Ocular involvement caused by tuberculosis (TB) is uncommon in the United States. In the last 6 decades, the TB incidence rate in the United States has decreased from 52.6 cases per 100,000 persons in 1953 to 2.9 cases per 100,000 in 2016. Worldwide, however, TB remains an important systemic infectious disease, with more than 10.4 million new cases and 1.7 million deaths reported annually. Nearly one-third of the world’s population is infected, and 95% of cases occur in resource-limited countries.
In the United States, important risk factors include ethnicity and country of birth, with increased prevalence among Asians, African Americans, and Hispanics, when compared to non-Hispanic whites. Diabetes mellitus and coninfection with HIV have also emerged as risk factors, in addition to substance abuse or residence in congregate settings, including correctional facilities, military barracks, homeless shelters, refugee camps, dormitories, and nursing homes, among others. Although the frequency of ocular disease parallels the prevalence of TB in general, it remains relatively uncommon both in endemic areas and among institutionalized populations with unequivocal systemic disease. In the United States, the incidence of uveitis attributable to TB at a large tertiary care facility was 0.6%, whereas at major referral centers in India, it ranged from 0.6% to 10%. In similar institutions in Japan and Saudi Arabia, the incidence was 7.9% and 10.5%, respectively.
Mycobacterium tuberculosis is an acid-fast–staining, obligate aerobe most commonly transmitted by aerosolized droplets. The organism has an affinity for highly oxygenated tissues. Tuberculous lesions are commonly found in the apices of the lungs as well as in the choroid, which has the highest blood flow rate in the body. Systemic infection may occur primarily, due to recent exposure; in 90% of patients, however, it occurs secondarily from reactivation of the disease with immune compromise. Widespread hematogenous dissemination of TB, known as miliary disease, likewise occurs most often in immunocompromised persons.
Pulmonary TB develops in approximately 80% of patients, whereas extrapulmonary disease occurs in about 20%, with one-half of these patients having a normal-appearing chest radiograph and up to 20% having a negative result on the purified protein derivative (PPD) skin test. Patients coinfected with HIV present more often with extrapulmonary disease, the frequency of which increases with deteriorating immune function. Only 10% of infected individuals develop symptomatic disease; one-half of these manifest illness within the first 1–2 years. Most, however, remain infected but asymptomatic. The classic presentation of symptomatic disease—fever, night sweats, and weight loss—occurs in both pulmonary and extrapulmonary infection. This fact is important to keep in mind when conducting a review of systems in patients suspected of tuberculous uveitis because histologically proven intraocular TB has been found in asymptomatic patients as well as in patients with extrapulmonary disease.
Centers for Disease Control and Prevention. Reported Tuberculosis in the United States 2016. Atlanta: US Department of Health and Human Services; 2017. Available at www.cdc.gov/tb/statistics/reports/2016/pdfs/2016_Surveillance_FullReport.pdf. Accessed September 12, 2018.
Yeh S, Sen HN, Colyer M, Zapor M, Wroblewski K. Update on ocular tuberculosis. Curr Opin Ophthalmol. 2012;23(6):551–556.
The ocular manifestations of TB may result from either active infection or an immunologic reaction to the organism. External ocular and anterior segment findings include scleritis, phlyctenulosis, interstitial keratitis, corneal infiltrates, anterior chamber and iris nodules, and isolated granulomatous anterior uveitis (Fig 10-9); the last is exceedingly uncommon in the absence of posterior segment disease.
Tuberculous uveitis is classically a chronic granulomatous disease that may affect the anterior and/or posterior segments. It may be replete with mutton-fat keratic precipitates, iris nodules, posterior synechiae, and secondary glaucoma, although nongranulomatous uveitis may also occur. Patients typically experience a waxing and waning course, with accumulation of vitreous opacities and macular edema (Fig 10-10).
Figure 10-9 Severe fibrinous inflammation and large iris nodules in a patient with ocular tuberculosis. Polymerase chain reaction testing was positive from aqueous.
(Courtesy of H. Nida Sen, MD, National Eye Institute.)
Figure 10-10 Chronic tuberculous uveitis. A, Fluorescein angiogram of chronic tuberculous uveitis with disc edema, periphlebitis, and macular edema. B, Spectral-domain optical coherence tomography confirms macular edema.
(Courtesy of Daniel V. Vasconcelos-Santos, MD, PhD.)
Disseminated choroiditis is the most common presentation and is characterized by multiple deep, discrete, yellowish lesions between 0.5 mm and 3.0 mm in diameter and numbering from 5 to several hundred (Fig 10-11). These lesions, or tubercles, are located predominantly in the posterior pole and may be accompanied by disc edema, nerve fiber layer hemorrhages, and varying degrees of vitritis and granulomatous anterior uveitis. Alternatively, they may present as a single, focal, large, elevated choroidal mass (tuberculoma) that varies in size from 4 mm to 14 mm and may be accompanied by neurosensory retinal detachment and macular star formation (Fig 10-12). Choroidal tubercles may be one of the earliest signs of disseminated disease and are more commonly observed among immunocompromised hosts. On FA, active choroidal lesions display early hypo-hyperfluorescence with late leakage, and cicatricial lesions show early blocked fluorescence with late staining. ICG angiography reveals early- and late-stage hypofluorescence corresponding to the choroidal lesions, which are frequently more numerous than those seen on FA or clinical examination (see Fig 10-12). Other manifestations include multifocal choroiditis, frequently with a serpiginoid patter (multifocal serpiginoid choroiditis, also called serpiginous-like choroiditis; Fig 10-13). In patients with HIV/AIDS, tuberculous choroiditis may progress despite effective antituberculous therapy.
Figure 10-11 Tubercular multifocal choroiditis with serous retinal detachment. Fundus photography shows multiple pockets of subretinal fluid overlying choroidal tubercles (top left). Fluorescein angiography reveals multifocal leakage (top middle), and indocyanine green angiography delineates hypocyanescence (top right), presumably corresponding to areas of choroidal inflammatory infiltration. Choroidal nodules (tubercles) are revealed by spectral-domain optical coherence tomography (bottom).
(Courtesy of Daniel V. Vasconcelos-Santos, MD, PhD.)
Figure 10-12 Fundus photograph of a choroidal tubercle with a macular star formation (tuberculoma).
Figure 10-13 Fundus photograph showing tuberculous choroiditis masquerading as atypical serpiginous-like choroiditis. The patient showed progression and recurrence while receiving immunomodulatory drugs; however, after antituberculous treatment was begun, the patient showed improvement in vision and resolution of the vitritis without recurrences.
(Courtesy of Narsing A. Rao, MD.)
Retinal involvement in TB is usually secondary to extension of the choroidal disease or an immunologic response to mycobacteria and should be differentiated from Eales disease, a peripheral retinal perivasculitis that presents in otherwise healthy young men aged 20–40 years with recurrent, unilateral retinal and vitreous hemorrhage and subsequent involvement of the fellow eye. The disease may be associated, at least in part, to some degree of tuberculin hypersensitivity. Interestingly a few studies employing PCR-based assays have detected M tuberculosis DNA from aqueous, vitreous, and epiretinal membranes of some patients with Eales disease. Periphlebitis is commonly observed in this setting, and may be accompanied by venous occlusion, peripheral nonperfusion, neovascularization (Fig 10-14), and eventual development of tractional retinal detachment in some cases (see also BCSC Section 12, Retina and Vitreous, for additional discussion of Eales disease). Other posterior segment findings of TB include subretinal abscess, CNV, optic neuritis, and panophthalmitis.
Figure 10-14 Eales disease. A, Wide-angle fundus photograph of Eales disease. B, Angiographic image shows peripheral retinal nonperfusion and neovascularization (temporally), in addition to perivenular hyperfluorescence (periphlebitis).
(Courtesy of Emilio Dodds, MD.)
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.