CMV retinitis is a severe opportunistic viral infection primarily occurring in advanced HIV disease when CD4 count falls below 50 cells/mm³. Untreated, it leads to progressive, irreversible retinal necrosis and blindness.

🦠 Aetiology & Pathophysiology

Caused by reactivation of latent CMV (a β-herpesvirus) in severely immunocompromised individuals.
Viral replication in retinal vascular endothelium → haemorrhagic necrosis, perivascular inflammation, and exudation.
May disseminate to involve optic nerve, brain (encephalitis), gastrointestinal tract, lungs, or other organs in disseminated CMV disease.

🧍‍♂️ Clinical Features

Typically occurs at CD4 <50 cells/mm³ (rare above 100 cells/mm³ with effective ART).
Symptoms: floaters, blurred vision, scotomas, photopsia (flashing lights), ocular pain (less common).
Often unilateral at presentation but progresses to bilateral in ~50% without treatment.
Fundoscopy: Classic “pizza-pie” or “cottage cheese and ketchup” appearance — confluent yellow-white areas of retinal necrosis with overlying retinal haemorrhages.

Characteristic Fundus Appearance:

Fundus photograph showing CMV retinitis with haemorrhagic necrosis

Classic CMV retinitis: haemorrhagic necrosis resembling a "pizza-pie" appearance (Wikipedia / public domain).

Another example of the "cottage cheese with ketchup" pattern — fluffy white necrosis with surrounding haemorrhages (MEDizzy).

Without therapy, rapid progression to retinal detachment, optic atrophy, and permanent blindness occurs.

🔍 Differential Diagnosis

HIV-associated toxoplasma chorioretinitis (more focal, less haemorrhagic).
Acute retinal necrosis (herpes simplex or varicella-zoster virus — peripheral, rapidly progressive).
Progressive outer retinal necrosis (VZV in profound immunosuppression).
Ischaemic or diabetic retinopathy.
Syphilitic or tuberculous chorioretinitis.

🧪 Investigations & Diagnosis

Clinical diagnosis: Characteristic fundoscopic findings are highly specific in the appropriate clinical context.
Dilated fundoscopy by ophthalmologist (gold standard).
Retinal photography and visual field testing for monitoring progression/response.
CMV PCR on vitreous fluid or aqueous humour (if diagnostic uncertainty).
Blood CMV PCR useful for systemic disease but poor predictor of retinitis relapse.
Urgent ophthalmology referral essential.

💊 Management (2025–2026 Guidelines)

Prevention

Routine dilated fundoscopic screening every 3–6 months in HIV patients with CD4 <100 cells/mm³ (or <50 in high-risk cases).
Primary prophylaxis not routinely recommended (no proven benefit vs toxicity).
Early initiation/optimisation of ART to maintain CD4 >100–200 cells/mm³ is most effective prevention.

Treatment

Preferred first-line (NIH Guidelines, July 2025; AI rating):

Regimen	Dosing	Indications/Notes
Valganciclovir (oral, preferred)	Induction: 900 mg PO twice daily × 14–21 days Maintenance: 900 mg PO once daily	Most cases; equivalent efficacy to IV; take with food.
Ganciclovir (IV)	Induction: 5 mg/kg IV every 12 hours × 14–21 days Maintenance: 5 mg/kg IV daily or switch to oral valganciclovir	Severe/sight-threatening (macula/optic disc involvement) or poor oral absorption; transition to oral when stable.

Sight-threatening lesions (within 1,500 microns of fovea or optic disc): Add intravitreal ganciclovir (2 mg/injection) or foscarnet (2.4 mg/injection) weekly during induction (BIII).

Alternatives (resistance, intolerance, or failure):

Foscarnet IV (BI): 60–90 mg/kg every 8–12 hours induction, then maintenance.
Cidofovir IV (CI): 5 mg/kg weekly × 2, then every 2 weeks (with probenecid; avoid if sulfonamide allergy).
Intravitreal foscarnet (for local control).

ART timing: Initiate/optimise HAART after initial CMV control (typically 2 weeks delay if sight-threatening) to reduce risk of immune reconstitution uveitis (IRU/IRIS).

Immune Recovery Uveitis (IRU)

Occurs post-ART with rising CD4; vitritis, macular oedema, even with inactive retinitis.
Treat active inflammation with corticosteroids (oral prednisone 1 mg/kg/day tapered, periocular, or intravitreal) + continue anti-CMV if needed (CIII).

Discontinuing Maintenance Therapy

After ≥3 months treatment, inactive lesions, and sustained CD4 ≥100 cells/mm³ on ART ≥3 months (AII).
Continue ophthalmologic monitoring (every 3 months initially, then yearly) for relapse/IRU (AIII).
Blood CMV PCR not recommended for relapse prediction (AII).

Monitoring & Follow-up

Close collaboration: HIV specialist + ophthalmologist.
Regular fundoscopy (weekly during induction if severe, then monthly).
Monitor for drug toxicities (e.g., neutropenia with ganciclovir/valganciclovir, nephrotoxicity with foscarnet/cidofovir).

📚 Key References (2025–2026)

NIH/CDC/HHS Opportunistic Infections Guidelines: Cytomegalovirus Disease (updated July 2025).
Asia-Pacific Vitreo-retina Society (APVRS) Consensus on CMV Retinitis (2025).
BHIVA Opportunistic Infection Guidelines (latest GI module 2024; aligns with valganciclovir preference).
EyeWiki & UpToDate: CMV Retinitis (updated 2025–2026).

This summary provides a concise, evidence-based overview suitable for clinical reference, teaching, or patient education.

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Cytomegalovirus (CMV) Retinitis ✅