A young adult presented with diminished vision. On examination he has anterior uveitis, vtritis, focal necrotizing granuloma & macular spot. Probable diagnosis is
D i.e. Ocular toxoplasmosis Ocular toxoplasmosis presents with localized necrotizing chorioretinitis involving macula, satellite lesions, spill over granular anterior uveitis, vitritisQ (1/t head light in fog appearance) with floaters (d/t vitritis), diminished vision(2, pain, redness and photophobia in young adults/ infantsQ. Panuveitis is commonly caused by VKH syndrome, sympathetic ophthalmia, sarcoidosis, syphilis, tuberculosis, toxoplasmosis, toxocariasisQ and endophthalmitis. Ocular Toxoplasmosis Ocular toxoplasmosis presents with necrotizing chorio-retinitis (destroying choroid & retina producing punched out heavily pigmented macular scar), satellite lesion (solitary inflammatory focus near old pigmented scar), spill over anterior uveitis (may be granular resembling Fuchs syndrome) and severe vitritis (so dense as to prohibit an adequate view of posterior segment i.e. head light in fog appearance). It usually presents in infants or adults between ages of 10-and 35 years. Bilateral macular involvement is common (in immune compromised). - Diagnosis of ocular toxoplasmosis is often made by clinical features alone. Active toxoplasmosis typically manifests localized necrotizing retinitis. The classical lesion is a grey white focus of retinal necrosis at the edge of pre existing pigmented chorioretinal scar. The entire thickness of choroid and retina is destroyed in a necrotizing inflammation so that a punched out heavily pigmented scar remains (often misdiagnosed White dot syndromes are caused by inflammation at the level of choriocapillaries resulting in non perfusion as congenital coloboma). In infants it is frequently a/w acute illness, convulsions, meningeal changes, hydrocephalus, calcification in brain and mental retardation. Diagnostic tests include demonstration of parasite, Sabin-Feldman dye test (serological test require live T. gondii organism with a titer >1:16), complement fixation test, indirect hemagglutination test and ELISA for IgG & IgM. - and secondary changes of choroid & outer retina. It includes multiple evanescent white dot syndrome (MEWDS), acute idiopathic blind spot enlargement syndrome, acute posterior multifocal placoid pigment epitheliopathy, multifocal choroiditis and panuveitis, punctuate inner choroidopathy, serpiginous choroidopathy, progressive subretinal fibrosis and uveitis syndrome, acute macular neuroretinopathy, and acute zonal occult outer retinopathy. - MEWDS is usually unilateral, self limiting disease predominantly involving females in 3,1-4th decade with sudden onset of decreased central vision & photopsia. It presents with mild vitritis, numerous tiny deep ill defined grey white dots at posterior pole and mid periphery. The blind spot is enlarged. The macula is spared but has a characteristic granular orange appearance which renders the foveal reflex abnormal or absent( 2. Over several weeks central vision recovers, dots fade. Fovea granularity may remain and enlarged blind spot may take much longer to diminish in size. Multifocal choroiditis and panuveitis is usually bilateral, recurrent / chronic, frequently asymmetrical disease that predominantly affects myopic females in their 3rd -4th decade with blurring of central vision, floater and photopsia. It presents with vitritis (universal), anterior uveitis (50%), and active lesions (bilateral, multiple, discrete, ovoid, yellowish grey) involving the posterior pole & periphery and arranged in clumps or linear streaks (Schlagel lines). Inactive lesions have sharp punched out margins and pigmented borders. Mild disc edema, disc enlargement and peripapillary fibrosis simulating napkin holder may develop.
Proteus syndrome
White dot syndrome
Multifocal choroiditis
Ocular toxoplasmosis