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SEXUALLY TRANSMITTED DISEASES
1. SEXUALLY TRANSMITTED DISEASES
INTRODUCTION
Sexually transmitted diseases (STDs) have been
described as “hidden epidemics,” comprising 5
of the top 10 most frequently reported diseases
in the United States. An estimated 12 million
new cases of STDs occur each year in the U.S.,
which has the highest rate among all developed
countries. In the developing world, STDs are an
even greater public health problem as the
second leading cause of healthy life lost among
women between 15 and 44 years of age. The
STD epidemic in the developing world, where
atypical presentations, drug resistant
2. organisms, and co-infections (especially with
HIV) are common, can have a potentially larger
impact on our population due to increased
international travel and migration. The health
consequences of STDs occur primarily in
women, children and adolescents especially
among racial/ethnic minority groups. In the
U.S., more than a million women are estimated
to experience an episode of pelvic
inflammatory disease (PID) per year. The
number of ectopic pregnancies has been
estimated as 1 in 50, and approximately 15% of
infertile American women are thought to have
tubal inflammation as a result of PID. Adverse
outcomes of pregnancy due to untreated STDs
include neonatal ophthalmia, neonatal
pneumonia, physical and mental
developmental disabilities, and fetal death
from congenital syphilis. Among all age groups,
3. adolescents (10- to 19-year-olds) are at
greatest risk for STDs, because of a greater
biologic susceptibility to infection and a greater
likelihood of having multiple sexual partners
and unprotected sexual encounters. Minority
groups such as African-Americans and Hispanic
Americans have the highest rates of STDs.
STDs and human immunodeficiency virus (HIV)
infections share common risk factors for
transmission. Genital ulcer disease increases
the risk of HIV acquisition and transmission by
2- to 5-fold; urethritis and cervicitis increase
the risk by 5-fold. Treatment and control of
STDs at the population level may result in
decreases in HIV incidence among populations
with high rates of STDs. STD control should be
considered an important component of HIV
4. prevention in public health as well as clinical
practice.
Effective clinical management of STDs should
include screening of sexually active individuals
with appropriate laboratory tests, providing
definitive diagnosis and treatment, client-
centered risk reduction and education, and
evaluation and treatment of partners.
Screening of asymptomatic patients is of
utmost importance in order to prevent
sequelae. Screening for STDs among sexually
active women, especially pregnant women, is
essential since roughly 70% of chlamydial
infections and 50% of gonococcal infections are
asymptomatic in this population.
Unfortunately, the barriers to effective STD
prevention are multiple, including the biological
characteristics of STDs, lack of public awareness
5. regarding STDs, inadequate training of health
professionals, and sociocultural norms related
to sexuality that can lead to misperception of
recognized risk and consequences.
Figure 1
Reported cases of syphilis by stage of infection:
United States, 1941–2006 CDC
GENITAL ULCER DISEASES: OVERVIEW
A genital ulcer is defined as a breach in the skin
or mucosa of the genitalia. Genital ulcers may
be single or multiple and may be associated
with inguinal or femoral lymphadenopathy.
Sexually transmitted pathogens that manifest
as genital ulcers are Herpes simplex virus (HSV),
Treponema pallidum, Haemophilus ducreyi, L-
6. serovars of Chlamydia trachomatis and
Calymmatobacterium granulomatis.
Genital ulcer diseases facilitate enhanced HIV
transmission among sexual partners. In the
presence of genital ulcers, there is a 5-fold
increase in susceptibility to HIV. In addition, HIV
infected individuals with genital ulcer disease
may transmit HIV to their sexual partners more
efficiently.
HSV is the most common cause of genital ulcers
in the US among young sexually active persons.
T. pallidum is the next most common cause of
GUD, and should be considered in most
situations despite the decline in cases of
syphilis nationwide (figure 1). Chancroid,
caused by H. ducreyi has infrequently been
associated with cases of GUD in the US, but has
been isolated in up to 10% of genital ulcers
7. diagnosed from STD clinics in Memphis and
Chicago. Chancroid is the most common genital
ulcer disease in many developing countries.
Lymphogranuloma venereum or LGV caused by
L-serovars of C. trachomatis and granuloma
inguinale (donovonosis) caused by
Calymmatobacterium granulomatis are
endemic in tropical countries and should be
considered in the differential diagnosis of
genital ulcers from a native in the tropics or in
travelers.
The prevalence of pathogens that cause GUD
varies according to the geographic area and the
patient population. A single patient can have
genital ulcers caused by more than one
pathogen. Despite laboratory testing,
approximately 25% of genital ulcers will have
no identifiable cause.
8. There is considerable overlap in the clinical
presentation of herpes, primary syphilis and
chancroid, the three most common causes of
genital ulcers in the U.S. Inguinal
lymphadenopathy is present in about 50% of
the patients with genital ulcer diseases. Genital
herpes typically presents with multiple, shallow
ulcers and bilateral lymphadenopathy. Primary
syphilis can usually be differentiated from
genital herpes by the presence of a single deep,
defined ulcer with induration. A distinction may
be made between syphilis and chancroid, which
commonly presents with a painful, undermined
ulcer with a purulent base and tender
lymphadenopathy unlike syphilis.
The cause of genital ulcers cannot be based on
clinical findings alone. Diagnosis based on the
classic presentation is only 30% to 34%
9. sensitive but 94% to 98% specific. Therefore,
diagnostic testing should be performed when
possible. Serologic testing for syphilis should be
considered even when lesions appear atypical.
If available, darkfield examination or direct
immunofluorescence on the lesion material
should be performed as the definitive tests for
T. pallidum. Genital herpes can be diagnosed in
the presence of typical lesions and/or positive
serology, but herpes culture should be
performed when the diagnosis is uncertain.
Figure 2
Transmission electron micrograph of herpes
simplex virus
CDC/Dr. Erskine Palmer
11. Genital herpes simplex virus infection affects
up to 60 million people in the U.S. and can be
caused by both herpes simplex virus type 1
(HSV-1) and type 2 (HSV-2) (figure 2). The
seroprevalence of HSV-2 has increased over the
past three decades to 22% among individuals
15 to 74 years of age (figure 3). Behavioral
factors correlated with seroprevalence include
cocaine use, multiple sexual partners and early
sexual activity. Most patients (40%) infected
with genital HSV-2 and two-thirds of the
patients infected with HSV-1 are asymptomatic.
Hence genital herpes is often acquired from
individuals who have never been clinically
diagnosed with herpes. Transmission of HSV
between sexual partners has been estimated at
12% per year but can be as high as 30% among
women who are partners of infected men.
Women have a 5% to 10% higher
12. seroprevalence of HSV-2 than men, suggesting
the increased risk of acquisition.
Genital lesions acquired through sexual contact
are typically caused by HSV-2 (figure 4-6), while
oropharyngeal lesions acquired through non-
genital personal contact are most commonly
due to HSV-1. However, both viruses can cause
genital and oral infections. HSV-2 causes the
vast majority of genital herpes in the U.S., but
HSV-1 accounts for 5% to 30% of first-episode
cases.
After mucosal or cutaneous contact, HSV
replicates in the dermis and epidermis and
ascends through the sensory nerve fibers to the
dorsal root ganglia. Once established in the
sensory ganglia, the virus remains latent for life
with periodic reactivation and spreads through
13. the peripheral sensory nerves to the
mucocutaneous sites.
Most patients seropositive for HSV-2 have
subclinical, undiagnosed genital herpes. About
one fourth of the patients with first episode of
genital herpes have positive HSV-2 serology
suggesting prior asymptomatic infection. Thus,
the first clinical episode of genital herpes could
reflect either primary infection or a first
recognized episode of a past infection.
Primary infection with HSV-2 is characterized
by a prodrome of systemic symptoms including
fever, chills, headache and malaise. Pain and
paresthesias around the outbreak site precede
the appearance of lesions by 12 to 48 hours.
The hallmark of genital herpes consists of
grouped vesicles or pustules that lead to
shallow ulcers. Atypical lesions of genital
14. herpes include linear fissures of the vulva,
cervical ulcerations, vaginal discharge, papules
and crusts. Patients may have accompanying
tender inguinal lymphadenopathy. Urethritis,
rectal or perianal symptoms may be present if
there is urethral or rectal involvement.
Immunocompromised patients may present
with extensive perianal and rectal
manifestations. Extragenital manifestations of
HSV include ulcerative lesions of the buttock,
groin, thighs, pharyngitis, aseptic meningitis,
transverse myelitis and sacral radiculopathy.
Primary infection with HSV-1 is manifested by
genital ulcers in about one-third of patients.
Another one-third may present with orolabial
lesions or pharyngitis and the remaining
patients are asymptomatic. The genital lesions
15. caused by HSV-1 are indistinguishable from
those of HSV-2.
Recurrent genital herpes is usually a milder
syndrome than primary infection. The
recurrence rate of genital herpes due to HSV-2
is much more frequent than due to HSV-1.
Similarly, the recurrence rate of orolabial
infection due to HSV-1 is much more frequent
than due to HSV-2.
Figure 7 Histopathology showing
Treponema pallidum spirochetes in testis of
experimentally infected rabbit. Modified Steiner silver
stain. CDC/Dr. Edwin P. Ewing, Jr. epe1@cdc.gov
Figure 8
Clinical presentation of syphilis
18. treatment, an infected person still has syphilis
even though there are no signs or symptoms. It
remains in the body, and it may begin to damage
the internal organs, including the brain, nerves,
eyes, heart, blood vessels, liver, bones, and
joints. CDC
Figure 16
A photograph of a patient with tertiary syphilis
resulting in gummas seen here on the nose. This
patient presented with tertiary syphilitic
gummas of the nose mimicking basal cell
carcinoma. The gummatous tumors are benign
and if properly treated, will heal and the patient
will recover in most cases. CDC
Figure 17
Gummas, or soft ”gummy” tumors, are seen
here on this liver specimen due to tertiary
syphilis. In this image two gummas are seen in
this liver specimen. At the lower periphery, one
19. is seen as a firm, white, somewhat irregular
nodule. The other is hemorrhagic and largely
necrotic. CDC
SYPHILIS
Treponema pallidum (figure 7), a spirochete, is
a major public health concern because of the
complications of untreated disease. In the
United States, the rates of primary and
secondary syphilis have declined significantly in
the past thirty years (figure 20-21). Some racial
and ethnic groups such as African Americans,
Native Americans and Alaskan natives continue
to have disproportionately high rates of syphilis
(figure 22). The incidence of primary and
secondary syphilis in non-Hispanic blacks
remains high at 17 cases per 100,000 persons
which is 34 times greater than the rate for non-
20. Hispanic whites. In the U.S., the Southeast has
the highest rates of syphilis perhaps due to
poor access to health care, unemployment and
the stigma associated with discussion of STDs
(figure 21). Untreated syphilis infection in
pregnancy can lead to congenital syphilis in
70% of the cases.
The prevalence of syphilis in HIV infected
individuals ranges from 14 to 22%. Syphilis,
along with other genital ulcer diseases,
facilitates transmission of HIV. A syphilitic
chancre not only increases transmission of HIV
by causing a breakdown of the skin, but also
increases the number of inflammatory cells
receptive to HIV. The transmission rate of
syphilis from an infected sexual partner has
been estimated at 30%.
21. T. pallidum is an exclusive human pathogen
that can be visualized by dark field microscopy.
It appears as a spiral bacterium with corkscrew
motility. After inoculation through abraded skin
or mucus membranes it attaches to the host
cells and disseminates within a few hours to the
regional lymph nodes and eventually to the
internal organs and the central nervous system.
The clinical presentation of syphilis is divided
into primary, secondary, early latent, late latent
and tertiary stages based on infectiousness and
for purposes of therapeutic decisions and
disease-intervention strategies (figure 8).
Primary syphilis
After an incubation period of 2 to 6 weeks
following exposure, a papule develops at the
site of inoculation, which will then ulcerate into
the characteristic syphilitic chancre (figure 9-
22. 11). The classic chancre is a painless, indurated
ulcer with well-defined borders and a clean
base. A chancre can develop on the oral (figure
11) or anorectal mucosa as well as in the
genital mucosa (figure 9-10). Prior application
of topical antibiotics or the use of systemic
antimicrobials, may change the typical
appearance of the lesion. Non-tender
lymphadenopathy may be present.
Secondary syphilis
Approximately 60% to 90% of patients with
untreated primary syphilis will develop
manifestations of secondary syphilis. Secondary
syphilis is a systemic disease that results from
dissemination of the treponemes. Systemic
symptoms include generalized
lymphadenopathy, fever, headache, sore throat
and arthralgias. Numerous clinical
manifestations occur 4 to 10 weeks after the
23. chancre disappears (or 2 to 6 months after
sexual contact). These involve dermatologic
(figure 12-13), central nervous system (aseptic
meningitis, cranial neuropathy), ocular (iritis,
uveitis or conjunctivitis), hepatic (hepatitis) and
renal (immune complex glomerulonephritis)
systems.
The most common manifestation of secondary
syphilis is the skin rash characterized by
macules and papules distributed on the head
and neck, the trunk and extremities including
the palms and soles. The rash may be confused
with pityriasis rosea, psoriasis or drug eruption.
Condyloma lata are large, raised whitish lesions
that are seen in warm, moist areas which occur
before or soon after the rash and are highly
infectious. These need to be distinguished from
condyloma acuminata of human papillomavirus
24. infections. Mucous patches are shallow,
painless ulcerations that can be found on the
oral or anorectal mucosa.
Latent syphilis
Latent syphilis is defined by reactive serology in
the absence of clinical signs or symptoms. After
resolution of early (primary or secondary)
syphilis, mucocutaneous lesions can recur for
up to 1 to 2 years in 25% of the patients. Early
latent syphilis is defined as the first year from
the suspected exposure when the patient is still
at risk for relapse of the manifestations of
secondary syphilis. Late latent syphilis is
defined as a time period of one year or more
after the primary infection and before the
onset of tertiary syphilis.
Tertiary syphilis
Tertiary syphilis or late syphilis can occur after
25. primary, secondary or latent syphilis. In the
pre-antibiotic era, 25% to 40% of all patients
with syphilis developed tertiary syphilis. It may
present with cardiovascular manifestations,
gummatous lesions or CNS disease.
Cardiovascular manifestations include aortic
aneurysms, aortic insufficiency or coronary
stenosis. Gummatous lesions are focal
inflammatory areas that can involve any organ
(e.g. the liver, figure 17) but usually involve the
skin (figure 15-16) and bones. Neurological
disease during the tertiary stage presents as
general paresis or tabes dorsalis.
Neurosyphilis
Infection of the CNS by the treponemes can
occur at any time during the course of syphilis
infection. In 15% to 40% of patients with
untreated primary and secondary syphilis, T.
pallidum was found in the CSF by animal
26. inoculation studies. Treponemal invasion of the
CNS during untreated early syphilis may have
the following outcomes: spontaneous
resolution, asymptomatic neurosyphilis (at any
time during syphilis infection), acute syphilitic
meningitis (in the first year), meningovascular
syphilis (5 to 12 years after primary infection),
and parenchymatous neurosyphilis (18 to 25
years after primary infection).
Diagnosis of syphilis
The definitive diagnosis of primary syphilis is
made by visualization of treponemes by dark
field microscopy or by direct
immunofluorescence (figure 18-19). The yield
of these tests is high provided that (1) there is
no prior topical or systemic antibiotic
treatment and that (2) the examination is done
by an experienced person. To obtain a
specimen, the lesion can be gently abraded
27. with gauze. The serous exudate is then applied
to a glass slide. Direct or indirect
immunofluorescence is recommended for oral
lesions as non-pathogenic treponemes may be
confused with T. pallidum on darkfield
microscopy.
Serological tests are the most widely used tests
for syphilis and are categorized into treponemal
and non-treponemal tests. The non-treponemal
tests detect anti-cardiolipin antibodies and
include RPR (Rapid Plasma Reagin), Toluidine
Red Unheated Serum Test (TRUST) and Reagin
Screen test (RST), VDRL (Venereal Disease
Research Laboratory) and Unheated Serum
Reagin (USR). The sensitivity of the non-
treponemal tests varies from 70% in primary
syphilis to 100% in secondary syphilis. These
tests are advantageous because they are
28. inexpensive, applicable for screening purposes,
and their titers tend to correlate with disease
activity. However, confirmation of the non-
treponemal tests is necessary with the specific
treponemal tests. The FTA-ABS (fluorescent
treponemal antibody absorption test), the
MHA-TP (microhemagglutination assay) and the
TP-PA (particle agglutination assay) are 80% to
100% sensitive depending on the stage of
disease. However, a positive MHA-TP alone
does not establish the diagnosis of primary
syphilis in a patient with genital ulcer, since the
MHA-TP can remain positive for life. Patients
suspected of having primary syphilis with a
negative darkfield examination, negative RPR
and MHA-TP should have follow up serologies
in 2 weeks, since detection by direct
microscopy depends on specimen collection
and the expertise of the microscopist, and since
29. serologies can be negative in the first two
weeks after a chancre appears. False-positive
non-treponemal and treponemal tests can
occur in a variety of disease conditions
including acute viral infections, autoimmune
diseases, vaccination, drug addiction and
malignancy.
Latent syphilis is diagnosed when a patient has
a reactive RPR and a confirmatory test in the
absence of signs or symptoms. The duration of
disease from exposure can be estimated if the
patient can recall specific signs or symptoms
consistent with primary syphilis, has a history of
exposure or previous serology. However, the
usual scenario is that of a patient with positive
serology and no clinical history suggestive of
syphilis.
30. Figure 18 Dark field photomicrograph
of Treponema pallidum bacteria. Nichol's strain
of T. pallidum from a rabbit testicle, and stained
by fluorescent antibody technique CDC
Figure 19 Treponema pallidum, IFA
stain for Fluorescent Treponemal Antibody
(FTA) antigen. CDC
Figure 20 Primary and secondary
syphilis — Rates: Total and by sex: United
States, 1987–2006
Figure 21 Primary and secondary
syphilis — Rates by state: United States and
outlying areas, 2006
Figure 22 Primary and secondary
syphilis — Rates by race/ethnicity: United
States, 1997–2006
31. Figure 23 Primary and secondary
syphilis—Age- and sex-specific rates: United
States, 2006
Figure 24
This direct smear microscopic exam revealed
the presence of Haemophilus ducreyi indicative
of a chancroid infection. CDC
Figure 25
A chancroid ulcer on the posterior vaginal wall
in a 25 year old female due to Haemophilus
ducreyi bacteria.
The first sign of a chancroid infection is usually
the appearance of one or more sores, or raised
bumps on the genital organs, surrounded by a
narrow red border. Eventually rupturing, these
lesions reveal a painful, open, pus-filled wound.
CDC
32. Figure 26
This patient presented with a chancroid lesion of
the groin and penis affecting the ipsilateral
inguinal lymph nodes. First signs of infection
typically appear 3 to 5 days after exposure,
although symptoms can take up to 2 weeks to
appear. In men, they are most common at the
base of the glans (head) of the penis, though
they can appear on the penis shaft. CDC
CHANCROID
The incidence of chancroid has been steadily
decreasing in the US. The disease is endemic in
some areas (New York City and Texas) and
tends to occur as outbreaks in other parts of
the US. Chancroid is a major cause of genital
ulcer diseases in the tropics.
33. Haemophilus ducreyi is a gram-negative rod
(figure 24) that requires abraded skin to
penetrate the epidermis and cause infection. It
is spread by sexual contact but autoinoculation
of other sites can occur.
After an incubation period of 3 to 10 days, a
papule surrounded by erythema develops at
the site of inoculation (figure 27). The papule
evolves to a pustule over 24 to 48 hours and
then ulcerates (figure 25-26). Men tend to note
significant pain with the ulcer whereas women
may not notice the ulcer. About 50% of patients
note tender unilateral inguinal adenopathy
(buboes). Buboes (figure 29-30) can become
fluctuant, undergo spontaneous drainage
(figure 28) and result in large ulcers. Systemic
symptoms are usually not a feature of
chancroid.
34. Chancroid is a clinical diagnosis based on:
(1) a tender painful ulcer with ragged borders
(2) tender lymphadenopathy
(3) negative darkfield examination of the ulcer
for T. pallidum (or negative syphilis serology
obtained at least 7 days after onset of the
ulcer)
(4) a negative test for herpes simplex virus
The presence of a painful ulcer along with
tender lymphadenopathy with suppuration is
highly suspicious for chancroid. A definitive
diagnosis is made by culture of H. ducreyi but
appropriate culture media are not widely
available.
Figure 27 A differential diagnosis
35. revealed that this was a chancroidal lesion, and
not a suspected syphilitic lesion, or chancre.
CDC
Figure 28 This patient presented with a
chancroid showing signs of a ruptured inguinal
lymph node. The ulcers usually begin as tender,
elevated bumps, or papules, that become pus-
filled, open sores with eroded or ragged edges.
Ruptured buboes, or swollen lymph nodes, are
susceptible to secondary bacterial infections.
CDC
Figure 29 This 52yr old female patient
presented with a chancroid and spontaneous
rupture of a left inguinal bubo. Chancroid is
characterized by painful genital ulcers, which
are associated with a unilateral painful inguinal
lymphadenopathy in 50% of those infected. Left
untreated, suppurative, spontaneously rupturing
36. buboes occur in approximately 25% of cases.
CDC
Figure 30 This photograph shows that a
chancroid infection has spread to the inguinal
lymph nodes, which have enlarged forming
buboes. Caused by the sexually transmitted
bacterium, Haemophilus ducreyi, in about half
of the untreated chancroid cases, the lymph
nodes in the groin develop into buboes that can
enlarge until they burst through the overlying
skin. CDC
Figure 31
This was a case of trichomonas vaginitis
revealing a copious purulent discharge
emanating from the cervical os. Trichomonas
37. vaginalis, a flagellate, is the most common
pathogenic protozoan of humans in
industrialized countries. This protozoan resides
in the female lower genital tract and the male
urethra and prostate, where it replicates by
binary fission. CDC
VAGINAL DISCHARGE (VAGINITIS):
OVERVIEW
Vaginal discharge is a frequent gynecologic
complaint, accounting for more than 10 million
office visits annually. Physiologic vaginal
discharge is white, odorless and increases
during midcycle due to estrogen. Abnormal
vaginal discharge may result from vaginitis or
vaginosis, cervicitis and occasionally
endometritis. Vaginitis presents with an
38. increase in the amount, odor or color of
discharge and may be accompanied by itching,
dysuria, dyspareunia, edema or irritation of the
vulva. The three most common causes of
vaginal discharge are bacterial vaginosis or BV
(40% to 50% of cases; associated with
Gardnerella vaginalis and overgrowth of
various bacteria including anaerobes),
vulvovaginal candidiasis (20% to 25% of cases)
and trichomoniasis (figure 31) (15% to 20% of
cases). While trichomoniasis is a sexually
transmitted disease, bacterial vaginosis occurs
in women with high rates of STDs as well as in
women who have never been sexually active.
Vaginitis may also result from infection with
Group A streptococci, Staphylococcus aureus
toxic shock syndrome and severe herpes
simplex virus infection. Non-infectious causes
of vaginal discharge include chemical or irritant
39. vaginitis, trauma, pemphigus, and collagen
vascular diseases. Vaginal discharge may result
from cervicitis caused by N. gonorrhoeae and C.
trachomatis. Severe genital herpes infection
can cause both cervicitis and vaginitis.
Figure 32
Gonorrhea Rates 1941-2006 CDC
Figure 33
A cervical smear photomicrograph reveals
extracellular diplococci determined to be
Neisseria gonorrhoeae bacteria.
Neisseria gonorrhoeae is a major cause of pelvic
inflammatory disease, ectopic pregnancy, and
infertility. It has been shown to facilitate the
transmission of the Human Immunodeficiency
Virus (HIV).
CDC/Joe Miller
40. Figure 34
Gonococcal arthritic patient who presented with
an inflammation of the skin of her right arm due
to a disseminated Neisseria gonorrhoeae
bacterial infection.
Although N. gonorrhoeae can infect the genital
tract, the mouth, and the rectum, they can
become disseminated throughout a person’s
bloodstream causing a widespread reaction.
CDC/Emory
Figure 35
Gonococcal urethritis can become systemically
disseminated leading to gonococcal
conjunctivitis of the right eye CDC
GONORRHEA
In the United States 355,642 cases of
gonorrhea were diagnosed in 1998, the first
increase since 1985 (figure 32). This increase is
41. thought to be from expansion of screening
programs and improved surveillance, increased
sensitivity of new diagnostic tests, and an
increase in morbidity. The risk factors for
gonorrhea include young age (15- to 19-year-
old age group in women and 20- to 24-year old
age group in men), low socioeconomic status,
early onset of sexual activity, unmarried marital
status, past history of gonorrhea and men who
have sex with men. Recently, there have been
reports of increased incidence of rectal
gonorrhea among men who have sex with men.
The rates of gonorrhea are highest among
minority races such as African-Americans,
Hispanics, Asians and Pacific Islanders. The
Southeastern region of the U.S. has the highest
rates of gonorrhea in the nation.
42. Transmission efficiency of N. gonorrhoeae
(figure 33) depends on the anatomic site of
infection and the number of sexual exposures.
Transmission by penile-vaginal intercourse has
been reported to be 50% to 90% among
women who are sexual contacts of infected
men compared to 20% among men who are
sexual contacts of infected women. The latter
can increase to 60% to 80% following 4
exposures. Transmission of rectal and
pharyngeal gonococcal infection is less well
defined, but appears to be relatively efficient.
Neisseria gonorrhoeae is almost always sexually
transmitted except in cases of neonatal
transmission. It causes a spectrum of mucosal
diseases including pharyngitis (figure 40),
conjunctivitis (figure 35), urethritis, cervicitis
and proctitis. It also causes disseminated
43. gonococcal infection (DGI), septic arthritis
(figure 34), endocarditis, meningitis and pelvic
inflammatory disease. Up to 30% people
infected with gonorrhea have concomitant
infection with Chlamydia trachomatis.
After an incubation period of 1 to 14 days, the
classic presentation of gonorrhea in men is the
presence of pus at the urethral meatus
accompanied by symptoms of dysuria, edema
or erythema of the urethral meatus. However,
a fourth of the patients may only develop scant,
mucoid exudate or no exudate at all.
Complications of gonococcal urethritis in men
include epididymitis, acute or chronic
prostatitis. Men who have sex with men may
also have rectal gonorrhea, which is usually
asymptomatic but may be associated with
tenesmus, discharge and rectal bleeding.
44. Oropharyngeal gonorrhea may manifest as
acute pharyngitis or tonsillitis, the large
majority of which are asymptomatic.
In women, the primary site of infection is the
endocervical canal, which may present with
purulent or mucopurulent discharge, erythema,
edema and friability of the cervix (figure 38).
Concurrent urethritis, infection of the
periurethral gland (Skene’s gland) or Bartholin’s
gland may also be present. Symptoms of
gonococcal infection in women may include
vaginal discharge, dysuria, menorrhagia or
intermenstrual bleeding. However, the majority
of women with gonorrhea have few symptoms.
Approximately one-third of women with
gonococcal cervicitis may also have positive
rectal cultures usually due to perineal
contamination with gonococci or due to rectal
45. intercourse. About 10% to 20% of women with
acute gonorrhea develop acute salpingitis or
pelvic inflammatory disease (see section on
pelvic inflammatory disease, below).
Systemic complications of gonorrhea include
perihepatitis (Fitz-Hugh-Curtis syndrome),
disseminated gonococcal infection (DGI),
endocarditis and rarely meningitis. The
incidence of DGI is 0.5% to 3% among patients
with untreated gonorrhea. Bacteremia begins 7
to 30 days after infection. In the majority of
patients mucosal infection is often
asymptomatic which may lead to
underdiagnosis of DGI. The most common
involvement is the skin and joints (figure 36-
37), which leads to arthralgias or arthritis,
tenosynovitis, and tender necrotic nodules with
an erythematous base in the distal extremities
46. (gonococcal arthritis-dermatitis syndrome).
Patients with DGI should also be examined for
endocarditis or meningitis.
Gonorrhea can also be maternally transmitted
(figure 41).
Figure 36 This patient presented with a
cutaneous gonococcal lesion due to a
disseminated Neisseria gonorrhea bacterial
infection. CDC
Figure 37 This cutaneous ecthyma
was caused by a systemically disseminated
Neisseria gonorrhea infection. When N.
gonorrhea bacteria become disseminated
throughout the body, they then can cause centers
of infection in all bodily regions. In this
47. patient’s case, the bacteria caused the formation
of a skin infection known as a pyoderma, or
ecthyma. CDC
Figure 38 This colposcopic view of
this patient’s cervix reveled an eroded ostium
due to Neisseria gonorrhea infection. A chronic
Neisseria gonorrhea infection can lead to
complications, which can be apparent such as
this cervical inflammation, and some can be
quite insipid, giving the impression that the
infection has subsided, while treatment is still
needed. CDC
Figure 39 This patient presented with
urogenital complications from a case of
gonorrhea including penile paraphimosis. Due
to the accompanying inflammation brought on
by the Neisseria gonorrhoeae infection, the
48. foreskin becomes adherent to the glans penis
resulting in a condition known as phimosis, and
cannot be retracted in order to expose the entire
glans. CDC
Figure 40 This patient presented with
symptoms later diagnosed as due to Gonococcal
pharyngitis.
Gonococcal pharyngitis is a sexually-
transmitted disease acquired through oral sex
with an infected partner. The majority of throat
infections caused by gonococci have no
symptoms, but some can suffer from mild to
severe sore throat. CDC
Figure 41 This was a newborn with
gonococcal ophthalmia neonatorum caused by a
maternally transmitted gonococcal infection.
Unless preventative measures are taken, it is
estimated that gonococcal ophthalmia
neonatorum will develop in 28% of infants born
to women with gonorrhea. It affects the corneal
49. epithelium causing microbial keratitis,
ulceration and perforation. CDC
Figure 42
Chlamydia trachomatis taken from a urethral
scrape. Untreated, chlamydia can cause severe,
costly reproductive and other health problems
including both short- and long-term
consequences, i.e. pelvic inflammatory disease
(PID), infertility, and potentially fatal tubal
pregnancy.
CDC/ Dr. Wiesner, Dr. Kaufman
Figure 43
This woman’s cervix has manifested signs of a
erosion and erythema due to chlamydial
infection.
An untreated chlamydia infection can cause
50. severe, costly reproductive and other health
problems including both short- and long-term
consequences, i.e. pelvic inflammatory disease
(PID), infertility, and potentially fatal tubal
pregnancy.
CDC/ Dr. Lourdes Fraw, Jim Pledger
CHLAMYDIA TRACHOMATIS INFECTION
Infections due to C. trachomatis (figure 42) are
one of the most prevalent STDs. The rates of
chlamydia infection among males and females
are highest in the age groups between 15 to 24
years (figure 44). The majority of chlamydia
urethritis in men and cervicitis in women are
asymptomatic. Women endure the most
morbidity and the most costly outcomes of
51. chlamydia infection due to pelvic inflammatory
disease (PID), ectopic pregnancy, tubal
infertility and chronic pelvic pain. In men,
chlamydia was formerly considered to be the
cause of most cases of non-gonococcal
urethritis (NGU) but recent data suggest that
only 10% to 20% of cases of NGU are caused by
Chlamydia (see section on urethritis in men).
Transmissibility of C. trachomatis has not been
well studied. However, a recent study has
shown that 68% of male partners of infected
women and 70% of female partners of infected
men are positive by PCR for C. trachomatis
suggesting that transmission from men or
women is equally efficient.
C. trachomatis infects the columnar or
squamocolumnar epithelium of the urethra,
cervix, rectum, conjunctiva and the respiratory
52. tract (in the neonate). All chlamydiae contain
DNA, RNA and cell walls that resemble those of
gram-negative bacteria and require
multiplication in eukaryotic cells. C. trachomatis
causes a spectrum of lower and upper genital
tract diseases in women: urethritis,
Bartholinitis, cervicitis (figure 43), endometritis,
salpingitis, tubo-ovarian abscess, ectopic
pregnancy, pelvic peritonitis and perihepatitis
(Fitz-Hugh-Curtis syndrome). About 75% to 90%
of cases of chlamydial cervicitis are
asymptomatic and may persist for years.
Among women with gonorrhea, 30% to 50%
have concomitant Chlamydia infection.
Approximately 40% to 50% of men with
chlamydial urethritis may be symptomatic with
dysuria or minimal urethral discharge. In 1% of
men, urethritis may lead to epididymitis.
53. C. trachomatis serovars L1-3 cause
Lymphogranuloma venereum (LGV), which is
characterized by a genital papule followed by
unilateral tender inguinal lymphadenopathy.
Other genital ulcer diseases such as syphilis,
chancroid or herpes should be considered in
the differential diagnosis of LGV. While LGV is
common in the tropical countries it is
uncommon in the United States.
Figure 44 Chlamydia — Age- and sex-
specific rates: United States, 2006
Figure 45 Chlamydia — Rates: Total
and by sex: United States, 1987–2006 CDC
54. Figure 46
Generalized peritonitis due to what was
diagnosed as a pelvic abscess.
A differential diagnosis included pelvic
inflammatory disease (PID), which if it had been
the root cause, could begin with a pelvic origin,
and become disseminated throughout the
abdominopelvic cavity, thereby, causing a
generalized peritonitis.
CDC/ Dr. James Curran
PELVIC INFLAMMATORY DISEASE
Pelvic inflammatory disease (PID) signifies
inflammation of the upper female genital tract
and its related structures. PID can manifest as
endometritis, salpingitis, adnexitis, tubo-
ovarian abscess, pelvic peritonitis (figure 46) or
55. perihepatitis. The most common manifestation
of PID is salpingitis, and these terms are used
synonymously in the literature. PID is one of
the most common causes of hospitalization
among women of reproductive age. Risk factors
for PID include young age, multiple sexual
partners, use of intrauterine devices, vaginal
douching, tobacco smoking, bacterial vaginosis,
HIV infection and STDs with gonorrhea or
chlamydia. Use of oral contraceptives has been
associated with a decreased rate of PID,
especially from infection with C. trachomatis.
Most cases of PID are secondary to C.
trachomatis or N. gonorrhoeae. C. trachomatis
is the most common cause of PID in the United
States. C. trachomatis is implicated with the
entity of “silent salpingitis” or subclinical PID.
Approximately 10% of women with chlamydial
56. cervicitis, and between 10% and 19% of women
with gonococcal cervicitis, can develop acute
PID. The pathogenesis of PID is not well
understood. In advanced cases, numerous
bacterial species are typically present as
“secondary invaders,” including anaerobes and
aerobic “bowel flora” bacteria. The chronic
sequelae of chlamydia-induced PID, such as
ectopic pregnancy and tubal infertility, are
thought to be due to an inflammatory reaction
to the chlamydial heat shock protein (HSP-60).
Certain characteristics of gonococcal strains
such as the serovar, the formation of
transparent colonies on agar, and penicillin
resistance have been correlated with a
propensity for causing tubal infection. Women
with PID and gonococcal infection tend to
present with pain during the first part of the
menstrual cycle suggesting the ascent of
57. gonococci into the upper genital tract through a
cervix with scant mucus during the menstrual
cycle.
Figure 47
This patient presented with a case of non-
specific urethritis with accompanying meatitis,
and a mucopurulent urethral discharge.
Non-specific urethritis merely means that upon
presentation, the cause of this given case of
urethral inflammation is unknown. A
differential diagnostic process will help to
narrow the possible causes by ruling out those
possibilities that do not provide respective
positive test results. CDC
URETHRITIS IN MALES
58. Urethritis (inflammation of the urethra) is
characterized by a burning sensation during
urination or itching or discharge at the urethral
meatus. The exudate (figure 47) may be
mucoid, mucopurulent or purulent.
Traditionally, urethritis has been differentiated
into gonococcal or nongonococcal urethritis.
When N. gonorrhoeae cannot be detected, the
syndrome is called non-gonococcal urethritis
(NGU). In the United States, the rates of NGU
have surpassed that of gonococcal urethritis in
the past 20 to 30 years. The 20- to 24-year-old
age group has the highest incidence of
gonococcal and non-gonococcal urethritis.
Up to 25% to 30% of men with gonococcal
urethritis also have concurrent Chlamydia
infection. In the past, the prevalence of C.
trachomatis as the cause of NGU has ranged
59. form 23% to 55%. Recent studies showed that
up to two-thirds of cases of NGU remain
undiagnosed. Ureaplasma urealyticum,
Mycoplasma genitalium and occasionally
Trichomonas vaginalis and Herpes simplex virus
have also been shown to cause NGU.
Gonococcal urethritis usually presents with a
purulent discharge and dysuria whereas NGU
usually presents with a scant, mucoid
discharge. However, in some patients the
inflammatory exudate may not be apparent on
examination. Patients with NGU may have a
discharge that is noted only in the morning or
as crusting at the meatus or as a stain on the
underwear. It is difficult to distinguish
gonococcal and non-gonococcal urethritis
based on physical examination alone. Patients
with gonococcal urethritis present with acute
60. urethritis and usually present within 4 days of
onset of symptoms. Patients with non-
gonococcal urethritis may present after 1 to 5
weeks after infection. Both groups may have
asymptomatic infection. Some patients present
with recurrent urethritis characterized by
persistent symptoms or frequent recurrences.
The symptoms of classic urinary tract infection
such as fever, chills, frequency, urgency,
hematuria is not a feature of urethritis.
Differential diagnosis of cystitis, prostatitis,
epididymitis, Reiter’s syndrome and bacterial
cystitis should be considered when evaluating a
patient with urethritis.
Figure 48
This patient presented with chemical dermatitis
61. of the perineum due to her extensive
treatment for labial venereal warts.
Condylomata acuminata, or genital warts, is a
sexually transmitted disease caused by the
Human Papilloma Virus, (HPV), which manifests
as bumps or warts on the genitalia, or within
the perineal region. CDC/JoeMillar
Figure 49
This patient presented with a penile tumor
differentially diagnosed as giant condyloma of
Buschke and Löwenstein (GCBL). Though
cancerous, giant condyloma of Buschke and
Löwenstein (GCBL) is seldom metastatic. It is
most commonly found originating on the glans
penis, but may be found on other perineal
surfaces including the anorectal, and
vulvovaginal mucosae. Though the etiology is
unknown, a viral cause is highly suspect, and
62. may include human papilloma virus, the cause
of condylomata. CDC
Figure 50
This HIV-positive patient was exhibiting signs
of a secondary condyloma acuminata infection,
i.e., venereal warts.
This intraoral eruption of condyloma acuminata,
or venereal warts was caused by the human
papilloma virus. Though oral HPV is a rare
occurrence, HIV reduces the body’s immune
response, and therefore, such secondary
infections can manifest themselves. CDC/ Sol
Silverman, Jr., DDS
HUMAN PAPILLOMAVIRUS INFECTION
Human papillomavirus (HPV) is the most
common viral sexually transmitted disease
63. worldwide. The prevalence ranges from 20% to
46% in young women worldwide. In the U.S.,
1% of sexually active persons between the ages
of 15 to 49 years are estimated to have genital
warts from HPV. The incidence of HPV infection
is high among college students (35% to 43%)
especially among minority races, individuals
with multiple sexual partners and alcohol
consumption. Immunocompromised persons
including those with HIV infection have
increased prevalence of HPV infection.
Most genital HPV infections are subclinical and
are transmitted primarily through sexual
contact. Several transmission studies noted
that 75% to 95% of male partners of women
with HPV-genital lesions also had genital HPV
infection. Vertical transmission can cause
laryngeal papillomatosis in infants and children.
64. Digital transmission of genital warts can also
occur.
Human papillomavirus is a double-stranded
DNA virus that infects the squamous
epithelium. It causes a spectrum of clinical
disease ranging from asymptomatic infection,
benign plantar and genital warts (figure 48),
squamous intra-epithelial neoplasia (bowenoid
papulosis, erythroplasia of Queyart, or Bowen’s
disease of the genitalia) and frank malignancy
(Buschke-Lowenstein tumor (figure 49), a form
of verrucous squamous cell carcinoma) in the
anogenital region. External genital warts have
various morphological manifestations such as
condyloma acuminata (cauliflower-like),
smooth dome-shaped papular warts, keratotic
warts and flat warts (squamous intra-epithelial
neoplasia). Condyloma acuminata tend to occur
65. on moist surfaces while the keratotic and
smooth warts occur on fully keratinized skin.
Flat warts can occur on either surface.
Approximately one hundred types of HPV have
been identified. The thirty types that infect the
anogenital area can be divided into low-risk
(e.g., 6, 11, 42, 43, 44) and high-risk types (e.g.,
16, 18, 31, 33, 35, 39, 45, 52, 55, 56, 58) based
on their association with anogenital cancer.
Types 6 and 11 are commonly associated with
external genital, cervical, vaginal, urethral and
anal warts as well as conjunctival, nasal, oral
and laryngeal warts. While HPV types 6 and 11
are found in 90% of condyloma acuminata, they
are rarely associated with squamous cell
carcinoma of the external genitalia. On the
other hand, HPV types 16, 18, 31, 33, 35 have
been associated with malignant
66. transformation, squamous intraepithelial
neoplasia and squamous cell carcinoma of the
vulva, vagina, cervix, penis and anus. About
95% of squamous cell carcinomas of the cervix
contain HPV-DNA. Most HPV infections do not
cause any clinical manifestations and mixed
types can be found in each lesion.
Most genital warts are asymptomatic but they
may cause itching, burning, pain and bleeding.
Condyloma acuminata (figure 50) can present
as multiple nodules or large, exophytic,
pedunculated, cauliflower like lesions in the
anogenital area. They are usually noted on the
penis, vulva, vagina, cervix, perineum and the
anal region. Flat condylomas are usually
subclinical and not visible to the naked eye.
They are most commonly noted on the cervix,
but may also be present on the vulva and the
67. penis. They may also present as white plaque
like lesions in the anogenital region.
