Intraocular Tuberculosis

Reema Bansal; Aman Sharma; Amod Gupta

Disclosures

Expert Rev Ophthalmol. 2012;7(4):341-349. 

In This Article

Pathogenesis of Intraocular TB

The pathogenesis of intraocular TB is not clear. In the absence of isolation of MTB from the ocular sites by either smear or cultures, pathogenesis of uveitis associated with TB has at best remained speculative. Pleural TB is believed to be caused by delayed type of hypersensitivity response to mycobacterial antigens and release of inflammatory cytokines by activated pleural cells.[17] If a similar mechanism is involved in tuberculous uveitis, it is difficult to prove due to the lack of opportunities of choroidal biopsy. In an enucleated eye of uveitis, Rao et al. documented the presence of MTB in the necrotic retinal pigment epithelium (RPE)which was confirmed by quantitative PCR.[18] They found 1.7 × 106 copies of MTB genome in the microdissected RPE cells. This location of the MTB may explain the nature of clinical lesions seen in patients with tuberculous uveitis. MTB is known to be a facultative intracellular parasite and multiplies in nonactivated macrophages.[19] The RPE cells that are known to express Toll-like receptors may actively phagocytose MTB that reaches the inner choroid via the hematogenous route. Once the intracellular MTB reaches a sufficient number in the macrophages, a cytotoxic cell-mediated response leads to destruction of the macrophages and surrounding tissue, and the formation of the caseum.[19] A similar mechanism may be operative in the eye as well. Rao et al. developed a model of intraocular TB by way of MTB aerosol infection in guinea pigs to mimic human infection.[20] MTB delivered via aerosol resulted in dissemination of the organisms to the eye besides the lungs. In the untreated animals, uveal TB developed in 42% of eyes, with the presence of acid-fast bacilli (AFB) and MTB DNA in uveal granulomas. Interestingly, in the animals given anti-TB drugs, none showed the presence of AFB but showed mild nongranulomatous inflammation.[20] In another study, Thayil et al. reported microbiological evidence of ocular TB within at least 4 weeks of aerosol infection.[21] Simultaneous with their appearance in the spleen and other organs, the organisms could be cultured form the eyes at 28 days after aerosol infection, thereby indicating that the ocular infection takes place by a hematogenous route. The resultant tuberculous granuloma lesions in the choroid were hypoxic, and the RPE and photoreceptors showed increasing levels of VEGF similar to what has been observed in the granulomas of lung TB.[21] While it is known that genotypic variations determine the clinical manifestations of TB,[22] there is as yet complete absence of data on the genetic types of MTB that cause various manifestations of intraocular TB.

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