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CYTOMEGALOVIRUS
Introduction
• CMV is a herpesvirus, has a double stranded RNA and renders infected cells 2-4
times the size of surrounding cells
• The cytomegalovirus cells contain an eccentrically placed intranuclear inclusion
surrounded by a clear halo with an “owl eye appearance”.
Mode of transmission
• Common in perinatal and childhood age groups. CMV is one of the TORCH infections.
• Most post-childhood infections are acquired from asymptomatic excreters who shed
virus in saliva, urine, semen and genital secretions.
• Sexual transmission and oral spread are common among adults and adolescent age
group.
• The virus can be spread in breast milk, saliva, feces and urine.
Pathogenesis
• Primary CMV infection is associated with vigorous T lymphocytes response and
activation of CD8+ T cells.
• Latent CMV infection persists throughout life and is oftren triggered by
depressed cell mediated immunity
• CMV also increases the risk of infection with opportunistic pathogens by
decreasing T cell responsiveness.
Clinical features
1. Congenital CMV Infection
o Petechiae, hepatosplenomegaly, and jaundice are present in 60–80% of cases; microcephaly
with or without cerebral calcifications, intrauterine growth retardation, prematurity, and
chorioretinitis are less common.
o The mortality rate is 20–30% among infants with severe disease; survivors have intellectual
or hearing difficulties.
2. Perinatal CMV Infection
o Perinatal infection with CMV is acquired by breast-feeding or contact with infected
maternal secretions (e.g., in the birth canal). Although most pts are asymptomatic, disease
similar to—but less severe than—congenital CMV can occur.
3. CMV Mononucleosis
o Symptoms last 2–6 weeks and include high fevers, profound fatigue and malaise, myalgias,
headache, and splenomegaly; in contrast to EBV infection, exudative pharyngitis and
cervical lymphadenopathy are rare in CMV infection.
4. CMV Infection in the Immunocompromised Host
o CMV is the most common and important viral pathogen complicating organ transplantation,
with the greatest risk of infection at 1–4 months after transplantation. HIV-infected pts with
CD4+ T cell counts of <50–100/μL are at risk for severe CMV disease.
Investigation
Congenital CMV
• Laboratory findings include elevated values in LFTs, thrombocytopenia, conjugated
hyperbilirubinemia, hemolysis, and increased CSF protein levels
CMV mononucleosis
• Laboratory findings include relative lymphocytosis with >10% atypical lymphocytes,
transaminitis, and immunologic abnormalities (e.g., the presence of cryoglobulins,
rheumatoid factor, or cold agglutinins). Recovery is generally complete, but postviral
asthenia can persist for months
Diagnosis requires isolation of CMV or detection of its antigens or DNA in appropriate clinical
specimens in conjunction with a compatible clinical syndrome. Immunofluorescence assays for
CMV antigens (pp65), PCR, viral culture, and serology are all useful means of detection.
Complications
1. Meningoencephalitis
2. Guillain–Barré syndrome
3. autoimmune haemolytic anaemia
4. Thrombocytopenia
5. myocarditis and
6. skin eruptions -such as ampicillin-induced rash.
7. Immunocompromised patients can develop hepatitis, oesophagitis, colitis,
pneumonitis, retinitis, encephalitis and polyradiculitis
Treatment
• Ganciclovir – 5mg/kg IV bid for 14-21 days
• Valganciclovir (the oral prodrug of ganciclovir)
• Foscarnet inhibits CMV DNA polymerase and is active against most ganciclovir-
resistant CMV isolates.
• Cidofovir is a nucleotide analogue that is also effective against CMV; however, it
can cause severe nephrotoxicity by proximal tubular cell injury.
• CMV immune or hyperimmune globulin may reduce the risk of CMV disease

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Cytomegalo vrius

  • 2. Introduction • CMV is a herpesvirus, has a double stranded RNA and renders infected cells 2-4 times the size of surrounding cells • The cytomegalovirus cells contain an eccentrically placed intranuclear inclusion surrounded by a clear halo with an “owl eye appearance”.
  • 3. Mode of transmission • Common in perinatal and childhood age groups. CMV is one of the TORCH infections. • Most post-childhood infections are acquired from asymptomatic excreters who shed virus in saliva, urine, semen and genital secretions. • Sexual transmission and oral spread are common among adults and adolescent age group. • The virus can be spread in breast milk, saliva, feces and urine.
  • 4. Pathogenesis • Primary CMV infection is associated with vigorous T lymphocytes response and activation of CD8+ T cells. • Latent CMV infection persists throughout life and is oftren triggered by depressed cell mediated immunity • CMV also increases the risk of infection with opportunistic pathogens by decreasing T cell responsiveness.
  • 5. Clinical features 1. Congenital CMV Infection o Petechiae, hepatosplenomegaly, and jaundice are present in 60–80% of cases; microcephaly with or without cerebral calcifications, intrauterine growth retardation, prematurity, and chorioretinitis are less common. o The mortality rate is 20–30% among infants with severe disease; survivors have intellectual or hearing difficulties. 2. Perinatal CMV Infection o Perinatal infection with CMV is acquired by breast-feeding or contact with infected maternal secretions (e.g., in the birth canal). Although most pts are asymptomatic, disease similar to—but less severe than—congenital CMV can occur. 3. CMV Mononucleosis o Symptoms last 2–6 weeks and include high fevers, profound fatigue and malaise, myalgias, headache, and splenomegaly; in contrast to EBV infection, exudative pharyngitis and cervical lymphadenopathy are rare in CMV infection. 4. CMV Infection in the Immunocompromised Host o CMV is the most common and important viral pathogen complicating organ transplantation, with the greatest risk of infection at 1–4 months after transplantation. HIV-infected pts with CD4+ T cell counts of <50–100/μL are at risk for severe CMV disease.
  • 6. Investigation Congenital CMV • Laboratory findings include elevated values in LFTs, thrombocytopenia, conjugated hyperbilirubinemia, hemolysis, and increased CSF protein levels CMV mononucleosis • Laboratory findings include relative lymphocytosis with >10% atypical lymphocytes, transaminitis, and immunologic abnormalities (e.g., the presence of cryoglobulins, rheumatoid factor, or cold agglutinins). Recovery is generally complete, but postviral asthenia can persist for months Diagnosis requires isolation of CMV or detection of its antigens or DNA in appropriate clinical specimens in conjunction with a compatible clinical syndrome. Immunofluorescence assays for CMV antigens (pp65), PCR, viral culture, and serology are all useful means of detection.
  • 7. Complications 1. Meningoencephalitis 2. Guillain–Barré syndrome 3. autoimmune haemolytic anaemia 4. Thrombocytopenia 5. myocarditis and 6. skin eruptions -such as ampicillin-induced rash. 7. Immunocompromised patients can develop hepatitis, oesophagitis, colitis, pneumonitis, retinitis, encephalitis and polyradiculitis
  • 8. Treatment • Ganciclovir – 5mg/kg IV bid for 14-21 days • Valganciclovir (the oral prodrug of ganciclovir) • Foscarnet inhibits CMV DNA polymerase and is active against most ganciclovir- resistant CMV isolates. • Cidofovir is a nucleotide analogue that is also effective against CMV; however, it can cause severe nephrotoxicity by proximal tubular cell injury. • CMV immune or hyperimmune globulin may reduce the risk of CMV disease