Abstract
Human immunodeficiency virus (HIV)-related uveitis may be due to specific infectious agents, to HIV, or to an immunologically mediated effect of HIV infection. Autoimmune phenomena are reported in HIV infection and may be responsible for the few cases of uveitis without focal posterior lesions in which an infectious agent other than HIV cannot be assigned. The retinal microangiopathy associated with HIV infection may reflect direct immunologic or infectious damage to the vascular endothelium or alterations in blood components that produce the same effect. Retinal perivasculitis, seen with and without intraocular infections, may represent an extreme form of microvascular change with exudation of inflammatory cells from vessel walls. Over the last 18 months, several case reports and series of HIV-related ocular infections have appeared. The number of cytomegalovirus retinitis cases now permits analysis of the effects of treatment on visual function and survival. Reports of herpes simplex, herpes zoster, toxoplasmosis, and syphilis emphasize the more severe tissue destruction and milder inflammation in HIV-infected patients than in patients with intact immune systems. Syphilitic ocular infection in particular appears to follow an unusual course, with occasional negative rapid plasmid reagin findings, a high rate of central nervous system involvement, and a relative dependence on high-dose penicillin for cure. Pneumocystis carinii, Mycobacterium species, and Cryptococcus neoformans round out the list of opportunistic infectious agents for which important natural history information is being gained. Because infection and not inflammation appears to cause tissue destruction in HIV-related ocular infections, use of specific antibiotic therapy rather than corticosteroids is appropriate in most cases of HIV-related uveitis.
