⬇ ⬇Herpes simplex genitalis is a genital disease caused most commonly by HSV-2, although HSV-1 can also infect genital skin. It is most commonly, but not invariably, sexually transmitted.
HSV is the most common cause of ulcerative genital lesions. The disease is highly contagious during its prodrome and while lesions are present.
HSV establishes latency in the dorsal root ganglia and reappears after different triggers in individual patients (see Chapters 6 and 17). Triggers include psychologic or physiologic stress, physical trauma such as from sexual intercourse, menses, and immunosuppression.
Affected patients may have recurrences that are infrequent or as common as once monthly. Patients who have six or more episodes per year are candidates for long-term suppressive therapy.
⬆ ⬇Most often, the diagnosis is based on the clinical appearance.
The Tzanck preparation (see Chapter 6: Superficial Viral Infections) may be helpful, but it lacks sensitivity.
Viral culture is the current standard of diagnosis, but the sensitivity declines rapidly as the lesions begin to heal.
Diagnosis in tissue culture using monoclonal antibodies or polymerase chain reaction is sensitive; however, it is very expensive and has not been approved by the U.S. Food and Drug Administration for the diagnosis of genital lesions.
Serologic testing may be useful, according to CDC guidelines, for those with (a) recurrent genital signs and symptoms and negative cultures, (b) a clinical diagnosis of genital herpes without laboratory confirmation, and (c) a partner with genital herpes. It is not recommended for screening of the general population.
Herpes Zoster (see Chapter 6: Superficial Viral Infections) |
⬆Initially, lesions appear as grouped vesicles on an erythematous base (Fig. 28.12).
Lesions may then become pustular, crusted, and eroded (Fig. 28.13).
Crusting of the lesions occurs over 15 to 20 days, before reepithelialization begins.
Chronic ulcerations or crusted or verrucous papules may develop in immunocompromised patients (see Figs. 33.3 and 33.4).
In women, the vulvae, perineum, inner thighs, buttocks, and sacral area (Fig. 28.14) are the most common sites of involvement.
In men, the penis, scrotum, thigh, and buttocks are the typical locations.
As with HSV-1, this may be more severe than recurrent infections (see Chapter 6: Superficial Viral Infections).
The duration is generally from 10 to 14 days. Regional adenopathy may be present.
Fever, dysuria, urinary retention, and constipation may also occur.
Alternatively, the initial outbreak may be mild or asymptomatic, so that the patient sheds virus intermittently without realizing that he or she is infected.
There is often a prodrome of itching, burning, numbness, tingling, or pain 1 to 2 days before a clinical outbreak.
Lesions are localized and recur at the same site or in close proximity each time.
Chronic ulcerative lesions are indicative of immunosuppression.
The risk of neonatal transmission is less than 3% and is greatest in patients with primary HSV at the time of delivery.
Genital ulcer disease puts the patient at an increased risk of HIV infection.
The risk of neonatal transmission depends on when the maternal infection is acquired. The risk to the neonate is less than 1% if the maternal infection is recurrent or is acquired at the beginning of pregnancy and is 30% to 50% if the maternal infection is acquired near term.
If maternal HSV is acquired near the time of delivery, cesarean section is usually advised.
Patients with certain skin diseases, such as atopic dermatitis, are in danger of developing dissemination of herpes simplex, also known as Kaposi varicelliform eruption or eczema herpeticum (see Figs. 6.14 and 17.29).
Differential Diagnosis 
Management 
Helpful Hints 
Points to Remember 