- Herpes simplex virus infections manifest as cold sores (on the face) and genital herpes (in the genital area).
- Infection is usually mild, but, rarely, it can cause more serious complications, especially in immunosuppressed people.
- Latent viral infection in the dorsal root ganglia results in cold sores. Reactivation may be precipitated by trauma, fever, intercurrent disease, or environmental factors such as windy days or sunburn.
- Severe cases may require systemic antiviral therapy.
Notification requirement for herpes simplex infections
Notification is not required.
Primary school and children’s services centre exclusion for herpes simplex infections
Young children with cold sores who are unable to comply with good hygiene practices should be excluded while the lesion is weeping. Lesions should be covered by a dressing, where possible.
Infectious agent of herpes simplex infections
Human herpes simplex virus (HSV) types 1 and 2 cause disease.
Identification of herpes simplex infections
HSV has been isolated from nearly all visceral and mucocutaneous sites. The clinical presentation depends on portal of entry, age, immune status and type of HSV (1 or 2) infection.
Cold sores are the most common manifestation of herpetic infection, and are characterised by a perioral primary lesion, latency and a tendency to local recurrence. Anal and perianal infections are common among sexually active populations of men who have sex with men.
In children with atopic dermatitis/eczema and immunosuppressed patients, HSV may cause a generalised eruption that requires hospitalisation for antiviral therapy. Cutaneous HSV infection may become chronic in patients with HIV infection or other immunosuppression, with recalcitrant crusted lesions and ulceration, or the infection may disseminate to cause severe extensive disease with visceral organ involvement. HSV infection may be complicated by erythema multiforme or Bell’s palsy, which is often more disabling than the infection itself.
HSV types 1 and 2 generally produce distinct clinical syndromes, depending on the portal of entry.
The primary infection may be mild and generally occurs in early childhood before the age of 5 years. About 10 per cent of primary infections cause a more severe form of disease manifested by fever and malaise. This may last a week or more, and can be associated with vesicular lesions leading to ulcers in and around the mouth (gingivostomatitis), eye infection (keratoconjunctivitis), a generalised vesicular skin eruption complicating chronic eczema or, more rarely, encephalitis. In immunosuppressed populations, syndromes such as pneumonitis or hepatitis may occur.
Features of gingivostomatitis include ulceration of the tongue, gums, lips and anterior buccal mucosa; severe systemic toxicity; and lymphadenopathy.
Reactivation of latent viral infection in the dorsal root ganglia results in cold sores appearing as clear vesicles on an erythematous base. These usually occur on the face and lips, and crust and heal in a few days. This reactivation may be precipitated by trauma, fever, intercurrent disease, or environmental factors such as windy days or sunburn.
This virus is the usual cause of genital herpes, although genital herpes can also be caused by type 1 virus. Genital herpes occurs mainly in adults and is sexually transmitted. Primary and recurrent infections occur, with or without symptoms.
The principal sites of primary disease in women are the cervix and vulva. Recurrent disease generally involves the vulva, perineal skin, legs and buttocks. In men, lesions appear on the glans penis or prepuce, and in the anus or rectum of those engaging in anal sex. Other genital or perineal sites, as well as the mouth, may also be involved in either gender, depending on sexual practices.
HSV-2 infection is, rarely, associated with aseptic meningitis and radiculitis. It can be a cause of recurrent aseptic meningitis (Mollaret’s) meningitis disease and transverse myelitis.
The diagnosis may be suggested by cytologic changes in tissue scrapings or biopsy. Confirmation is made by direct fluorescent antibody tests, by isolation of the virus from oral or genital lesions or other sites, or by detection of HSV DNA by nucleic acid testing of lesion fluid or cerebrospinal fluid. Techniques are also available to differentiate type 1 from type 2 antibody, if required. HSV infections are best confirmed by isolation of virus in tissue culture or lesion scrapings, with the greater yield from vesicular lesions. More than 90 per cent of the population has antibodies to HSV-1 by the fifth decade of life.
Incubation period of herpes simplex viruses
The incubation period varies from 2 to 12 days.
Public health significance and occurrence of herpes simplex infections
Asymptomatic infections with HSV-1 are common. Seventy to ninety per cent of adults have circulating antibodies to HSV-1, indicating previous infection.
HSV-1 is a common cause of meningoencephalitis. Vaginal delivery in pregnant women with active genital infection carries a high risk of disseminated visceral infection, encephalitis and death to the newborn.
HSV-2 is frequently associated with sexually transmitted infections, and 12–15 per cent of adults have antibody evidence of exposure. The prevalence is greater in socioeconomically disadvantaged groups and those with multiple sexual partners.
Reservoir of herpes simplex viruses
Humans are the reservoir.
Mode of transmission of herpes simplex viruses
Transmission of HSV infections occurs through close contact with a person shedding virus from a peripheral site, at a mucosal surface, or in genital or oral secretions. Inoculation of virus onto susceptible surfaces such as oropharynx, cervix, conjunctivae or small cracks in skin is required for infection. Contact with HSV-1 in the saliva of carriers is the most important mode of spread. Contact of healthcare workers with patients who are shedding HSV may result in an infection of the tip of the finger (herpetic whitlow). It begins with intense itching and pain, and is followed by vesicle formation and then ulceration.
Transmission of HSV-2 to nonimmune adults is usually by sexual contact.
Period of communicability of herpes simplex infections
Secretion of virus in the saliva may occur for up to 7 weeks after recovery from stomatitis.
Patients with primary genital lesions are infective for 7–10 days. Those with recurrent disease are infectious for 4–7 days with each episode.
Susceptibility and resistance to herpes simplex infections
Everyone is susceptible to infection. The disease does not usually confer protective immunity because the virus tends to become latent in dorsal root ganglia of the spine, where it may be reactivated at a later date.
Control measures for herpes simplex infections
No vaccine is currently available.
Health education and personal hygiene should be directed towards minimising transfer of infectious material and reducing the risk of exposure of high-risk groups.
Emphasise personal hygiene to minimise the transfer of infectious material. Avoiding skin contact from the time of first symptoms (warning 'tingle') on the mouth, genitals or anus, and for a week after the symptoms have gone helps prevent transmission. Wear gloves when in direct contact with infectious lesions, and wash hands with soap and water afterwards.
Correct and consistent use of condoms during sexual intercourse decreases the risk of infection.
Preventive antiviral medication (suppressive therapy) when recurrences are frequent can reduce the risk of transmission.
Control of case
For symptomatic treatment of minor attacks, use Betadine (povidone iodine) 10 per cent paint applied three times daily, and/or topical antiviral therapy. Therapy should be self-initiated and commenced at the earliest sign of onset. Consult the current version of the .
Sun protection is important in preventing recurrences of facial herpes simplex.
Specialist advice on systemic antiviral treatment should be sought for:
- severe primary or severe recurrent attacks
- attacks complicated by erythema multiforme
- primary or recurrent attacks in HIV-infected patients or the immunosuppressed.
- recurrent episodes of lymphocytic meningitis (Mollaret’s meningitis).
Patients with active lesions should have no contact with newborns, children with burns or eczema, or immunosuppressed patients. Consider caesarean section before the membranes rupture when primary or recurrent genital infections occur in late pregnancy, to minimise the risk of neonatal infection.
Cases of disseminated severe infection and cases in neonates should be managed in isolation under contact precautions because of the risks to other neonates or pregnant women.
Patients should be fully screened for other sexually transmissible infections, including HIV infection, on their first presentation.
Treatment usually consists of valaciclovir, famciclovir or aciclovir. The choice and duration of treatment varies for initial attacks, infrequent recurrent attacks (episodic therapy) or suppression of frequent recurrent attacks (chronic suppressive therapy). Consult the current version of the .
If there is breakthrough during prophylaxis, higher doses may be successful. Relapse may occur at the cessation of prophylaxis.
Control of contacts
Control of environment
Outbreak measures for herpes simplex infections
Reviewed 05 May 2023