Ocular TB was described first in 1711 by Maitre-Jan (
4) and it was in 1855 that Eduard von Jaeger first detected the Choroidal tubercles (
5) which appeared to be similar microscopically to tubercles elsewhere in the body by Cohnheim in 1867 (
6). In 1882, Julius van Michel identified
tubercle bacillus in the eye (
7). Mechanisms which may cause eye infection by TB are hematogenous spread as the most common form of ocular involvement, primary exogenous infection when the involved part is conjunctiva or eye lid, direct extension, and hypersensitivity reaction which is assumed to be responsible for Phlyctenular or Eales diseases (
8-
10).
TB can invade one eye or both in any part, but focal or multifocal choroiditis is the most frequent form, estimated at 78% and 94% (
11,
12). Differential diagnosis of TB
choroiditis based on lesion appearance includes Sarcoidosis, Syphilis and rarely metastatic diseases (
13). Chronic anterior uveitis, usually granulomatous and retinal vasculitis or periphlebitis, are the second and third common manifestations. Other manifestations include scleritis, interstitial keratitis and optic neuritis (
14). Eales` disease, which is mostly common in patients from India, Pakistan and Afghanistan typically, manifests itself with vascular sheathing of retinal veins (periphlebitis), vitreous inflammation and peripheral retinal capillary occlusion. Noteworthily, the last one leads to neovascularization and subsequent retinal hemorrhage (
14). Before the discovery of Polymerase Chain Reactions (PCR) technology, the majority of cases were considered to have "presumed ocular TB”, because (
15):
- Biopsies and culture are practical in cases of lid involvement, keratitis or Orbital tuberculosis although the majority of cases present with intraocular involvement.
- Aqueous and vitreous paracentesis generally fails to result positive bacterial cultures (
16).
- Isolating the microorganism is difficult technically.
- The features are similar to other granulomatous inflammations of eye.
- And the ocular manifestations of TB are extremely variable.
The initial evaluation of suspected patient (which the ocular involvement usually accompanies with systemic disease) requires the complete history including exposure, physical examination, sputum smear and culture, PPD test, chest X-radiography and ruling out the other causes for granulomatous inflammations (
15). Recently, PCR and ELISA play important roles in detection of mycobacterial DNA or antigens in ocular tissues including eyelid skin, conjunctiva, aqueous and vitreous with unproven specificity and sensitivity (
17-
24). The main treatment of ocular TB is the same systemic anti-Tuberculosis therapy which can lead to remission of inflammation and improvement in visual acuity to nearly premorbid levels. Topical ointment and subconjunctival injection can contribute to adequate intraocular drug levels especially in anterior segments. Furthermore, parenteral administration is the method of choice in posterior intraocular TB which leads to higher vitreous drug levels (
15).
TB in endemic areas rare manifestations are more likely to be seen due to high prevalence of infection. Hence, TB should be considered as a differential diagnosis, especially when the symptoms are progressing gradually and response to treatment is not satisfactory. In ocular involvement the important issue is the possibility of accompanying no systemic manifestations, and other difficulties in diagnosis as mentioned before. All in all, ocular TB must not be ruled out rapidly if history and/or early paraclinic findings are not in favor of TB infection, especially in endemic areas.