Disseminated herpes zoster encephalitis induced by low-dose corticosteroids.

Introduction

Herpes zoster (HZ) is caused by reactivation of the varicella-zoster virus (VZV) and typically presents as a unilateral, vesicular, painful rash with a dermatomal distribution. Immunocompromised patients are especially susceptible to VZV reactivation. In rare cases, the infection can progress to encephalitis, pneumonia, hepatitis, retinal necrosis causing blindness, and cerebral ataxia, among others. 1 Disseminated herpes zoster (DHZ) is characterized by widespread vesicular lesions beyond the primary dermatome, often with the involvement of other organs, and is predominantly observed in immunocompromised individuals.

Corticosteroids have been used since the 1950s for a range of illnesses, including inflammatory and arthritic disorders, as well as in palliative care. Although effective, they are known to suppress immune function, predisposing to infections, including viral reactivations. High-dose corticosteroids are a well-established risk factor for DHZ, but the threshold for clinically significant immunosuppression remains uncertain. This report describes a rare case of disseminated HZ encephalitis occurring in an elderly patient on a low-dose prednisone regimen of 5 mg daily, possibly challenging our view of what qualifies as immunosuppression.

Case report

An 89-year-old woman presented to the emergency department for sudden-onset altered mental status and inability to walk or talk. She was reportedly fully independent at baseline. Due to her symptoms, a comprehensive stroke workup was completed (computed tomography head and neck) and showed no acute findings. On the first day of admission, a nonpainful, nonpruritic, bullous rash developed on her right occipital scalp, face, and neck which continued to spread to her bilateral lower extremities ( Fig 1 ). There were no mucosal lesions. Due to the concern for bullous pemphigoid by the primary team, dermatology was consulted. She had received her annual influenza and COVID-19 vaccines but had not received the shingles vaccine. Her medication history included prednisone 2.5 mg twice daily, newly prescribed within the prior 2 months for the pain associated with degenerative disc disease. On physical examination, the patient was afebrile, normotensive, and nontachycardic. Labs showed a normal complete blood count, mild hyponatremia, and hyperglycemia. The patient was not diabetic, and her blood glucose was 144 on admission. No recent hemoglobin A1c was available. Autoimmune blistering diseases were ruled out with negative desmoglein 1 and 3 and bullous pemphigoid antigens. VZV/herpes simplex virus polymerase chain reaction swab was taken from a bullae on the neck. VZV polymerase chain reaction was found to be positive and the patient was promptly initiated on intravenous acyclovir 10 mg/kg every 8 hours. Due to the mental status change in the face of a positive VZV swab, a lumbar puncture was performed revealing elevated glucose, protein, red blood cell counts, white blood cell counts, and lymphocytes, with cerebrospinal fluid polymerase chain reaction confirming central nervous system VZV infection. Over the next 48 hours, the patient’s mental status rapidly improved. The final diagnosis was disseminated HZ encephalitis immunosuppression secondary to steroids.

Discussion

Although most cases of HZ infection are self-limited, systemic corticosteroids and other immunosuppressive drugs can worsen the severity of the infection. To our knowledge, this is the first case report to document significant immunosuppression resulting in DHZ with a cumulative corticosteroid dose of 5 mg daily. While higher-dose corticosteroids are well-documented for VZV reactivation, our case shows that even minimal dosage can have profound immunosuppressive effects, prompting the reconsideration of what it means to be immunosuppressed from oral corticosteroids. Current literature on corticosteroid-induced DHZ involves patients receiving moderate to high doses, often in the setting of chronic inflammatory conditions or organ transplantation. A brief literature review of previously reported cases shows that systemic corticosteroid administration ranging from 7.5 mg to 20 mg daily ( Table I ) has contributed to the development of HZ. Our case demonstrates that doses as low as 5 mg daily can be sufficient to result in immunosuppression, resulting in VZV reactivation with dissemination and central nervous system involvement.

Herein, we describe how seemingly low doses of systemic corticosteroids can predispose patients to varicella reactivation and, in some cases, dissemination. Although these outcomes may be uncommon, they warrant consideration, especially in the elderly. Health care providers must remain judicious when prescribing systemic corticosteroids, regardless of dosage, and they should closely monitor patients for potential complications, including VZV. This is particularly applicable to geriatric and immunocompromised populations. The patient in our case had been vaccinated for both influenza and COVID-19 but had no documented HZ vaccination. This underscores the importance of routine health maintenance and age-appropriate vaccination in the elderly, as this patient’s elderly age may alone have accounted for her risk of DHZ. Our case expands the understanding of corticosteroid-induced immunosuppression and its potential consequences. Nonetheless, the level at which systemic corticosteroids cause significant immunosuppression remains unknown and should be further investigated, especially in the geriatric and immunocompromised population.

Conflicts of interest

None disclosed.

Footnotes

Funding sources: None.

Patient consent: The authors obtained written consent from patients for their photographs and medical information to be published in print and online and with the understanding that this information may be publicly available. Patient consent forms were not provided to the journal but are retained by the authors.

IRB approval status: Not applicable.

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