In our case, at the first visit, she was misdiagnosed as having phacolytic glaucoma because she had a mature cataract and elevated intraocular pressure. However, the persistent post-operative inflammation and progressive scleral abscesses made us reconsider the possibility that the origin of the disease may be infectious, especially an atypical one. Apart from the chronic post-operative endophthalmitis, atypical infectious pathogens such as Nocardia spp. and Mycobacterium spp. initially were included in our differential diagnosis. Endophthalmitis was later ruled out by negative bacteria and fungus culture results. Moreover, the location of vitreous haze was localized only in the retrolental area instead of the vitreous chamber and the normal retinal-choroidal thickness from ultrasonography suggested that the vitreous cells were the reaction to a marked anterior segment inflammation rather than endophthalmitis, a vitreous infection in origin. Our initial differential diagnosis was Nontuberculous mycobacterium because a prolonged steroid use and prior ocular surgery were identified as the risk factors for developing this group of mycobacterium especially the rapid growers [10]. However, when the culture results came back as Mycobacterium tuberculosis, her past clinical course started to make sense.
It should be noted that cataract can frequently develop in the eyes followed by chronic or recurrent uveitis [11]. Severe intraocular inflammation can raise the intraocular pressure due to either the blockage of the intertrabecular space by inflammatory cells or edema of the trabecular meshwork which is the main route for aqueous drainage. The prolonged course of inflammation can permanently damage these meshwork functions. In our case, the patient seemed to have the uveitis for a long period prior to visiting the ophthalmology clinic. These two clinical manifestations, a consequence of a long-run untreated uveitis as aforementioned, misled us to diagnose the patient with phacolytic glaucoma because she had a cataract with high intraocular pressure.
In general phcolytic cases, after cataract surgery, the inflammation should rapidly subside in the first month because the lens, which are the cause of the inflammation, have been removed. Even though the inflammation persisted to 7–8 weeks, it should have been very low grade. However, for this patient, the inflammation subsided a bit in the first week after the cataract surgery when compared to the pre-operative state, but continued to persist at a moderate to high grade throughout the next 7 weeks. Thus, we believe that this inflammation was caused by a pre-existing infection rather than the secondary one.
There are a few cases of intraocular tuberculosis presented with anterior uveitis [6]. Presentation usually includes granuloma of the iris or inflammatory cells at the angle of the anterior chamber previously described as mutton fat KP. Its characteristics are greasy clumps of inflammatory cells at the posterior cornea [6]. This type of KP indicates that it is a granulomatous inflammation, which can also be found in toxoplasmosis and sarcoidosis [10]. However, for this patient, the characteristics of the typical mutton fat KP were absent. Instead, the KPs were heavily pigmented and inferiorly located. The presence of KPs in this patient probably was an important sign that was overlooked which indicated that the etiology was uveitis rather than phacolytic glaucoma. Therefore, we suggest that differential diagnosis of tuberculous uveitis must be kept in mind despite of the absence of a typical mutton fat KP, especially when a prominent pigment is observed.
Mycobacterium tuberculosis can also cause scleritis but this is rare [12]. The anterior part of the sclera is affected more frequently than the posterior. Examination may reveal necrotizing nodular scleritis along with scleral ulceration [5]. Kesen, et al. [13] reported, in 2009, a case of atypical drug-resistant tuberculous scleritis presented with masses at the anterior sclera. The masses subsequently progressed to a large area of necrotic sclera. Damodaran, et al. [14] also reported, in 2012, a case with severe intraocular inflammation and a large mass lesion in the globe detected by ultrasonography. The patient did not respond to anti-inflammatory or immunosuppressive agents resulting in perforation of the eye. In both cases, the diagnoses of tuberculous scleritis were confirmed afterward by histopathology of the enucleated eyes.
As far as we are aware, this is the first report that demonstrates the progression of untreated Mycobacterium tuberculosis uveitis to scleral abscesses. The progression can be the course of the disease itself when there is a migration of an increasing number of organisms into the adjacent structure, from the intraocular to sclera. It is also possible that the scleral involvement may have been the consequence of a direct inoculation of the organisms during the cataract surgery which could have spread the mycobacterium-filled aqueous to the sclera.
Diagnostic tests for tuberculosis in endemic area are very different compared to non-endemic areas. For example, the tuberculin skin tests and interferon-gamma release assays may be useful for diagnosing tuberculosis in non-endemic area, but the use of these tests are limited and cannot differentiate between the latent tuberculous infection and disease in endemic area such as Thailand [5, 6, 15]. Therefore, in order to diagnose tuberculosis disease in an endemic country, Mycobacterium tuberculosis culture, the gold standard, is needed to detect ocular tuberculosis even though the sensitivity of the culture is low for the detection of paucibacillary infection in which case a molecular technique may be helpful bearing in mind the limitation of false-positive results [6].
