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CMV infection

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CMV infection

Epidemiology

- worldwide distribution
- once infected an individual probably carries virus for life. Usually these infections remain latent. However if cell mediated immunity becomes impaired CMV reactivation syndromes may develop
- most primary CMV infections in organ transplant recipients result from transmission of the virus in the graft itself. In CMV seropositive transplant recipients infection results from reactivation of latent virus or, less commonly, from reinfections by a new strain of CMV

- about 25% of bone marrow and organ transplant recipients develop CMV pneumonitis. Infection may be primary/reactivation/superinfection
- incidence of clinical disease differs in 3 forms of infection: 60%, <20% and 20-50% respectively
- type of immunosuppression has important effect on incidence and severity of infection. Antilymphocyte antibodies have greatest effect in inducing CMV disease; cyclosporin, azathioprine, cyclophosphamide have intermediate effect; steroid minimal effect
- tends to cause infection 1-6 months post transplant
- transplanted organ particularly vulnerable as a target for CMV infection (ie CMV hepatitis follows liver transplantation)

Clinical features

In immunosuppressed patients CMV induces a variety of syndromes including:

  • fever and leucopaenia
  • hepatitis
  • pneumonitis
  • oesophagitis
  • gastritis
  • colitis
  • retinitis

Often begin with prolonged fever, malaise, anorexia, fatigue, night sweats, myalgia and arthralgia. Liver function abnormalities, leucopaenia, thrombocytopaenia and atypical lymphocytosis may be observed during these episodes
- dry cough, dyspnoea and hypoxia in pneumonitis. CXR: bilateral interstitial or reticulonodular infiltrates beginning in the periphery of the lower lobes and spreading centrally and superiorly. Localized segmental, nodular or alveolar patterns less commonly involved. Diagnosis requires lung biopsy or BAL. Most cases associated with bacterial, fungal or protozoal superinfection so it can be difficult to assess the clinical relevance of CMV isolation from respiratory secretions or positive serology.
- GI involvement may be localized or extensive
- fatal CMV infections often associated with persistent viraemia and multiple organ involvement. Progressive pulmonary infiltrates, pancytopaenia, hyperamylasaemia and hypotension are characteristic. Superinfection with bacterial, protozoa and fungi common.
- other early manifestations (1-6 months post transplant) of CMV infection include:

  • encephalitis
  • transverse myelitis
  • cutaneous vasculitis

Investigations

  • Diagnosis cannot usually be made reliably on clinical grounds alone.
  • Virus isolation from appropriate clinical specimens, together with demonstration of a fourfold or greater rise in antibody titre or persistently elevated titres is preferred diagnostic approach
  • Shell vial assay may expedite diagnosis when virus titres are too low to produce rapid diagnosis from tissue culture
  • CMV in blood more clinically significant than in oropharyngeal secretions/urine as excretion from the latter sites may continue for months to years following illness
  • Detection of CMV immediate-early antigens or DNA in peripheral WBCs may hasten diagnosis of disease in certain populations (eg organ transplant recipients). Positivity in such assays may antedate culture positivity by several days
  • Rises in Ab titres may not be detectable for up to 4 weeks after primary infection and titres often remain high for years after infection. Detection of CMV-specific IgM sometimes useful in the diagnosis of recent or active infection

Treatment

- ganciclovir (2-3 week course) and hyperimmune globulin to CMV or (pooled immunoglobulin). Latter thought to act as a modulator of the immune response as pneumonitis is mainly mediated by immunopathological mechanisms rather than the viral infection that causes damage in other tissues
- foscarnet is an alternative. Also inhibits viral DNA polymerase but because it does not phosphorylation to an active form it is effective against ganciclovir-resistant CMV. Adverse effects include renal dysfunction, hypomagnesaemia, hypokalaemia, hypocalcaemia, fits, fever and rash. All occur in >5% of patients

Prevention

- use of seronegative donors and blood products for seronegative recipients
- acyclovir in high dose from time of transplantation decreases risk of CMV disease significantly in BMT recipients and patients receiving kidney transplants from seropositive donors
- acyclovir does not prevent CMV disease in HIV positive patients
- conflicting results regarding effectiveness of ganciclovir, interferon and immune globulin in prophylaxis

Further reading

Ong ELC. Viral infections in the immunocompromised host. Hospital Update Apr '95

http://www.cdc.gov/ncidod/diseases/cmv.htm


© Charles Gomersall November 1999

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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