Source; Robbins Basic Pathology, 9th Edition.

1. Male Genital System and
Lower Urinary Tract
Mohammad Sadeq Disomangcop

2. PENIS

3. Malformations
• Hypospadias
– the more common of the two conditions, the
abnormal opening of the urethra is on the ventral
aspect of the penis anywhere along the shaft
• Epispadias
– the abnormal urethral orifice is on the dorsal
aspect of the penis.

4. Hypospadias.

5. Epispadias.

6. Inflammatory Lesions
• Balanitis and balanoposthitis
– refer to local inflammation of the glans penis and
of the overlying prepuce, respectively.
– Candida albicans, anaerobic bacteria, Gardnerella,
and pyogenic bacteria.
– poor local hygiene in uncircumcised males, with
accumulations of desquamated epithelial cells,
sweat, and debris, termed smegma, acting as a
local irritant.

7. • Phimosis
– condition in which the prepuce cannot be
retracted easily over the glans penis.
– most cases are acquired from scarring of the
prepuce secondary to previous episodes of
balanoposthitis.

8. Neoplasms
• Squamous cell carcinoma in situ of the penis
– Bowendisease
– older uncircumcised males
– grossly as a solitary plaque on the shaft of the
penis.
– Histologic examination reveals morphologically
malignant cells throughout the epidermis with no
invasion of the underlying stroma

9. Carcinoma in situ (Bowen disease) of the penis. The epithelium
above the intact basement membrane shows delayed
maturation and disorganization (left). Higher magnification
(right) shows several mitotic figures, some above the basal
layer, a dyskeratotic cell, and nuclear pleomorphism.

10. • Invasive squamous cell carcinoma of the
penis
– appears as a gray, crusted, papular lesion, most
commonly on the glans penis or prepuce.
– Infiltration of the underlying connective tissue
produces an indurated, ulcerated lesion with
irregular margins.
– Histologically, it is a typical keratinizing squamous
cell carcinoma.

11. Carcinoma of the penis. The glans penis is
deformed by an ulcerated, infiltrative mass

12. • Verrucous carcinoma
– variant of squamous cell carcinoma characterized
by a papillary architecture, virtually no cytologic
atypia, and rounded, pushing deep margins.
– Locally invasive but do not metastasize.

13. SCROTUM, TESTIS, AND
EPIDIDYMIS

14. Cryptorchidism
• Cryptorchidism
– represents a failure of testicular descent into the
scrotum.
– The diagnosis of cryptorchidism is only established
with certainty after the age of 1 year, particularly in
premature infants, because testicular descent into the
scrotum is not always complete at birth.
– Majority of cases, the cause of the cryptorchidism is
unknown.
– bilateral cryptorchidism causes sterility
– failure of descent is associated with a 3- to 5-fold
increased risk of testicular cancer.

15. Inflammatory Lesions
• Epididymitis and orchitis
– begin as a primary urinary tract infection that then
spreads to the testis through the vas deferens or
the lymphatics of the spermatic cord.
– The involved testis typically is swollen and tender.
– Histologic examination reveals a predominantly
neutrophilic inflammatory infiltrate.

16. Vascular Disturbances
• Torsion
– twisting of the spermatic cord,
– results in obstruction of testicular venous drainage
while leaving the thick-walled and more resilient
arteries patent, so that intense vascular
engorgement and venous infarction follow unless
the torsion is relieved.
– Neonatal torsion- in utero orshortly after birth.
– Adult torsion- in adolescence and manifests with
sudden onset of testicular pain.

17. Testicular Neoplasms
• Testicular neoplasms occur in roughly 6 per
100,000 males.
• Males In the 15- to 34-year-old age group, when
these neoplasms peak in incidence, they are the
most common tumors of men
• In postpubertal males, 95% of testicular tumors
arise from germ cells, and all are malignant.
• The cause of testicular neoplasms remains
unknown.

18. – more common in whites than in blacks
– Cryptorchidism is associated with a three- to five-fold
increase in the risk of cancer in the
undescended testis, as well as an increased risk of
cancer in the contralateral descended testis.
– Family history is important, because brothers of
males with germ cell tumors have an 8- to 10-fold
increased risk over that of the population at large,
presumably owing to inherited risk factors.
– Most testicular tumors in postpubertal males arise
from the in situ lesion intratubular germ cell
neoplasia.

20. Morphology
• Pure- composed of a single histologic type
• Mixed- seen in 40% of cases
1. Seminoma
– are soft, well-demarcated, gray-white tumors that
bulge from the cut surface of the affected testis

21. Seminoma
Appearing as a well-circumscribed, pale,
fleshy, homogeneous mass.

22. – Microscopically, seminomas are composed of
large, uniform cells with distinct cell borders,
clear, glycogen-rich cytoplasm, and round nuclei
with conspicuous nucleoli
– The cells often are arrayed in small lobules with
intervening fibrous septa. A lymphocytic infiltrate
usually is present and may, on occasion,
overshadow the neoplastic cells.

23. Seminoma of the testis.
Microscopic examination reveals large cells with distinct
cell borders, pale nuclei, prominent nucleoli, and a
sparse lymphocytic infiltrate.

24. Morphology
2. Embryonal Carcinoma
– are ill-defined, invasive masses containing foci of
hemorrhage and necrosis.
– The tumor cells are large an primitivelooking,
with basophilic cytoplasm, indistinct cell borders,
and large nuclei with prominent nucleoli.
– The neoplastic cells may be arrayed in
undifferentiated, solid sheets or may contain
primitive glandular structures and irregular
papillae

25. Embryonal carcinoma.
In contrast with the seminoma, this tumor is a
hemorrhagic mass.

26. Embryonal carcinoma.
Note the sheets of undifferentiated cells and primitive
gland-like structures. The nuclei are large and
hyperchromatic.

27. Morphology
3. Yolk sac tumors
– Are the most common primary testicular neoplasm in children
younger than 3 years of age; in this age group it has a very good
prognosis.
– In adults, yolk sac tumors most often are seen admixed with
embryonal carcinoma.
– 90% of patients have elevated AFP
– On gross inspection, these tumors often are large and may be
well demarcated.
– Histologic examination discloses low cuboidal to columnar
epithelial cells forming microcysts, lacelike (reticular) patterns,
sheets, glands, and papillae.
– Schiller-Duvall bodies- distinctive structure resembling
premitive glomeruli

28. Yolk sac tumor
Yolk sac tumor demonstrating areas of loosely textured,
microcystic tissue and papillary structures resembling a
developing glomerulus (Schiller-Duval bodies).

29. Morphology
4. Choriocarcinomas
– are tumors in which the pluripotential neoplastic germ
cells differentiate along trophoblastic lines.
– 100% of patients have elevated HCG
– Grossly, the primary tumors often are small, nonpalpable
lesions, even those with extensive systemic metastases.
– Microscopic examination reveals that choriocarcinomas
are composed of sheets of small cuboidal cells irregularly
intermingled with or capped by large, eosinophilic
syncytial cells containing multiple dark, pleomorphic
nuclei.
– cytotrophoblastic and syncytiotrophoblastic

30. Choriocarcinoma.
Both cytotrophoblastic cells with central nuclei (arrowhead,
upper right) and syncytiotrophoblastic cells with multiple
dark nuclei embedded in eosinophilic cytoplasm (arrow,
middle) are present. Hemorrhage and necrosis are
prominent.

31. Morphology
5. Teratomas
– are tumors in which the neoplastic germ cells
differentiate along somatic cell lines. These
tumors form firm masses that on cut surface often
contain cysts and recognizable areas of cartilage.
– They may occur at any age frominfancy to adult
life.
– Pure forms of teratoma are fairly common in
infants and children, being second in frequency
only to yolk sac tumors.

32. – Teratomas are composed of a heterogeneous,
helterskelter collection of differentiated cells or
organoid structures, such as neural tissue, muscle
bundles, islands of cartilage, clusters of squamous
epithelium, structures reminiscent of thyroid
gland, bronchial epithelium, and bits of intestinal
wall or brain substance, all embedded in a fibrous
or myxoid stroma.
– In prepubertal males, teratomas are typically
benign, whereas teratomas in postpubertal males
are malignant, being capable of metastasis
regardless of whether they are composed of
mature or immature elements.

33. Teratoma.
Testicular teratomas contain mature cells from endodermal, mesodermal, and
ectodermal lines. A–D, Four different fields from the same tumor specimen contain
neural (ectodermal) (A), glandular (endodermal) (B), cartilaginous (mesodermal) (C),
and squamous epithelial (D) elements.

34. PROSTATE

35. • The prostate can be divided into several
biologically distinct regions, the most important
of which are the peripheral and transition zones.
• The types of proliferative lesions are different in
each region.
• Most hyperplastic lesions arise in the inner
transition zone, while most carcinomas (70% to
80%) arise in the peripheral zones.
• The normal prostate contains glands with two cell
layers, a flat basal cell layer and an overlying
columnar secretory cell layer.

36. Prostatitis
Categories:
• acute bacterial prostatitis (2% to 5% of cases)
– caused by the same organisms associated with other acute
urinary tract infections
– is associated with fever, chills, and dysuria; it may be
complicated by sepsis. On rectal examination, the prostate
is exquisitely tender and boggy.
• chronic bacterial prostatitis (2% to 5% of cases)
– also caused by common uropathogen
– is associated with recurrent urinary tract infections
bracketed by asymptomatic periods. Presenting
manifestations may include with low back pain, dysuria, and
perineal and suprapubic discomfort.

37. • chronic nonbacterial prostatitis, or chronic pelvic
pain syndrome (90% to 95% of cases),
- in which no uropathogen is identified despite the
presence of local symptoms
• asymptomatic inflammatory prostatitis (incidence
unknown)
- associated with incidental identification of leukocytes in
prostatic secretions without uropathogens.

38. Benign Prostatic Hyperplasia
(Nodular Hyperplasia)
• BPH is characterized by proliferation of both stromal
and epithelial elements, with resultant enlargement of
the gland and in some cases, urinary obstruction.
• It is present in a significant number of men by the age
of 40, and its frequency rises progressively with age,
reaching 90% by the eighth decade of life.
• Dihydrotestosterone (DHT), the ultimate mediator of
prostatic growth, is synthesized in the prostate from
circulating testosterone by the action of the enzyme
5α-reductase, type 2.

39. Morphology
– BPH virtually always occurs in the inner, transitional zone
of the prostate.
– weighing between 60 and 100 g
– The nodules may appear solid or contain cystic spaces, the
latter corresponding to dilated glandular elements.
– The urethra is usually compressed by the hyperplastic
nodules, often to a narrow slit.
– Microscopically the hyperplastic nodules are composed of
variable proportions of proliferating glandular elements
and fibromuscular stroma. The hyperplastic glands are
lined by tall, columnar epithelial cells and a peripheral
layer of flattened basal cells

40. Nodular prostatic hyperplasia.
Well-defined nodules compress the urethra into a
slitlike lumen.

41. Nodular hyperplasia of the prostate.
Low-power photomicrograph demonstrates a well-demarcated nodule
at the right of the field with a portion of urethra seen to the left.

42. Carcinoma of the Prostate
• Adenocarcinoma of the prostate occurs mainly
in men older than 50 years of age.
• It is the most common form of cancer in men,
accounting for 25% of cancer in men in the
United States in 2009.

43. Morphology
• Carcinoma of the Prostate
– Most carcinomas detected clinically are not visible grossly. More
advanced lesions appear as firm, gray-white lesions with ill-defined
margins that infiltrate the adjacent gland.
– On histologic examination, most lesions are moderately
differentiated adenocarcinomas that produce well-defined
glands.
– The glands typically are smaller than benign glands and are lined
by a single uniform layer of cuboidal or low columnar epithelium,
lacking the basal cell layer seen in benign glands.
– In further contrast with benign glands, malignant glands are
crowded together and characteristically lack branching and
papillary infolding. The cytoplasm of the tumor cells ranges from
pale-clear (as in benign glands) to a distinctive amphophilic (dark
purple) appearance. Nuclei are enlarged and often contain one or
more prominent nucleoli

45. Adenocarcinoma of the prostate demonstrating small
glands crowded in between larger benign glands

46. Adenocarcinoma
Higher magnification shows several small malignant
glands with enlarged nuclei, prominent nucleoli, and
dark cytoplasm, as compared with the larger, benign
gland

47. Adenocarcinoma of the prostate.
Carcinomatous tissue is seen on the posterior aspect (lower left). Note the
solid whiter tissue of cancer, in contrast with the spongy appearance of the
benign peripheral zone on the contralateral side.

48. URETER, BLADDER, AND
URETHRA

49. Ureter
• Ureteropelvic junction (UPJ) obstruction
– usually manifests in infancy or childhood, much more commonly in
boys. It is the most frequent cause of hydronephrosis in infants and
children.
• Primary malignant tumors
– follow patterns similar to those arising in the renal pelvis, calyces, and
bladder, and a majority are urothelial carcinomas
• Retroperitoneal fibrosis
– is an uncommon cause of ureteral narrowing or obstruction
characterized by a fibrous proliferative inflammatory process encasing
the retroperitoneal structures and causing hydronephrosis.
– middle to old age.

50. Urinary Bladder
(Non-neoplastic Conditions)
• A bladder or vesical diverticulum
– consists of a pouchlike evagination of the bladder
wall. Diverticula may be congenital but more
commonly are acquired lesions that arise as a
consequence of persistent urethral obstruction
– lead to urinary stasis and predispose to infection.

51. Urinary Bladder
(Non-neoplastic Conditions)
Cystitis
• Interstitial cystitis
– (i.e., chronic pelvic pain syndrome) is a persistent,
painful form of chronic cystitis occurring most
frequently in women. It is characterized by
intermittent, often severe suprapubic pain, urinary
frequency, urgency, hematuria and dysuria without
evidence of bacterial infection
– cystoscopic findings of fissures and punctate
hemorrhages (glomerulations) in the bladder mucosa.

52. Urinary Bladder
(Non-neoplastic Conditions)
• Malakoplakia
– most commonly occurs in the bladder and results
from defects in phagocytic or degradative function
of macrophages, such that phagosomes become
overloaded with undigested bacterial products.
– Michaelis-Gutmann bodies
• laminated mineralized concretions resulting from
deposition of calcium in enlarged lysosomes are
present within the macrophages

53. Urinary Bladder
(Non-neoplastic Conditions)
• Polypoid cystitis
– is an inflammatory condition resulting from
irritation to the bladder mucosa in which the
urothelium is thrown into broad bulbous polypoid
projections as a result of marked submucosal
edema.

54. Urinary Bladder
(Neoplasms)
• Bladder cancer accounts for approximately 7%
of cancers. The vast majority of bladder
cancers (90%) are urothelial carcinomas.
• Carcinoma of the bladder is more common in
men than in women, in industrialized than in
developing nations, and in urban than in rural
dwellers
• About 80% of patients are between the ages
of 50 and 80 years.

55. Morphology
• Noninvasive papillary urothelial neoplasms
demonstrate a range of atypia and are graded
to reflect their biologic behavior
– (1) papilloma
– (2) papillary urothelial neoplasm of low
malignant potential (PUNLMP)
– (3) low-grade papillary urothelial carcinoma
– 4)high-grade papillary urothelial carcinoma

56. Noninvasive low-grade papillary urothelial carcinoma.
Higher magnification (right) shows slightly
irregular nuclei with scattered mitotic figures.

58. Morphology
• Carcinoma in situ
– defined by the presence of cytologically malignant
cells within a flat urothelium Like high-grade papillary
urothelial carcinoma, CIS tumor cells lack
cohesiveness. This leads to the shedding of malignant
cells into the urine, where they can be detected by
cytology.
– commonly is multifocal and sometimes involves most
of the bladder surface or extends into the ureters and
urethra.
– Without treatment, 50% to 75% of CIS cases progress
to muscle-invasive cancer.

59. Carcinoma in situ (CIS) with enlarged hyperchromatic
nuclei and a mitotic figure

60. SEXUALLY TRANSMITTED
DISEASES

62. Syphilis
– Syphilis, or lues, is a chronic venereal infection
caused by the spirochete Treponema pallidum.
– T. pallidum is a fastidious organism whose only
natural host is man. The usual source of infection
is contact with a cutaneous or mucosal lesion in a
sexual partner in the early (primary or secondary)
stages of syphilis.
– The organism is transmitted from such lesions
during sexual activity through minute breaks in
the skin or mucous membranes.

63. Primary Syphilis
• The chancre of syphilis is characteristically indurated and
has been referred to as a “hard chancre,” to distinguish it
from the “soft chancre” of chancroid caused by
Haemophilus ducreyi.
• The chancre begins as a small, firm papule, which gradually
enlarges to produce a painless ulcer with well-defined,
indurated margins and a “clean,” moist base.
• Histologic examination of the ulcer reveals the usual
lymphocytic and plasmacytic inflammatory infiltrate and
proliferative vascular changes.
• Even without therapy, the primary chancre resolves over a
period of several weeks to form a subtlescar.

64. Syphilitic chancre of the scrotum.
Such lesions typically are painless despite the
presence of ulceration, and they heal
spontaneously

65. Histologic features of the chancre include
a diffuse plasma cell infiltrate beneath
squamous epithelium of skin.

66. Secondary Syphilis
• Within approximately 2 months of resolution of
the chancre, the lesions of secondary syphilis
appear.
• The manifestations of secondary syphilis are
varied but typically include a combination of
generalized lymph node enlargement and a
variety of mucocutaneous lesions.
• Skin lesions usually are symmetrically distributed
and may be maculopapular, scaly, or pustular.
Involvement of the palms of the hands and soles
of the feet is common

67. Secondary Syphilis
• Histologic examination of mucocutaneous lesions during the
secondary phase of the disease reveals the characteristic
proliferative endarteritis, accompanied by a
lymphoplasmacytic inflammatory infiltrate.
• Spirochetes are present and often abundant within these
mucocutaneous lesions; they are therefore contagious.
• Lymph node enlargement is most common in the neck and
inguinal areas.
• The mucocutaneous lesions of secondary syphilis resolve over
several weeks, at which point the disease enters its early
latent phase, which lasts approximately 1 year.

68. Tertiary Syphilis
• Tertiary syphilis develops in approximately one third of untreated
patients, usually after a latent period of 5 years or more.
• Complications:
– Cardiovascular syphilis- syphlitic aortitis and accounts 80% of
tertiary cases.
– Neurosyphilis- accounts for 10% of cases of tertiary syphilis overall
but occurs at increased frequency in those with concomitant HIV
infection
– Benign tertiary syphilis- is an uncommon form marked by the
development of gummas in various sites. Emergence of these lesions
probably is related to the development of delayed hypersensitivity.
• Gummas occur most commonly in bone, skin, and the mucous
membranes of the upper airway and mouth, but any organ may
be affected

69. Congenital Syphilis
• T. pallidum may be transmitted across the placenta from an
infected mother to the fetus at any time during pregnancy.
• The likelihood of transmission is greatest during the early
(primary and secondary) stages of disease, when spirochetes
are most numerous.
• Routine serologic testing for syphilis is mandatory in all
pregnancies. The stigmata of congenital syphilis typically do
not develop until after the fourth month of pregnancy.
• Manifestations:
– Stillbirth syphilis
– Infantile syphilis
– Late (tardive) congenital syphilis

70. • Still birth syphilis
– Among infants who are stillborn, the most
common manifestations are hepatomegaly, bone
abnormalities, pancreatic fibrosis, and
pneumonitis.
– Spirochetes are readily demonstrable in tissue
sections. In cases of congenital syphilis, the
placenta is enlarged, pale, and edematous.

71. • Infantile syphilis
– Refers to congenital syphilis in liveborn infants
that is clinically manifest at birth or within the first
few months of life.
– Affected infants present with chronic rhinitis
(snuffles) and mucocutaneous lesions similar to
those seen in secondary syphilis in adults.

72. • Late, or tardive, congenital syphilis
– Refers to cases of untreated congenital syphilis of
more than 2 years’ duration.
– Hutchinson triad:
• notched central incisors
• interstitial keratitis with blindness,
• deafness from eighth cranial nerve injury
– Other changes include a so-called saber shin
deformity caused by chronic inflammation of the
periosteum of the tibia, deformed molar teeth
(“mulberry molars”), chronic meningitis,
chorioretinitis, and gummas of the nasal bone and
cartilage with a resultant “saddlenose” deformity.

73. Serologic Tests for Syphilis
• serology remains the mainstay of diagnosis.
• Serologic tests for syphilis include nontreponemal antibody tests
and antitreponemal antibody tests.
• Nontreponemal tests measure antibody to cardiolipin, an antigen
that is present in both host tissues and the treponemal cell wall.
These antibodies are detected by the rapid plasma reagin (RPR)
and Venereal Disease Research Laboratory (VDRL) tests.
• Nontreponemal antibody tests are usually positive by 4 to 6 weeks
of infectio and are strongly positive in the secondary phase of
infection.
– However, nontreponemal antibody test results may revert to
negative during the tertiary phase or, conversely, may on
occasion be persistently positive in some patients after
successful treatment.

74. • Nontreponemal antibody test results often are
negative during the early stages of disease, even
in the presence of a primary chancre.
– direct visualization of the spirochetes by darkfield or
immunofluorescence microscopy may be the only way
to confirm the diagnosis.
• Treponemal antibody tests also become positive
within 4 to 6 weeks after an infection, but, unlike
those for nontreponemal an
• tibody tests, they usually remain positive
indefinitely, even after successful treatment.

75. Gonorrhea
• is a sexually transmitted infection of the lower
genitourinary tract caused by Neisseria gonorrhoeae.
• Humans are the only natural reservoir for N.
gonorrhoeae.
• The organism is highly fastidious, and spread of
infection requires direct contact with the mucosa of
an infected person, usually during sexual activity.
• Pregnant women can transmit gonorrhea to
newborns during passage through the birth canal.
• Diagnosis can be made by culture of the exudates as
well as by nucleic acid amplification techniques.

76. Morphology
• N. gonorrhoeae provokes an intense,
suppurative inflammatory reaction.
• In males this manifests most often as a purulent
urethral discharge, associated with an
edematous, congested urethral meatus.
• Gram-negative diplococci, many within the
cytoplasm of neutrophils, are readily identified in
Gram stains of the purulent exudate
• Ascending infection may result in the
development of acuteprostatitis, epididymitis or
orchitis.

77. Neisseria gonorrhoeae.
Gram stain of urethral discharge demonstrates
characteristic gram-negative, intracellular
diplococci.

78. Acute epididymitis caused by gonococcal infection.
The epididymis is involved by an abscess.
Normal testis is seen on the right.

79. Nongonococcal Urethritis and
Cervicitis
• Nongonococcal urethritis (NGU) and cervicitis are the
most common forms of STD.
• C. trachomatis, Trichomonas vaginalis, U. urealyticum,
and Mycoplasma genitalium.
• Most cases are apparently caused by C. Trachomatis
– is a small gram-negative bacterium that is an
obligate intracellular pathogen. It exists in two
forms. The infectious form, the elementary body, is
capable of at least limited survival in the
extracellular environment.

80. – The elementary body is taken up by host
cells, primarily through a process of
receptor-mediated endocytosis.
– Once inside the cell, the elementary body
differentiates into a metabolically active
form, termed the reticulate body.
– Using energy sources from the host cell, the
reticulate body replicates and ultimately
forms new elementary bodies capable of
infecting additional cells.

81. Chancroid (Soft Chancre)
• Chancroid, sometimes called the “third” venereal
disease (after syphilis and gonorrhea), is an acute,
ulcerative infection caused by Haemophilus ducreyi, a
small, gram-negative coccobacillus.
• The disease is most common in tropical and subtropical
areas and is more prevalent in lower socioeconomic
groups, particularly among men who have regular
contact with prostitutes.
• A definitive diagnosis of chancroid requires the
identification of H. ducreyi on special culture media.

82. Morphology
• At 4 to 7 days after inoculation, a tender, erythematous papule
develops on the external genitalia. In male patients, the
primary lesion is usually on the penis; in female patients, most
lesions occur in the vagina or periurethral area.
• the primary lesion erodes to produce an irregular ulcer, which is
more likely to be painful in males than in females.
• The base of the ulcer is covered by shaggy, yellow-gray exudate.
The regional lymph nodes, particularly in the inguinal region,
become enlarged and tender in about 50% of cases within 1 to 2
weeks of the primary inoculation.
• On microscopic examination, the ulcer of chancroid contains a
superficial zone of neutrophilic debris and fibrin, with an
underlying zone of granulation tissue containing areas of
necrosis and thrombosed vessels.

83. Chancroid.

84. Genital Herpes Simplex
• Genital herpes infection, or herpes genitalis, is a
common STD. 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.
• Recent years have seen a rise in the number of genital
infections caused by HSV-1, in part due to the
increasing practice of oral sex.
• 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.

85. Morphology
• The initial lesions of genital HSV infection are painful,
erythematous vesicles on the mucosa or skin of the lower
genitalia and adjacent extragenital sites.
• Histologic changes include the presence of intraepithelial
vesicles accompanied by necrotic cellular debris, neutrophils,
and cells harboring characteristic intranuclear viral inclusions.
• The classic Cowdry type A inclusion appears as a light purple,
homogeneous intranuclear 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, specific diagnosis of HSV infection in histologic
sections or smears.

86. Genital herpes simplex.

87. Human Papillomavirus Infection
• HPV causes a number of squamous proliferations
in the genital tract, including precancerous
lesions that commonly undergo transformation to
carcinomas; these most commonly involve the
cervix 18), but also occur in the penis, vulva, and
oropharyngeal tonsils.
• Condylomata acuminata
– also known as venereal warts, are caused by HPV
types 6 and 11. These lesions occur on the penis as
well as on the female genitalia.

88. 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.

89. Condyloma acuminata.