Diagnostic hallmarks
- Distribution - perioral, genital, and perigenital skin
- Tight clustering of small vesicles
- Recurrent episodes in the same location
Clinical Presentation
Cutaneous infection with Herpesvirus hominis (HSV 1 and HSV 2) results in the appearance of small vesicles of uniform size and shape. Two clinical patterns are commonly seen, herpes labialis and herpes genitalis.
Herpies labialis consists of three to eight small, tightly clustered vesicles at the vermilion border of the lips. Occasionally, the grouped vesicles are found elsewhere on the face, particularly around the nose. The individual vesicles are 1-3 mm in diameter and are so closely set that sometimes the appearance is that of a single, irregularly shaped multiloculated bulla. The vesicles usually appear to arise from normal skin, but occasionally a narrow ring of erythema surrounds the base.
The vesicles of herpes simplex are quite fragile, and patients often present with one or more erosions rather than with intact vesicles. The erosion is usually 1.0-1.5 cm in diameter. The configuration of the erosion is distinctive, since it reflects the multiple vesicles that led to its formation and is thus irregular rather than round in outline. The eroded surface may be covered by a loosely adherent yellow crust simulating the appearance of impetigo. The history of a preceding multivesicular stage helps to identify the lesion as herpes simplex.
The lesions of herpes labialis are relatively asymptomatic, but patients often describe a preeruptive sensation of mild burning or tingling that precedes the appearance of the vesicles by several hours. Regional, somewhat tender lymphadenopathy is sometimes present.
The lesions of herpes genitalis are entirely analogous to those of herpes labialis. Multiple small vesicles suddenly appear on genital or perigenital skin. The appearance differs from herpes labialis, in that more vesicles may be present and there may be less tightness to the clustering. This is particularly true for women experiencing their initial attack. In this situation, 20 or more vesicles may be scattered in a random, bilateral distribution over the entire vulva. These severely painful initial episodes may be accompanied by lymphadenopathy, malaise, meningismus, urethritis, cystitis, and cervicitis. In both men and women, these recurrent lesions are less troublesome but remain more painful than the recurrent lesions of herpes labialis.
Because of trauma from movement and the rubbing of clothing, intact vesicles are not often seen. Here too, the irregular shape of the resultant erosion is a clue to the fact that the lesion was originally composed of clustered, confluent vesicles.
The diagnosis of herpes simplex is usually made on a clinical basis. A suspected diagnosis can be confirmed by means of a Tzanck smear, viral culture, or biopsy.
Uncommon Clinical Presentations. In children, initial exposure to herpesvirus occasionally results in widespread oral and genital lesions with fever and malaise. This syndrome of primary herpes infection is, fortunately, rather rare.Herpes simplex infection occuning in patients with atopic disease or Darier’s disease sometimes develops into a disseminated cutaneous infection known as eczema herpeticum or Kaposi’s varicelliform eruption.
Older patients with depressed immune response and patients treated with cancer chemotherapeutic drugs may have difficulty clearing their herpes simplex lesions. In such nstances, seemingly trivial infections develop into widespread erosive disease or chronic, deep, burrowing ulcers.
Recurrent clustered herpes simplex vesicles sometimes occur on other than perioral or genital skin. These infections appear as bright-red inflammatory plaques 3-6 cm in diameter. Vesiculation is often rather inapparent; instead, the lesions appear eczematous or urticarial. Such lesions are particularly common over the sacrum and buttocks.
Rarely, recurrent herpes simplex occurs entirely as an intraoral process with no lip involvement. These lesions must be differentiated from recurrent aphthous ulcers.
Course and Prognosis
Individual episodes of recurrent herpes labialis last 5-10 days. During the first few days viral replication takes place and contagion is possible. By the third or fourth day the vesicles have usually broken and cruisting develops. Healing occurs without scarring. Repeated episodes, occurring as a result of viral reactivation rather than exogenous reinfection, follow sunburn, coryza, fever, and psychologic stress. These recurrent episodes tend to involve the same skin location each time and may continue intermittently for many years.
Individual episodes of herpes genitalis last 7-14 days; this longer duration occurs as a result of the extra heat, maceration, and trauma that are present in the groin. Viral particles are present during the first 5-7 days, and contagion is likely during this time. Healing eventually occurs without scarring. Approximately 50% of the patients will have one or more recurrences. The recurrence rate for those with HSV 2 infections is much higher than that for those with HSV 1 infections. Generally, these develop at the same site as the original lesion. Recurrent episodes occur as a result of trauma during intercourse, vaginitis, menses, and psychologic stress. These recurrences are less severe than the original infection, and by the end of 3 years, approximately half of the affected individuals will cease having recurrent episodes.
For purposes of counseling, one generally assumes that there is no risk of contagion during the asymptomatic intervals between attacks. Actually, some asymptomatic viral shedding, especially in women, does occur, but it is not known to what degree these patients are contagious. Obtaining proof of a patient’s status as a “shedder” or “nonshedder” would be impractical, as it would require multiple viral cultures during asymptomatic intervals. Herpes infection at or just before parturition may result in severe neonatal infection.
Pathogenesis
Herpes simplex infections are due to the enveloped DNA virus Herpesvirus hominis (HSV) types 1 and 2. These two organisms are identical in appearance under electron microsÂcopy but differ biochemically and antigenically. Both are transmitted as a result of close human-to-human contact. Type I infections tend to occur in childhood and are extremely common. Antibody studies suggest that by the time of adult life, 70-90% of the population has been infected. Type 2 infections tend to occur in early adult life. They are considerably less common, affecting 10-20% of sexually active adults. Antibody studies suggest that the likelihood of infection is directly related to the number of sexual partners. Approximately 80% of the cases of herpes labialis will be due to type 1 infection, and about 20% will be due to type 2 infection. These proportions are reversed for herpes genitalis. It is extremely important to realize that the initial infection with either type of virus may be entirely asymptomatic and that the pool of those infected is considerably larger than the number of people who experience visible lesions.
After initial infection (which may be either symptomatic or asymptomatic), the virus resides in a latent, nonreplicating phase in one or more of the dorsal root ganglia. Reactivation of the infection results in the movement of viral particles along the sensory nerves such that witllin a matter of hours they arrive at the terminal branches at the dermal-epidermal junction. At that point, viral particles infect the nuclei of epithelial cells wherein they replicate and infect adjoining cells. Matter several days of replication, the cell-mediated immune response of the host halts the process, and slow resolution of the disease ensues. Humoral immune response does not seem to control cutaneous infection, since recurrent episodes can take place in the face of high antibody titers. Antibody response, however, does seem to playa role in restricting the viral infection to the skin. Those without antibody response are at considerable risk of developing herpes encephalitis or other systemic infection. Immune responsiveness to type1 infection confers only a modest degree of protection against subsequent type 2 infection.
From an epidemiologic standpoint, it should be recognized that there are several mechanisms through which a person might develop his or her first clinically recognizable infection. Infection might occur as a result of:
- exposure to a clinically infected person 3-5 days earlier,
- exposure to an asymptomatic viral shedder 3-5 days earlier, or
- reactivation of a latent infection that had been acquired asymptomatically months or even years earlier.
As a result of these latter two mechanisms, contact tracing in individuals with herpes genitalis is often unproductive.
Therapy
Availability of the antiviral antibiotic acyclovir 10 years ago has greatly improved the therapeutic possibilities for patients with herpes simplex infections. Initial attacks of herpes genitalis (and herpes labialis if they are sufficiently symptomatic) can be treated with the oral administration of acyclovir in a dosage of 200 mg 5 times/day. This treatment rapidly reduces the severity of symptoms and reduces the number of days of viral replication. Similar but lesser improvement occurs when recurrent episodes are treated at the time of the prodromal stage.
Patients who experience multiple episodes of recurrent herpes genitalis can also be treated prophylactically. In this situation, a dose of 200 mg of acyclovir is taken 3 times/day. Such treatment reduces the recurrence rate essentially to zero and appears to decrease (but probably not stop) asymptomatic shedding. In some patients, lower daily doses will be equally effective. Currently, the Food and Drug Administration (FDA) has approved continuous treatment for 1 year; studies, however, have demonstrated safety and efficacy for as much as 4 years. There is, unfortunately, no long-term effect on the recurrence rate, once the medication has been stopped, new episodes generally ensue a short time later.
For some patients, acyclovir therapy may not be desirable or practical. Patients with mild initial episodes, patients with infrequent recurrences, and patients in monogamous relationships may find that concerns about safety, viral resistance, and high cost outweigh potential benefits. For these patients, local symptomatic treatment with soaks followed by a thin layer of a bland cream or ointment may be all that is necessary.
The recurrence rate for herpes labialis is most effectively reduced through the frequent application of sunscreen to the lips and by the avoidance of local mechanical trauma. It is harder to reduce the recurrence rate of herpes genitalis. Reduction in genital trauma through the use of condoms in the male and treatment of even trivial vaginitis in the female is of help, as is the use of added lubrication during intercourse. However, perhaps the most productive approach is attempted reduction in the stress that seems to account for such a large percentage of recurrent episodes.
An important component of therapy for patients with genital herpes is the provision of advice to reduce the likelihood of transfer to a sexual partner. Certainly, intercourse ought to be avoided during symptomatic episodes. It is probably safe for infected men to have intercourse when no penile lesions are present, since asymptomatic shedding in men seems to occur infrequently. This may not be true for women because intermittent shedding from the cervix seems to occur in a larger percentage of affected individuals. Women, therefore, should use a diaphragm and/or should encourage their consorts to use a condom. The degree of protection offered by these mechanical barriers is not known with certainty, but anecdotal evidence suggests that it is quite good.
Tags:erythema, herpes Simplex, herpesvirus, herpesvirus hominis, herpie labialis, lymphadenopathy, perigenital skin Vesiculobullous Diseases
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