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CCBS - PELVIC INFECTIONS-7

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CCBS-3
PELVIC INFECTIONS
1. GENITAL ULCER DISEASE
Manifests as a breach in the skin or mucosa of the genitalia
Herpes simplex virus type 2 (HSV-2) is the most common etiology in most geographic
areas
Followed by syphilis and chancroid
The most important noninfectious cause is behçet’s disease
In chancroid, a cytotoxin secreted by Haemophilus ducreyi - important in epithelial cell
injury
Pathogens
Common infectious etiologies of genital ulcer disease include:
HSV-2 - genital herpes
Treponema pallidum - primary syphilis
H. ducreyi – chancroid
Less common pathogens include:
Chlamydia trachomatis serovars L1–3 - lymphogranuloma venereum
Klebsiella granulomatis - granuloma inguinale/ donovanosis
STD’S
Diagnosis
Sexual and medical history
Physical examination
Clinical characteristics
Often overlap in presentation
May also be multiple syndromes copresenting
Therefore, diagnostic testing is highly recommended
Testing for other Sexually transmitted diseases including human immunodeficiency virus
(HIV) is also important because there is often cotransmission of multiple pathogens
Treatment & Prevention
Genital herpes is acyclovir, famciclovir or valacyclovir
Primary and secondary syphilis – long acting penicillin, benzathine penicillin G
Chancroid - azithromycin
Lymphogranuloma venereum – doxycycline
Consistent use of condoms
Partner notification and treatment
2. VAGINITIS
Inflammation of the vagina that can result in discharge, itching, and pain
Common causes of vaginitis are:
 Candidiasis
 Trichomoniasis
 Bacterial vaginosis
Noninfectious causes - lichen planus and certain medications (e.g., oral contraceptives
Patients are usually prompted to seek medical attention because of an abnormal vaginal
discharge
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This may be accompanied by pruritus, pain (including dyspareunia), and symptoms of
vaginal irritation
Pathophysiology
The use of antibiotics that inhibit the normal flora of the vagina, especially lactobacilli,
predisposes to Candida vaginitis
Candida is a member of the normal flora of many women
The pathogenesis of bacterial vaginosis is uncertain, but it does not appear to be a
sexually transmitted disease
Trichomoniasis - sexually transmitted disease
Pathogens
Candida albicans is the most common cause of vaginal candidiasis
Trichomonas vaginalis is the cause of trichomoniasis
Overgrowth of bacteria such as Gardnerella vaginalis is implicated in bacterial vaginosis,
but anaerobes such as Mobiluncus are also involved
Diagnosis
Careful history - time of last menstrual period, medications, and sexual activity
Physical examination - microscopic examination of the vaginal discharge itself on a glass
slide using a drop of 0.9% saline solution (to look for motile trichomonads or clue cells),
followed by a drop of 10% potassium hydroxide (to look for Candida)
Clue cells as large, vaginal epithelial cells dotted with bacteria - Gardnerella
Appearance of the yeasts and pseudohyphae of Candida
Cultures for Gardnerella are not done because at least 50% of asymptomatic women
carry the organism
Treatment
Metronidazole is the drug of choice for both bacterial vaginosis and trichomoniasis
For candidiasis, either oral fluconazole or vaginally administered miconazole or
butoconazole is the drug of choice
T. vaginalis is a sexually transmitted infection, so a one-time treatment regimen of
patient and partner is preferred
3. CERVICITIS
Cervicitis is inflammation of the uterine cervix
Acute cervicitis is usually due to a sexually transmitted infection caused by either C.
trachomatis or Neisseria gonorrhoeae or both
Other less common etiologies include HSV and T. vaginalis
Clinical Manifestations
A large proportion of women with cervicitis are asymptomatic
In many cases, cervicitis is detected on speculum examination and/or following routine
screening for C. trachomatis and N. gonorrhoeae
Women who have concomitant urethral infection may have dysuria
On physical examination, increased friability of the cervical tissue after a swab is
inserted may be a clue to the diagnosis
Diagnosis
A clinical diagnosis may be made based on increased friability of the cervix, with or
without mucopurulent discharge
 To make a laboratory diagnosis, nucleic acid amplification testing (NAAT) for C.
trachomatis and N. gonorrhoeae is routinely performed in many centers
 If NAAT testing is not available, then Gram stain and culture may be performed
 Treatment
 If there is clinical evidence of cervicitis, empiric treatment for both C. trachomatis and N.
gonorrhoeae (ceftriaxone intramuscularly plus azithromycin orally) is recommended,
particularly if follow-up of test results by the patient is uncertain
 Sex partners of patients with a confirmed diagnosis should also be notified and treated
 Prevention
 Consistent use of condoms is an important measure that can prevent sexually
transmitted diseases
 Partner notification and treatment are important prevention strategies as well
 4. PELVIC INFLAMMATORY DISEASE
 Pelvic inflammatory disease (PID) is a polymicrobial infection of upper genital tract
structures, namely the uterus, fallopian tubes, and ovaries
 Pathophysiology
 When the endocervical canal barrier is compromised, vaginal bacteria can ascend into
the normally sterile space of the upper genital tract (uterus, fallopian tubes, and
ovaries)
 A sexually transmitted infection affecting the cervix (e.g., N. gonorrhoeae and C.
trachomatis) can initiate the process, permitting the anaerobic bacteria of the vagina to
ascend
 Having multiple sex partners increases the risk of PID
 Multiple episodes of PID lead to scarring of the fallopian tubes and an increased risk of
ectopic pregnancy and sterility
 Clinical Manifestations
 Patients can present with a range of symptoms, from lower back pain to fever, chills,
lower abdominal pain, and cervical and adnexal tenderness
 On physical exam, pain and tenderness on motion of the cervix are important diagnostic
signs
 Pathogens
 PID is primarily associated with N. gonorrhoeae and C. trachomatis, together with
enteric gram-negative rods and anaerobes
 Diagnosis
 Because it is often difficult to diagnose PID precisely (given the nonspecific findings) and
because the consequences of not treating PID can be grave, many opt to treat with
minimum diagnostic criteria such as uterine, adnexal, or cervical motion tenderness
 Fever, the presence of leukocytes on cervical or vaginal discharge, elevated C-reactive
protein, and laboratory evidence of cervical infection with N. gonorrhoeae or C.
trachomatis can increase the specificity of the diagnosis
 Treatment
 If symptoms are mild, women can be treated as outpatients with cefoxitin or ceftriaxone
(one dose) plus doxycycline (14 days)
 Metronidazole is sometimes added to the regimen
 In the inpatient setting, intravenous therapy is preferred
 Cefoxitin or cefotetan with doxycycline, or clindamycin plus gentamicin are initial
options with oral antibiotics only after 24 hours of improvement of the patient
 5. URETHRITIS
 Urethritis is inflammation of the urethra
 It is usually caused by a sexually transmitted infection, particularly in sexually active men
 A noninfectious cause is Reiter’s syndrome, an autoimmune disease that includes
urethritis, uveitis, and reactive arthritis
 Clinical Manifestations
 Dysuria is a common presenting complaint
 Discharge from the urethra, pruritus, and burning are also common complaints
 Pathogens
 N. gonorrhoeae and C. trachomatis are the most common organisms implicated
 Other organisms include Mycoplasma genitalium and T. vaginalis
 Diagnosis
 Nucleic acid amplification testing (NAAT) for C. trachomatis and N. gonorrhoeae is
routinely performed in many centers
 Treatment
 If there is clinical evidence of urethritis such as a purulent urethral discharge, empiric
treatment for both N. gonorrhoeae and C. trachomatis (ceftriaxone intramuscularly plus
azithromycin orally) is recommended
 Prevention
 Consistent use of condoms is an important measure that can prevent sexually
transmitted diseases
 Partner notification and treatment are important prevention strategies as well
 CASE
 A 24-year-old man is referred to the local genito-urinary medicine (GUM) clinic. He has
been complaining of recent onset of dysuria and has also noticed a yellowish urethral
discharge. He denies any constitutional symptoms, frequency or haematuria. He has not
noticed any rash, conjunctivitis or joint pains. His background history is unremarkable.
He is heterosexual with a number of sexual partners, and admits to practising unsafe sex
 Examination
 General examination is normal. There is a small amount of muco-purulent discharge
evident from the urethra, which was mildly erythematous around the meatus. There is
no rash visible, nor any evidence of genital ulceration or inguinal lymphadenopathy. The
testes and prostate are non-tender and not enlarged. Urine and urethral swabs are
taken for investigation. Due to his risky sexual behaviour, blood is taken for syphilis, HIV
and hepatitis B. A list of his sexual contacts is requested for contact tracing.
 INVESTIGATIONS
 Microbiology
 Urethral swab
 Microscopy (performed in the clinic) WBC +++
 Epithelial cells ++
 Intracellular diplococci (coffee-bean shaped)
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Microscopy (performed in the lab) WBC +++
Epithelial cells ++
Gram-negative intracellular diplococci
Culture: Neisseria gonorrhoeae
Urine MC&S
Microscopy WBC +++
RBC +
Epithelial cells +
Bacteria +++
Culture: No growth
Urine nucleic acid amplification test (NAAT): positive for Neisseria gonorrhoeae,
negative for Chlamydia trachomatis
 Questions
1. What is the differential diagnosis for a urethral discharge?
2. How is this condition diagnosed?
3. How would you manage this patient?
 The differential diagnosis of a urethral discharge is classically divided into gonococcal
urethritis (GU) and non-gonococcal urethritis (NGU)
 GU is a sexually transmitted infection caused by the gram-negative diplococcus
Neisseria gonorrhoeae
 There is generally a short history of dysuria and a thick urethral discharge occurring
after a recent contact
 In women the presentation can be slower, and may be asymptomatic
 Disseminated infection occurs if the organism spreads to the systemic circulation
 This is characterized by fever, rash and suppurative arthritis
 NGU presentation tends to be more indolent, with a 3–4-week history being usual
 The dysuria and discharge are less prominent, and the discharge is more watery than for
GU
 Causes of NGU include:
• Chlamydia trachomatis, the most common cause of sexually transmitted infection reported in
the UK, especially in young adults and adolescents. Symptoms may come and go over several
weeks, and it may appear to spontaneously resolve in some. It may also be asymptomatic,
especially in women. There is co-infection with N. gonorrhoeae in about 20% of patients, and
empiric treatment will usually treat both these infections simultaneously
 Mycoplasma genitalium, emerging as a common cause of NGU, and is more commonly
symptomatic than C. trachomatis. It is more difficult to diagnose and is therefore
sometimes treated empirically
• Trichomonas vaginalis infection, a common cause of vaginitis in women and also an important
source of urethritis in men. A 22% urethral prevalence was found among male partners of
women with known trichomonal infection. The condition should be suspected in patients with
symptoms but little or no discharge on physical examination
 Ureaplasma urealyticum, more recently thought to be a cause of NGU. It may account
for 10–40% of NGU cases and is sexually transmitted
• Herpes simplex virus infection, most often associated with painful superficial genital ulcers
that are usually visible on the external genitalia
• Prostatitis, especially in older men with enlarged prostates, predisposing to obstruction and
infection. Minor penile discharge may be present. Symptoms of urinary outflow obstruction and
perineal discomfort may be the predominant symptoms
 No test is currently 100% sensitive or specific for N. gonorrhoeae
 Routine urine MC&S culture media does not support its growth
 Options for diagnosis of urethritis are microscopy, culture and molecular tests:
• Microscopy: staining of the urethral discharge is helpful in looking for pus cells as well as the
typical intracellular, bean-shaped diplococci of N. gonorrhoeae
If a gram stain is performed the bacteria will look pink in colour (gram-negative)
Microscopy has a sensitivity of 90–95% in symptomatic men for N. gonorrhoeae
Sensitivity is poor for endocervical (<50%), rectal and throat swabs, and in asymptomatic men
(50–75%)
 Culture: using specific selective media, N. gonorrhoeae will grow if plated soon after the
specimen is taken
 It is a fragile organism and a delay in the specimen reaching the lab will result in a false
negative culture, as it will have died en route
 Thus some GUM clinics plate the specimens directly onto culture plates in the clinic
 It is not practical to culture for Chlamydia or Ureaplasma because it is technically
difficult, takes two to three days to get a result, and is expensive
 Molecular tests: Nucleic acid amplification test (NAAT) is the standard diagnostic and
screening test used for N. gonorrhoeae and C. trachomatis
 It is >96% sensitive even on asymptomatic cases and can be performed on swabs from
any site as well as urine samples from men
 Sensitivity on urine samples from women is significantly lower than from an
endocervical swab and is not recommended
 N. gonorrhoeae has become significantly resistant to a spectrum of antibiotics
 There are no longer any oral antibiotics that can be recommended alone for first-line
treatment with the certainty of curing the infection
 First-line treatment for uncomplicated gonococcal infection is currently a single dose of
parenteral ceftriaxone with oral azithromycin
 The azithromycin is thought to have a synergistic effect with the cephalosporin, and is
also used to try to delay emergence of resistance to the cephalosporin
 Testing for cure and contact tracing is recommended after treatment
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