosis in the absence of obvious animal exposure.

In its typical presentation, ocular toxoplasmosis causes a white, focal area of chorioretinal necrosis.[3] It is usually accompanied by overlying vitritis, causing a classic "headlight in the fog" appearance. Patients experience decreased vision but can have discomfort from anterior uveitis and elevated intraocular pressure. The lesions often heal within 2-4 months, resulting in a hyperpigmented scar. Reactivation of the disease typically manifests with a new lesion adjacent to the old scar. Less commonly, T gondii may cause punctate outer retinal toxoplasmosis, neuroretinitis, or scleritis.[1]

The diagnosis of ocular toxoplasmosis can be made clinically with or without corroboration of serum T gondii IgG and IgM antibodies. The absence of IgG antibodies can help rule out infection, because they last a lifetime after exposure. IgM antibodies are associated with acute infection, but their positive predictive value for acute infection is limited by their highly variable lifespan in the blood. However, negative results can rule out acute infection.

When the diagnosis is less clear, testing the aqueous humor for T gondii DNA or anti-T gondii antibodies can be useful; however, T gondii DNA detection in the blood is inadequate for diagnosis, particularly in immunocompetent patients.[4,5] Such infections as tuberculosis, cytomegalovirus, herpes virus, and syphilis should always be considered in the differential diagnosis of a patient with suspected ocular toxoplasmosis.[5] In this case, because of the patient's history of latent tuberculosis, an interferon-gamma release assay and rapid plasma reagin test were obtained, along with T gondii IgG and IgM serology studies.

Although no consensus exists on the most effective treatment, traditional therapy for ocular toxoplasmosis consists of systemic pyrimethamine, sulfadiazine, folinic acid, and corticosteroids.[6] Oral azithromycin and clindamycin have been effective in patients with sulfa drug allergies, whereas trimethoprim-sulfamethoxazole and intravitreal clindamycin have been shown to be equivalent to classic therapy.[7,8,9] Adjunct corticosteroid therapy is generally initiated within a few days of antibiotic therapy; however, its use in the absence of antimicrobials increases the risk for retinal damage and should be avoided.[1,10]

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