RESPIRATORY
SYNCYTIAL VIRUS
|
Structure
& Property |
Transmission |
Pathogenesis |
Clinical
findings |
Laboratory
diagnosis |
Treatment |
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Family: paramyxovirus Genome: one piece of single-stranded RNA Nucleocapsid: helical Lipoprotein envelope: - only fusion proteins - cause cells to fuse, forming syncytia Only one antigenic type Antibody against fusion protein neutralizes infectivity. |
Humans and chimpanzees are natural hosts. Transmission occurs via respiratory droplets and by direct contact of contaminated hands with nose or mouth. Causes outbreaks of respiratory infections every winter. Causes outbreaks of respiratory infections in hospitalized infants. Infected children shed virus in respiratory secretions for 3-8 days. |
Invade lower respiratory tract. Infants: - more severe - involves lower respiratory tract - localized infection - viremia does not occur Immunopathogenesis: - maternal antibody passed to infant react with virus & damage respiratory tract cells - immune complexes (IgG + virus), IgE, and histamine may be involved. Multiple RSV infections – incomplete immunity |
Bronchiolitis: - young children with peak at age 3 months. - fever - cough -dyspnea - tachypnea -wheezing - cyanosis Complications: - pneumonia - secondary bacterial infections - otitis media - cardiac failure -apnea Up to 5% mortality in bronchiolitis & pneumonia High mortality associated with CNS malformations, congenital disease of heart and lung Upper respiratory tract infection in older children and adults |
Tissue culture: - inoculate HeLa or Hep-2 cells - highly characteristic refractile syncytium formation of multinucleated giant cells Immunofluoresence: on smears of respiratory epithelium or by isolation in cell culture. A rise in antibody titer of at least 4-fold Does not haemagglutinate Isolation: - mouth washings - nasal secretions |
Ribavirin aerosol therapy Ventilatory support No effective vaccine Isolate infected hospitalized children |