Synopsis
Distinguish benign primary cytomegalovirus from tissue-invasive and congenital disease, choose the diagnostic compartment correctly, and deliver safe specialist antiviral treatment.
- CMV is a betaherpesvirus that remains latent after primary infection and reactivates most dangerously when T-cell immunity is impaired.
- Primary infection in an immunocompetent adult is often asymptomatic or produces a heterophile-negative mononucleosis with fever, fatigue, lymphocytosis and mild hepatitis.
- Blood quantitative CMV PCR measures replication and treatment response in immunocompromised hosts, but DNAaemia alone does not prove gastrointestinal, pulmonary or retinal tissue disease.
Key red flags
New floaters, flashing lights, visual-field loss or reduced acuity in advanced HIV or transplantation requires same-day ophthalmology for possible CMV retinitis.
Painless floaters, blurred vision, photopsia or field loss accompanies haemorrhagic white retinal necrosis in severe cellular immune deficiency.
Investigation priorities
Assess prior exposure and support timing of primary maternal or immunocompetent infection.
Management branches
A person with HIV, transplantation or major immunosuppression has compatible symptoms or a rising CMV viral load.
- Assess visual, gastrointestinal, respiratory, neurological and graft symptoms alongside immune status, current prophylaxis and competing opportunistic infections.
- Send quantitative blood CMV PCR, FBC, renal and liver tests, but arrange the relevant retinal examination, endoscopy or organ sample when tissue invasion is suspected.
Key medicines
Intravenous ganciclovirGive 5 mg/kg intravenously every 12 hours for induction, with course length set by organ response; CMV colitis usually requires two to four weeks or until symptoms resolve.
Oral valganciclovir inductionGive 900 mg orally twice daily with food for 21 days for active CMV retinitis when creatinine clearance is at least 60 mL/min; use the SmPC renal table below that threshold.