This is typically granulomatous though the nongranulomatous form has also been described. Granulomatous uveitis is identified by presence of mutton-fat keratic precipitates and iris nodules (Koeppe and Busacca) and may be associated with broad posterior synechiae (Fig. 15.1).

TB can account for nearly half the cases of intermediate uveitis in high-endemic countries [10]. It presents as chronic, low-grade inflammation associated with vitritis, and ‘snowballs’ in vitreous cavity. ‘Snow-banking’ is less commonly seen. Long-standing disease may lead to cystoid macular edema, complicated cataract, elevated intraocular pressure, epiretinal membrane, and peripheral retinal neovascularization.

The most common manifestations of tubercular posterior uveitis in ophthalmic practice are retinal vasculitis and multifocal serpiginoid choroiditis. Different manifestations of posterior uveitis may co-exist in the same or opposite eye (Fig. 15.2). The posterior uveitis can be accompanied by generalized intraocular inflammation (panuveitis), anterior, and intermediate uveitis.

Theses may range from papillitis and neuroretinitis to optic nerve granuloma [14]. They are usually associated with some form of uveitis. Most cases recover well after appropriate therapy.

These present acutely with hypopyon and dense vitritis. Subretinal or choroidal abscess can be present that may burst into the vitreous cavity. Unlike the previously mentioned clinical manifestations, acid-fast bacilli may be demonstrated in aqueous or vitreous samples in such cases.

The pathogenesis of ocular TB in the form of intraocular inflammation/uveitis has long been debated. The identification of M. tuberculosis in enucleated eyes and amplification of mycobacterial DNA from ocular fluid samples suggest that this condition results from an inflammatory response to the bacteria in ocular tissues [15, 16]. Animal models have shown that mycobacteria are disseminated to the eye from pulmonary foci, as in other cases of extrapulmonary TB [17]. It has been suggested that mycobacteria remain sequestered in the RPE in a dormant form for long periods and on their activation they lead to recurrent inflammation [18]. Most recently, it has been shown that RPE cells are better able to control growth of M. tuberculosis than macrophages, which helps them survive longer in the presence of infection [19].

However, ocular TB is also paucibacillary, as noted in a large series of 42 patients with histopathologically proven ocular TB [20]. Thus the organism is rarely found in ocular tissues. This has led many authors to believe that ocular TB results from immune reaction to tubercular antigens released from extraocular foci. Such a phenomenon is not seen in any other form of TB and has not been validated for ocular TB.

Although ocular TB is a clinical diagnosis in the majority of patients, imaging studies can be helpful in assessing disease activity, and evaluating associated complications of intraocular inflammation.