They can be unilateral or bilateral, up to five in number although there may be as many as 50–60 in the same eye. They usually range from 0.5 to 3 mm in diameter and may be associated with an overlying serous retinal detachment. These tubercles heal within 12–14 weeks and leave behind pale atrophic areas with variable pigmentation. Active choroidal tubercles usually respond well to antitubercular treatment (ATT).

These tuberculomas may be located anywhere in the choroid, in the macula, the posterior pole, the equator, or in a juxtapapillary location. The tuberculomas generally present as a large solitary mass and may mimic a tumor. Hemorrhages and retinal folds may be seen on the tuberculoma surface, and in later stages, the overlying retina may detach. The tuberculoma may measure up to 14 mm in diameter. They may give the classical “ring of fire” appearance in fundus fluorescein angiogram. Large tuberculomas may present as yellowish subretinal mass lesions accompanied by exudative retinal detachment that shows good resolution with antitubercular treatment and steroids.

Multiplication of the bacilli in the caseous material of the granulomas can lead to liquefaction necrosis and abscess formation. Patients with disseminated tuberculosis may present with subretinal abscess with little overlying vitreous inflammation [21]. These necrotizing granulomas may be seen in isolation in the eye, with no evidence of tuberculosis in any other part of the body [22]. These abscesses are more yellowish in color indicating liquefaction necrosis and overlying retinal hemorrhages. These lesions usually heal with antitubercular therapy and healed lesions may show pigmentation and atrophy with chances of good visual recovery [7]. It may be seen in both immunocompetent and immunocompromised patients. Although uncommon, these may rupture into the vitreous cavity, resulting in the development of endophthalmitis/panophthalmitis leading to removal of the eye.

Serpiginous-like choroiditis is a rare, usually bilateral, chronic, progressive, recurrent inflammation of the retinal pigment epithelium, choriocapillaris, and choroid of unknown etiology. The earliest description of the condition, known as “peripapillary retinochoroiditis,” was coined in 1932 by Junius. Laatikainen and Erkkila were the first to describe the association of serpiginous choroiditis with TB [23]. Presumed tubercular serpiginous-like choroiditis has been classified into three morphologic variants (Fig. 15.2): multifocal choroiditis progressing to diffuse lesions resembling serpiginous choroiditis, diffuse choroiditis resembling serpiginous at initial presentation, and mixed variants in which opposite eyes had features of multifocal and diffuse lesions [24]. Although the precise cause of serpiginous choroiditis is thought to arise on an autoimmune basis and treatment classically mandates multiple systemic immunosuppressive medications or alkylating agents in some cases [25], presumed tubercular serpiginous-like choroiditis requires an anti-TB strategy sometimes in combination with corticosteroids (Fig. 15.3). Therefore, distinction between these two entities, which may be quite similar in appearance, is of paramount importance. Clinical features that may help to clinically distinguish tubercular serpiginous-like choroidopathy from serpiginous choroidopathy include the country of origin of the patient (i.e., patients from areas where TB is endemic), significant vitritis, and the presence of multifocal lesions in the posterior pole and periphery or juxtapapillary lesions sparing the periphery in serpiginous. The lesions appear as gray-white to yellow with ill-defined edges, classically begin in a peripapillary location, and spread centrifugally with multiple recurrences. The fluorescein angiographic appearance is distinctive, with the acute lesions showing early hypofluorescence and progressive late staining [26, 27].

Tubercular vasculitis presents with vitreous infiltrates (vitritis), retinal hemorrhages, neovascularization, and neuroretinitis. The presenting features are often similar to another common vasculitis, Eales’ disease, which by definition is idiopathic in nature and presents with recurrent vitreous hemorrhage in young patients. The eye usually does not show other signs of intraocular inflammation, for instance, the active or healed patches of focal choroiditis which are seen in patients with tubercular retinal vasculitis. Both diseases share the extensive capillary closure which may require laser photocoagulation. Tubercular vasculitis responds well to a combination of ATT and oral corticosteroids [28, 29].

Ocular TB can present as acute-onset endogenous endophthalmitis, due to rapidly progressive disease, which does not respond to ATT. This may occur due to rapid multiplication of bacilli or in patients who receive corticosteroid therapy without concomitant antitubercular drugs.