A Case of Ill-Defined Erythematous Plaques Scattered on the Scalp

What Is Your Diagnosis?

Question

A 55-year-old woman from Cuba presented with a 2-week history of asymptomatic scalp lesions associated with headaches and left-sided otalgia. Scalp examination revealed several asymptomatic erythematous plaques with ill-defined borders lacking scales, vesicles, crusts, or hair loss (shown in Fig. 1a, b). Dry trichoscopy showed nonspecific simple loops and hairpin vessels, dilated thick vessels with lakes of blood, and brown/yellow blotches as shown in Figure 2. Hair shaft findings were unremarkable. A lesional scalp biopsy was evaluated and showed mid-level and upper level follicular necrosis and a dense peribulbar lymphocytic infiltrate.

Fig. 1.

a, b Ill-defined erythematous plaques scattered on the scalp.

Fig. 2.

Dry trichoscopy: simple loops and hairpin vessels, dilated thick vessels with lakes of blood, and brown/yellow blotches.

What is your diagnosis?

Answer

Herpes zoster (HZ) infection of the scalp.

Discussion

Our unusual case of HZ infection of the scalp presented with ill-defined plaques in a C2 dermatomal distribution and ipsilateral otalgia underlies the value of obtaining a scalp biopsy in patients with non-vesicular plaques − where Tzanck smear is not feasible. Atypical scalp presentations of HZ infection have been reported in the literature as localized or dermatomal folliculitis [1, 2, 3]. Nonspecific urticarial-like plaques have been reported in early HZ and have required confocal microscopy to detect the acantholytic and ballooned keratinocytes [4]. The folliculosebaceous unit is the first epithelial structure targeted in HZ infection resulting in erythematous plaques, which differs from the epidermal involvement seen in herpes simplex and varicella infections that manifests as vesicles [3, 5, 6].

The histological findings observed in our patients biopsy, specifically the peribulbar infiltrates, are similar to those observed in early stages of alopecia areata (AA), although lacking telogen shift [7]. In HZ infection, the peribulbar infiltrate is predominant in T-lymphocytes (including CD 30 + lymphoid cells) and B-lymphocytes [8], whereas in AA the peribulbar infiltrate is composed of autoreactive CD4+ and CD8+ T-lymphocytes (Fig. 3).

Fig. 3.

a H&E stain complete necrosis of the follicular epithelium. b H&E stain of the peribulbar inflammation.

The patient's epidermis showed reticular degeneration with ballooned keratinocytes, acantholytic keratinocytes with slate gray nuclei, and multinucleated keratinocytes. Absence of dermoscopic signs of AA was noted. A diagnosis of HZ infection of the scalp was rendered after confirmation with varicella zoster virus immunostaining shown in Figure 4. A retrospective analysis of the clinical findings showed that the lesions were restricted to the left half of the scalp in a C2 dermatomal distribution. Systemic acyclovir and prednisone therapy resulted in complete resolution.

Fig. 4.

VZV immunostaining. VZV, varicella zoster virus.

Some studies have reported an association between AA and HZ infection with AA developing after HZ infection [9, 10]. However, a large population-based study from Taiwan found that patients diagnosed with AA within a 3-year window had an increased odds ratio for HZ infection [11]. The evidence of HZ infection triggering AA or, conversely, AA predisposing to HZ is inconclusive. More studies are needed in order to clearly identify the association between HZ and AA.

Statement of Ethics

Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

Conflict of Interest Statement

The authors have no conflicts of interest to disclose.

Funding Sources

There was no funding for this work.

Author Contributions

Rebecca L. Quiñonez, MD, MS: corresponding author; Naiem T. Issa, MD, PhD: co-author; Mariya Miteva, MD: co-author.