Varicella Zoster virus culture
Detection of varicella-zoster virus in clinical specimens for laboratory confirmation of disease due to this virus. Please note that Direct Fluorescent Antibody assay (DFA) is a more rapid and sensitive detection method (see VZV DFA) for vesicular lesions. For body fluid (including CSF and vitreous fluid) viral culture is the preferred method.
Indications for Testing
– Rash of chikenpox (varicella) or shingles (zoster) is usually a clinical diagnosis
- Chickenpox – skin lesions are in different stages of development (papule, vesicle, pustule, umbilication, and crusting) concurrently
- Shingles – painful vesicles in a dermatomal distribution
– Most common indication is to confirm severe or atypical disease and VZV encephalitis, congenital varicella syndrome and disseminated VZV in immunocompromised host
VZV causes both varicella (chickenpox) and herpes zoster (shingles). During acute infection, highly infectious cell-free VZV is produced in skin vesicles,
accounting in large part for the high degree of contagion of varicella and zoster. VZV produces a generalized vesicular rash on the dermis (chickenpox) in normal children, usually before 10 years of age. After primary infection with VZV, the virus persists in latent form and may emerge (usually in adults 50 years of age and older) clinically to cause a unilateral vesicular eruption, generally in a dermatomal distribution (shingles).
Varicella presents with fever, headache, and a rash that is maculopapular for a few hours, vesicular for 3-4 days and leaves a granular scab. The vesicles collapse when punctured. These lesions mostly occur in successive crops, with various stages of maturity all at the same time. The lesions may be present on the scalp, axilla, mucous membrane of the mouth upper respiratory tract and the conjunctivae. They may be abundant or mild and not profuse enough to note that an infection is present. Complications are seen more frequently if the infections occur in adolescence, adulthood or immunocompromised host, with higher rates of encephalitis, pneumonia and death. Babies who develop varicella within the first 28 days are at higher risk from developing severe generalized varicella. Complications from infection include secondary bacterial skin infections, otitis media, bacteraemia, osteomyelitis, septic arthritis, endocarditis, necrotizing fasciitis, toxic shock like syndrome, mild hepatitis and thrombocytopenia. Infections that occur early in pregnancy may result in congenital varicella syndrome in 0.7% of cases. After 13-20 weeks gestation the incidence is 2%.
Herpes Zoster or shingles is a reactivation of latent varicella infection in the dorsal root ganglia in a localized area. The lesions are restricted to an area supplied by the sensory nerves along nerve pathways and are usually unilateral causing severe pain.
In Newfoundland and Labrador, among a cohort of 586 children, 565 (96.4%) did not have detectable VZV antibody at one year of age. The proportion with VZV antibody increased thereafter to 12.8% and 33.9%, respectively, at age two and four years, indicating the extent of exposure to VZV at these ages. Among 1135 school-age children, the proportion testing positive for VZV antibody increased from 44% at five years of age to 88.9% at 15 years of age, indicating the cumulative incidence of varicella in this age group. Among pregnant women, 92.1% tested positive for VZV antibody, and the corresponding figure for health care providers was 93.1%. In both groups, the proportion testing positive for VZV antibody increased with advancing age, from 89.6% for the 15- to 19-year age group to 96.5% for those over the age of 40 years. The risk of VZV infection increases steadily from one year of age, reaching a peak during school years. This data support the recent Canadian recommendation to vaccinate any person older than 12 months of age who is susceptible to VZV. Among the adult population, the proportion susceptible will be under 10% for the foreseeable future, and for those at risk, selective vaccination based on their immune status would be a cost effective approach.
Varicella-zoster virus (VZV) is a member of the Herpesviridae. It is classified as an alphaherpesvirus along with the herpes simplex viruses (HSV). VZV is a highly cell-associated virus that is spread through the body by cell-to-cell contact.
Demonstration of virus by culture provides confirmation of VZV disease.
Gershon, A. A., Chen, J., LaRussa, P., and Steinberg, S. P. 2007. Varicella-Zoster Virus, p. 1537-1548. In Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., and Pfaller, M. A. Manual of Clinical Microbiology, 9th ed., vol. 2. ASM Press, American Society for Microbiology, Washington, DC.
Whitley, R. J. 2010. Varicella-Zoster Virus, p. 1963-1969. In Mandell, D., Bennett, J. E., and Dolin, R. 2010. Principles and practice of infectious diseases, 7th ed., vol. 2. Churchill Livingstone, Elsevier, Philadelphia, PA.
Puchhammer-Stöckl, E., and Aberle, S. W. 2011. Varicella-Zoster Virus, p. 1545-1557. In Versalovic, J., Carroll, K. C., Funke, G., Jorgensen, J, H., Landry, M. L., and Warnock, D, W. Manual of Clinical Microbiology, 10th ed., vol. 2. ASM Press, American Society for Microbiology, Washington, DC.
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