Chapter 172 Herpes Simplex
• Acute or recurrent viral infection of the skin or mucous membranes characterized by the appearance of grouped vesicles on an erythematous base frequently occurring about the mouth (herpes gingivostomatitis), lips (herpes labialis), genitals (herpes genitalis), and conjunctiva and cornea (herpes keratoconjunctivitis)
More than 70 viruses compose the Herpesviradae family. Of these, four are important in human disease: herpes simplex virus (HSV), varicella zoster virus, Epstein-Barr virus, and cytomegalovirus. Serologic methods have distinguished two types of HSV, which have been designated HSV-1 and HSV-2. HSV-1 is frequently acquired in early childhood, with evidence of serologic infection approaching 90% in adults. More than one-third of the world’s population has recurrent HSV. Although 80% of seropositive individuals do not have clinically apparent recurrences, they still shed virus asymptomatically. Current estimates indicate that 20% to 40% of people in the United States have recurrent HSV infections.1 Previously, HSV-1 was primarily isolated from extragenital sites, while genital infections were caused primarily by HSV-2. By the year 2000, however, HSV-1 had replaced HSV-2 as the primary cause of genital lesions, likely due to orogenital contact.2 A retrospective review of genital HSV isolates collected in a university student health service showed that HSV-1 accounted for 78% of all genital isolates in this population by 2001, compared with 31% of isolates in 1993.3 Individuals who are exposed to HSV and have asymptomatic primary infections may experience an initial clinical episode of genital herpes months to years after becoming infected.
Herpes outbreaks on the hands and fingers (herpes whitlow) is increasingly recognized, probably owing to digital–genital contact. Cigarette smoking is a risk factor because a nicotine by-product concentrates in genital secretions and suppresses T-cell function.
HSV-1 genital lesions have a recurrence rate of 14%, whereas the HSV-2 recurrence rate is 60%. Men seem more susceptible to recurrences. After resolution of the primary infection, HSV probably becomes a dormant inhabitant within sensory or autonomic trigeminal or lumbosacral ganglia or both. Recurrences develop at or near the sites of primary infection and may be precipitated by many different stimuli:
Because not everyone exposed to HSV develops clinical infection, it appears that host defense mechanisms are paramount in protecting against infection. Chronic, persistent labial and genital infections are seen in immunosuppressed individuals. The cell-mediated immune system is undoubtedly the major factor in determining the outcome of herpes exposure; that is, whether it leads to resistance, latent infection, or clinical disease.
Isolation of HSV from tissue scrapings is the gold standard for diagnosis. Cytopathic effects are typically seen within 2 to 7 days. A more rapid diagnostic test for mucocutaneous lesions is direct staining of skin scrapings. Type-specific serologic tests are now widely used to diagnose unrecognized HSV-1 and HSV-2 infections or to confirm suspected cases.
Prevention of recurrent herpes is recommended to decrease the number and severity of outbreaks, reduce asymptomatic viral shedding, and prevent transmission to partner and/or fetus. Three or more people may benefit when one person takes preventive measures. Education regarding transmission and asymptomatic viral shedding is imperative.
Enhancement of the host’s immunologic status is a key goal in the control of herpes infection. In addition to general immune support (for a complete discussion, see Chapter 56) one of the key natural measures to strengthen cell-mediated immunity is the use of polypeptide-rich bovine thymus extracts. These have been shown to be effective in preventing both the number and severity of recurrent infections in immune-suppressed individuals.4 Thymus extract appears to increase the lymphoproliferative response to HSV, natural killer cell activity, and interferon production, thus preventing viral activation by potentiating these cell-mediated immune responses.