Human herpes virus 3 (HHV-3) of the Herpesviridae family is an exclusively human virus that causes chicken pox and varicella zoster (also referredto as shingles) [1]. A single serotype of a virus can have varying presentations depending on the immune status of the host. In immunocompromised hosts, varicella demonstrates a disseminated presentation ratherthan the classic dermatomal distribution. In our case, a young male with HIV presented with a wide-spread, disseminated case of VZV despite treatment with newer combination HIV multi-drug therapy. The patient's CD4 count had dropped significantly since his diagnosis, and start of the multi-drug medication, increasing his susceptibility to opportunistic infections. A 2013 study showed that HAART therapy might have different effects on VZV depending on the duration of the treatment, which could potentially explain the presentation in our patient [2].

A 30-year-old male presented to the emergency department complaining of a painful rash. He was diagnosed with HIV three months prior to his admittance and was compliant at the time with HAART therapy taking Stribild (a combination of elvitegravir, cobicistat, emtricitabine and tenofovir). In addition, he was compliant with azithromycin and bactrim for prophylaxis.

The rash started on his forehead and, within 48 hours, had spread down his to neck, upper chest, and lower extremities. His latest CD4 count (obtained three months ago upon diagnosis) was 132 cells/mm3 and viral load was 36 copies/mL. He had no recent sick contacts, and denied any tick bites, recent travel, fever, chills or nausea/vomiting.

Upon admission, laboratory findings showed: blood pressure 125/74 mmHg and pulse 91 bpm 1 Resp:18 breaths/min, SaO2 98% on room air, temperature 36.4C, white blood cell count 3×10⁹/L, platelet 122×10³/µL, absolute neutrophil count 1.5, CD4 count 65 cells/mm³, viral load 1639 copies/mL. On physical examination, the rash was composed of small vesicles with surrounding erythema, and was painful to the touch. It was located mainly on the forehead (Figure 1), between the patient's toes (Figure 2) and plantar aspect of the foot (Figure 3), with scattered lesions on his legs, back (Figure 4), and abdomen (Figure 5). The vesicular lesions appeared to be in varying stages with no umbilication. The patient was immediately started on intravenous acyclovir 10 mg/kg IV q8hr [3], placed in isolation, and was monitored for progression of the lesions into the mouth or eyes. Within 24–36 hours, half of the body lesions had begun to crust over with no newly forming lesions. After 48 hours of treatment, all of the lesions crusted without further vesicle progression.

Normally, VZV is a clinical diagnosis; however, laboratory diagnosis becomes necessary in cases of infection control, or immunocompromised patients such as this case [4]. Several days after admission and initial treatment, polymerase chain reaction (PCR)---the diagnostic treatment of choice-confirmed the presence of varicella zoster.

Varicella Zoster (VZV) is a member of the herpesviridae family (HHV-3) known to affect humans [5]. Depending on age, its presentation varies causing chicken pox in the young and shingles in the elderly. Once infected, the virus remains dormant in the dorsal root ganglion of nerves, only to be re-activated at a later time (typically along the dermatome for which it lay dormant).

In aging adults, or immunocompromised individuals, the body cannot suppress the virus and a reactivation of zoster can present as a widespread rash-referred to as disseminated. The level of the absolute CD4 count can also alter the severity of presentation in an immunocompromised state [6]. When this occurs, the painful lesions are diffuse, at varying stages of development, and affect all parts of the body.

Treatment is aimed at minimizing the patient's pain and shortening the duration of the episode. Over-the-counter pain medications are typical first line treatment, but the use of anti-virals such as acyclovir and its derivatives may be necessary. In an immunocompromised patient, anti-virals can be used as primary treatment in the acute setting, as well as prophylaxis to prevent recurrent episodes.

Varicella zoster virus (VZV), a member of the Herpesviridae family, can vary in presentation depending on the patient's age and immune status. Early detection and treatment with analgesics and antivirals is important to limit the pain and duration of each episode. In an immunocompromised patient, early treatment is even more imperative as the presentation is typically more severe. In our case, the clinical outcome was excellent due to the rapid diagnosis and treatment by the medical team.

Paloma Kennedy - Technical assistance and editing.

1. Kramer JM, LaRussa P, Tsai WC, et al. Disseminated vaccine strain varicella as the acquired immunodeficiency syndrome-defining illness in a previously undiagnosed child. Pediatrics 2001 Aug;108(2):E39.   [CrossRef]   [Pubmed]    
2. Gershon AA, Gershon MD. Pathogenesis and current approaches to control of varicella-zoster virus infections. Clin Microbiol Rev 2013 Oct;26(4):728–43.   [CrossRef]   [Pubmed]    
3. Liu C, Wang C, Glesby MJ, et al. Effects of highly active antiretroviral therapy and its adherence on herpes zoster incidence: a longitudinal cohort study. AIDS Res Ther 2013 Dec 27;10(1):34.   [CrossRef]   [Pubmed]    
4. Malkud S, Patil SM. Disseminated Cutaneous Herpes Zoster in a Patient with Uncontrolled Diabetes Mellitus. J Clin Diagn Res 2015 Jul;9(7):WD01–2.   [CrossRef]   [Pubmed]    
5. Pergam SA, Limaye AP, AST Infectious Diseases Community of Practice. Varicella zoster virus (VZV) in solid organ transplant recipients. Am J Transplant 2009 Dec;9 Suppl 4:S108–15.   [CrossRef]   [Pubmed]    
6. Levy O, Orange JS, Hibberd P, et al. Disseminated varicella infection due to the vaccine strain of varicella-zoster virus, in a patient with a novel deficiency in natural killer T cells. J Infect Dis 2003 Oct 1;188(7):948–53.   [CrossRef]   [Pubmed]