Tubercular panophthalmitis: Case report of a rare entity
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/MJDRDYPU.MJDRDYPU_267_16
Tuberculosis (TB) remains the leading cause of infection-related deaths in adults worldwide. The ocular involvement in TB is extremely rare. The incidence of ocular TB is reported to be 1%–2% of ocular diseases. We report an interesting case of mycobacterial panophthalmitis in an adult male who presented with painful red eye with loss of vision. Keywords: Acid-fast bacilli, panophthalmitis, tuberculosis
Tuberculosis (TB) remains the leading cause of infection-related deaths in adults worldwide. The incidence is increasing by 8 million new cases annually with over 2 billion people affected by the disease.[1] The ocular involvement in TB is extremely rare. The incidence of ocular TB is reported to be 1%–2% of ocular diseases.[2],[3] Moreover, very few case reports are available in literature. Endogenous panophthalmitis is most frequently caused by fungi, followed by virulent bacteria (Pseudomonas, Clostridia, and Bacillus).[4] TB is a very rare cause of panophthalmitis and it mostly occurs in immunocompromised patients.[5] We report an interesting case of TB panophthalmitis in an adult male.
A 26-year-old male presented with painful red eye with loss of vision in the left eye for the last 1 month. He also complained of low-grade fever on and off for the last 2 months. The patient was a known case of pulmonary TB and was on antitubercular treatment for the last 2 months. At the time of presentation, ocular examination of the left eye revealed no perception of light, circumcorneal congestion with ciliary staphyloma, fixed and dilated pupil, and marked limitation of eye movements. Intraocular tension was raised to 29.4 mmHg. Anterior chamber had exudates, cells 2+, and flare 2+, in addition to complicated cataract. In the left eye, vision was 6/6 unaided, intraocular tension was within normal range (14.6 mmHg), and pupillary consensual reaction was absent. Posterior segment could not be evaluated because of media haze. Ultrasound revealed features suggestive of vitreous hemorrhage. There was no evidence of calcification. A routine hemogram was within normal limits, and erythrocyte sedimentation rate was 84 mm in the 1st h by Westergren method. Liver and kidney function tests were within normal limits. The chest X-ray showed bilateral upper lobe infiltration and hilar lymphadenopathy. Sputum examination was negative for acid-fast bacilli (AFB). The patient was HIV negative. Clinical diagnosis of endogenous panophthalmitis was made and considered for evisceration of the left eye in view of painful blind eye. Grossly, multiple gray-brown pieces were received for histopathological examination. Microscopy revealed extensive necrotizing granulomatous inflammation involving all the layers of the eye ball [Figure 1]. Occasional epithelioid cell granulomas and Langhan's giant cells were seen, along with the areas of caseous necrosis. Ziehl–Neelsen staining for AFB was positive [Figure 2]. Culture revealed colonies of Mycobacterium TB (MTB). A diagnosis of tubercular panophthalmitis was made.
There is marked diversity in the ocular manifestation of TB and it largely depends on the variables such as immunological status of the patient, virulence of the bacteria, and epidemiological factors.[6] Ocular involvement in TB is uncommon and may be both primary and secondary.[7] Cornea and conjunctiva are the preferred sites of involvement in case of primary ocular TB whereas the secondary involvement usually manifests as anterior uveitis, choroiditis, choroidal tubercles, vasculitis, vitritis, and papillitis. TB panophthalmitis is a rare entity. It may be diagnosed only after histopathological examination or suspected in an immunocompromised patient or known case of TB. A painless, progressive loss of vision, decreased motility of the eye, cloudy cornea, and low intraocular pressure favor tubercular etiology.[8] However, pain could be present if the patient develops secondary glaucoma.[9] Our patient was on antitubercular treatment for 2 months and presented with redness and pain due to glaucoma. There has been a resurgence of TB due to AIDS epidemic with one study quoting an incidence of TB as 18%.[5] Our patient was HIV negative. Rich vascular plexus within choroid makes it prone to be the most common site of involvement in hematogenous spread of tubercular bacilli from primary focus in the lung. Due to painless presentation, the disease progresses to panophthalmitis, leading to loss of vision. However, our case presented with painful red eye with loss of vision and hence was difficult to diagnose. Ocular complications of AIDS are common, seen in 70%–80% of patients in Western countries before the advent of antiretroviral therapy.[10] Marked variation in the clinical presentation and nonspecific manifestation of the ocular TB delays the correct diagnosis and hence strong clinical suspicion is required for timely diagnosis.[11] Definitive diagnosis requires demonstration of either AFB in tissue sections or bacterial genome by nucleic acid amplification procedures.[12] A newer test based on the detection of anti-cord factor antibody through enzyme-linked immunosorbent assay is also being used.[13] Balne et al. studied various factors influencing the outcomes of polymerase chain reaction in patients with clinically suspected ocular TB.[14] Fewer new techniques are available for TB detection such as interferon gamma release assay which is based on gamma interferon production by T-cells sensitized to specific antigens to MTB and therefore not influenced by bacille Calmette–Guérin and most non-TB bacteria. These tests include QuantiFERON-TB Gold In-Tube and ELISpotPLUS.[15] Polymerase chain reaction techniques are also used for the detection of MTB in aqueous and vitreous samples from patients with presumed TB uveitis. Detection of antibodies against purified cord factor, the most antigenic and abundant cell wall component of MTB, can provide strong evidence of the infection. However, the sensitivity was reported to be low, as many ocular manifestations may represent a delayed hypersensitivity reaction rather than a direct mycobacterial infection, making the analysis of a fluid sample from the eye less sensitive.[15] It is recommended that in all susceptible individuals (immunocompromised/known cases of TB), a routine ocular examination is a must. At the clinical suspicion of ocular TB, early antitubercular treatment should be started to prevent the progression to panophthalmitis and loss of vision. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
[Figure 1], [Figure 2]
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