Fig. 1.14 Candida vitritis (a) and retinitis (b). (a) Gross examination shows multifocal candidal retina abscess with “cotton ball” vitreous opacities (Courtesy of Dario Savino-Zari, MD). (b) Candida retinitis (Reprinted with permission from Arevalo

JF, ed. Manifestaciones Oculares del SIDA en el Nuevo Milenio: Texto y Atlas [Ocular manifestations of AIDS in the New Milenium: Text and Atlas]. Panama City, Panama: Highlights of Ophthalmology 2004 [55]

5–10 mg). Other agents, such as fluconazole, ketoconazole, and miconazole, have been used successfully to treat Candida chorioretinitis. Recently, there is experience using intravitreal voriconazole (50–100 mg/0.1 mL) combined successfully with oral voriconazole, but the experience is still limited. In addition, intravitreal voriconazole has been found effective in cases resistant to amphotericin B and fluconazole. A vitrectomy is of great help in these cases followed by intravitreal antifungal therapy. Vitreous biopsy and blood cultures may be useful in the diagnosis of systemic candidemia.

Drug addicts (intravenous drug abusers) who develop AIDS are likely to present an increased risk of ocular infection by Candida.

Pneumocystis carinii Choroiditis

Pneumocystis carinii pneumonia (PCP) has been the most common systemic opportunistic infection associated with AIDS. It affected more than 60% of patients with AIDS in the 1980s, but with the advent of effective prophylaxis using trimethoprim/sulfamethoxazole in HIV-positive patients with a count of CD4 + <200 cells/uL, the incidence of systemic disease by Pneumocystis has decreased significantly. Pneumocystis carinii choroiditis (PCC) was described in 1989 [90, 91]. Lesions respond to systemic treatment (intravenous or oral) with pentamidine (4 mg/kg/day) or a combination of trimethoprim (15–20 mg/kg/day)

and sulfamethoxazole (75–100 mg/kg/day) for 3–4 weeks. PCC has become very rare, and this is likely because it is almost exclusively seen as a disseminated form of Pneumocystis that has been controlled with local inhalational pentamidine. That therapy is rarely used since the disease does disseminate. Systemic treatment of Pneumocystis likely prevents the appearance of choroiditis and other disseminated infections in most patients.

The clinical appearance of the PCC is very characteristic. The lesions are yellow-white, round, circumscribed, flat, or slightly elevated, located at the posterior pole with a diameter ranging between 500 m and 3,000 m (Fig. 1.15). They are usually multifocal and bilateral but may be unifocal and unilateral. Rarely lesions are visually significant, although foveal and optic nerve lesions can sometimes cause visual impairment. The lesions occur with little or no vitritis [90–93].

Cryptococcus neoformans Chorioretinitis

Cryptococcus neoformans is a yeast that rarely is associated with disease in humans but can cause opportunistic infection in the immunocompromised patient. CNS involvement with Cryptococcus infection is relatively common in AIDS patients and often results in meningitis and secondary ocular findings (in 75% of cases) [94]. Choroiditis and chorioretinitis by Cryptococcus has been reported in patients with AIDS and appears to be associated with central nervous sys-

Fig. 1.15 Deep lesions in the posterior pole corresponding to the diagnosis of Pneumocystis carinii choroiditis. (a) Accompanied by papilledema by Cryptococcus neoformans. (b) Very subtle. (c) Large, confluent, and accompanied by a “patch” caused by cytomegalovirus retinitis

tem involvement (Fig. 1.16a). The typical lesions of this entity are located in the choroid and retina; the appearance is of multiple yellowish spots, circumscribed, with a variable diameter of 500– 3,000 m (Fig. 1.16b–d). They may be accompanied by perivascular sheathing (vasculitis), vitritis, and anterior uveitis with keratic precipitates mutton fat (granulomatous). Papilledema may be

present owing to increased intracranial pressure caused by meningitis. Visual loss may occur as a result of cryptococcal involvement of the optic nerve, chiasm, and optics tracts [94].

Treatment in patients with AIDS and cryptococcal ocular involvement has included amphotericin B and 5-fluorocytosine; the combination of these two drugs has been effective in the treatmentofcryptococcalchorioretinitis.Ketoconazole also appears to be effective and appears to be synergistic with 5-fluorocytosine.

Mycobacterium Choroiditis

The mycobacterial ocular infections in AIDS patients are infrequent and are caused primarily by Mycobacterium tuberculosis or Mycobacterium avium intracellulare (MAI) [95–97]. In either case, the eye infection is a manifestation of disseminated systemic disease. MAI ocular infections have only been described in autopsy series; however, clinically apparent cases of ocular infection by Mycobacterium tuberculosis have been described. Ocular findings in Mycobacterium tuberculosis infection in AIDS patients (similar to those of immunocompetent patients) include a prominent granulomatous reaction of the anterior chamber with posterior synechiae, a moderate vitritis and yellowish-white choroidal elevated lesions (granulomas) with retinal spearing (Figs. 1.17 and 1.18).

Treatment is focused on control of systemic disease, although topical corticosteroids can be used to help control the anterior chamber reaction. The lesions caused by MAI described in autopsies are choroidal granulomas that are slightly elevated. The organisms were observed in choriocapillaris and choroidal vessels. The lesions do not appear to be of clinical significance unless accompanied by vitritis.

Tuberculosis remains common throughout Latin America. The impact of HIV and multidrug resistance on tuberculosis control has been enormous. HIV-positive patients may be at ten times greater risk of multidrug-resistant tuberculosis than HIV-negative patients. Hopefully, improved diagnostic techniques will allow more rapid diagnosis of tuberculosis. However, in alarming reports, only 58% of patients were

treated with the recommended treatment regimen in a Brazilian study, and dropout from treatment in parts of Bolivia was common. Many failings could be combated by rigorous education of patients and physicians. In an encouraging advance, multidrug-resistant tuberculosis was successfully treated in a community-based program, saving an estimated 90% of the cost of hospital-based treatment. An opportunity to identify treatment failure earlier is demonstrated by the finding that 2 months after the initiation of therapy, positive smears were found in only 3% of those whose treatment was successful, but 74% of those whose treatment failed [98].

B-Cell Lymphoma

While obviously this entity is not an infectious manifestation associated with AIDS, we wanted to include it in this review as it is one of the most frequent pathologies of the posterior pole in these

patients that may mimic atypical infectious retinitis and therefore we keep it on our list of differential diagnoses.

HIV-infected patients are at increased risk for developing non-Hodgkin’s lymphoma [99], which tends to occur at a younger age than in their immunocompetent counterparts [100–102]. B-cell non-Hodgkin’s lymphoma is a cancer more frequently associated with AIDS. Lymphoma can be visceral or affect the CNS [103]. Ocular B-cell lymphoma in AIDS patients (similar to those of immunocompetent patients) consists of a mild- to-moderate vitritis, lesions of the uvea and retina. Ocular manifestations in this disease occur more frequently when there is a CNS involvement than when there is a systemic involvement. While intraocular lymphoma typically develops late in the course of HIV/AIDS, it can occur as an AIDSdefining illness [104, 105]. The incidence of HIV-associated primary intraocular and CNS