Published on 19/03/2015 by admin
Filed under Dermatology
Last modified 19/03/2015
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Jane C. Sterling
Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports
Herpes simplex virus (HSV) infects skin and mucous membranes damaging keratinocytes and causing intense inflammation, seen as small blisters on a background of erythema. Infections around the mouth or elsewhere on the skin are almost always due to HSV-1, whilst genital infection is most commonly caused by HSV-2. The primary infection may be obvious or subclinical; once latency is established in sensory ganglia, the virus may reactivate at variable intervals to produce visible lesions. In immunosuppression, disease can be chronic and antiviral resistance can develop.
Both primary and reactivation episodes are usually self-limiting and may require no treatment. Soothing antiseptic creams, alcohol-based tinctures or surface dressings may be used as self-help remedies. Antiviral therapy, in the form of acyclovir and related drugs, is available for topical and systemic use and is usually the most effective form of treatment. Although anogenital herpes will frequently respond to topical acyclovir applied five times daily for 5 days, its efficacy in cutaneous herpes is less certain, resulting in marginal benefit. Acyclovir 5% in combination with 1% hydrocortisone cream, appears to reduce the risk of ulceration. Oral acyclovir, 200 mg five times daily for 5 days, will usually reduce the time to healing and duration of virus shedding and is more effective than topical treatment. Shorter treatment courses with higher dose acyclovir produce similar effects. Topical or systemic treatment for an acute episode should be started early in the episode to have most benefit. In addition, pain relief may be necessary.
A failure of response to acyclovir may be due to the poor absorption and rapid clearance following ingestion or to the emergence of acyclovir resistance. Valacyclovir, a prodrug of acyclovir, and famciclovir, a prodrug of penciclovir, have improved bioavailability and are alternatives to acyclovir with the additional benefit of a once or twice daily dosing. Short course (single day) treatment with oral famciclovir can hasten healing if taken at the start of a reactivation episode. Efficacy of oral valacyclovir can be as good as intravenous acyclovir.
In frequently recurrent disease, or in immunosuppressed individuals when episodes may be severe, prophylactic antiviral treatment can be considered and measures taken to avoid any precipitating factors. UV protection may help to reduce viral reactivation in herpes labialis. To reduce frequency and severity of attacks, antiviral treatment needs to be continuous for several weeks or months. The dose of 400 mg twice daily for acyclovir is most likely to produce a decrease in the frequency of reactivation episodes. Oral valacyclovir or famciclovir can also be used for long-term suppression of viral reactivation. There is a potential risk of selection of resistant strains of virus with long-term therapy, but this is rare even in immunosuppressed patients. Oral antivirals may be taken as a relatively short-term course to reduce the risk of a reactivation episode before and during intense sun exposure, or before dental or cosmetic procedures.
In immunosuppressed individuals, with spreading or persistent infection, intravenous therapy with acyclovir, or the more toxic foscarnet or cidofovir, may be necessary. Topical preparations of cidofovir have been shown to have effect but are not commercially available. Vidarabine, interferons, and interleukin-2 and other agents have also been used, but without reliable effect. Herpes simplex is a common precipitating cause of episodes of recurrent erythema multiforme (see chapter on erythema multiforme), which can be reduced in frequency by prophylactic antiviral therapy.
Other treatments reported to have some effect in acute attacks include the antivirals idoxuridine, trifluorothymidine (TFT) and docosanol used topically and low-level laser light therapy.
Electron microscopy of blister fluid
PCR of blister fluid or biopsy
Viral culture from swab of lesion
Immunocytology of blister floor cells
Skin biopsy of atypical lesion
Herpes simplex serology
Assessment of immune function
The diagnosis is usually obvious clinically. In atypical disease, laboratory confirmation is essential. In unexplained persistent or severe disease, immunodeficiency should be excluded.
Amir J, Harel L, Smetana Z, Varsano I. BMJ 1997; 314: 1800–3.
A total of 61 children with herpetic gingivostomatitis were treated with acyclovir suspension 15 mg/kg or placebo five times daily for 7 days. Acyclovir reduced the duration of lesions from 10 to 4 days and reduced the period of viral shedding.
Treatment of Skin Disease Comprehensive Therapeutic Strategies 4e
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Topical acyclovir
Oral acyclovir
