|
Herpes comes from the Greek word meaning "to creep" and is used to describe two distinct but antigenically related serotypes of herpes simplex virus. Herpes simplex virus type 1 (HSV-1) is most commonly associated with oropharyngeal disease, and herpes simplex virus type 2 (HSV-2) is most closely associated with genital disease; however, each virus is capable of causing infections clinically indistinguishable in both anatomic areas.(1, 2)
Humans are the sole known reservoir for HSV. Infection is transmitted via inoculation of virus from infected secretions onto mucosal surfaces (e.g., urethra, oropharynx, cervix, conjunctivae) or through abraded skin.(3) The virus can exist for a limited time on environmental surfaces, suggesting possible transfer by means other than the venereal route.
Infections of herpes simplex occur in cycles. The first stage is primary mucotaneous infection. Exposure at mucosal surfaces or abraded skin permits entry of the virus and replication in cells of the epidermis and dermis. Initial infection is often subclinical. Whether clinical, or subclinical, sufficient viral replication occurs to cause infection of either sensory or autonomic nerve endings. This is followed by infection of the ganglia and establishment of latency. The time period involved from mucosal inoculation to transport and replication in the ganglion is unknown. The virus may then spread to distant locations through peripheral sensory nerves. At some point, the disease is reactivated causing recurrent infection. It is unclear what factors occur that cause or maintain latency, and what factors trigger reactivation. It is believed, however, that physical and emotional stresses contribute to reactivation of latent virus.
Host responses to infection with HSV influence the acquisition of the disease, the severity of infection, resistance to the development of latency, the maintenance of latency, and the frequency of recurrences.(4) While both cell-mediated immunity and antibody-mediated immunity are important, immunocompromised patients with defects in cell-mediated immunity appear to have a greater recurrence and greater severity of HSV disease than those with deficits in humoral immunity, such as gammaglobulinemia.
First episode primary infections are classified as infections occurring in persons lacking antibody to either type of HSV.(3) First episode infections are typically more severe than recurrent infections and include systemic as well as local symptoms. Many patients experience flu-like symptoms of fever, myalgia, headache, and malaise, in addition to pustular or ulcerative local lesions. Both subtypes can cause oral-facial or genital lesions that are clinically indistinguishable. However, the frequency of reactivation of infection is influenced by anatomic site and virus type. Genital HSV-2 infection is twice as likely to reactivate and recurs eight to 10 times more frequently than genital HSV-1 infection. Conversely, oral-labial HSV-1 infection recurs more frequently than oral-labial HSV-2 infection.(4) First episodes of genital herpes in patients who have had prior HSV-1 infection are associated with faster healing of lesions and less frequent systemic symptoms than in primary genital herpes.
Other herpes infections include herpetic whitlow, or HSV infection of the finger. This may occur as a complication of primary oral or genital herpes via a break in the epidermal surface, or it may occur by direct exposure to the hand through occupational or other exposure. Herpes gladitorum has been most frequently described in association with wrestlers. HSV may infect any area of the skin. Mucotaneous infection of the thorax, ears, face, and hands is facilitated by trauma to the skin sustained during wrestling. Prompt diagnosis and treatment should be obtained to prevent the spread of infection.
HSV infectio
|
