Infectious Posterior Uveitis & Choroiditis

Overview

Infectious causes account for a substantial share of posterior uveitis worldwide, and the differential is unusually organism-diverse: parasites, viruses, bacteria, and spirochetes can all produce chorioretinal inflammation that looks superficially similar on a first glance at the fundus. Getting the diagnosis right matters because the treatments don't overlap — an antiviral does nothing for a spirochete, and a corticosteroid given before antimicrobial coverage is established can make several of these substantially worse.

The most useful discriminators tend to be the same three questions in every case: what is the patient's immune status (a healthy host vs. AIDS with a low CD4 count vs. a transplant recipient), what does the lesion actually look like (a fresh white infiltrate vs. an old pigmented scar vs. a geographic pattern), and is there a relevant exposure or travel history (soil, ticks, blackflies, cats, a specific region). The entities below are grouped roughly by how often they appear on differentials and how distinctive their classic findings are.

Toxoplasma Retinochoroiditis

Toxoplasma gondii is the leading cause of infectious posterior uveitis globally. Infection can be acquired postnatally, but a large share of cases trace back to congenital toxoplasmosis, acquired when a mother has a primary infection during pregnancy and the parasite crosses the placenta to infect the fetus — this can lie dormant and re-present as chorioretinitis years or decades later in childhood or adulthood.

A healed lesion appears as a well-circumscribed, pigmented, atrophic chorioretinal scar, often with central pigment clumping and satellite lesions from earlier episodes of reactivation. Reactivation itself has a classic look: a new focus of fluffy, white, actively necrotizing retinitis appears adjacent to an old pigmented scar, with overlying vitreous inflammation that gives the hazy "headlight in the fog" appearance — one of the more recognizable descriptive terms in posterior uveitis.

Not every reactivation needs treatment. Many clinicians observe a small peripheral lesion in an immunocompetent patient when vision, the macula, and the optic nerve are spared and vitreous haze stays mild, since these typically resolve on their own within one to two months. Treatment is reserved for lesions that threaten central vision, sit near the optic disc or vascular arcades, cause heavier vitritis, or arise in an immunocompromised host. The classic regimen pairs pyrimethamine and sulfadiazine with folinic acid to offset pyrimethamine's marrow toxicity, usually with a systemic corticosteroid added once antiparasitic coverage is established rather than given on its own.

Cytomegalovirus (CMV) Retinitis

CMV retinitis is a disease of severe immunosuppression — classically HIV/AIDS patients with a CD4 count below 50 cells/µL, as well as transplant recipients on immunosuppressive therapy. It's the most common ocular opportunistic infection in advanced AIDS and the leading cause of vision loss in that population.

The fundus appearance is distinctive: dense retinal hemorrhages following the vascular arcades combined with granular, fluffy white retinal necrosis, classically described as a "pizza pie" or "cottage cheese and ketchup" appearance. Treatment is antiviral — systemic and/or intravitreal ganciclovir, valganciclovir, or foscarnet — paired with restoration of immune function whenever possible, since the antiviral alone doesn't address the underlying immunosuppression driving reactivation.

Acute Retinal Necrosis

Acute retinal necrosis (ARN) is caused by herpesviruses — most often varicella-zoster virus or herpes simplex virus — producing a rapidly progressive, peripheral necrotizing retinitis with an associated retinal vasculitis. Unlike CMV retinitis, ARN can occur in immunocompetent patients, and its rapid peripheral-to-central progression and vasculitic component make prompt treatment time-sensitive.

First-line treatment for VZV-associated ARN is intravenous acyclovir, often transitioned to an oral antiviral, to achieve therapeutic antiviral levels quickly and reduce the risk of fellow-eye involvement. Systemic corticosteroids are added only after antiviral coverage is established — adding steroids first risks accelerating unchecked viral replication.

Syphilitic Uveitis

Syphilitic uveitis is caused by the spirochete Treponema pallidum and has earned syphilis its reputation as "the great masquerader" in ophthalmology — it can mimic nearly any pattern of intraocular inflammation, anterior, posterior, or panuveitic, with no single pathognomonic appearance.

A reactive treponemal test in a patient with uveitis should prompt a lumbar puncture to evaluate for concurrent neurosyphilis via CSF-VDRL — many experts consider ocular syphilis itself a manifestation of neurosyphilis, but confirming CNS involvement matters clinically because confirmed neurosyphilis mandates the more intensive intravenous penicillin regimen rather than outpatient intramuscular therapy.

Ocular Tuberculosis

Mycobacterium tuberculosis elicits a granulomatous immune response, and ocular TB follows suit: it classically presents with mutton-fat keratic precipitates, iris nodules, and choroidal granulomas or tubercles. As with pulmonary TB, ocular involvement should prompt a workup for systemic disease rather than being treated as an isolated ocular finding.

Lyme Disease-Associated Uveitis

Lyme disease is caused by the spirochete Borrelia burgdorferi, transmitted by Ixodes ticks. Ocular involvement is variable in pattern — it can produce anterior, intermediate, or panuveitis — so a tick exposure history in an endemic region is often the strongest clue toward the diagnosis rather than any single characteristic fundus finding.

Herpetic Anterior & Posterior Uveitis

Beyond ARN, HSV and VZV also produce a distinctive anterior uveitis. Herpetic anterior uveitis classically causes trabeculitis with markedly elevated intraocular pressure during an acute flare, patchy or sectoral iris atrophy from ischemic vasculitis, and granulomatous keratic precipitates — a combination that sets it apart from most other causes of anterior uveitis, where IOP is typically normal or low.

When the clinical picture is atypical or the diagnosis uncertain, herpetic uveitis (anterior or posterior) is often confirmed by PCR testing of aqueous or vitreous fluid to detect HSV, VZV, or CMV DNA directly, rather than relying on clinical appearance alone.

Other Infectious Causes: West Nile, Cat-Scratch, HTLV-1

West Nile Virus Chorioretinitis

West Nile virus chorioretinitis classically produces multiple round-to-oval chorioretinal lesions with a target or "bull's-eye" appearance, often distributed along the retinal vascular arcades — a pattern distinct enough that it's frequently recognizable on fundus photography alone in the right epidemiologic setting.

Cat-Scratch Disease Neuroretinitis

Bartonella henselae, transmitted through cat scratches or bites, causes cat-scratch disease neuroretinitis, characterized by optic disc edema followed by a macular star — a radiating pattern of hard exudates at the macula that develops as fluid from the leaking disc tracks along the outer plexiform layer.

HTLV-1-Associated Uveitis

Human T-lymphotropic virus type 1 (HTLV-1) associated uveitis is a retroviral cause of uveitis that is particularly endemic in southwestern Japan and the Caribbean, regions with high seroprevalence of the virus — geography is often the key clue pointing toward this diagnosis.

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