56.1 Features
Mycobacterium tuberculosis (MTB) infects one-third of the world’s population. In the United States, the overall case rate of active TB is rare. Foreign-born persons constitute approximately two-thirds of those cases and as a group had 13 times higher incidence rate than those born in the United States (15.6 vs. 1.2 per 100,000 persons). Human immunodeficiency virus (HIV) positive patients are also at high risk of developing active disease.
The reported prevalence of intraocular tuberculosis (IOTB) varies from 1% in patients with pulmonary TB to over 20% in those with extrapulmonary infection. IOTB accounts for 0.5% of uveitis cases without a known active systemic disease. There are two possible pathophysiological mechanisms: active mycobacterial infection (hematogenous spread of TB into local ocular tissues [choroidal granuloma] or direct exogenous infection of TB into local ocular tissues [conjunctivitis/scleritis/keratitis]) and immunological response without local replication of the infectious agent causing delayed hypersensitivity reaction to TB situated elsewhere in the body (e.g., conjunctival phlyctenule/Eales disease).
56.1.1 Common Symptoms
Systemic
Mostly asymptomatic; cough (sometimes blood-tinged), weight loss, night sweats, and fever when symptoms present.
Ocular
Most commonly blurred vision and light sensitivity.
56.1.2 Exam Findings
Anterior Segment Findings
Broad posterior synechiae, necrotizing and non-necrotizing diffuse or nodular scleritis, episcleritis, and peripheral ulcerative keratitis. Other rare forms can include interstitial keratitis, phlyctenulosis, iris or ciliary body granulomas, and dacryoadenitis.
Posterior Segment Findings
Posterior uveitis is the most common presentation; may manifest as choroidal tubercles, occlusive retinal vasculitis (affecting venous structures, includes chorioretinal inflammation adjacent to the involved vessels), serpiginous-like choroiditis or multifocal serpiginoid choroiditis (MSC), choroidal or optic disc granuloma(s), and optic neuropathy (papillitis, neuroretinitis, and retrobulbar optic neuropathy) (▶ Fig. 56.1).
Fig. 56.1 (a) Fundus photograph demonstrating a temporal midperipheral fibrovascular proliferation along with sclerosed blood vessels. (b) Fluorescein angiography shows the area of capillary nonperfusion and hyperfluorescence from the leaking neovascularization. (Courtesy of J. Fernando Arevalo, MD.)
Retinal Perivasculitis and Multifocal Serpiginoid Choroiditis
Strongly suggestive of ocular tuberculosis.
Choroidal Tuberculomas
Identified in the context of systemic TB (pulmonary/extrapulmonary). Choroidal granulomas may be unifocal or multifocal; typically, white-, cream-, or yellow-colored and may be associated with an exudative retinal detachment.
56.2 Key Diagnostic Tests and Findings
56.2.1 Optical Coherence Tomography
TB choroidal granulomas present as a localized area of adhesion between the retinal pigment epithelium (RPE)–choriocapillaris layer and the overlying neurosensory retina (“contact sign”), surrounded by an area of exudative retinal detachment. Anterior segment optical coherence tomography of anterior lesions reveals a poorly demarcated amorphous lesion in the iridocorneal angle, corneal edema, narrowing and synechiae of the iridocorneal angle, anterior chamber exudates, and cells in presumed ocular TB. Active areas reveal irregular disruption of the outer retinal hyper-reflective bands associated with both the photoreceptors and RPE, as well as pronounced thickening of the underlying choroid. Granularity of the outer photoreceptor layer and proliferating RPE cells indicate the chronicity of the underlying choroidal pathology in cases of TB choroidal granulomas. Inactive areas show atrophy of the outer retina and underlying choroid.
56.2.2 Fluorescein Angiography or Ultra-Widefield Fluorescein Angiography
Active choroidal granulomas exhibit early hypofluorescence and late hyperfluorescence (▶ Fig. 56.2a,c). Inactive healed tubercles show transmission hyperfluorescence (▶ Fig. 56.2b,d). Large choroidal granulomas may show early hyperfluorescence with a dilated capillary bed, progressive increase in hyperfluorescence, and late pooling of dye in the subretinal space. Serpiginous-like choroiditis shows an initial hypofluorescent active edge with late hyperfluorescence and diffuse staining of the active advancing edge. Active retinal vasculitis shows focal or diffuse staining and leakage from the retinal vasculature, mainly from the veins, and optic disc hyperfluorescence (associated with focal or diffuse capillary leakage), and also identifies the extent of areas of capillary nonperfusion, as well as retinal (border of inactive lesion) and/or optic disc neovascularization. Papillitis and neuroretinitis show early optic disc hyperfluorescence with leakage in the late frames. Fluorescein angiography is also useful in identifying cystoid macular edema characterized by progressive leakage and accumulation of dye in cystic spaces surrounding the fovea with a characteristic “petaloid pattern.” Ultra-widefield fluorescein angiography identifies the entire extent of choroidal lesions, areas of retinal capillary nonperfusion, peripheral neovascularization, and detection of disease activity (Fig. 56.1a,b).
Fig. 56.2 Ocular tuberculosis. (a) Fundus color photograph demonstrating active white/yellowish lesion underneath temporal vessels. (b) Same eye with healed lesion, pigmentary changes around and radial folds involving the fovea. (c) Fluorescein angiography (FA) shows hypofluorescence corresponding to the active lesion. (d) FA demonstrates hyperfluorescence around the healed lesion.
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