In pulmonary tuberculosis and other forms of extra-pulmonary tuberculosis, it is easy to monitor the response because of the availability of clinical specimens in the form of sputum and tissue specimens, respectively. However, in the case of ocular tuberculosis, as intraocular tissues are not easily available, response is analysed completely based on clinical evaluation. It is important to assess the therapeutic response to ATT and monitor ocular toxicity of these drugs without compromising on the therapeutic effect. In case of favourable response within 2 months, ATT for 6 months might be enough. Patients who do not respond to ATT even at 2–3 months might need second line of therapy or alternative treatment along with complete systemic re-evaluation by an infectious disease specialist [5]. The end point for the therapy is assessed by the ophthalmologist in terms of resolution of intraocular inflammation. In case of poor response, a severe form of disease or an alternate diagnosis should be considered. If there is no reduction in intraocular inflammation after the 2-month initiation phase, the utility of continuing ATT should be reassessed as the likelihood of intraocular tuberculosis is low. Gupta et al. referring to their unpublished data have demonstrated resolution of intraocular inflammation in nearly 95% of their patients after 6–15 months of treatment with four drug regimens [31]. There are clear-cut guidelines for patients with pulmonary tuberculosis who are defaulters or previously treated cases who relapse in various tuberculosis control programmes all over the world. In case of intraocular tuberculosis, the role of restarting ATT in previously treated patients or in case of reactivation of previous lesions is not yet clear.

All these side effects can lead to compliance issues. Poor compliance in turn leads to poor response to therapy, increased chances of recurrences and development of drug-resistant tuberculosis.

Nanotechnology-related rational drug delivery has improvised the therapeutic success and also has reduced the systemic toxicity and frequency of drug administration. In spite of emergence of newer antitubercular antibiotics , the real challenge is to target the intracellular pathogen. Most of the antibiotics are unable to actively pass through the cell membranes. Antitubercular drugs are loaded in the carrier system so that, once they get endocytosed by the phagocytic cells, they can prolong the release of the drugs and decrease the frequency of doses and drug toxicity (Table 6.3).

One of the main aims of therapy for intraocular tuberculosis is to control the intraocular inflammation for which oral steroids are mainstay of treatment. Gupta et al. showed superior clinical outcomes following concurrent treatment with steroids and anti-TB treatment in patients with uveitis in comparison to patients who received ATT alone [33]. When ocular tuberculosis is misdiagnosed as some other uveitic entity, inflammation may recur in spite of steroid therapy or ocular disease may worsen, as underlying tubercular aetiology is not taken care of. Antitubercular drugs decrease the microbial as well as antigen load by actively killing the microbes. The decrease in antigen load in turn leads to fewer chances of hypersensitivity and recurrences. Steroids are well known to modify the immune response and decrease the inflammation and chances of recurrences when given along with antitubercular drugs. However few studies have reported no role of corticosteroid treatment in tuberculous optic neuropathy [34], poorer visual outcome in cases of initiation of corticosteroids prior to ATT [8], reactivation of latent TB with concurrent use of ATT and corticosteroids [5] and higher rate treatment failure in patients on immunosuppressants [35].