Herpesvirus Infections and Herpetic Wounds

Advances in Skin & Wound Care,  Sep/Oct 2003  by Trent, Jennifer T,  Kirsner, Robert S

• E-mail
• Print
• Link

AT THE PRESENT TIME, 8 different viruses have been described within the human herpcsvirus (HHV) family (Table 1). All of these viruses produce cutaneous manifestations to varying degrees. However, HHV-1 and HHV-2, known as herpes simplex virus (HSV) types 1 and 2 (HSV-1, HSV-2), and HHV-3, known as varicella-zoster virus (VZV), are most commonly known to cause cutaneous ulcers and will be the focus of this article (Figures 1-3).

Herpes Simplex Virus Types 1 and 2 Incidence and prevalence

More than 85% of the world's population is estimated to be seropositive for HSV-1.1 However, only 25% to 40% of seropositive individuals suffer from recurrent cold sores. HSV-1 affects lower socioeconomic groups to a slightly greater extent. For example, one third of children younger than age 5 in lower socioeconomic groups are seropositive for HSV-1, compared with 20% of 5-year-olds in middle-class groups. Similarly, although 80% of adolescents in lower socioeconomic groups are seropositive, 40% to 60% of adolescents in middle-class groups are seropositive for HSV-1.

The scroprevalcnce for HSV-2 in the United States is 21.9% (45.9% black, 17.6% white) and is higher in developing countries, where scroprevalcnce is 40% to 60%.2 One study that reported a 16% seroprevalencc of HSV-2 among individuals aged 15 to 74 years found that 78% of these individuals never developed evidence of infection. In addition, Brown et al3 found 25% of women seropositive for HSV-2, but only one quarter of those women exhibited signs of infection.

Clinical presentation

HSV-1 and HSV-2 are double-stranded DNA viruses that carry only 1 type-specific surface glycoprotein: gG-1 for HSV-1 and gG-2 for HSV-2.4 Therefore, cross-reactivity between the 2 viruses is considerable. The genome of the viruses encode for several enzymes, which become targets for certain antiviral medications used in the treatment of HSV infections.

In general, HSV-1 is thought to be largely responsible for orolabial ulcerations and HSV-2 primarily causes genital ulcerations.5 However, this is not true in a small percentage of cases. HSV-2 can cause orolabial lesions6 and HSV-1 causes about 30% of genital herpes lesions. In cases in which HSV-1 is responsible for lesions of genital herpes, less recurrence, shedding, symptoms, and transmission of the virus occurs than when HSV-2 causes the disease.2,5 Prior infection with HSV-1 confers some protection against infection with HSV-2; however, when concurrent infections do occur, genital lesions are less symptomatic.

Herpes labialis (orolabial herpes) appears most commonly on the lips and in the mouth.7 Clinical presentation often begins with burning pain, which may, at times, herald the development of cutaneous lesions. The lesions may begin as macules or papules, which become vesicles, or patients may develop vesicles de novo. These vesicular lesions can ulcerate, causing considerable pain and gingivostomatitis. Fever, sore throat, malaise, lymphadenopathy, and anorexia can accompany a herpetic outbreak. Lesions on children classically involve the buccal and gingival mucosa. Recurrences usually present on the vermillion border of the lips.

Herpes genitalis (genital herpes) presents with lesions on the penis, scrotum, and/or perianal areas in men and on the cervix, vulva, and/or perianal areas in women.8 Herpes genitalis may begin in a similar fashion to herpes labialis, often with pain. Painful papules then occur, which progress to vesicles that ulcerate and eventually heal by developing crusts. Patients may less commonly experience dysuria, urinary retention, autonomie dysfunction, vulvar adhesions, urethra) strictures, constipation, rectal pain and bleeding, and transverse myelitis.5

Immunocompromised patients usually have more pain in both forms of HSV; larger, more necrotic lesions; more lesions that may disseminate; slower healing times; and lesions in atypical locations? In addition to the classic appearance of herpetic lesions, immunocompromised patients may have verrucous or hyperkeratotic lesions. Acyclovir resistance occurs more frequently in this population of patients.

Transmission of HSV from mother to fetus may lead to serious complications.3,9,10 Vertical transmission occurs in 1 case per 2000 to 1 case per 15,000 of all births.3 Newborns usually become ill 5 to 21 days after birth. HSV-2 can produce developmental disorders, central nervous system complications, and even death, whereas HSV-1 can cause lesions on skin, eyes, and mucosa. Transmission of HSV-1 occurs more easily than HSV-2. Only 5% of transmissions occur in utero; the rest (95%) occur during labor and transvaginal delivery.3 In most cases, infected mothers are asymptomatic. Timing of viral infection also appears critical in transmission to newboms. Infections occurring during the third trimester of pregnancy have led to a 50% transmission rate, compared with a 3% transmission rate for mothers who are infected earlier in pregnancy. All pregnant women should be screened for HSV at their first prenatal examination.