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Dermatologic Manifestations of Herpes Simplex

  • Author: Joseph S Eastern, MD; Chief Editor: William D James, MD  more...
 
Updated: Mar 07, 2016
 

Background

Herpes simplex viruses (HSVs) are DNA viruses that cause acute skin infections and present as grouped vesicles on an erythematous base. Rarely, these viruses can cause serious illness and can affect pregnancy, leading to significant harm to the fetus. Most infections are recurrent and tend to reappear at or near the same location. Herpes labialis is the most common infection caused by HSV type 1 (HSV-1), whereas genital herpes is usually caused by HSV type 2 (HSV-2). Other clinical manifestations of HSV infection are less common.

Characteristic cluster of vesicles on an erythemat Characteristic cluster of vesicles on an erythematous base. Photo courtesy of Dr. John Reeves.
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Pathophysiology

Intimate contact between a susceptible person (without antibodies against the virus) and an individual who is actively shedding the virus or with body fluids containing the virus is required for HSV infection to occur. Contact must involve mucous membranes or open or abraded skin.

HSV invades and replicates in neurons as well as in epidermal and dermal cells. Virions travel from the initial site of infection on the skin or mucosa to the sensory dorsal root ganglion, where latency is established. Viral replication in the sensory ganglia leads to recurrent clinical outbreaks. These outbreaks can be induced by various stimuli, such as trauma, ultraviolet radiation, extremes in temperature, stress, immunosuppression, or hormonal fluctuations. Viral shedding, leading to possible transmission, occurs during primary infection, during subsequent recurrences, and during periods of asymptomatic viral shedding.

HSV-1 reactivates most efficiently from trigeminal ganglia (affecting the face and the oropharyngeal and ocular mucosae), while HSV-2 has a more efficient reactivation in the lumbosacral ganglia (affecting the hips, buttocks, genitalia, and lower extremities). The clinical difference in site-specific reactivation between HSV-1 and HSV-2 appears to be due, in part, to each virus establishing latent infection in different populations of ganglionic neurons.[1]

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Epidemiology

Frequency

United States

HSV-1 infection is acquired by early childhood, and evidence of serologic infection with HSV-1 approaches 80% in the general adult population. Only about 30% of these individuals have clinically apparent outbreaks. In the United States, approximately 1 in 4-5 adults (21-25%) is serologically positive for HSV-2. For adolescents in the United States, studies have found rates up to 49-53% for HSV-1 and 12-15% for HSV-2. More than half the seropositive individuals do not experience clinically apparent outbreaks, but these individuals still have episodes of viral shedding and can transmit the virus. The incidence of HSV-2 infection is one of the most rapidly increasing rates among sexually transmitted diseases in this country. Independent predictors of HSV-2 seropositivity include female sex, black race, older age, lower education, more lifetime sex partners, prior diagnosis of sexually transmitted disease, and lack of HSV-1 antibody.

International

Serologic evidence of HSV-1 infection by early adulthood ranges from 56-85%, varying by country.[2, 3] HSV-2 seroprevalence has been reported to vary from 13-40% worldwide. More than one third of the world's population has recurrent clinical HSV infections.

In the developing world, HSV-2 is becoming a common cause for genital ulcer disease,[4] especially in countries with a high prevalence of HIV infection. International studies show seroprevalence in people co-infected with HIV being close to 90% for HSV-1 and up to 77% for HSV-2.[5]

Race

African Americans have a higher prevalence of antibodies against HSV-1 than whites. Nonwhite race has been reported as a risk factor for HSV-2 seropositivity.

Sex

The frequency of HSV-1 and HSV-2 antibodies is slightly higher in females than in males. However, women are more likely than men to be protected from genital HSV infection by the use of barrier methods.

In a study of more than 600 pregnant women, 63% were seropositive for HSV-1, 22% for HSV-2, and 13% for both, and 28% were seronegative. Nonwhite race and having had 4 or more sex partners independently correlated with increased HSV-2 infection. Non-Hispanic white pregnant women had the highest percentage of seronegativity for both HSV-1 and HSV-2. However, this group had the highest risk of having a child with neonatal herpes, indicating their susceptibility for new HSV infection during their third trimester of pregnancy (when a mother is most likely to transmit infection to her neonate).[6]

Age

The frequency of HSV-1 infection in children varies with the socioeconomic status. Approximately, one third of children from lower socioeconomic families exhibit some evidence of HSV-1 infection by age 5 years. The frequency increases to 70-80% by early adolescence/adulthood. In contrast, only 20% of children from middle-class families seroconvert. The frequency of infection remains fairly stable until the second to third decade of life when it increases to 40-60%. The rate of HSV-2 seroconversion is highest in sexually active young adults.

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Contributor Information and Disclosures
Author

Joseph S Eastern, MD Clinical Assistant Professor, Department of Internal Medicine, Section of Dermatology, University of Medicine and Dentistry of New Jersey; Clinical Assistant Professor, Seton Hall University School of Graduate Medical Education

Joseph S Eastern, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, International Society for Dermatologic Surgery, Medical Society of New Jersey

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael J Wells, MD, FAAD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

Rosalie Elenitsas, MD Herman Beerman Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System

Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society of Dermatopathology, Pennsylvania Academy of Dermatology

Disclosure: Received royalty from Lippincott Williams Wilkins for textbook editor.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Sungnack Lee, MD Vice President of Medical Affairs, Professor, Department of Dermatology, Ajou University School of Medicine, Korea

Sungnack Lee, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Malcolm Schinstine, MD, PhD; Paul Krusinski, MD; Gisela Torres, MD; and Stephen K Tyring, MD, PhD, MBA, to the development and writing of this article.

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Characteristic cluster of vesicles on an erythematous base. Photo courtesy of Dr. John Reeves.
 
 
 
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