C h a p t e r 4 1
Sexually Transmitted Infections
1051
Diagnosis andTreatment
Diagnosis of genital warts is usually made by visualiza-
tion or palpation of nontender papillomatous genital
lesions. A diagnosis of genital warts may be confirmed by
biopsy. There are no approved serologic tests for HPV or
routine methods for culturing the virus.
7
As HPV infec-
tion is confined to the epithelium and cells are shed, the
infection results in a minimal immune response and not
all those infected produce antibodies to the virus that
are detected using serology tests. HPV tests are available
for women older than 30 years of age who are under-
going cervical cancer screening. These tests detect HPV
nuclear DNA, ribonucleic acid (RNA), or capsid pro-
teins. Four tests have been approved by the Food and
Drug Administration (FDA), two of which indicate the
presence of one or more high-risk HPV types, and two
which provide individual detection of HPV 16 and 18.
7
None of these tests have been approved for use in men,
for women older than 20 years of age, or as a general
test for STIs.
The choice of treatment for genital warts is based on
the number, size, site, and morphology of the lesions,
as well the person’s preference. If left untreated, the
warts may resolve spontaneously, so expectant manage-
ment is acceptable if the person is comfortable with this
approach. Evaluation and treatment of sexual partners
may be suggested, although this may be difficult consid-
ering that warts often do not become clinically apparent
for several years after exposure.
Treatment regimens canbe classified as patient-applied
or provider-applied. Patient-applied products include
cytoxic agents (podofilox [5%]), an immune enhancer
(imiquimod), or a green tea extract (sinecatechin).
4–6
Podofilox is a topical antimitotic agent that results in
visible necrosis of wart tissue. The safety of podofilox
during pregnancy has not been established. Imiquimod
stimulates the body’s immune system (i.e., production
of interferon-
α
and other cytokines). Imiquimod is a
category B drug and therefore potentially safe for use
in pregnancy. Sinecatechins are thought to destroy wart
tissue by inducing cell cycle arrest and apoptosisis.
5
The
safety of sinecatechins during pregnancy has not been
established.
6
Provider-administered treatments include podophyl-
lin resin [10% or 25%], trichloroacetic acid (TCA), or
bichloracetic acid (BCA). Podophyllin resin is a topical
cytotoxic agent that has long been used for treatment of
visible external growths. Multiple applications may be
required for resolution of lesions. The amount of drug
used and the surface area treated should be limited with
each treatment session to avoid systemic absorption and
toxicity. This treatment is contraindicated in pregnancy
for the same reason. An alternative therapy involves the
topical application of a solution of TCA or BCA. These
weak destructive agents produce an initial burning in the
affected area, followed in several days by a sloughing of
the superficial tissue. Several applications at 1- to 2-week
intervals may be necessary to eradicate the lesion. Sexual
abstinence is suggested during any type of treatment to
enhance healing.
Genital warts also may be removed using cryotherapy
(i.e., freezing therapy) with liquid nitrogen or a cyro-
probe, laser vaporization, electrocautery, or surgical
excision.
4
Cryotherapy and BCA or TCA are the recom-
mended treatments for cervical HPV lesions. Laser sur-
gery can be used to remove large or widespread lesions
of the cervix, vagina, or vulva, or lesions that have failed
to respond to other first-line methods of treatment.
Electrocautery treatment has become more widespread
for these types of lesions because it does not require
suturing and is beneficial for persons who have a large
number of warts.
4
Vaccination is currently regarded as one of the most
effective strategies for controlling HPV-related diseases.
Two vaccines are available to protect females against the
type of HPV that causes cervical cancer—a quadrivalent
vaccine (Gardasil) that protects against HPV types 6, 11,
16, and 18.
8
and a bivalent vaccine (Cevarix) that pro-
tects against HPV types 16 and 18.
7
The quadrivalent
(Gardasil) vaccine can be given to males for protection
from genital warts.
8
There is no treatment, however, to
eradicate the virus once a person has become infected.
Genital Herpes
Genital herpes is a common cause of genital ulcers,
affecting more than 50 million people in the United
States.
1,2
Because herpesvirus infection is not reportable
in all states, reliable data on its true incidence and prev-
alence are lacking.
Etiology and Pathogenesis
Genital herpes is caused by the herpes simplex virus
(HSV), a large double-stranded DNA virus.
9–13
Herpes
simplex infections are highly contagious. There are eight
types of HSV; however, only two are considered sexu-
ally transmitted. These are HSV-1 (usually associated
with fever blisters and cold sores) and HSV-2 (usually
associated with genital herpes).
13
HSV-1 and HSV-2 are
genetically similar; both cause a similar set of primary
and recurrent infections; and both can cause oropharyn-
geal and genital lesions, but HSV-2 is most commonly
found only in the genitals.
12
HSV-1 and HSV-2 are
neurotropic
viruses, meaning
that they grow in neurons and share the biologic prop-
erty of latency.
9
Latency refers to the ability to maintain
disease potential in the absence of clinical signs and
symptoms. In genital herpes, the virus ascends through
the peripheral nerves to the sacral dorsal root ganglia
(Fig. 41-2). The virus can remain dormant in the dor-
sal root ganglia, or it can reactivate, in which case the
viral particles are transported back down the nerve root
to the skin, where they multiply and cause a lesion to
develop. During the dormant or latent period, the virus
replicates in a different manner so that the immune sys-
tem or available treatments have no effect on it. It is
not known what reactivates the virus. It may be that
the body’s defense mechanisms are altered. Numerous
studies have shown that host responses to infection
influence initial development of the disease, severity of
