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U N I T 1 1
Genitourinary and Reproductive Function
infection, development and maintenance of latency, and
frequency of HSV recurrences.
Herpes simplex virus is transmitted by contact with
infectious lesions, but may also be transmitted when no
symptoms or lesions are present. Although most HSV
genital infections were once caused by HSV-2, it is now
increasingly common for infections to be caused by both
HSV-1 and HSV-2, particularly among adolescents and
young women.
12
Persons infected with HSV-1 remain at
risk for acquiring HSV-2. Most cases of HSV-2 infec-
tion are subclinical, manifesting as asymptomatic or
symptomatic but unrecognized infections. These sub-
clinical infections can occur in people who have never
had a symptomatic outbreak or they can occur between
recognized clinical recurrences. Up to 70% of genital
herpes is spread through asymptomatic shedding by
people who do not realize they have the infection.
11,12
This “unknown” transmission of the virus to sex part-
ners explains why this infection has reached epidemic
proportions throughout the world.
12
The incubation period for HSV is 2 to 12 days.
11
Genital HSV infection may manifest as a first-episode
or recurrent infection. The initial symptoms of primary
genital herpes infections include tingling, itching, and
pain in the genital area, followed by eruption of small
pustules and vesicles. These lesions rupture on approxi-
mately the 5th day to form wet ulcers that are excru-
ciatingly painful to touch and can be associated with
dysuria, dyspareunia, and urine retention. This period
is followed by a 10- to 12-day interval during which
the lesions crust over and gradually heal. Involvement
of the cervix, vagina, urethra, and inguinal lymph nodes
is common in women with primary infections. In men,
the infection can cause urethritis and lesions of the penis
and scrotum. Rectal and perianal infections are possible
with anal contact. Systemic symptoms associated with
primary infections include fever, headache, malaise,
muscle ache, and lymphadenopathy. Primary infections
may be debilitating enough to require hospitalization,
particularly in women. First episodes of nonprimary
infections (acquisition of HSV-2 in persons with preex-
isting antibodies to HSV-1 or, more rarely, acquisition
of HSV-1 in persons with preexisting HSV-2 antibodies)
are associated with fewer lesions, a shorter duration of
disease, and a lower rate of complications than primary
infections.
Recurrent HSV episodes are usually milder than the
initial episode—there typically are fewer lesions, and
viral shedding occurs at a lower concentration and for a
shorter duration (about 3 days). However, the prodro-
mal symptoms of itching, burning, and tingling at the
lesion site are similar. Except for the greater tendency
of HSV-2 to recur, the clinical manifestations of genital
HSV-2 and HSV-1 infections are similar. The frequency
and severity of recurrence vary from person to person.
Numerous factors, including emotional stress, lack of
sleep, overexertion, other infections, vigorous or pro-
longed coitus, and premenstrual or menstrual distress,
have been identified as triggering mechanisms.
Diagnosis andTreatment
Diagnosis of genital herpes is based on symptoms,
appearance of the lesions, and identification of the
virus taken from the lesions. Viral culture can gener-
ally isolate the virus in 5 days, is relatively inexpensive,
and is highly specific. However, it is not very sensitive,
with false-negative results of 25% with primary infec-
tions and as high as 50% with recurrent infections.
Polymerase chain reaction (PCR), which can detect sin-
gle copies of viral DNA by amplifying the DNA many
millions of times, has a higher sensitivity and has become
the preferred method to confirm a diagnosis of genital
HSV infection.
4,11
In addition to identifying the virus
from a sample taken from the herpes lesion, detection
of type-specific antibodies to HSV-1 and HSV-2 from a
blood sample also can help to establish the diagnosis.
These tests yield false-negative results when used in the
early stages of infection, since it takes approximately
22 days for the body to produce antibodies to the virus.
2
Approximately 20% of patients may remain seronega-
tive for 3 months, particularly if they have received anti-
viral medications.
2
This type of testing may prove useful
in confirming infection in persons with recurrent genital
symptoms and negative HSV testing, or in establishing
a clinical diagnosis of genital herpes in a partner of a
person with genital herpes.
4
There is no known cure for genital herpes, and the
methods of treatment are largely symptomatic. The oral
antiviral drugs acyclovir, valacyclovir, and famciclovir
have become the cornerstone for management of geni-
tal herpes.
2,11
By interfering with viral DNA replication,
these drugs decrease the frequency of recurrences, shorten
the duration of active lesions, reduce the number of new
lesions formed, and decrease viral shedding. Valacyclovir,
the active component of acyclovir, and famciclovir have
greater bioavailability, which enables improved dosing
1. Penetration of virus into skin.
Local replication and entry of
virus into cutaneous neurons
2. Centripetal migration in the
axon of uncoated
nucleocapsids
3. Synthesis of
infectious
virions
4. Centrifugal migration of
infectious virions to epidermis
FIGURE 41-2.
Pathogenesis of primary mucocutaneous herpes
simplex virus infection. (From Corey L, Spear PG. Infections with
herpes simplex viruses: Part 1. N Engl J Med. 1986;314:686.)
