Human Herpesviruses

Published on 05/03/2015 by admin

Filed under Dermatology

Last modified 22/04/2025

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67

Human Herpesviruses

Herpes Simplex Viruses (HSV-1/HHV-1 and HSV-2/HHV-2)

Ubiquitous pathogens that produce primarily orolabial (HSV-1 > HSV-2) and genital infections (HSV-2 > HSV-1) characterized by recurrent vesicular eruptions (Table 67.1).

Transmission can occur during both symptomatic and asymptomatic periods of viral shedding.

Reactivation can occur either spontaneously or due to an appropriate stimulus (e.g. stress, UVR, fever, tissue trauma, or immunosuppression).

A wide range of clinical presentations exist, with asymptomatic infection being the most common.

In primary infection.

Onset is usually 3–7 days after exposure.

Generalized prodrome (before the onset of mucocutaneous lesions) of tender lymphadenopathy, fever, and malaise; localized pain, burning, and tenderness.

Initial lesions: small round vesicles on an erythematous base; often painful or burning; the grouping of these vesicles is a clue to the diagnosis; vesicles may become umbilicated or pustular, followed by erosions or ulcerations with hemorrhagic crusts, often with a scalloped border; lesions resolve over 2–6 weeks (Fig. 67.1).

In reactivation infection.

Localized prodrome of dysesthesia (e.g. burning/tingling, pain, pruritus) and tenderness.

Mucocutaneous lesions similar as in primary but fewer in number, less severe, and shorter duration (Fig. 67.2).

In addition to the classic orolabial and genital infections, HSV can cause other infections (Table 67.2; Figs. 67.367.7).

DDx and Dx: see Table 67.1 and Fig. 67.8.

Rx: outlined in Table 67.3.

Varicella–Zoster Virus (VZV or HHV-3)

Primary varicella infection (chickenpox).

Usually self-limited in otherwise healthy children but more severe with more numerous lesions and a greater risk for complications in adults (including pregnant women) and immunocompromised individuals (Table 67.4; Fig. 67.9).

Herpes zoster (shingles) – reactivation of VZV.

Incidence, severity, and risk of complications increase significantly with age and immunosuppression due to a decline in specific cell-mediated immune response to VZV.

Reactivation results in a sensory neuritis and painful neuralgia, followed by a dermatomal vesicular eruption; clinical course is outlined in Table 67.4 (Figs. 67.1067.12).

Exposure of a susceptible person to an individual with chickenpox or zoster can lead to primary varicella but not zoster.

Rx: early antiviral treatment (within 72 hours of the onset of the first vesicle) is ideal, but initiation after 72 hours but within 7 days may also be helpful (see Table 67.3).

Selected complications of herpes zoster:

1. Disseminated zoster.

Defined as >20 vesicles outside the area of the primary or adjacent dermatomes.

Implies viremia and an increased risk for visceral or CNS involvement (see Table 67.4).

Requires intravenous acyclovir.

2. Post-herpetic neuralgia (PHN) and post-herpetic itch (PHI).

Affects 10–15% of patients; incidence and severity increase with age.

Characterized by persistent pain, dysesthesia (PHN) or pruritus (PHI) along the affected dermatome for weeks to years after the resolution of the eruption.

Rx: gabapentin, tricyclic anti­depressants (e.g. amitriptyline, nortriptyline); topical agents (e.g. lidocaine patch, capsaicin); oral analgesics (e.g. ibuprofen, opioids).

Note that opioids are typically ineffective or even aggravating in patients with PHI.

3. Ocular involvement (see Fig. 67.10F).

Occurs in ~10% of patients, with 20–70% developing ocular disease (occasionally blindness).

Due to VZV reactivation in the first division of the trigeminal nerve (V1).

Clues to its diagnosis include lesions in the V1 distribution (see Fig. 67.11), which may be accompanied by unilateral eye pain or conjunctivitis.

Hutchinson’s sign is the presence of vesicles at the tip, side, or bridge of the nose, indicating involvement of the nasociliary branch of the trigeminal nerve, which also innervates the cornea.

Initial and longitudinal evaluation by ophthalmology is required.

4. Ramsay–Hunt syndrome (herpes zoster oticus).

Due to VZV reactivation in the geniculate ganglion.

Clues to its diagnosis: vesicles in the ear canal, tongue, and/or hard palate.

Patients may have severe ear pain, acute facial nerve paralysis, and/or taste loss of the anterior two-thirds of the tongue.

If the vestibulocochlear nerve is also affected, may have tinnitus, hearing loss, or vertigo.

Consider referral to otolaryn­gology.