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CYTOMEGALOVIRUS DISEASE

CYTOMEGALOVIRUS DISEASE. In normal hosts: (a) If acquired by contact -- 1 o attack is asymptomatic or mononucleosis with subclinical hepatitis. (b) If by transfusion -- “post-transfusion syndrome”: fever and mononucleosis, FUO, granulomatous hepatitis.

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CYTOMEGALOVIRUS DISEASE

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  1. CYTOMEGALOVIRUS DISEASE In normal hosts: • (a) If acquired by contact -- 1o attack is asymptomatic or mononucleosis with subclinical hepatitis. • (b) If by transfusion -- “post-transfusion syndrome”: fever and mononucleosis, FUO, granulomatous hepatitis. In hosts with impaired T-cell immunity and in fetuses: • Fetus -- cytomegalic inclusion disease (TORCH) syndrome: petechial rash, hepatosplenomegaly, thrombocytopenia, anemia, CNS damage, low birth weight. Most congenital CMV infections are subtle (mental retardation, partial deafness, eye disease or asymptomatic). CMV is a common infectious cause of congenital abnormality.

  2. CMV Routes of Infection 1. Saliva 2. Sexual contact 3. Transfusion 4. Organ transplant (usually renal)

  3. CMVDiagnosis Difficult on clinical data alone…viral culture (2-4 weeks), serology by indirect immunofluorescence, cytology on concentrated urine

  4. CMV Treatment The antiviral drugs, cidofovir and ganciclovir, are the drugs of choice for CMV retinitis and pneumonitis- ganciclovir is more toxic than cidofovir. Experimental live attenuated vaccines are being developed but unknown efficacy or safety.

  5. EPSTEIN-BARR VIRUS • EBV is a herpesvirus first seen by electron microscopy of neoplastic cells from a Burkitt’s lymphoma (BL) in 1964. • Antibody to EBV is found in sera of almost all patients with BL or nasopharyngeal carcinoma. • Antibody to EBV was found in 80% of low-income adults in Philadelphia and 100% of adults in developing countries; most didn’t have BL. • EBV usually results in infectious mononucleosis (IM) in North America and BL in Africa and other parts of the world.

  6. EBV Disease Characteristics • EBV can be cultured in normal human B lymphocytes (virus attaches to complement C3b receptor) which then begin to behave like neoplastic lymphoma cells. These cells undergo blastogenesis and begin secreting vast amounts of polyclonal (heterophile) immunoglobulins. • Infection is followed by the prompt appearance of cytotoxic T cells which proceed to turn off activated B cells (the “atypical lymphocytes” are the T cells). • Heterophil Ab ( IgM antibodies which agglutinate sheep and horse RBCs) appears in 80% of patients with IM. These antibodies appear approximately four weeks after onset of symptoms, but are not EBV specific antibodies.

  7. Epatein-Barr Virus (EBV) Infection

  8. Diagnostic Procedures For Herpesviruses 1. Cell Culture: Cell rounding > fusion > giant cell formation (HSV) 2. Immunofluorescence: Intense nuclear staining for all herpesviruses 3. ELISA and Western Blot: Specificity based on glycoprotein 4. PCR 5. TORCH: Serologic assay

  9. TORCH - Syndrome Toxoplasma To Rubella R Cytomegalovirus C Herpes Simplex H

  10. Chickenpox lesions Zoster lesions

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