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Herpes Simplex in Emergency Medicine

  • Author: Rahul Sharma, MD, MBA, FACEP; Chief Editor: Steven C Dronen, MD, FAAEM  more...
Updated: Oct 27, 2015


The herpes simplex viruses comprise 2 distinct types of DNA viruses: herpes simplex virus 1 (HSV-1) and herpes simplex virus 2 (HSV-2). The epidemiology of herpes infection has dramatically changed over the past several decades.[1] HSV-1 causes oral lesions in approximately 80% of cases and genital lesions in 20% of cases. In adolescents, as many as 30-40% of genital herpes is caused by HSV-1, as this proportion is thought to be increasing in the developed world, due to increased oro-genital contact. The reverse is true for HSV-2, which causes genital lesions in 80% and oral lesions in 20%. Cutaneous herpes is shown in the image below.

Cutaneous vesicles characteristic of herpes simple Cutaneous vesicles characteristic of herpes simples virus infection

Approximately 65% of the United States population is seropositive for HSV-1 by the fourth decade of life. Approximately 25% of the United States population is seropositive for HSV-2 by the fourth decade of life, with women being infected more frequently than men.[1] The indirect and direct costs of incident HSV genital infection in the United States are presently approximately $1.8 billion and expected to be greater than $2.7 billion by the year 2015.

Herpes viruses cause a wide range of diseases, including the following:

  • Gingivostomatitis
  • Keratoconjunctivitis
  • Encephalitis
  • Genital disease
  • Newborn infection

Primary infection

Primary infections usually are mild and, in many cases, asymptomatic. Patients who are immunocompromised may develop severe infections involving multiple organ systems. Immunocompetent individuals also may have severe primary infections.

Latency and recurrence

After the patient begins to produce antibodies, the infection becomes latent in the sensory ganglia. HSV-1 infection remains latent in the trigeminal ganglia and HSV-2 in the sacral ganglia. The viruses become reactivated secondary to certain stimuli, including fever, physical or emotional stress, ultraviolet light exposure, and axonal injury.

Recurrent infections tend to be less severe because of existing cellular and humoral immunity from prior exposures. Although many persons are seropositive for HSV-1, the recurrence rates range from 10-40% after the primary infection. Infection by HSV requires a break in the skin's barrier; intact skin is resistant to the virus.



HSV-1 infections are spread via respiratory droplets or direct exposure to infected saliva. HSV-2 usually is transmitted via genital contact. The contact must involve mucous membranes or open or damaged skin. The incubation period may last from 2-12 days, and vesicles typically erupt 6-48 hours after the onset of a prodrome.

Herpes viruses cause cytolytic infections; therefore, pathologic changes are due to cell necrosis as well as inflammatory changes. Fluid accumulates between the dermis and the epidermal skin layers, causing vesicle formation. The fluid then is absorbed, scabs are formed, and healing is completed without evidence of scarring. Shallow ulcers form after the vesicles rupture on mucous membranes.

Lesions from primary herpes infection typically take longer to form and usually persist for a longer duration of time.

The virus travels from the site of infection in the skin or mucosa to the sensory dorsal root and remains latent until a recurrent outbreak. Outbreaks are usually due to some sort of stress including ultraviolet radiation, trauma, emotional or psychological stress, or immunosuppression.




United States

Approximately 80% of adults have antibodies to HSV-1, whereas antibodies to HSV-2 are found in approximately 20% of the population.

The incidence of genital herpes has been estimated to be 500,000-1,000,000 cases per year with a prevalence of 40-60 million affected individuals.

In sexually transmitted disease (STD) clinics, HSV-2 seropositivity approaches 40-50%.

Encephalitis develops in 1 per 250,000-500,000 patients per year.

Neonatal HSV develops in 1 per 2,000-10,000 live births per year. Approximately 70% of cases of neonatal HSV occur when the mother is asymptomatically shedding virus near time of delivery. The risk of neonatal transmission is increased if vaginal delivery occurs during acute maternal infection.

Approximately 90% of HIV-positive individuals are seropositive for HSV-1, and about 77% of HIV-positive individuals are seropositive for HSV-2.


Greater than one third the world's population has recurrent clinical HSV infections. Reportedly, 13-40% of the world's population is seropositive for HSV-2 and 56-85% is seropositive for HSV-1, varying by country.


Most patients with herpetic infection experience short-term local pain and irritation, with mild constitutional symptoms.

Infection occasionally may become life threatening.

Immunocompromised patients are at increased risk of developing severe HSV infections.

HSV-1 is a common cause of fatal encephalitis in the US, with a mortality rate 60-80%. Fewer than 10% of patients are left without significant neurologic sequelae.

Keratoconjunctivitis may be caused by HSV-1. It is second only to trauma as a cause of corneal blindness in the US.


African Americans are more likely to be infected with HSV-2 than any other racial or ethnic group.[2] HSV-2 antibodies are present in approximately 20% of Caucasian adults and 65% of African American adults. Some experts consider nonwhite race as a risk factor to contract genital HSV-2.


Men are 20% more likely to develop recurrences of HSV-2 than are women.


Highest incidence of HSV-1 occurs in children aged 6 months to 3 years.[3, 4]

HSV-2 most commonly occurs in those aged 18-25 years.

Contributor Information and Disclosures

Rahul Sharma, MD, MBA, FACEP Medical Director and Associate Chief of Service, NYU Langone Medical Center, Tisch Hospital Emergency Department; Assistant Professor of Emergency Medicine, New York University School of Medicine

Rahul Sharma, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Association for Physician Leadership, Phi Beta Kappa, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Eric L Weiss, MD, DTM&H Medical Director, Office of Service Continuity and Disaster Planning, Fellowship Director, Stanford University Medical Center Disaster Medicine Fellowship, Chairman, SUMC and LPCH Bioterrorism and Emergency Preparedness Task Force, Clinical Associate Professor, Department of Surgery (Emergency Medicine), Stanford University Medical Center

Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Oncology Association of Practices, Southern Clinical Neurological Society, Wilderness Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Lawrence C Brilliant, MD Clinical Assistant Professor, Department of Primary Care and Community Services, MCP Hahnemann University; Attending Physician, Department of Emergency Medicine, Doylestown Hospital

Lawrence C Brilliant, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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Cutaneous vesicles characteristic of herpes simples virus infection
Herpes labialis
Penile infection with herpes simplex virus type 2
Tzanck smear showing a multinucleated giant cell
Herpes simplex virus dendritic ulcer with fluorescein staining.
Genital herpes infection
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