Herpes Simplex in Emergency Medicine

Updated: Jun 26, 2017
  • Author: Melissa Kohn, MD, MS, FACEP, EMT-T/PHP; Chief Editor: Steven C Dronen, MD, FAAEM  more...
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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

  • Chickenpox

  • Shingles

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 neural ganglia. Most commonly, 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, unless the person is immunocompromised. 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 that comes into contact with genital or oral secretions or an HSV lesion. The incubation period may last from 2-12 days, and vesicles typically erupt 6-48 hours after the onset of a prodrome. An asymptomatic individual without an open lesion can still transmit the HSV-2 virus through genital shedding. [2]

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 type of stress including ultraviolet radiation, trauma, emotional or psychological stress, or immunosuppression.




United States

Epidemiologic data may be incomplete, as HSV is not currently a nationally reportable condition.

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%. Overall, the seroprevalence of HSV-2 is declining, especially within specific cultural groups. [3]

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.


Just over two thirds of the world's population has recurrent clinical HSV infections. Reportedly, 13-40% of the world's population is seropositive for HSV-2 and 67% is seropositive for HSV-1, varying by country. Africa has higher rates of both HSV-1 and HSV-2. For HSV-2, the second highest rates are found in the Americas, but those countries have the lowest rates of HSV-1. [4]


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. [5] 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, although women have higher rates of HSV-2 infection. [3]


Highest incidence of HSV-1 occurs in children aged 6 months to 3 years. [6, 7]

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