Cytomegalovirus Retinitis

CMV is one of the most puzzling members of the Herpesviridae family. Ocular involvement has been reported during congenital infection and in patients with acquired immunodeficiency syndrome (AIDS) [34]. Primary infection during pregnancy is the major cause of in-trauterine infection in developed countries, with a mortality rate of 20 % and a risk of retinitis in 15% of children. Before the use of highly active antiretroviral therapy (HAART) in AIDS patients, CMV disease was the major cause of blindness. CMV retinitis was observed late during the disease and the risk was significant when the level of CD4 lymphocytes dropped below 50-100/mm3. In a small percentage of patients, CMV retinitis may be the first clinical manifestation of AIDS. CMV retinitis is probably secondary to the passage of the virus across the blood retinal barrier, when local defense mechanisms are almost completely abolished. Viral progression into the retina seems to occur in a polarized manner. The internal blood-retinal barrier is initially disrupted after primary replication in endothelial cells, allowing viral particles to reach retinal glial cells. CMV then spreads towards the retinal pigment epithelium. The retinal site of HCMV latency is still under debate: retinal pigment epithelium or glial cells are two putative candidates. CMV retinitis occurs initially in the peripheral retina. Visual complaints remain rare for a long period of time. Systematic fundus examination should be performed every 3 months if CD4 lymphocytes counts are below 50/mm3. Active CMV retinitis is usually diagnosed on ophthalmoscopic signs, such as white fluffy areas of necrotizing retinitis associated with haemorrhages and vascular sheathing. Early CMV retinitis may begin with a small, white retinal infiltrate. The lesion may masquerade as a cotton-wool spot present in HIV-related microvasculopathy. Fundus examination must be controlled in order to confirm a putative CMV retinitis. Two distinct subtypes of CMV retinitis have been described. The fulminant or edematous variant is the classic appearance of disease (Fig. 10.6). Dense, white confluent opacifications of the retina without any central atrophic lesion occur usually along vessels associated with retinal haemorrhages and inflammatory vascular sheathing. The indolent or granular variant of disease associates granular foci of retinal necrosis with a central atroph-ic zone, fewer haemorrhages and less vascular sheathing. The border of retinal necrosis is usually irregular in both variants, surrounded by

Cytomegalovirus Retinitis

Fig. 10.7. Atypical aspect of VZV-associated retinitis with diffuse retinal hemorrhages 2 weeks after an episode of varicella

Fig. 10.6. PCR-proven CMV retinitis in a patient with a previous history of macular toxoplasmosis satellite infiltrates. The optic disk is rarely infiltrated initially, but papillitis may be observed when retinitis progresses toward the posterior pole. Mild vitritis is associated with minor anterior segment inflammation. Despite slow progression of retinitis, destruction of the entire retina occurs within 3-6 months in the absence of anti-CMV therapy. Cicatricial lesions are at-rophic retina with vessel rarefaction. Fluores-cein angiography may be helpful in complex cases, when other differential diagnoses such as retinochoroidal toxoplasmosis, candida en-dophthalmitis, syphilitic retinitis, herpes simplex and herpes zoster retinitis are suspected.

The administration of HAART to AIDS patients has dramatically changed the course of CMV disease by improving the function of the immune system and increasing survival [37,55]. If CD4 cell counts increase after HAART, a beneficial effect on viral recurrences may be observed and anti-CMV maintenance therapy can be discontinued [69]. In patients presenting with previous areas of CMV retinitis before immune restitution under HAART, episodes of posterior uveitis, vitritis, retinal vasculitis, papillitis and macular edema have been reported [12, 38]. The patho-physiology of disease, known as immune recovery uveitis, remains controversial [57]. However, personal data and results reported recently seem to exclude viral replication and highlight an immune reaction due to restoration of lymphocytes recognizing chronically infected retinal cells expressing CMV antigens at their surface.

Fig. 10.7. Atypical aspect of VZV-associated retinitis with diffuse retinal hemorrhages 2 weeks after an episode of varicella

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