In immunocompetent individuals herpes zoster usually
presents with typically grouped vesicles on erythematous base involving single
dermatome with self-limiting nature, while it may present in extensive form
involving multiple dermatomes or disseminated form in immunocompromised,
especially in Human Immunodeficiency Virus (HIV). HIV-positive patients with
lower CD4 counts have higher risk of HZ. Disseminated and multiple dermatomal
involvement, with more severity is more commonly involved among HIV-positive
patients when compared to HIV-negative patients and they also have higher
incidence of post herpetic neuralgia.
Keywords: Herpes
zoster, Human immunodeficiency virus, Immunosuppression
INTRODUCTION
Herpes Zoster (HZ)
is characterized by unilateral radicular pain and grouped vesicular eruption
involving dermatome innervated by a single spinal or cranial sensory ganglion,
as a result of reactivation of persistent latent form of Varicella Zoster Virus
(VZV) within the sensory ganglion [1]. Although more than 90% of adults have
serologic evidence of VZV infection and are therefore are at risk of developing
HZ, many times HIV-positive patients have been found to have higher incidence
than the general population [2]. HZ usually occurs as an early manifestation in
the course of HIV infection and when compared to HIV-negative individuals it
shows higher incidence of post herpetic neuralgia, recurrences, disseminated
zoster, ulcerated lesions and chronic verrucous lesions [3]. There have been
various studies showing the difference in HZ presentation between HIV positive
and negative individuals.
DISCUSSION
Herpes zoster is a
viral infection caused by varicella-zoster virus, which occurs more frequently
in the elderly and those with any form of immunodeficiency. Hence, the
incidence of HZ is observed to be higher in the immune-deficient condition
‘Acquired Immuno-Deficiency Syndrome’ (AIDS) with more severity, multiple
dermatomal involvement, dissemination and systemic involvement [4]. The
prevalence of HIV in general population of Gujarat is around 0.38% [5]. It
ranges from 5.6% to 22.5% in various similar studies [6]. HZ occurs primarily
in adults older than 50 years although it can occur at any age [7]. Its
incidence rate ranges from 1.2 to 3.4 per 1,000 person-years among younger
healthy individuals, increasing to 3.9-11.8 per 1,000 person-years among those
older than 65 years [8]. Association of VZV reactivation with immunosuppression
and age suggests if the immune system is effective, it prevents viral
replication [9]. Therefore immunosuppression, especially organ transplantation,
hematologic malignancy and HIV infection increases the rates of HZ occurrence.
One study has showed that 30% of the AIDS cases have history of HZ [10]. Unlike
typical HZ which is characterized by unilateral, segmental painful vesicles
over certain affected dermatomal region, HZ in the immunosuppressed can be
ulcerative and necrotic and scar more severely. These patients have relatively
increased severity of cutaneous lesions and course of disease is prolonged,
persistent or recurrent with attacks, showing unusual morphologies like
verrucous and hyperkeratotic lesions [11]. HZ has high risk of dissemination up
to 40%, in immunocompromised persons and in HIV infections [12], which is defined as more
than
20 vesicles outside the
CONCLUSION
Although multi-dermatomal
and disseminated involvement is more commonly seen in HIV-infected patients,
they can also present with typical presentation of herpes zoster. Hence, the
physician should screen every case of herpes zoster for HIV infection to detect
the disease earlier.
1. Straus SE, Schmader KE, Oxman MN
(2003) Varicella and herpes zoster. In: Freedberg IM, Eisen AZ, Wolff K, Austen
KF, Goldsmith LA, Katz SI, editors. Fitzpatrick's Dermatology in General
Medicine. 6th Edn. New York: McGraw Hill 2: 2070-2085.
2. Gebo KA, Kalyani R, Moore RD,
Polydefkis MJ (2005) The incidence of, risk factors for and sequel of herpes
zoster among HIV patients in the highly active antiretroviral therapy era. J
Acquir Immune Defic Syndr 40: 169-174.
3. Jacobson MA, Berger TG, Fikrig S,
Becherer F, Moohr JW, et al. (1990) Acyclovir resistant varicella zoster virus
infection after chronic oral acyclovir therapy in patients with the acquired
immuno deficiency syndrome (AIDS). Ann Intern Med 112: 187-191.
4. Tappero JW, Perkins BA, Wenger JD,
Berger TG (1995) Cutaneous manifestations of opportunistic infections in
patients infected with human immunodeficiency virus. Clin Microbiol Rev 8:
440-450.
5. National AIDS Control
Organization, Ministry of Health and Family Welfare, Government of India (2008)
HIV estimates during surveillance in 2006.
6. Sharvadze L, Tsertsvadze T,
Gochitashvili N, Stvilia K, Dolmazashvili E (2006) HIV prevalence among high
risk behavior group persons with herpes zoster infection. Georgian Med News
132: 60-64.
7. McCrary ML, Severson J, Tyring SK
(1999) Varicella zoster virus. J Am Acad Dermatol 41: 1-14.
8. Dworkin RH, Johnson RW, Breuer J,
Gnann JW, Levin MJ, et al. (2007) Recommendations for the management of herpes
zoster. Clin Infect Dis 44: S1-26.
9. James WD, Berger TG, Elston DM,
Odam RB (2006) Andrews' diseases of the skin: Clinical dermatology. 10th
Edn. Philadelphia: WB Saunders, pp: 379-384.
10. Hira SK, Wadhawan D, Kamanga J,
Kavindele D, Macuacua R, et al. (1988) Cutaneous manifestations of human
immunodeficiency virus in Lusaka, Zambia. J Am Acad Dermatol 19: 451-457.
11. Grossman MC, Grossman ME (1993)
Chronic hyperkeratotic herpes zoster and human immunodeficiency virus infection
(review). J Am Acad Dermatol 28: 306-308.
12. Webre DM, Pelechia JA (1965)
Varicella pneumonia: Study of prevalence in adult men. JAMA 192: 572-573.
13. Vora RV, Anjaneyan G, Kota RKS,
Pilani AP, Diwan NG, et al. (2017) Study of clinical profile of herpes zoster
in human immunodeficiency virus positive and negative patients at a rural-based
tertiary care center, Gujarat. Indian J Sex Transm Dis AIDS 38: 65-68.
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