Page 692 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster

678 C H A P T E R 17 Male Genital System and Lower Urinary Tract
of acid-producing Döderlein bacilli. It may be asymptom-
atic or be associated with pruritus and a profuse, frothy,
yellow vaginal discharge. Urethral colonization may cause
urinary frequency and dysuria. T. vaginalis infection typi-
cally is asymptomatic in males but in some cases may
manifest as NGU. The organism usually is demonstrable
in smears of vaginal scrapings.
Genital Herpes Simplex
Genital herpes infection, or herpes genitalis, is a common
STD that affects an estimated 50 million people in the
United States. Although both herpes simplex virus 1
(HSV-1) and HSV-2 can cause anogenital or oral infections,
most cases of anogenital herpes are caused by HSV-2.
However, recent years have seen a rise in the number of genital
infections caused by HSV-1, in part due to the increasing prac-
tice of oral sex. Genital HSV infection may occur in any sexu-
ally active population. As with other STDs, the risk of
infection is directly related to the number of sexual con-
tacts. Up to 95% of HIV-positive men who have sex with
men are seropositive for HSV-1 and/or HSV-2. HSV is
transmitted when the virus comes into contact with a
mucosal surface or broken skin of a susceptible host. Such
transmission requires direct contact with an infected
person, because the virus is readily inactivated at room
temperature, particularly if dried.
MORPHOLOGY
The initial lesions of genital HSV infection are painful, ery-
thematous vesicles on the mucosa or skin of the lower
genitalia and adjacent extragenital sites. The anorectal area is as several precancerous lesions that commonly undergo
a particularly common site of primary infection among men
who have sex with men. Histologic changes include the pres-
ence of intraepithelial vesicles accompanied by necrotic
cellular debris, neutrophils, and cells harboring characteristic also known as venereal warts, are caused by HPV types 6
intranuclear viral inclusions. The classic Cowdry type A
inclusion appears as a light purple, homogeneous intranu-
clear structure surrounded by a clear halo. Infected cells
commonly fuse to form multinucleate syncytia. The inclusions
readily stain with antibodies to HSV, permitting a rapid, spe-
cific diagnosis of HSV infection in histologic sections or
smears. Immunohistochemical tests have largely replaced
detection of HSV infection by cytologic examination, which
is less sensitive and prone to false-positive results.
Clinical Features
As mentioned earlier, both HSV-1 and HSV-2 can cause
genital or oral infection, and both can produce primary
or recurrent mucocutaneous lesions that are clinically
indistinguishable. The manifestations of HSV infection
vary considerably, depending on whether the infection is
primary or recurrent. Primary infection with HSV-2 often
is mildly symptomatic. In persons experiencing their first
episode, locally painful vesicular lesions are often accom-
panied by dysuria, urethral discharge, local lymph node
enlargement and tenderness, and systemic manifestations,
such as fever, muscle aches, and headache. HSV is actively
shed during this period and continues to be shed until the
mucosal lesions have completely healed. Signs and
symptoms may last for several weeks during the primary
phase of disease. Recurrences are much more common
with HSV-1 than with HSV-2 and typically are milder and
of shorter duration than in the primary episode. As with
primary infection, HSV is shed while active lesions are
present.
In immunocompetent adults, herpes genitalis generally
is not life-threatening. However, HSV does pose a major
threat to immunosuppressed patients, in whom fatal, dis-
seminated disease may develop. Also life-threatening is
neonatal herpes infection, which occurs in about half of
infants delivered vaginally of mothers suffering from either
primary or recurrent genital HSV infection. The viral infec-
tion is acquired during passage through the birth canal. Its
incidence has risen in parallel with the rise in genital HSV
infection. The manifestations of neonatal herpes, which typically
develop during the second week of life, include rash, encephalitis,
pneumonitis, and hepatic necrosis. Approximately 60% of
affected infants die of the disease, with significant morbid-
ity occurring in about half of the survivors. The laboratory
diagnosis of genital herpes relies on viral culture. Of note,
however, the sensitivity of culture is low, especially for
recurrent lesions, and declines rapidly as lesions begin to
heal. Molecular diagnostic tests also are available but are
used mostly in diagnosis of extragenital herpes, particu-
larly with central nervous system infections.
Human Papillomavirus Infection
HPV causes a number of squamous proliferations in the
genital tract, including condyloma acuminatum, as well
transformation to carcinomas; these most commonly
involve the cervix (Chapter 18), but also occur in the penis,
vulva, and oropharyngeal tonsils. Condylomata acuminata,
and 11. These lesions occur on the penis as well as on the
female genitalia. They should not be confused with the
condylomata lata of secondary syphilis. Genital HPV infec-
tion may be transmitted to neonates during vaginal deliv-
ery. Recurrent and potentially life-threatening papillomas
of the upper respiratory tract may develop subsequently in
affected infants.
MORPHOLOGY
In males, condylomata acuminata usually occur on the coronal
sulcus or inner surface of the prepuce, where they range in
size from small, sessile lesions to large, papillary proliferations
measuring several centimeters in diameter. In females, they
commonly occur on the vulva. Examples of the microscopic
appearance of these lesions are presented in Chapter 18.
S U M M A RY
Herpes Simplex Virus and Human Papillomavirus
Infections
• HSV-2 and, less commonly, HSV-1 can cause genital infec-
tions. Initial (primary) infection causes painful, erythema-
tous, intraepithelial vesicles on the mucosa and skin of
external genitalia, along with regional lymph node