METHODS OF ACQUIRING KNOWLEDGE IN NURSING.pptx by navdeep kaur
Sexually Transmitted Diseases Introduction
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
2. 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 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
3. 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
4. death from congenital
syphilis. Among all age
groups, 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
5. 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
prevention in public
health as well as clinical
practice.
Effective clinical
management of STDs
6. 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
7. 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
regarding STDs,
inadequate training of
health professionals, and
sociocultural norms
related to sexuality that
can lead to
misperception of
recognized risk and
consequences.
GENITAL ULCER
Figure 1
8. DISEASES:
Reported cases of
OVERVIEW
syphilis by stage
of infection:
A genital ulcer is defined
United States,
as a breach in the skin or
1941–2006 CDC
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-serovars of
Chlamydia trachomatis
and
Calymmatobacterium
9. 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
10. 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
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
11. 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
12. testing, approximately
25% of genital ulcers
will have no identifiable
cause.
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
13. 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% sensitive but
94% to 98% specific.
14. 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
15. diagnosis is uncertain.
GENITAL HERPES
SIMPLEX
Figure 2
Transmission Genital herpes simplex
electron virus infection affects up
micrograph of to 60 million people in
herpes simplex the U.S. and can be
virus caused by both herpes
CDC/Dr. Erskine simplex virus type 1
Palmer (HSV-1) and type 2
(HSV-2) (figure 2). The
Figure 3 seroprevalence of HSV-2
Genital herpes — has increased over the
Initial visits to past three decades to
physicians’ 22% among individuals
offices: United 15 to 74 years of age
States, 1966–2006 (figure 3). Behavioral
factors correlated with
Figure 4 seroprevalence include
17. Management Forum 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%
18. 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 the peripheral
sensory nerves to the
mucocutaneous sites.
Most patients
seropositive for HSV-2
have subclinical,
undiagnosed genital
19. 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
20. 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 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
21. 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
22. asymptomatic. The
genital lesions 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.
23. SYPHILIS
Figure 7
Treponema pallidum
Histopathology
(figure 7), a spirochete,
showing Treponema
is a major public health
pallidum spirochetes
concern because of the
in testis of
complications of
experimentally
untreated disease. In the
infected rabbit.
United States, the rates
Modified Steiner
of primary and
silver stain. CDC/Dr.
secondary syphilis have
Edwin P. Ewing, Jr.
declined significantly in
epe1@cdc.gov
the past thirty years
(figure 20-21). Some
Figure 8 racial and ethnic groups
Clinical such as African
presentation of Americans, Native
syphilis Americans and Alaskan
natives continue to have
disproportionately high
Figure 9
rates of syphilis (figure
Primary syphilis.
22). The incidence of
25. syphilis in HIV infected
Figure12 individuals ranges from
This photograph 14 to 22%. Syphilis,
shows a close-up along with other genital
view of keratotic ulcer diseases, facilitates
lesions on the transmission of HIV. A
palms of this syphilitic chancre not
patient’s hands only increases
due to a secondary transmission of HIV by
syphilitic infection causing a breakdown of
CDC the skin, but also
increases the number of
inflammatory cells
receptive to HIV. The
Figure 13
transmission rate of
This patient
presented with a syphilis from an infected
sexual partner has been
secondary
estimated at 30%.
syphilitic rash
covering his back T. pallidum is an
representing the exclusive human
systemic spread of pathogen that can be
26. the Treponema visualized by dark field
pallidum bacteria. microscopy. It appears as
These a spiral bacterium with
papulosquamous corkscrew motility. After
lesions often inoculation through
appear as rough, abraded skin or mucus
red, or reddish membranes it attaches to
brown spots that the host cells and
usually form on disseminates within a
the palms of the few hours to the regional
hands, soles of the lymph nodes and
feet, the chest and eventually to the internal
back, but can organs and the central
nervous system.
manifest upon
other regions of
The clinical presentation
the body. CDC
of syphilis is divided into
primary, secondary,
early latent, late latent
Figure 14
and tertiary stages based
Secondary syphilis -
on infectiousness and for
mouth mucosa
purposes of therapeutic
28. remains in the 10). Prior application of
body, and it may topical antibiotics or the
begin to damage use of systemic
the internal antimicrobials, may
organs, including change the typical
the brain, nerves, appearance of the lesion.
eyes, heart, blood Non-tender
vessels, liver, lymphadenopathy may
be present.
bones, and joints.
CDC
Secondary syphilis
Approximately 60% to
90% of patients with
Figure 16
untreated primary
A photograph of a
syphilis will develop
patient with
manifestations of
tertiary syphilis
secondary syphilis.
resulting in
Secondary syphilis is a
gummas seen here
systemic disease that
on the nose. This
results from
patient presented
dissemination of the
with tertiary
treponemes. Systemic
29. syphilitic gummas symptoms include
of the nose generalized
mimicking basal lymphadenopathy, fever,
cell carcinoma. headache, sore throat and
The gummatous arthralgias. Numerous
tumors are benign clinical manifestations
and if properly occur 4 to 10 weeks after
treated, will heal the chancre disappears
and the patient (or 2 to 6 months after
will recover in sexual contact). These
most cases. CDC involve dermatologic
(figure 12-13), central
nervous system (aseptic
Figure 17 meningitis, cranial
Gummas, or soft neuropathy), ocular
‖gummy‖ tumors, (iritis, uveitis or
are seen here on conjunctivitis), hepatic
this liver specimen (hepatitis) and renal
due to tertiary (immune complex
syphilis. In this glomerulonephritis)
image two systems.
30. gummas are seen The most common
in this liver manifestation of
specimen. At the secondary syphilis is the
lower periphery, skin rash characterized
one is seen as a by macules and papules
firm, white, distributed on the head
somewhat and neck, the trunk and
irregular nodule. extremities including the
The other is palms and soles. The
hemorrhagic and rash may be confused
largely necrotic. with pityriasis rosea,
CDC 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
31. acuminata of human
papillomavirus
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
32. 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
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
33. 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
34. 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 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),
35. 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
36. an experienced person.
To obtain a specimen,
the lesion can be gently
abraded 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
37. 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 inexpensive,
applicable for screening
purposes, and their titers
38. 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
39. 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
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
40. 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
41. patient with positive
serology and no clinical
history suggestive of
syphilis.
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
42. (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
Figure 23
43. Primary and secondary
syphilis—Age- and sex-
specific rates: United
States, 2006
Figure 24 CHANCROID
This direct smear
The incidence of
microscopic exam
chancroid has been
revealed the
steadily decreasing in the
presence of
US. The disease is
Haemophilus
endemic in some areas
ducreyi indicative
(New York City and
of a chancroid
Texas) and tends to
infection. CDC
occur as outbreaks in
other parts of the US.
Figure 25
Chancroid is a major
A chancroid ulcer cause of genital ulcer
on the posterior diseases in the tropics.
vaginal wall in a
44. 25 year old female Haemophilus ducreyi is a
due to gram-negative rod
(figure 24) that requires
Haemophilus
ducreyi bacteria. abraded skin to penetrate
The first sign of a the epidermis and cause
chancroid infection. It is spread by
infection is sexual contact but
usually the autoinoculation of other
appearance of one sites can occur.
or more sores, or
After an incubation
raised bumps on
period of 3 to 10 days, a
the genital organs,
papule surrounded by
surrounded by a
erythema develops at the
narrow red border.
site of inoculation (figure
Eventually
27). The papule evolves
rupturing, these
to a pustule over 24 to 48
lesions reveal a
hours and then ulcerates
painful, open, pus-
(figure 25-26). Men tend
filled wound.
to note significant pain
CDC
with the ulcer whereas
women may not notice
45. the ulcer. About 50% of
Figure 26 patients note tender
This patient unilateral inguinal
presented with a adenopathy (buboes).
chancroid lesion Buboes (figure 29-30)
of the groin and can become fluctuant,
penis affecting the undergo spontaneous
ipsilateral inguinal drainage (figure 28) and
lymph nodes. First result in large ulcers.
signs of infection Systemic symptoms are
typically appear 3 usually not a feature of
to 5 days after chancroid.
exposure,
Chancroid is a clinical
although
diagnosis based on:
symptoms can
take up to 2 weeks (1) a tender painful ulcer
to appear. In men, with ragged borders
they are most (2) tender
common at the lymphadenopathy
base of the glans (3) negative darkfield
(head) of the examination of the ulcer
46. penis, though they for T. pallidum (or
can appear on the negative syphilis
penis shaft. CDC 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.
47. Figure 27 A
differential diagnosis
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
48. 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
49. 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
50. VAGINAL
Figure 31 DISCHARGE
This was a case of (VAGINITIS):
trichomonas OVERVIEW
vaginitis revealing
a copious purulent Vaginal discharge is a
frequent gynecologic
discharge
emanating from complaint, accounting
for more than 10 million
the cervical os.
office visits annually.
Trichomonas
Physiologic vaginal
vaginalis, a
flagellate, is the discharge is white,
odorless and increases
most common
during midcycle due to
pathogenic
estrogen. Abnormal
protozoan of
vaginal discharge may
humans in
result from vaginitis or
industrialized
vaginosis, cervicitis and
countries. This
51. protozoan resides occasionally
in the female endometritis. Vaginitis
lower genital tract presents with an increase
and the male in the amount, odor or
urethra and color of discharge and
prostate, where it may be accompanied by
replicates by itching, dysuria,
binary fission. dyspareunia, edema or
CDC 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
52. 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
53. irritant 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
Gonorrhea Rates In the United States
1941-2006 CDC 355,642 cases of
gonorrhea were
Figure 33 diagnosed in 1998, the
A cervical smear first increase since 1985
photomicrograph (figure 32). This increase
is thought to be from
reveals
54. extracellular expansion of screening
diplococci programs and improved
determined to be surveillance, increased
Neisseria sensitivity of new
gonorrhoeae diagnostic tests, and an
bacteria. increase in morbidity.
Neisseria The risk factors for
gonorrhoeae is a gonorrhea include young
major cause of age (15- to 19-year- old
pelvic age group in women and
inflammatory 20- to 24-year old age
disease, ectopic group in men), low
pregnancy, and socioeconomic status,
infertility. It has early onset of sexual
been shown to activity, unmarried
facilitate the marital status, past
transmission of history of gonorrhea and
the Human men who have sex with
Immunodeficiency men. Recently, there
Virus (HIV). have been reports of
CDC/Joe Miller increased incidence of
55. rectal gonorrhea among
men who have sex with
Figure 34
men. The rates of
Gonococcal
gonorrhea are highest
arthritic patient
among minority races
who presented
such as African-
with an
inflammation of Americans, Hispanics,
Asians and Pacific
the skin of her
right arm due to a Islanders. The
Southeastern region of
disseminated
the U.S. has the highest
Neisseria
rates of gonorrhea in the
gonorrhoeae
bacterial infection. nation.
Although N. Transmission efficiency
gonorrhoeae can of N. gonorrhoeae
infect the genital (figure 33) depends on
tract, the mouth, the anatomic site of
and the rectum, infection and the number
they can become of sexual exposures.
disseminated Transmission by penile-
throughout a vaginal intercourse has
56. person’s been reported to be 50%
bloodstream to 90% among women
causing a who are sexual contacts
widespread of infected men
reaction. compared to 20% among
CDC/Emory men who are sexual
contacts of infected
women. The latter can
Figure 35 increase to 60% to 80%
Gonococcal following 4 exposures.
urethritis can Transmission of rectal
become and pharyngeal
systemically gonococcal infection is
disseminated less well defined, but
leading to appears to be relatively
gonococcal efficient.
conjunctivitis of
Neisseria gonorrhoeae is
the right eye
almost always sexually
CDC
transmitted except in
cases of neonatal
transmission. It causes a
57. spectrum of mucosal
diseases including
pharyngitis (figure 40),
conjunctivitis (figure
35), urethritis, cervicitis
and proctitis. It also
causes disseminated
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
58. 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
59. and rectal bleeding.
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.
60. 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 intercourse. About
10% to 20% of women
with acute gonorrhea
develop acute salpingitis
61. 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
62. 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
(gonococcal arthritis-
dermatitis syndrome).
Patients with DGI should
also be examined for
endocarditis or
meningitis.
Gonorrhea can also be
maternally transmitted
(figure 41).
63. 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
64. in all bodily regions. In
this 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
65. 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 foreskin becomes
adherent to the glans
penis resulting in a
66. 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
67. 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
epithelium causing
microbial keratitis,
ulceration and
perforation. CDC
68. Figure 42
CHLAMYDIA
Chlamydia
TRACHOMATIS
trachomatis taken
INFECTION
from a urethral
scrape. Untreated, Infections due to C.
chlamydia can trachomatis (figure 42)
cause severe, are one of the most
costly prevalent STDs. The
reproductive and rates of chlamydia
other health infection among males
problems and females are highest
including both in the age groups
short- and long- between 15 to 24 years
term (figure 44). The majority
consequences, i.e. of chlamydia urethritis in
pelvic men and cervicitis in
inflammatory women are
disease (PID), asymptomatic. Women
infertility, and endure the most
69. potentially fatal morbidity and the most
tubal pregnancy. costly outcomes of
CDC/ Dr. chlamydia infection due
Wiesner, Dr. to pelvic inflammatory
Kaufman disease (PID), ectopic
pregnancy, tubal
Figure 43 infertility and chronic
pelvic pain. In men,
This woman’s
chlamydia was formerly
cervix has
manifested signs considered to be the
of a erosion and cause of most cases of
erythema due to non-gonococcal
urethritis (NGU) but
chlamydial
recent data suggest that
infection.
only 10% to 20% of
An untreated
cases of NGU are caused
chlamydia
by Chlamydia (see
infection can
section on urethritis in
cause severe,
men).
costly
reproductive and Transmissibility of C.
other health trachomatis has not been
70. problems well studied. However, a
including both recent study has shown
short- and long- that 68% of male
term partners of infected
consequences, i.e. women and 70% of
pelvic female partners of
inflammatory infected men are positive
disease (PID), by PCR for C.
infertility, and trachomatis suggesting
potentially fatal that transmission from
tubal pregnancy. men or women is equally
efficient.
CDC/ Dr. Lourdes
Fraw, Jim Pledger
C. trachomatis infects
the columnar or
squamocolumnar
epithelium of the urethra,
cervix, rectum,
conjunctiva and the
respiratory tract (in the
neonate). All chlamydiae
contain DNA, RNA and
71. 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
72. 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.
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
73. 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
74. PELVIC
Figure 46
INFLAMMATORY
Generalized
DISEASE
peritonitis due to
what was Pelvic inflammatory
diagnosed as a disease (PID) signifies
pelvic abscess. inflammation of the
A differential upper female genital
diagnosis included tract and its related
pelvic structures. PID can
inflammatory manifest as endometritis,
disease (PID), salpingitis, adnexitis,
which if it had tubo-ovarian abscess,
been the root pelvic peritonitis (figure
cause, could begin 46) or perihepatitis. The
with a pelvic most common
origin, and manifestation of PID is
become salpingitis, and these
disseminated terms are used
throughout the synonymously in the
abdominopelvic literature. PID is one of
75. cavity, thereby, the most common causes
causing a of hospitalization among
generalized women of reproductive
peritonitis. age. Risk factors for PID
CDC/ Dr. James include young age,
Curran 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.
76. 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
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
77. 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
78. 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 gonococci into
the upper genital tract
through a cervix with
scant mucus during the
menstrual cycle.
URETHRITIS IN
MALES
Figure 47
This patient Urethritis (inflammation
presented with a of the urethra) is
case of non- characterized by a
specific urethritis burning sensation during
urination or itching or
with
discharge at the urethral
accompanying
79. meatitis, and a meatus. The exudate
mucopurulent (figure 47) may be
urethral discharge. mucoid, mucopurulent or
Non-specific purulent. Traditionally,
urethritis merely urethritis has been
means that upon differentiated into
presentation, the gonococcal or
cause of this given nongonococcal urethritis.
case of urethral When N. gonorrhoeae
inflammation is cannot be detected, the
unknown. A syndrome is called non-
differential gonococcal urethritis
diagnostic process (NGU). In the United
will help to States, the rates of NGU
narrow the have surpassed that of
possible causes by gonococcal urethritis in
ruling out those the past 20 to 30 years.
possibilities that The 20- to 24-year-old
do not provide age group has the highest
respective positive incidence of gonococcal
test results. CDC and non-gonococcal
80. 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 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
81. 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
82. based on physical
examination alone.
Patients with gonococcal
urethritis present with
acute 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,
83. 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.
HUMAN
PAPILLOMAVIRUS
Figure 48
INFECTION
This patient
Human papillomavirus
presented with
(HPV) is the most
chemical
common viral sexually
dermatitis of the
transmitted disease
perineum due to
worldwide. The
her extensive
prevalence ranges from
treatment for
84. labial venereal 20% to 46% in young
warts. women worldwide. In
Condylomata the U.S., 1% of sexually
acuminata, or active persons between
genital warts, is a the ages of 15 to 49
sexually years are estimated to
transmitted have genital warts from
disease caused by HPV. The incidence of
the Human HPV infection is high
Papilloma Virus, among college students
(HPV), which (35% to 43%) especially
manifests as among minority races,
bumps or warts on individuals with multiple
the genitalia, or sexual partners and
within the perineal alcohol consumption.
region. Immunocompromised
CDC/JoeMillar persons including those
with HIV infection have
increased prevalence of
HPV infection.
Figure 49
This patient Most genital HPV
85. presented with a infections are subclinical
penile tumor and are transmitted
differentially primarily through sexual
diagnosed as giant contact. Several
condyloma of transmission studies
Buschke and noted that 75% to 95%
Löwenstein of male partners of
(GCBL). Though women with HPV-
cancerous, giant genital lesions also had
condyloma of genital HPV infection.
Buschke and Vertical transmission can
Löwenstein cause laryngeal
(GCBL) is seldom papillomatosis in infants
metastatic. It is and children. Digital
most commonly transmission of genital
warts can also occur.
found originating
on the glans penis,
Human papillomavirus is
but may be found
a double-stranded DNA
on other perineal
virus that infects the
surfaces including
squamous epithelium. It
the anorectal, and
causes a spectrum of
86. vulvovaginal clinical disease ranging
mucosae. Though from asymptomatic
the etiology is infection, benign plantar
unknown, a viral and genital warts (figure
cause is highly 48), squamous intra-
suspect, and may epithelial neoplasia
include human (bowenoid papulosis,
papilloma virus, erythroplasia of Queyart,
or Bowen’s disease of
the cause of
condylomata. the genitalia) and frank
CDC malignancy (Buschke-
Lowenstein tumor
(figure 49), a form of
verrucous squamous cell
Figure 50 carcinoma) in the
This HIV-positive anogenital region.
External genital warts
patient was
exhibiting signs of have various
morphological
a secondary
manifestations such as
condyloma
condyloma acuminata
acuminata
87. infection, i.e., (cauliflower-like),
venereal warts. smooth dome-shaped
This intraoral papular warts, keratotic
eruption of warts and flat warts
condyloma (squamous intra-
acuminata, or epithelial neoplasia).
venereal warts Condyloma acuminata
was caused by the tend to occur on moist
human papilloma surfaces while the
virus. Though oral keratotic and smooth
HPV is a rare warts occur on fully
occurrence, HIV keratinized skin. Flat
reduces the body’s warts can occur on either
immune response, surface.
and therefore,
Approximately one
such secondary
hundred types of HPV
infections can
have been identified. The
manifest
thirty types that infect
themselves. CDC/
the anogenital area can
Sol Silverman, Jr.,
be divided into low-risk
DDS
(e.g., 6, 11, 42, 43, 44)
88. 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
89. with malignant
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)
90. 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 penis. They may also
present as white plaque
like lesions in the
anogenital region.
