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Infectious Diseases
Transplant Medicine
Ophthalmology
Neonatology

Cytomegalovirus (CMV)

High EvidenceUpdated: 2025-12-24

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Red Flags

  • CMV Retinitis (Visual Loss in HIV/AIDS)
  • Congenital CMV (Leading Cause of Congenital Deafness)
  • CMV Pneumonitis (Post-Transplant)
  • CMV Colitis (Severe GI Disease)
Overview

Cytomegalovirus (CMV)

1. Clinical Overview

Summary

Cytomegalovirus (CMV), also known as Human Herpesvirus 5 (HHV-5), is a ubiquitous herpesvirus that establishes lifelong latent infection after primary exposure. Most immunocompetent individuals are infected asymptomatically or with a mild mononucleosis-like illness. However, CMV causes severe disease in immunocompromised patients: CMV Retinitis (Blindness in AIDS, CD4 less than 50), CMV Colitis, CMV Pneumonitis (Transplant recipients), and CMV Encephalitis. Congenital CMV is the leading infectious cause of congenital deafness and neurodevelopmental disability worldwide. Diagnosis is by CMV PCR (Blood/Tissue) or Histopathology (Owl's Eye inclusions). Treatment is with Ganciclovir (IV) or Valganciclovir (Oral); Foscarnet or Cidofovir are second-line. Prevention in transplant includes CMV prophylaxis or pre-emptive monitoring. [1,2]

Clinical Pearls

"Monospot-Negative Mono": Primary CMV in immunocompetent adults presents like Glandular Fever (EBV) but with Negative Monospot (Heterophile antibody test).

CMV Retinitis = CD4 less than 50: In HIV/AIDS, CMV retinitis occurs at very low CD4 counts. "Pizza Pie" or "Cottage Cheese and Ketchup" fundus appearance.

Congenital CMV = Commonest Congenital Infection: Leading infectious cause of sensorineural hearing loss. Screen neonates with symptoms.

Transplant CMV: Major cause of morbidity. D+/R- (Donor positive, Recipient negative) highest risk. Prophylaxis or Pre-emptive strategy.


2. Epidemiology

Prevalence

  • Highly Prevalent: 50-80% of adults seropositive by age 40 (Higher in developing countries).
  • Transmission: Saliva, Urine, Sexual contact, Blood transfusion, Organ transplant, Vertical (Congenital).

At-Risk Groups

GroupRisk
ImmunocompetentAsymptomatic or Mild mononucleosis. Self-limiting.
HIV/AIDS (CD4 less than 50)CMV Retinitis, Colitis, Encephalitis. Opportunistic infection.
Solid Organ Transplant (SOT)CMV Syndrome, Tissue-Invasive Disease. D+/R- highest risk.
Haematopoietic Stem Cell Transplant (HSCT)CMV Pneumonitis (High mortality).
Congenital (In Utero)Primary maternal infection during pregnancy → Congenital CMV.
Neonates (Perinatal)Breast milk transmission. Usually asymptomatic in term infants.

3. Pathophysiology

Virology

  • CMV = Human Herpesvirus 5 (HHV-5).
  • Latency: After primary infection, establishes lifelong latency in myeloid progenitor cells (Monocytes).
  • Reactivation: When immune control is lost (Immunosuppression, HIV, Transplant).

Mechanism of Disease

  1. Primary Infection: Usually asymptomatic or mild mononucleosis in immunocompetent.
  2. Latency Establishment: Virus persists in myeloid cells.
  3. Reactivation (Immunosuppression): Virus replicates, causes end-organ disease.
  4. Tissue Tropism: Retina, GI tract, Lung, Liver, CNS.
  5. Histopathology: Owl's Eye Inclusions (Large cells with intranuclear inclusions). Pathognomonic.

4. Clinical Syndromes

Immunocompetent Host

PresentationNotes
AsymptomaticMost common.
CMV MononucleosisFever, Fatigue, Lymphadenopathy, Hepatosplenomegaly. Monospot Negative (Unlike EBV). Atypical Lymphocytes on blood film. Self-limiting.

Immunocompromised Host (HIV, Transplant)

SyndromeClinical FeaturesNotes
CMV RetinitisFloaters, Visual field defects, Blindness. "Pizza Pie" / "Cottage Cheese & Ketchup" fundus (Haemorrhages + Exudates).CD4 less than 50 in HIV. Ophthalmology emergency.
CMV ColitisDiarrhoea (May be bloody), Abdominal pain, Fever. Colonic ulceration.Biopsy shows Owl's Eye inclusions.
CMV OesophagitisOdynophagia, Dysphagia. Large shallow ulcers.Differentiate from Candida (White plaques) and HSV (Small ulcers).
CMV PneumonitisCough, Dyspnoea, Hypoxia. Interstitial infiltrates.High mortality in HSCT.
CMV EncephalitisConfusion, Altered consciousness, Seizures.Rare. PCR on CSF.
CMV Syndrome (Post-Transplant)Fever, Malaise, Leucopenia, Thrombocytopenia. No specific organ involvement.Common after SOT.

Congenital CMV

FeatureNotes
Asymptomatic (~90%)May still develop late sequelae (Hearing loss).
Symptomatic (~10%)IUGR, Microcephaly, Periventricular Calcifications (Imaging), Hepatosplenomegaly, Jaundice, Thrombocytopenia (Petechiae/Purpura – "Blueberry Muffin" rash), Chorioretinitis.
Late SequelaeSensorineural Hearing Loss (Leading cause of non-genetic congenital deafness – ~20% of asymptomatic, ~50% of symptomatic). Developmental delay.

5. Investigations

Diagnosis

TestUseNotes
CMV DNA PCR (Blood/Plasma)Detect viraemia. Quantitative. Monitor treatment.Gold standard for transplant monitoring.
CMV IgG / IgM SerologyDetermine serostatus (Prior exposure). Primary infection (IgM positive + IgG seroconversion).Limited use in immunocompromised (Antibody production impaired).
CMV PCR (CSF)CMV Encephalitis.
Tissue Biopsy + HistopathologyCMV Colitis, Pneumonitis.Owl's Eye Inclusions (Large intranuclear + Cytoplasmic inclusions in enlarged cells). Immunohistochemistry.
FundoscopyCMV Retinitis.Ophthalmology referral. Characteristic appearance.

Congenital CMV

TestUse
Urine CMV PCR (Within first 3 weeks of life)Gold standard for diagnosis of Congenital CMV. Saliva CMV PCR also used.
Cranial Imaging (USS/MRI)Periventricular calcifications, Microcephaly.
Hearing Assessment (ABR)Screen for SNHL.

Transplant Monitoring

  • CMV PCR Viral Load: Monitored regularly post-transplant (Weekly).
  • Pre-Emptive Strategy: Initiate treatment if viraemia rises above threshold.

6. Management

Management Algorithm

       CMV INFECTION IDENTIFIED
       (PCR Positive / Tissue-Invasive Disease / Retinitis)
                     ↓
       ASSESS IMMUNE STATUS & SYNDROME
    ┌────────────────┴────────────────┐
 IMMUNOCOMPETENT                IMMUNOCOMPROMISED
    ↓                           (HIV, Transplant)
 USUALLY SELF-LIMITING              ↓
 Supportive Care Only       TREAT CMV DISEASE

Treatment of CMV Disease

AgentRouteDoseNotes
GanciclovirIV5mg/kg BD x 14-21 days (Induction), then 5mg/kg OD (Maintenance)First-line for serious CMV disease.
ValganciclovirOral900mg BD x 21 days (Induction), then 900mg OD (Maintenance)Oral prodrug of Ganciclovir. Used for less severe disease or as step-down.
FoscarnetIV60mg/kg TDS or 90mg/kg BDSecond-line. Ganciclovir-resistant CMV. Renal dose adjustment essential.
CidofovirIV5mg/kg weekly x 2 weeks, then 5mg/kg every 2 weeksThird-line. Nephrotoxic. Must give with Probenecid + IV fluids.

Key Side Effects

AgentMajor Side Effects
Ganciclovir / ValganciclovirBone Marrow Suppression (Neutropenia, Thrombocytopenia, Anaemia). Monitor FBC.
FoscarnetNephrotoxicity, Electrolyte abnormalities (Hypocalcaemia, Hypomagnesaemia).
CidofovirNephrotoxicity (Dose-limiting).

Duration of Treatment

  • CMV Retinitis (AIDS): Induction x 14-21 days, then Maintenance until Immune Reconstitution (CD4 >100 for 3-6 months on ART).
  • CMV Colitis/Pneumonitis: 14-21 days (May be longer if severe).

CMV in HIV/AIDS

  • Immune Reconstitution: Start/Optimise ART. Primary goal is to raise CD4.
  • CMV Retinitis: Urgent Ophthalmology. Treat with Ganciclovir/Valganciclovir.

CMV Prevention in Transplant

StrategyDescription
ProphylaxisGive Valganciclovir to all at-risk patients (D+/R-, etc.) for 3-6 months post-transplant.
Pre-Emptive TherapyMonitor CMV PCR weekly. Treat if viraemia rises above threshold.

Congenital CMV Treatment

  • Symptomatic Congenital CMV: Valganciclovir 6 months (Improves hearing outcomes). Start within first month of life.

7. Complications
ComplicationNotes
Blindness (Retinitis)Permanent if untreated.
Colonic Perforation (Colitis)Severe ulcerative disease.
Respiratory Failure (Pneumonitis)High mortality in HSCT.
Sensorineural Hearing Loss (Congenital)Progressive. Leading infectious cause of congenital deafness.
Neurodevelopmental Delay (Congenital)Microcephaly, Cerebral Palsy.

8. Prognosis and Outcomes
  • Immunocompetent: Excellent. Self-limiting.
  • Immunocompromised: Dependent on immune reconstitution / Transplant function. CMV Retinitis can be controlled with treatment and ART.
  • Congenital CMV: Symptomatic infants have ~50% risk of significant sequelae. Asymptomatic infants have ~10-15% risk of late-onset hearing loss.

9. Evidence and Guidelines

Key Guidelines

GuidelineOrganisationKey Recommendations
BHIVA Guidelines: CMV in HIVBHIVAART + Ganciclovir/Valganciclovir for Retinitis. Maintenance until immune reconstitution.
Transplant Society GuidanceInternationalProphylaxis or Pre-emptive monitoring. D+/R- highest risk.
AAP / CDC Congenital CMVAAP/CDCValganciclovir for symptomatic congenital CMV. Universal screening debated.

10. Patient and Layperson Explanation

What is CMV?

CMV (Cytomegalovirus) is a very common virus that most people catch at some point in their lives. In healthy people, it usually causes no symptoms or a mild flu-like illness. Once you've had it, the virus stays in your body for life but doesn't usually cause problems.

When is CMV a problem?

It becomes serious in people with weak immune systems (e.g., HIV/AIDS, organ transplant recipients), where it can cause eye problems (CMV Retinitis, which can cause blindness), gut problems (diarrhoea, bleeding), and lung problems.

It is also important in pregnancy – if a mother is infected for the first time during pregnancy, the baby can be affected (Congenital CMV), which can cause hearing loss and developmental problems.

How is it treated?

Antiviral medications (Ganciclovir or Valganciclovir) are used to treat CMV in people with weakened immune systems. These can have side effects on blood counts, so regular monitoring is needed.


11. References

Primary Sources

  1. Griffiths P, et al. The pathogenesis of human cytomegalovirus. J Pathol. 2015;235(2):288-297. PMID: 25205268.
  2. BHIVA Guidelines on Opportunistic Infections in HIV: CMV. 2021.

12. Examination Focus

Common Exam Questions

  1. CMV Retinitis CD4 Count: "At what CD4 count does CMV Retinitis typically occur?"
    • Answer: CD4 less than 50 cells/μL.
  2. Histopathology Finding: "What is the pathognomonic histopathological finding in CMV infection?"
    • Answer: Owl's Eye Inclusions – Large cells with intranuclear and cytoplasmic inclusions.
  3. Monospot-Negative Mono: "A patient presents with a mononucleosis-like illness but Monospot is negative. What is the likely cause?"
    • Answer: CMV (Primary Cytomegalovirus infection).
  4. Congenital CMV Sequelae: "What is the leading infectious cause of congenital sensorineural hearing loss?"
    • Answer: Congenital CMV.

Viva Points

  • Ganciclovir Side Effect: Bone marrow suppression (Neutropenia).
  • Transplant CMV Risk: D+/R- (Donor CMV positive, Recipient negative) is highest risk.

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.

Last updated: 2025-12-24

At a Glance

EvidenceHigh
Last Updated2025-12-24

Red Flags

  • CMV Retinitis (Visual Loss in HIV/AIDS)
  • Congenital CMV (Leading Cause of Congenital Deafness)
  • CMV Pneumonitis (Post-Transplant)
  • CMV Colitis (Severe GI Disease)

Clinical Pearls

  • **"Monospot-Negative Mono"**: Primary CMV in immunocompetent adults presents like Glandular Fever (EBV) but with **Negative Monospot (Heterophile antibody test)**.
  • **CMV Retinitis = CD4 less than 50**: In HIV/AIDS, CMV retinitis occurs at very low CD4 counts. "Pizza Pie" or "Cottage Cheese and Ketchup" fundus appearance.
  • **Congenital CMV = Commonest Congenital Infection**: Leading infectious cause of sensorineural hearing loss. Screen neonates with symptoms.
  • **Transplant CMV**: Major cause of morbidity. D+/R- (Donor positive, Recipient negative) highest risk. Prophylaxis or Pre-emptive strategy.

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines