Choroidal neovascularization secondary to tuberculosis: Presentation and management☆

Purpose While there are many known etiologies of choroidal neovascularization (CNV), tuberculosis is not a well-known causative agent. In this case series, we highlight CNV occurring secondary to tuberculous chorioretinitis, its presentation, and its management. Observations We retrospectively reviewed the charts and imaging of four patients who presented with presumed tuberculous chorioretinitis and CNV. Three of these patients had signs of intraocular inflammation and were also found to have active macular CNV. The one remaining patient had chorioretinal scars from prior posterior uveitis and previously treated macular CNV membranes. The three patients with active disease were started on anti-tuberculosis medications and oral corticosteroids, and they also received intravitreal anti-vascular endothelial growth factor (VEGF) injections as needed for the CNV. There was a significant improvement in the clinical course of all three patients with active disease—the intraocular inflammation subsided, and CNV recurrences were mitigated. Upon completion of systemic treatment, all patients have remained quiescent. Conclusions and importance Our findings demonstrate that CNV may occur in the course of tuberculous chorioretinitis with marked loss of vision, and management with anti-tuberculosis medications, oral corticosteroids, and intravitreal anti-VEGF injections results in notable improvement in their clinical course

Dark hypopyon in Streptococcus bovis endogenous endophthalmitis: clinicopathologic correlations

# The Author(s) 2010. This article is published with open access at Springerlink.com Purpose The aim of this report is to present a previously unreported causative organism associated with brownpigmented hypopyon in a patient with endophthalmitis. Methods This is a retrospective case report which includes clinicopathologic correlations. Results Vitreous cultures demonstrated Streptococcus bovis infection resulting in a brown-pigmented hypopyon, with uveal pigment found intra- and extracellularly on pathologic examination of the pupillary membrane. Conclusions S. bovis endophthalmitis may be a cause of dark hypopyon, especially in patients with a history of liver disease, and, when identified, warrants colonoscopy and cardiac workup. Keywords Streptococcus bovis. Brown/dark hypopyon

Direct Detection of Reactive Nitrogen Species in Experimental Autoimmune Uveitis

PURPOSE: Demonstrate unequivocally the generation of nitric oxide in experimental autoimmune uveoretinitis by electron spin resonance spectroscopy (ESR) using ferrous iron complex of N-methyl-D-glucamine dithiocarbamate, (MGD)(2)-Fe(2+), as a spin trap. METHODS: Experimental autoimmune uveitis was induced in Lewis rats, and at the peak of the intraocular inflammation, the animals received intravitreous injections of the spin trap. The retina and choroid dissected from the enucleated globes were subjected to ESR. Similarly, the retina and choroid obtained at the peak of experimental autoimmune uveo-retinitis (EAU) were placed in a vial containing luminal, and chemiluminescence was counted on a Packard liquid scintillation analyzer. RESULTS: The ESR three-line spectrum (g=2.04; a(N)=12.5 G) obtained was characteristic of the adduct [(MGD)(2)-Fe(2+)-NO]. The majority of this signal was eliminated by the inducible nitric oxide synthase (iNOS) specific inhibitor aminoguanidine injected inflamed retina was detected when compared with that of the non inflamed controls. The chemiluminescent activity was further increased two-fold by the addition of bicarbonate to the inflamed retina; the phenomenon is attributable only to the presence of a high steady-state concentration of peroxynitrite. CONCLUSIONS: The study shows an unequivocal presence of nitric oxide in EAU retina and choroid and the generation of peroxynitrite. High levels of these reactive nitrogen species generated in the inflamed retina and choroids are certain to cause irreversible tissue damage, especially at the susceptible sites such as photoreceptors

Polarization-Sensitive Optical Coherence Tomographic Documentation of Choroidal Melanin Loss in Chronic Vogt–Koyanagi–Harada Disease

Purpose: Vogt–Koyanagi–Harada (VKH) disease is a systemic autoimmune disorder that affects organs with melanocytes. The sunset glow fundus (SGF) in VKH disease was evaluated with polarization-sensitive optical coherence tomography (PS-OCT).Methods: The study involved 28 eyes from 14 patients with chronic VKH disease, 21 eyes from 21 age-matched controls, and 22 eyes from 22 high-myopic patients with a tessellated fundus. VKH eyes were grouped into sunset or non-sunset groups on the basis of color fundus images. The presence of melanin in the choroid was determined by using the degree of polarization uniformity (DOPU) obtained by PS-OCT. The sunset glow index (SGI) was calculated by using color fundus images. Presence of an SGF was evaluated by using DOPU, SGI, subfoveal choroidal thicknesses, near-infrared images, and autofluorescence images at 488 nm (SW-AF) and 785 nm (NIR-AF).Results: There were 16 eyes in the sunset group and 12 eyes in the non-sunset group. For all eyes in the sunset group, the disappearance of choroidal melanin was clearly detected with PS-OCT. Percentage areas of low DOPU in the choroidal interstitial stroma of the sunset group were significantly lower than those of other groups and showed no overlap with other groups. The distribution of choroidal thicknesses and SGI in the sunset group substantially overlapped with other groups. The subjective analyses of the sunset and non-sunset groups, using near infrared, SW-AF, or NIR-AF, showed substantial inconsistencies with the PS-OCT results.Conclusions: PS-OCT provides an in vivo objective evaluation of choroidal melanin loss of the SGF in chronic VKH disease

Small Heat Shock Protein αA-Crystallin Prevents Photoreceptor Degeneration in Experimental Autoimmune Uveitis

The small heat shock protein, αA-crystallin null (αA−/−) mice are known to be more prone to retinal degeneration than the wild type mice in Experimental Autoimmune Uveoretinitis (EAU). In this report we demonstrate that intravenous administration of αA preserves retinal architecture and prevents photoreceptor damage in EAU. Interestingly, only αA and not αB-crystallin (αB), a closely related small heat shock protein works, pointing to molecular specificity in the observed retinal protection. The possible involvement of αA in retinal protection through immune modulation is corroborated by adaptive transfer experiments, (employing αA−/− and wild type mice with EAU as donors and Rag2−/− as the recipient mice), which indicate that αA protects against the autoimmune challenge by modulating the systemic B and T cell immunity. We show that αA administration causes marked reduction in Th1 cytokines (TNF-α, IL-12 and IFN-γ), both in the retina and in the spleen; notably, IL-17 was only reduced in the retina suggesting local intervention. Importantly, expression of Toll-like receptors and their associated adaptors is also inhibited suggesting that αA protection, against photoreceptor loss in EAU, is associated with systemic suppression of both the adaptive and innate immune responses