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A number of infectious diseases cause uveitis (see Table: Infectious Causes of Uveitis). The most common are herpes simplex virus, varicella-zoster virus, and CMV infection and toxoplasmosis. Different organisms affect different parts of the uveal tract.
Infectious Causes of Uveitis
Herpes simplex virus (see also Herpes Simplex Virus (HSV) Infections) causes anterior uveitis. Varicella-zoster virus does so less commonly, although the prevalence of zoster-associated anterior uveitis increases with age. Symptoms include ocular aching, photophobia, and decreased vision. Signs include redness; conjunctival injection and anterior chamber inflammation (cells and flare), often accompanied by corneal inflammation (keratitis); decreased corneal sensation; and patchy or sectorial iris atrophy. Intraocular pressure may be elevated as well; elevation can be detected by using applanation tonometry with, for example, a Goldmann tonometer, a pneumotonometer, an electronic indentation tonometer, or, if these are not available, a Schiotz tonometer.
Treatment should generally be initiated by an ophthalmologist and should include a topical corticosteroid and a cycloplegic-mydriatic drug. Acyclovir (400 mg po 5 times/day for herpes simplex virus and 800 mg po 5 times/day for herpes zoster virus) may also be given. Drops to lower intraocular pressure may be required in patients with ocular hypertension.
Much less commonly, varicella-zoster and herpes simplex viruses cause a rapidly progressing form of retinitis called acute retinal necrosis (ARN), which typically manifests as confluent retinitis, occlusive retinal vasculitis, and moderate to severe vitreous inflammation. One third of ARN cases become bilateral, and in three fourths of eyes, retinal detachment occurs. ARN may also occur in patients with HIV/AIDS, but severely immunocompromised patients can have less prominent vitreous inflammation. Vitreous biopsy for culture and PCR analysis may be useful in diagnosing ARN. Treatment options include IV acyclovir, IV ganciclovir or foscarnet, intravitreal ganciclovir or foscarnet, and oral valacyclovir or valganciclovir.
Toxoplasmosis (see also Toxoplasmosis) is the most common cause of retinitis in immunocompetent patients. Most cases are acquired postnatally; however, congenital cases occur as well, particularly in countries where infection is endemic. Symptoms of floaters and decreased vision may be due to cells in the vitreous humor or to retinal lesions or scars. Concurrent anterior segment involvement can occur and may cause ocular ache, redness, and photophobia. Laboratory testing should include serum anti- Toxoplasma gondii antibody titers.
Treatment is recommended for patients with posterior lesions that threaten vital visual structures, such as the optic disk or macula, and for immunocompromised patients. Multidrug therapy is commonly prescribed; it includes pyrimethamine, sulfonamides, clindamycin, and, in select cases, systemic corticosteroids. Corticosteroids should not, however, be used without concurrent antimicrobial coverage. Long-acting periocular and intraocular corticosteroids (eg, triamcinolone acetonide) should be avoided. Patients with small peripheral lesions that do not directly threaten vital visual structures may be observed without treatment and should begin to show slow improvement in 1 to 2 mo.
CMV (see also Cytomegalovirus (CMV) Infection) is the most common cause of retinitis in immunocompromised patients, but prevalence has decreased among patients with HIV/AIDS receiving highly active antiretroviral therapy (HAART). Currently, ≤ 5% of these patients are affected. Most affected patients have a CD4+ count < 100 cells/μL. CMV retinitis may also occur in neonates and in pharmacologically immunosuppressed patients but is uncommon.
The diagnosis is largely clinical based on direct or indirect ophthalmoscopic examination; serologic tests are of limited use. Treatment in patients with HIV/AIDS is with systemic or local (implant) ganciclovir, systemic foscarnet, or valganciclovir. Therapy is typically continued indefinitely, unless immune reconstitution is achieved with combination antiretroviral therapy (typically a CD4+ count > 100 cells/μL for at least 3 mo).
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