LAUSR

T hank you Drs. Fung and Pradeep for sharing a fascinating case of retrobulbar optic neuritis due to tuberculosis, in an immunocompetent patient (1). Infective causes of optic neuritis pose a significant challenge in the context of systemic illness. There were a number of points I thought deserved further comment. The authors have commented on difficulties proving causation of the retrobulbar optic neuritis by Mycobacterium tuberculosis (TB) and therefore it is presumed in this case, such as we often see in TB uveitis. Most TB uveitis is termed Presumed Intraocular TB as sampling of the ocular fluids to identify TB on microscopy, culture, or polymerase chain reaction is of low sensitivity (2). Clinicians are therefore often reliant on a positive interferon gamma release assay in conjunction with supportive clinical features to make a diagnosis. In addition, exclusion of other causes adds weight and so it would be helpful in a case of severe bilateral optic neuritis to exclude neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein neuritis. Aside from the mentioned possibility of optic nerve sheath biopsy, lumbar puncture may be considered, as identification of the organism would be consistent with central nervous system involvement. As with other extrapulmonary sites of infection, the sensitivity of testing is low because of potential paucibacillary infection (3,4). Similarly, clues to a treatment approach may be sought from the literature on TB meningitis where it has been reported that the severity of the inflammatory response seen in the brain parenchyma and meninges suggests an immune phenomenon rather than direct effects of M. tuberculosis (5). Continued cytokine release despite treatment with anti-TB treatment has led to the widespread use of high-dose steroids with an associated reduction in mortality, in the shortterm (6). The largest of these trials used an intravenous starting dose of 0.4 mg/kg of dexamethasone for Grade II or III TB meningitis (focal neurological deficit e.g., cranial nerve palsy is classed Grade II) (4). In a 70 kg adult, this would equate to 28 mg dexamethasone, which is equivalent to approximately 180 mg prednisolone, 3 times the received steroid dose for the patient in question and closer to the dosage that is commonly used in other causes of atypical optic neuritis. Rifampicin as a potent enzyme inducer may also lend weight to using a higher steroid dose, with many doubling the dose of oral prednisolone when treating TB uveitis. The resolution of pulmonary symptoms would make the possibility of a multi drug resistant strain of TB accounting for the poor visual outcome, unlikely. Finally, the authors have classed this patient as immunocompetent, presumably based on being HIV negative and a medical history. However, given that the patient denies travel to a TB endemic area or exposure to an index case, immune dysfunction may be investigated for by checking serum immunoglobulins and lymphocyte markers. It is thus clear that there is no consensus for treatment of presumed TB optic neuritis, but it may be that clinicians should consider higher doses of steroids, with close input from a physician, to try to maximize the visual outcome and minimize adverse effects. Thank you to the authors for bringing this interesting case and its challenges to our attention.