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U N I T 1 1
Genitourinary and Reproductive Function
Infections of the External
Genitalia
Sexually transmitted infections can selectively infect the
mucocutaneous tissues of the external genitalia, rectum,
and oral pharynx, or produce both genitourinary and
systemic effects. These infections include condylomata
acuminata, genital herpes, chancroid, and lymphogran-
uloma venereum.
Human Papillomavirus Infection
and Genital Warts
Genital warts (condylomata acuminata) are caused by
the human papillomavirus (HPV) that infects epithelial
cells and can cause a number of benign and malignant
growths.
2–8
Although recognized for centuries, HPV-
induced genital warts have become one of the fastest-
growing STIs of the past decade. The Centers for Disease
Control and Prevention (CDC) estimates that 360,000
million Americans are currently infected with the HPV.
3
Etiology and Pathogenesis
Transmission of HPV is usually through skin-to-skin
contact, most often through penetration (oral–genital,
manual–genital, and genital–genital contact). HPV can
also be transmitted though nonsexual routes including
mother to newborn (vertical transmission) and fomites
(objects such as clothing, towels, or utensils that har-
bor the agent). Prevention of HPV transmission through
condom use has not been adequately demonstrated.
Most HPV infections are asymptomatic and transient,
and resolve without treatment. In some cases, how-
ever, HPV infection results in genital warts, abnormal
Papanicolaou (Pap) test abnormalities, or, rarely, cervical
cancer.
Human papillomaviruses are nonenveloped dou-
ble-stranded deoxyribonucleic acid (DNA) viruses that
cause proliferative lesions of the squamous epithelium.
1,2
Human papillomavirus is species specific, meaning it only
affects humans.
2
More than 100 distinct HPV subtypes
have been identified, over 40 of which affect the ano-
genital area.
2–6
These subtypes are routinely classified into
low-risk and high-risk categories. Low-risk types such as
HPV 6 and 11 are typically associated with genital warts.
Types 16, 18, 31, 33, and 45 are considered to be high
risk because of their association with cervical dysplasia
and cervical cancer. Of the high-risk types, HPV 16 and
18 account for approximately two thirds of cervical can-
cer.
2
Only a subset of women infected with HPV go on
to develop cervical cancer, however, suggesting that even
the most virulent HPV strains may vary in terms of their
oncogenic potential. Cofactors that may increase the risk
for cancer include smoking, immunosuppression, and
exposure to hormonal alteration (e.g., pregnancy, oral
contraceptives).
2
Human papillomavirus infection begins with viral
inoculation into squamous epithelial cells, where infec-
tion stimulates replication of the squamous epithelium,
producing the various HPV-proliferative lesions.
5
The
incubation period for HPV-induced genital warts ranges
from 6 weeks to 8 months, with a mean of 2 to 3 months.
Genital warts typically present as soft, raised, fleshy
lesions on the external genitalia, including the penis
(Fig. 41-1), vulva, scrotum, perineum, and perianal skin.
External warts may appear as small bumps, or they may
be flat, rough surfaced, or pedunculated. Less commonly,
they can appear as smooth reddish or brown raised
papules or as dome-shaped lesions on keratinized skin.
Internal warts are cauliflower-shaped lesions that affect
the mucous membranes of the vagina, urethra, anus, or
mouth. They may cause discomfort, bleeding, or painful
intercourse.
6
Although warts can be a disturbing clinical feature
of HPV infection, subclinical infection is common.
Approximately 70% of women with HPV become HPV
DNA negative within 1 year, and as many as 91% of
them become negative within 2 years.
1
Many women
with transient HPV infections develop atypical squa-
mous cells of undetermined significance (ASC-US) or
low-grade squamous intraepithelial lesions (LSILs) of the
cervix as detected on a Pap test, colposcopy, or biopsy
(see Chapter 40). In men, transient HPV infection may
be associated with intraepithelial neoplasia of the penis
and anus.
1
Although many individuals will clear the virus
and become negative within 1 to 2 years, it is unclear if
development of an effective immune response completely
clears the infection. In some individuals the virus may
remain dormant for years and reactivate at a later time.
While some of these later lesions may be reactivations,
others may be re-infections from an affected partner.
FIGURE 41-1.
Condylomata of the penis. Raised circumscribed
lesions are seen on the shaft of the penis. (From Damjanov I,
McCue PA.The lower urinary tract and male reproductive system.
In: Rubin R, Strayer DS, eds. Rubin’s Pathology: Clinicopathologic
Foundations of Medicine. 6th ed. Philadelphia, PA:Wolters
Kluwer Health | LippincottWilliams &Wilkins; 2012:825.)
