Introduction
Disseminated cutaneous herpes zoster is a potentially serious infection which has been described in persons with low immunity due to Human Immunodeficiency Virus (HIV), hematological malignancy, chemotherapy, renal transplant, or type II diabetes and dyslipidemia (1) (2) (3) (4). However, it is uncommon to see this particular disease in healthy individuals. In this report, we describe the clinical course of a patient who was diagnosed with disseminated cutaneous herpes zoster in the absence of unknown immunosuppressive conditions.
Case Report
A 33 year old Saudi male, who was not leukemic and did not have any immunological disorder, was seen in the dermatology clinic with generalized and widespread vesicular rash covering his entire body with a few Bullae lesions appearing in the chest, abdomen, and one of his legs (Figure 1 & 2). On examination, he complained that he visited the hospital’s Emergency Room 5 days prior complaining of fever, weakness, and lethargy. The doctor who examined him that day informed him that there was nothing to worry about and wrote in his notes; nothing remarkable and advised him to go home and rest. The patient however insisted that he needed treatment and because of that a single dose of hydrocortisone was given to him intravenously.
During his second visit where he was seen in the dermatology clinic, a Complete Blood Count (CBC) was requested in addition to skin biopsy, antinuclear antibody test (ANA), and hemagglutination assay (HI). The patient stated that he had chickenpox during his childhood and he had just come back from a trip abroad before he came to the ER but he mentioned no possible exposure to the disease during his travel.
A microscopic examination of the skin biopsy revealed: ballooning degeneration in the epidermis with margination of chromatin in nucleous of keratinocyte (Figure 3). HIV was none reactive, both Red Blood Cells (RBCs) test and HI were normal and there was no record of elevated ANA. Liver enzymes, kidney functions, and chest x-ray were all normal.
A diagnosis of disseminated cutaneous herpes zoster was confirmed, and 800 mg of Acyclovir, 5 times per day for 7 days was prescribed for the patient. Two months later, the patient retuned to the clinic for a follow-up. A skin wise procedure depicted only post-inflammatory hyperpigmentation. No other signs or symptoms of incomplete recovery or remarkable skin disorders were evident (Figure 4). The patient tolerated the treatment very well and no further action was done.
Discussion
Disseminated cutaneous herpes zoster or shingles is the consequence of the reactivation of latent Varicella Zoster Virus (VZV) from the dorsal root ganglia. The disease is usually seen more in senior patients than young adults who are immunocompromised and is reported to be as common as 10- 40% in them (5) (6). Our case study however is an uncommon scenario as the patient was not immunocompromised, on long immunosuppressive therapy or even elderly. He was diagnosed at the clinic with disseminated cutaneous herpes zoster and it was later confirmed through a skin biopsy. Based on the patient’s history, it did not reveal any significant evidence that might stimulate the cause of such a disease. Physical stress and/or emotional stress are often cited as precipitating factors for herpes zoster (6). Yet, the patient during his history recall stated that he had no emotional problems that might have triggered the viral activation. Hence, there was no clear contributing factor that could explain the cause of the disease at this stage.
As stated earlier in this report, the patient was given a single dose of hydrocortisone intravenously on his first visit to the ER. It is not clear why it was prescribed to him especially since hydrocortisone is usually given on a long term basis (7, 8). Moreover, administration of a single dose of intravenous hydrocortisone is usually used to treat acute asthmatic patients (9). This however was not the case with our patient. He did not complain from any respiratory symptoms as was evident from his notes. Moreover, a single dose of hydrocortisone is not known to play a major role in the activation of the virus (10). Therefore, there must have been an undetected reason that helped activate the virus and cause the eruption of the symptoms. One argument could be that he might have had an immunological disorder that was not identified during his examination and which might have led to his severe condition.
Although our patient’s case is considered uncommon, we argue that it should not be listed as “rare” any more. A literature search between clearly identified more than 9 similar cases around the world (11) (12) (13). We believe further intensive immunological research is needed to identify the real cause of this disease and treating clinicians should not put such a condition in the “rare category” anymore. Thus, disseminated cutaneous herpes zoster should not be limited to immunocompromised patients as it can target healthy individuals. To sum up, the main aim of any clinician is to identify the disease if present in immunocompetent patient and not consider it as a rare case.
Conclusion
Disseminated herpes zoster is a potentially serious infection that can be present in the absence of immunosuppression. Early diagnosis and aggressive treatment with intravenous acyclovir can reduce morbidity and help stop the severity of possible complications.