DR8.2 | Herpes Simplex Recognition — Summary & Reflection

KEY TAKEAWAYS

Herpes simplex is recognised by grouped vesicles on an erythematous base, preceded by a tingling prodrome and recurring at the same site — the visible signature of a herpesvirus that lies latent in a sensory ganglion and reactivates with fever, UV, stress, menstruation or immunosuppression. HSV-1 classically causes orolabial infection (herpes labialis) and HSV-2 genital infection, though either type can affect either site. Primary infection (gingivostomatitis, vulvovaginitis) is more severe and systemic than localised recurrent disease. A Tzanck smear shows multinucleate giant cells (confirming a herpesvirus, not the subtype); PCR is the gold standard. Key differentials are herpes zoster (dermatomal), aphthous ulcer, impetigo and — critically for genital lesions — the painless indurated syphilitic chancre. Treatment is early aciclovir or valaciclovir (episodic for infrequent, suppressive for frequent recurrences), with intravenous therapy and referral for severe, neonatal, disseminated or immunocompromised disease, alongside counselling on incurability, contagiousness and triggers.

REFLECT

Think of a patient you have seen with a cold sore or a genital ulcer — or imagine the next one you will meet. At the time, were you able to name the morphological signature (grouped vesicles on an erythematous base, prodrome, recurrence) with confidence, or did you reach for a label without reading the lesion? For a genital ulcer in particular, did you actively distinguish painful herpetic vesicles from a painless syphilitic chancre? Consider how you would explain to that patient, in plain language, why the infection recurs and why treatment controls rather than cures it. Tying this recognition skill to a real or anticipated encounter is what turns it into the everyday clinical reflex it needs to become.