Ocular Involvement in HIV/AIDS

From EyeWiki
Assigned editor:
Assigned status Update Pending
 by Marissa Larochelle, MD on December 22, 2022.

HIV infection can manifest in a variety of ways in and around the eyes, and these manifestations vary according to HIV disease severity, specifically, CD4+ T lymphocyte counts. In general, Kaposi sarcoma, herpes zoster ophthalmicus, candidiasis, and lymphoma are more common in earlier stages whereas tuberculosis, toxoplasmosis, and pneumocystosis occur with more impairment. Cytomegalovirus retinitis and mycobacterium-avium complex disease are usually seen in patients with profound reductions of CD4 counts. Achievement of a non-detectable HIV viral load is associated with a better prognosis.



The identification in 1981 of a cluster of gay men with unusual clinical manifestations later ascribed to infection with human immunodeficiency virus-I (HIV-I) was followed within a year by publication of typical ocular manifestations: cotton wool spots, cytomegalovirus, periphlebitis, and conjunctival Kaposi sarcoma. [1] The acquired cellular immunodeficiency syndrome, rapidly became the world-wide focus of numerous surveys of eye disease, randomized clinical trials, and case series detailing optimal management of the ocular complications of AIDS. After 1996 ocular manifestations were modified by the improved immune status achieved by many patients who were treated with highly active anti-retroviral therapy (HAART). [2] In 2007, a large observational study reported 9.2% of patients with visual impairment in the better eye and 41.4% of patients with other major ocular complications.[3]  HIV infection remains a significant clinical problem for ophthalmologists. Ocular manifestations occur mainly in adults but can also occur in children with HIV/AIDS.[4] 

Incidence and prevalence of HIV infection

In 2007, there were 33 million people worldwide with HIV/AIDS, 2.7 million people newly infected with HIV, 2 million death. Ninety-five per cent of infections and deaths occurred in developing countries. In the US, 1.1 million people are estimated to have HIV/AIDS in 2016 with approximately 37,832 new infections, disproportionately affecting African Americans.[5][6] Transmission occurs by sexual contact, by exposure to infected blood or blood products typically through needle-sharing, or through vertical transmission from an infected mother. Diagnosis is made by detection of virus-specific antibodies and confirmed by Western blot. After diagnosis patients are monitored by quantitative HIV-RNA determinations by PCR.

Spectrum of HIV disease

Acute infection with HIV causes nonspecific symptoms of viral infection and lymphadenopathy, followed by a minimally symptomatic phase during which CD4+ T lymphocyte counts decline from the normal values of 600 to 1500 cells/mm3. Below 200 cells/mm3, symptoms occur frequently from opportunistic infections, malignancies, and generalized malaise. Ocular manifestations attributable to HIV infection vary according to CD4+ T lymphocyte counts.[7]  In general, Kaposi sarcoma, herpes zoster ophthalmicus, candidiasis, and lymphoma are more common in earlier stages whereas tuberculosis, toxoplasmosis, and pneumocystosis occur with more impairment. Cytomegalovirus retinitis and mycobacterium-avium complex disease are usually seen in patients with profound reductions of CD4 counts.[8]  Achievement of a non-detectable HIV viral load is associated with a better prognosis.

Treatment of HIV

Current medical therapy of HIV infection is updated periodically by the International AIDS Society. [9]

Anatomic Categorization of Ocular Manifestations

Adnexa and orbit

Molluscum contagiosum presents as small, painless papules 1-3 mm in size with a central depression. The lesions are more likely to be numerous and bilateral in HIV infection but patients may be asymptomatic unless the eyelid margin is involved. Crusted, painful vesicles suggest herpetic infection. Herpes zoster ophthalmicus in individuals less than 50 years of age is suggestive of HIV infection and HIV infected patients are more likely to develop sequential necrotizing herpetic retinitis following HZO. [10] HZO has both an elevated risk ratio and increased incidence rate in HIV infected patients compared to immunocompetent individuals. [11] Kaposi sarcoma is an opportunistic malignancy produced by HHV-8 infection. The tumors are highly vascular with deep red or purple color and may distort the eyelid contours. [12] The orbit can become infected secondary to contiguous sinus disease. Aspergillosis is the most common orbital infection in HIV/AIDS. [13] Anterior and external disorders associated with AIDS were the subject of a comprehensive review. [14]


Malignant tumors can affect the conjunctiva in HIV/AIDS. Kaposi sarcoma has the same intense red, hemorrhagic appearance as the adnexal lesions. Conjunctival intraepithelial neoplasia (CIN) typically occurs at the conjunctival/corneal junction, causes mild redness and foreign body sensation; it may mimic pterygium or pinguecula. [15] Squamous cell carcinoma is elevated with an irregular, roughened surface and typically invasive. Excision is indicated for most neoplastic complications; local administration of interferon alfa-2b has efficacy for KS and CIN. Qureshi 2009, [16][17] Radiation and cryotherapy is useful in more advanced KS; disseminated KS is treated with chemotherapy. Conjunctival lymphoma has a characteristic salmon-patch appearance.


Corneal manifestations range from relatively benign dry eye symptoms to severe, blinding bacterial pseudomonal keratitis. Recurrences of herpes simplex keratitis are more common in HIV/AIDS, but the clinical course and incidence differs little from HSV keratitis in immunocompetent individuals. [18] The intracellular, protozoal parasite Microsporidia causes a coarse, superficial punctate keratitis.

Iris and ciliary body

Iritis can accompany bacterial or viral keratitis or posterior segment infections or may be associated solely with HIV infection and improve with treatment of the underlying HIV disease. Certain drugs used in the treatment of HIV-related conditions can cause drug-induced iritis. Rifabutin is used in the treatment of mycobacterium-avium complex infection and can produce severe hypopyon iritis that may be confused with endogenous endophthalmitis. [19] Cidofovir, used in the treatment of cytomegalovirus retinitis (CMVR), can also cause iritis and occasionally hypotony. [20][21]


In a subset of patients with HIV/AIDS, a disorder called HIV associated neuroretinal disorder has been described. It is defined as loss of the nerve fiber layer which manifests clinically as decreased contrast sensitivity, abnormal color vision, and visual field loss. Jab et al described risk factors for development which include Hepatitis C infection, detectable viral load, and low Cd4 T cells.[22]

Retina - Non-infectious

Microangiopathy is the most common ocular manifestation of HIV infection. Cotton wool patches are the most typical. They can be distinguished from infectious retinitis by a size less than 500 microns, a feathered edge, and transience, with fading over 6 to 8 weeks. Although microangiopathy is generally not felt to be visually threatening, permanent structural damage has been documented with scanning laser ophthalmoscopy and OCT. [23] Microangiopathy may also be responsible for alterations in visual function. In a large series of AIDS patients without retinitis, 3% of eyes had vision worse than 20/40, nearly 40% had some abnormal visual field, and 12% had low contrast sensitivity. [24]Decreasing visual function correlated with some measures of increasing disease severity.

Retina – Infectious - Cytomegalovirus retinitis (CMVR)

Prior to HAART therapy, CMVR occurred in 15 to 40% of HIV infected patients and was associated with increased mortality and death within 6 months for many patients. [25] Pre-HAART, patients with CMVR in three large clinical trials had 51.7 to 97.67 events per 100 eye-years for loss of visual acuity to worse than 20/40. [26] Use of HAART is associated with fewer symptoms, reduced border opacification, and better vision even in patients who acquire CMVR because they are failing HAART therapy. [25] HAART has also resulted in a decline in the incidence of CMVR by 80%. [27] CMVR is spread by contact with body fluids and has a high seroprevalence in the same populations at high risk for HIV infection. [28]The lesions follow a vascular distribution because the virus is endothelial-tropic. Depending on the size of the vessels infected, the retinitis can be either fulminantly hemorrhagic and exudative and follow the major vascular arcades, or superficial and granular. Clearing within lesions is typical because slow viral replication allows central healing. The border is yellow-white and studded with small satellite lesions marking progression of retinal necrosis into adjacent retina. Clinical diagnosis is considered adequate; PCR confirmation of CMV infection from aqueous humor is available if needed. [29]

Treatment of CMVR

Treatment of CMV retinitis is with intravenous ganciclovir administered as an initial, high-dose induction therapy (5 mg/kg twice daily for 2 weeks) followed by long-term maintenance therapy (5 mg/kg once daily). Oral valganciclovir is more commonly used because it is more convenient and achieves equivalent blood levels equivalent to intravenous administration. Induction therapy is 900 mg twice daily for 21 days followed by 900 mg once daily. [30] Both drugs can produce myelosuppression. Foscarnet is an intravenous alternative used mainly for virologic resistance and for synergistic therapy with ganciclovir in clinical resistance. It requires an initial 2-week, high- dose induction therapy (90 mg/kg every 12 hours for 2 weeks) followed by long-term maintenance therapy (90–120 mg/kg daily). Renal dysfunction and metabolic abnormalities of calcium and magnesium have been reported in up to 30% of patients. Intravitreal injections of 2.0 mg ganciclovir in 0.05 mL once per week can provide adequate maintenance therapy for control of CMV retinitis. Salvage or induction therapy with two to three injections per week for up to two weeks is safe. [31]Foscarnet, 2.4 mg in 0.1 mL, can be used intravitreally instead of ganciclovir or combined with ganciclovir, 1.2 mg in 0.05 mL, mixed immediately prior to injection to avoid crystallization. Intravitreal implantation of the ganclovir intraocular device is less frequently used due to the high cost and limited duration of 8 months, but has a good safety profile. [32][33]Cidofovir, administered intravenously or intraocularly, has largely been abandoned because of both systemic and ocular toxicity.

Monitoring of treatment response

Monitoring of response to treatment is done by assessing border activity and position. Photographic monitoring is helpful to detect subtle changes in the border that may indicate progression. Patients with low CD4+ T lymphocyte counts, positive blood CMV by PCR, and longer duration of AIDS are more likely to progress. [34]With therapy, healing is generally expected in 4 to 6 weeks, although activity commonly recurs unless the underlying immunosuppression is effectively treated. Strategies for recurrence include reinduction, addition of foscarnet to ganciclovir, intravitreal injections, and implantation of the ganciclovir intraocular device. A recent review summarizes current treatment strategies for CMV retinitis. [35]

Discontinuation of anti-CMV therapy

Discontinuation of anti-CMV therapy can be considered in patients with stable retinitis who have CD4+ T lymphocyte counts ≥ 100 if they are taking HAART. [36]A nondetectable viral load increases the chances of success. Even with stability of the retinitis, patients may still experience vision loss from complications related to CMVR. [37] Elevated CD4+ T lymphocyte counts associated with immune recovery may lead to macular edema and epiretinal membrane. [34] Risk of immune recovery vitritis and uveitis increases with CMVR surface area greater than 30%. [38]Other risk factors are posterior pole involvement and treatment with intravitreal cidofovir. [39] Overall, immune recovery is associated with a decreased risk visual acuity loss in patients with CMVR. [40]

Retinal detachment

Retinal detachment is associated with CMVR in up to 50% of cases and is the third most common cause of vision loss in AIDS patients after posteriorly located CMVR and cataract. [41]Laser photocoagulation of retinal holes or partial detachments may reduce the risk of progression and need for vitrectomy with silicone oil tamponade. [20][42][43] HAART therapy is also associated with a 60% reduction in risk of retinal detachment, presumably due to better control of the retinitis. [44]

Retinitis – Infectious – Necrotizing Herpetic Retinitis

Progressive outer retinal necrosis (PORN) is the usual term used to describe necrotizing herpetic retinitis due to varicella zoster. It is characterized by rapid progression and minimal anterior or vitreous inflammation. There is a high frequency of no light perception in patients treated with intravenous acyclovir by one month. [45] It often occurs in the setting of cutaneous zoster infection. There is a high incidence of retinal detachment and bilateral involvement. Intravitreal antiviral treatment or combined intravenous ganciclovir and foscarnet seem to control the infection better than intravenous acyclovir.[46] Because of the rapidity of progression, very aggressive initial therapy is usually selected.

Retinitis – Infectious - Toxoplasma retinochoroiditis

Toxoplasmic chorioretinitis has an increased incidence in HIV-positive compared to HIV-negative patients. [11] Large lesion sizes and bilateral involvement are more common in immunocompromised patients. A distinctive pattern of diffuse toxoplasmic chorioretinitis mimicking a viral necrotizing retinitis and involving more than 3 clock hours of the fundus can be seen. [47] Preexisting scars may be less common in HIV/AIDS, suggesting that acquired disease or dissemination from remote sites may be the initiating factor. [48] Patients with HIV infection may be more prone to progression if left untreated. Standard anti-toxoplasmosis regimens are used. In addition, ocular toxoplasmosis may be associated with cerebral or toxoplasmosis in immunocompromised patients. MRI of the brain to rule out CNS involvement can be considered.

Retinitis – Infectious - Syphilitic chorioretinitis

Manifestations of ocular syphilis include anterior or intermediate uveitis, optic neuritis, and chorioretinitis. The chorioretinitis typically presents as placoid subretinal lesions in the posterior pole. OCT examination often shows outer retinal and subretinal fluid. Geographic areas of non-necrotizing retinitis can also occur that heal with stippled hyperpigmentation of the RPE over time. Relapse and negative nontreponemal serology may be more common in HIV infected patients. [49] Treatment with a neurosyphilis regimen is required: either 24 million units of intravenous penicillin G daily for 10–14 days, followed by 2.4 million units of intramuscular benzathine penicillin G administered weekly for 3 weeks or 2.4 million units of procaine penicillin G intramuscularly for 10 days with probenecid 500 mg orally four times daily.

Choroiditis – Infectious

Pneumocystis carinii choroiditis was relatively common in the early years of the HIV pandemic because of ineffective prophylaxis against P carinii pneumonia. Use of systemic antimicrobials such as trimethoprim-sulfamethoxazole rather than aerosolized pentamidine essentially eradicated this ocular manifestation. Deep orange lesions are characteristic of P carinii choroiditis; they generally do not affect vision and fade with antimicrobial treatment. Cryptococcus neoformans choroiditis is also much less common in the HAART era. It can occur from systemic dissemination or from optic nerve involvement via the central nervous system in the setting of cryptococcal meningitis. Optic nerve edema from increased intracranial pressure with risk of optic atrophy is likely a more common complication of CNS cryptococcosis than intraocular invasion. [50]

Other choroidal infections

Ocular tuberculosis is rare even in HIV-infected patients residing in endemic areas. Prevalence was 15 (19 eyes) in 766 HIV/AIDS patients (1.95%) in India. [51]Choroidal granuloma was the most common manifestation, present in more than 50% of eyes. Subretinal abscess in 7 eyes worsed to panophthalmitis in 3. The average CD4+ T lymphocyte count was 160, indicating that marked immunocompromised is not necessary for ocular tuberculosis to develop in patients with active pulmonary tuberculosis and HIV. Autopsy studies have identified histoplasma capsulatum, candida, aspergillus, toxoplasma, and mycobacterium avium-intracellulare in the choroid of patients with HIV/AIDS. [52]

Additional Resources


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