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History: 21 year-old male with decreased vision in both eyes for 3 months.  Redness and pain present mostly in the left eye.  No fever or systemic symptoms.  Seen by several local ophthalmology services and treated with several unknown drugs.

Epidemiology: Born and living in Lima with his family.  Father had a “neurological problem” 3 years ago and was treated for several months.  No family history of TB; not sexually active.

Physical Examination: Afebrile.  General examination unremarkable.  Visual acuity was 20/50 right eye and limited to counting fingers in the left eye.  On slit lamp examination there was 2+ vitreous haze in the right eye and 3+ in the left eye.  Intraocular pressure was: 14 mm Hg in both eyes both eyes.  On fundoscopy there were multi-focal choroidal lesions in right eye [Image A] and a localized exudative choroidal detachment in the left eye [Image B].  On retinal angiography there were active multiple foci in both eyes [Images C, D] with an exudative choroidal detachment, a pattern for Harada disease.  The clinical impression was bilateral posterior uveitis.

Laboratory Examination: Chest x-ray normal.  HIV negative.  HTLV-1 negative.  CBC and routine biochemistry normal.  A diagnostic test was performed on an aspirate of aqueous humor.

Discussion: The aqueous fluid was positive on PCR for M. tuberculosis.  PPD was positive at 18 mm.  Other tests performed on serum included a negative VDRL, negative toxoplasma IgG, negative brucella agglutinins.

Posterior uveitis, as in this patient, refers to inflammation involving the choroid, retina, or both (chorioretinitis) as well as retinal vasculitis.  There may also be inflammation of the posterior vitreous.  In addition to location uveitis can either be granulomatous or non-granulomatous.  Granulomatous uveitis as in this patient does not refer to histological finding of granulomas but rather to aggregates of white blood cells and not uniform dispersement of inflammation throughout the lesion.

Most uveitis is either idiopathic or autoimmune and non-granulomatous, though two types of autoimmune uveitis, Harada syndrome and sarcoid, can cause a granulomatous uveitis.  For the infectious causes of posterior granulomatous uveitis the differential diagnosis includes: toxoplasmosis, CMV (in HIV patients), Toxocara, brucellosis, syphilis, leprosy, Bartonella henselae, Borrelia, Yersinia, histolplasmosis, and cryptococosis.  We have noted in a number of our patients concomitant uveitis of infectious origin together with the exudative choroidal detachment that is diagnostic of Harada syndrome.

At our tropical medicine institute in Lima, we evaluate about 30 patients per year referred from the National Opthalmology Institute for evaluation of possible infectious etiologies in patients with uveitis, and about one-third are found to be infectious.  Of these about 20% are due to TB.  It is not possible to culture TB from the eye, so in the past, the diagnosis has usually been made on the basis of clinical suspicion, exclusion of other infectious and non-infectious causes and in the setting of a highly reactive PPD.  More recently, we have been using PCR, as in this patient.  Most HIV negative patients have no other obvious manifestation of tuberculosis infection.  In patients with HIV our experience is that other concomitant manifestations are more common.  Several large studies suggest ocular complications in 1% of all patients with clinical tuberculosis.  Our experience in a highly endemic country such as Peru suggests that this number is between 0.1 and 0.5%.

The patient was started on standard 4-drug TB therapy and on prednisone. Our usual practice is to treat with high dose prednisone for 2-3 weeks before tapering.  After 1 month, his vision improved in the right eye to 20/20 [Images E, G] without evidence of retinal detachment.  However, the left eye developed a scar in the central macula with vision remaining at counting fingers [Images F, H].