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LETTER TO EDITOR
Year : 1991  |  Volume : 57  |  Issue : 1  |  Page : 52

Herpes zoster associated with varicelliform eruptions



Correspondence Address:
S Talwar


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How to cite this article:
Talwar S. Herpes zoster associated with varicelliform eruptions. Indian J Dermatol Venereol Leprol 1991;57:52

How to cite this URL:
Talwar S. Herpes zoster associated with varicelliform eruptions. Indian J Dermatol Venereol Leprol [serial online] 1991 [cited 2020 Jul 12];57:52. Available from: http://www.ijdvl.com/text.asp?1991/57/1/52/3626


Antigenic stimulation due to endogenous reactivation of varine)ka zos*arvirus (VZV) ap­pears to be responsible for natural resistance to herpes zoster (HZ). Molecular fingerprinting has demonstrated hetrogenecity between strains of VZV, therefore exogenous reinfection is possible with different strains of VZV 1. This subclinical exogenous reinfection further boosts the resistance. However, during periodic reaction of the virus, haematogenous dissemi­nation of virus also takes place which is nor­mally neutralized by the host immune response, If the host's immune response during reactivation is delayed, the haematogenous dissemi­nation causes disseminated lesions. A case of HZ associated with such disseminated lesions is being reported.

Forty two-year-old male presented with painful grouped vesiculobullous lesions along right thoracic-7 dermatome. One day later be developed painless generalised pupulo-vesicu!er lesions involving trunk (predominantly), extremities and face. Oral mucosa and eyes were not involved. There was no evidence of immunosuppression. Tzanck smear from the lesions revealed presence of balloned-up acantholytic cells containing one to many nu­clei. Blood sugar was within normal limits. The case was diagnosed as herpes zoster with varicelliform eruptions. Vericelliform eruptions regressed fully after 11 days while herpes zoster lesions regressed in 14 days with no residual sequelae

Haematngenous dissemination during re­activation of the virus takes place from the af­fected ganglion, nerve or skin.[2],[3] Depending upon the rapidity of host immune response during haematogenous dissemination we may get no clinical lesion, scattered vesicles with­out zosteriform lesion[2] , zoster sine herpete, or disseminated HZ. Careful examination may reveal few scattered vesicles away from the involved dermatome in 17-35 percent of cases. [3] This dissemination, commonly observed in immunocompromised patients may also be seen in non-compromised individuals[2]. A se­lective decline of cell mediated immunity to VZV in elderly patients may be responsible for commonly observed dissemination in immunocompetent elderly patients[4]. Cases reported as HZ associated with chickenpox may actually be disseminated herpes as observed in our case. In all cases with significant dissemina­tion, one has to look for visceral and CNS in­volvement.




 

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