Varicella-Zoster Virus Infection in Children and Adolescents
Varicella-Zoster Virus Infection in Children and Adolescents
Varicella is primarily transmitted human-to-human via the nasopharynx or conjunctiva, through mucosal inoculation with droplets and aerosols from VZV- or HZ- infected persons. The infectious period occurs within 1 to 2 days before the onset of rash (through nasopharyngeal secretions) or within 5 to 7 days after appearance of rash (through skin lesions). This period of contagiousness can be extended in immunocompromised persons. The virus has an average incubation period of 14 to 16 days (range: 10–21 days).
After inoculation, there is a primary viremia phase where the virus disseminates and multiplies in the viscera and reticuloendothelial tissues. A secondary viremia phase occurs at about 14 days post infection where there is a viral spread to the nasopharyngeal surface and the skin, leading to the appearance of typical maculopapular vesicular rashes. These vesicular rashes are highly concentrated with the virus and are very contagious until crusted. The virus can also infiltrate the CNS and become dormant in the dorsal root and cranial nerve ganglia, to be reactivated at a later period in the human life cycle as HZ infection. While there is a favorable outcome with the primary infection, children with underlying HIV infection showed a higher incidence of the secondary zoster infection in early stages of life.
Transmission and Pathophysiology
Varicella is primarily transmitted human-to-human via the nasopharynx or conjunctiva, through mucosal inoculation with droplets and aerosols from VZV- or HZ- infected persons. The infectious period occurs within 1 to 2 days before the onset of rash (through nasopharyngeal secretions) or within 5 to 7 days after appearance of rash (through skin lesions). This period of contagiousness can be extended in immunocompromised persons. The virus has an average incubation period of 14 to 16 days (range: 10–21 days).
After inoculation, there is a primary viremia phase where the virus disseminates and multiplies in the viscera and reticuloendothelial tissues. A secondary viremia phase occurs at about 14 days post infection where there is a viral spread to the nasopharyngeal surface and the skin, leading to the appearance of typical maculopapular vesicular rashes. These vesicular rashes are highly concentrated with the virus and are very contagious until crusted. The virus can also infiltrate the CNS and become dormant in the dorsal root and cranial nerve ganglia, to be reactivated at a later period in the human life cycle as HZ infection. While there is a favorable outcome with the primary infection, children with underlying HIV infection showed a higher incidence of the secondary zoster infection in early stages of life.
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