SN3 SHORT NOTE 5M ★ High-yield

Describe cytomegalovirus infection with its clinical forms, diagnosis and treatment.

Microbiology · 2nd Professional — Para-Clinical

The Virus and its Transmission

Cytomegalovirus (HHV-5) — the largest of the herpesviruses, an enveloped double-stranded DNA virus establishing lifelong latency in monocytes and their precursors
Highly species-specific and slow-growing in culture, producing a characteristic cytopathic effect with cell enlargement — "cytomegaly"
Seroprevalence exceeds 80 to 90% in Indian adults, acquisition occurring in childhood; primary infection in the immunocompetent is almost always silent
Transmission — saliva, urine, breast milk, sexual contact, blood transfusion, organ transplantation, and transplacentally. Infected children excrete virus in urine and saliva for months to years, which is why young children are a major source

Clinical Disease

Setting	Features
Immunocompetent	Usually asymptomatic. May cause a mononucleosis-like illness with fever and atypical lymphocytes but a negative Paul-Bunnell (heterophile) test — the commonest cause of "heterophile-negative mononucleosis"
Congenital	The commonest congenital viral infection and a leading infectious cause of sensorineural deafness and of neurodevelopmental disability. Risk is highest with primary maternal infection. Features: intrauterine growth restriction, microcephaly, periventricular calcification, chorioretinitis, hepatosplenomegaly, jaundice, thrombocytopenia with a "blueberry muffin" rash. Most infected infants are asymptomatic at birth, yet a proportion develop late deafness
Transplant recipients	The single most important infection after solid organ and stem cell transplantation — fever, leucopenia, pneumonitis, hepatitis, colitis, retinitis; and it also predisposes to graft rejection and to other infections
Advanced HIV (CD4 below 50)	CMV retinitis — a progressive "pizza pie" or "cottage cheese and ketchup" retinopathy causing blindness; also colitis, oesophagitis and encephalitis
Transfusion-associated	Prevented by leucodepletion or by CMV-negative products for at-risk recipients

CLINICAL PEARL

Most congenitally infected infants look normal at birth and some go deaf later, which is why screening matters. Roughly 90% are asymptomatic at delivery, and a proportion of those develop progressive sensorineural hearing loss over the following years — after the newborn hearing screen has been passed. Congenital CMV is therefore a leading cause of non-genetic deafness that is invisible at the one moment everybody is looking.

Diagnosis and Treatment

Histology — large cells with the characteristic "owl eye" intranuclear inclusion surrounded by a clear halo
PCR for CMV DNA with quantitative viral load is the mainstay, used both to diagnose and to monitor treatment and to guide pre-emptive therapy in transplant recipients
Pp65 antigenaemia assay in leucocytes; culture on human fibroblasts, with the shell vial method giving a faster result
Serology — IgM and IgG with avidity testing to distinguish primary from past infection in pregnancy, which is the key distinction for fetal risk
Congenital infection is confirmed by detecting virus in urine or saliva within the first 3 weeks of life; after that, a positive result cannot distinguish congenital from perinatal acquisition
Treatment — ganciclovir and oral valganciclovir (limited by myelosuppression); foscarnet (nephrotoxic and causes electrolyte disturbance) and cidofovir as alternatives; letermovir for prophylaxis in stem cell transplantation. Valganciclovir in symptomatic congenital infection improves hearing and developmental outcomes

Applied Aspects

Test the urine or saliva within 3 weeks in a suspected congenital infection; after that window the opportunity to prove it is lost, and with it the case for antiviral treatment
Arrange long-term audiological follow-up for congenitally infected infants, including those who are asymptomatic and pass the newborn screen
Advise pregnant women on hygiene — handwashing after nappy changes, not sharing utensils or food with toddlers, and avoiding kissing young children on the mouth; these simple measures reduce seroconversion and there is no vaccine
Monitor transplant recipients with quantitative PCR and use pre-emptive or prophylactic antiviral therapy, which has substantially improved outcomes
Examine the fundus in any patient with advanced HIV and visual symptoms; CMV retinitis is sight-threatening, progresses rapidly and is treatable, and antiretroviral therapy restoring the CD4 count is the definitive answer
Use leucodepleted or CMV-negative blood for neonates, transplant recipients and other at-risk patients

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