Dr Dora Milman
Kaplan Medical Center
Rehovot
 Vulvar secretions from sebaceous, sweat, Bartholin,
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Skene glands
Transudate from vaginal wall
Exfoliated vaginal & cervical cells
Cervical mucus
Endometrial & oviductal fluids
Micro-organisms and their metabolic products
 The type, amount of cells, mucus and fluids are
determined by biochemical processes that are
influenced by hormone levels
 Vaginal secretions may increase in the middle cycle
due to increase in the amount of cervical mucus
 These cycle variations do not occur when oral
contraceptives are used
The vaginal desquamative epithelial cells are responsive
to amounts of estrogen and progesterone:
 Superficial cells – the main type in the reproductive
age, predominate when estrogen stimulation is present
 Intermediate cells – during the luteal phase –
stimulation by progesterone
 Parabasal cells – absence of either hormone, in
postmenopausal without HRT
 The normal vaginal flora – mostly aerobic
 An average of six types of bacteria
 The most common – Hydrogen peroxide-producing
lactobacilli
 Normal vaginal pH is lower than 4.5 (due to
production of Lactic acid by lactobacilli and vaginal
epithelial cells)
 Normal vaginal secretions are floccular, white, usually
located in the posterior fornix
Microscopy of normal vaginal secretions:
 Many superficial epithelial cells
 Few white blood cells
 Few, if any, Clue cells (superficial vaginal epithelial
cells with adherent bacteria, usually Gardnerella
vaginalis, wich obliterates the crisp cell border)
 An alternation of normal vaginal flora: loss of
lactobacilli, overgrowth of predominantly anaerobic
bacteria
 The most common form of vaginitis
 Anaerobes, G. vaginalis, Mycoplasma hominis – 1001,000 times higher than in normal women
 The possible triggers: repeated alkalinization of the
vagina (frequent sexual intercourse or use of douches)
Increased risk for:
 Pelvic inflammatory disease (PID)
 Postabortal PID
 Postoperative cuff infections after hysterectomy
 Abnormal cervical cytology
In pregnancy:
 PROM
 Preterm labor and delivery
 Chorioamnionitis
 Postcesarean endometritis
 A fishy vaginal odor, particularly following coitus
 Vaginal secretions – gray, thinly coat the vaginal wall
 The pH higher than 4.5
 Microscopy: increased number of clue cells and
leukocytes
 The addition of KOH to the vaginal secretions releases
a fishy, aminelike odor (the “whiff” test)
Inhibition of anaerobes but not vaginal lactobacilli.
 Metronidazole – orally 500 mgX2 for 7 days or
vaginal gel 0.75% for 5 days
 Clindamycin – 100 mg ovules intravaginally for 3
nights or 2% vaginal cream for 7 nights or 300 mg X2
for 7 days
 No need of treatment of male sexual partner (no
improvement of therapeutic results)
 Sexually transmitted flagellated parasite
Trichomonas vaginalis
 High transmission rate
 An anaerobe, with ability to generate Hydrogene to
combine with Oxygen to create an anaerobic
environment
 Often accompanies BV (as many as 60% of cases of
trichomoniasis)
 Local immune factors and inoculum size influence the
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appearance of symptoms
Profuse, purulent, malodorous vaginal discharge,
vulvar pruritus
A patchy vaginal erythema and colpitis macularis
(“strawberry” cervix)
The pH of vaginal secretions higher than 5.0
Microscopy: motile trichomonads, increased
number of WBC
Clue cells may be present
The whiff test may be positive
Morbidity (in association with BV) – postoperative cuff
cellulitis after hysterectomy, P-PROM, preterm
delivery
Tests for other STD: Neisseria gonorrhoeae, Chlamydia
trachomatis
Serologic testing for Syphilis and HIV should be
considered
 Metronidazole – the drug of choice: a single-dose (2 g
orally) or 500 mg twice daily for 7 days - a cure rate
95%
 The sexual partner should be treated!
 Vaginal treatment is not effective
An estimated 75% of women experience at least one
episode of VVC during lifetimes
Candida albicans – 85-90% of vaginal yeast infections
C. glabrata, c. tropicalis – rare, tend to be resistant to
therapy
Predisposing factors: antibiotic use, pregnancy,
diabetes
Decrease in cell-mediated immunity (pregnancy,
diabetes) leads to higher incidence of candidiasis
 Vulvar pruritus, vaginal discharge – “cottage cheese”
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or watery, or homogeneously thick
External dysuria, vulvar burning, dyspareunia
Erythema and edema of the vulva, vagina. The cervix
appears normal
The pH of the vagina is usually normal (<4.5)
Fungal elements appear in as many as 80% of cases
The whiff test is negative
A fungal culture
 Topically applied azole – 80-90% relief of symptoms
 Oral fluconazole in a single 150-mg dose
 Complicated VVC – an additional 150-mg dose of
fluconazole 72 hours after the first dose or 10-14 days
of topical treatment
 Ajunctive treatment – a weak topical steroid – 1%
hydrocortisone cream – for relieve of external
irritation
 4 or more episodes in a year – a small number of
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women
Persistent irritative symptoms of the vestibule and
vulva
Diff. diagnosis with chronic atopic dermatitis or
atrophic vulvovaginitis
Fluconazole 150 mg every 3 days for 3 doses and
supression with 150 mg weekly for 6 months
One half – recurrence of the symptoms
 In Menopause – naturally or secondary to
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oophorectomy
Inflammatory vaginitis
Increased purulent vaginal discharge
Dyspareunia
Postcoital bleeding
A result of atrophy of the vaginal and vulvar
epithelium
Topical Estrogen – cream or tablets, or systemic HRT
 Two types of cervical epithelium: squamous –
ectocervical – an extension of vaginal epithelium, and
glandular - in endocervix
 the ectocervical infections – as in the vagina –
Trichomonas, Candida, HSV
 The endocervical infections –N. gonorrhoeae, C.
trachomatis
 A purulent endocervical discharge, yellow or green –
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“mucopus”
Gram stain
Increased number of neutrophils
Intracellular G- diplococci (gonorrhea)
If negative for gonococci, the presumptive diagnosis is
chlamydial cervicitis
Nucleic acid amplification tests for gonorrhea and
chlamydia
The etiology of 50% of endocervicitis is unknown
 Treatment of Gonorrhea and Chlamydia
 Treatment of sexual partners!
 Treatment of BV, commonly associated with cervicitis
 Fluoroquinolone resistance is common in N.
gonorrhoeae
 N. gonorhoeae – Ceftriaxone, 250 mg IM – single
dose
 C. trachomatis – Doxycycline, 100 mg X2 for 7 days
 Azithromycin, 1 g orally as single dose
 Acute infection of the upper female genital tract –
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uterus, oviducts, ovaries, often involvement of
neighboring pelvic organs
Endometritis,salpingitis, oophoritis, tubo-ovarian
abscess, peritonitis, perihepatitis
N. gonorhoeae, C. trachomatis are often implicated
Vaginal flora (BV micro-organisms)
Haemophilus influenzae, group A streptococci,
pneumococci
 Chronic pelvic pain – as many as one-third of women
with PID.
 Infertility - injury to fallopian tube – loss of ciliary
action, fibrosis, occlusion - hydrosalpinx (in IVF –
negative consequences on the rates of pregnancy,
implantation, early pregnancy loss, preterm birth, and
live delivery)
 Ectopic pregnancy - 7.8% after laparoscopicallyconfirmed PID versus 1.3% without PID at
laparoscopy.
 Lower abdominal pain– may be subtle, worsens
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during coitus, may onset during or shortly after
menses, usually bilateral
Abnormal uterine bleeding – in one-third of
patients with PID
New vaginal discharge
Fever, chills
Non of these signs is neither sensitive nor specific
There is NO single diagnostic
gold standard
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Previous episode of PID
Sex during menses
Vaginal douching
Bacterial vaginosis
Intrauterine device
Age less than 25 years
Young age at first sex
Nonbarrier contraception
Oral contraception
New, multiple, or symptomatic sexual partners
 Fever – only about one-half
 Diffuse tenderness greatest in the lower quadrants
 Rebound
 Right upper quadrant tenderness – Fitz-Hugh-Curtis
syndrome – perihepatitis – 10% of patients with PID
 Purulent endocervical discharge
 Cervical motion and adnexal tenderness
 Low-grade fever, weight loss, abdominal pain – susp.
Actinomycosis (IUD?)
 Leukocytosis
 Elevated CRP or ESR
 Positive test for Gonorrhea or Chlamydia
 Ultrasound documenting tubo-ovarian abscess
 Laparoscopy visually confirming salpingitis
Empirical, broad-spectrum coverage of likely
pathogens, including
N. Gonorrhoeae
C. Trachomatis
M. Genitalium
Gram-negative facultative bacteria
Anaerobes
Streptococci
 Mild – outpatient regimen
 Hospitalization – when:
- the diagnosis is uncertain
- pelvic abscess is suspected
- clinical disease is severe
- poor compliance
 Evaluate sexual partners for gonococcal and
chlamydial urethritis
 An end-stage process of acute PID
 A palpable pelvic mass - agglutination of pelvic organs
 Hospitalization!
 About 75% respond to antimicrobial therapy alone
 Failure to respond to antimicrobial therapy after 72
hours – the need for drainage – percutaneous,
transvaginal or surgical exploration (laparoscopy)
Infectious:
 Herpes simplex – HSV – type 1, type 2
 Syphilis – Treponema pallidum
 Chancroid – Haemophilus ducreyi
 Lymphogranuloma Venerum – Chlamydia
trachomatis serovars L1-3
 Granuloma Inguinale (Donovanosis) – Klebsiella
granulomatis
Noninfectious:
 Fixed drug reactions
 Behchet’s disease
 Neoplasms
 Trauma
HSV
 Type-2, type-1
 Multiple small grouped vesicles - ulcers; erythematous
base
 Usually painful
 Occasionally single lesion/fissures
 Can be painless or pruritic
 Reactive lymphadenopathy
Syphilis:
 Ulcer – usually a single, indurated, with smooth firm
borders
 Usually painless
 Inguinal lymphadenopathy
Chancroid:
 Begin as papules that go on to ulcerate
 Sharply circumscribed or irregular, ragged
undermined edges
 Multiple ulcers
 Not indurated
 Base with gray or yellow exudate
 Very painful
 50% with inguinal adenopathy
Granuloma inguinale:
 One or more nodular lesions that ulcerate
 Usually painless
 Slowly enlarge friable ulcers, with raised, rolled
margins
 Granulation-like lesions
 “kissing” lesions
 Lymphadenopathy – less common, though nodular
lesions may appear as pseudobuboes
LGV – Lymphogranuloma venerum:
 Often begins as a single papule or a small and shallow
ulcer
 Usually painless
 Rapid spontaneous healing
 Tender lymphadenopathy
 Suppuration of the lymph nodes
 A painful “buboe”
 Infectious or noninfectious
 Sexual and medical history
 Ulcer - single or multiple? Recurrent? Painful?
Indurated or no? Suppurative? Lymphadenopathy?
 Underlying HIV infection? (oropharyngeal thrush,
significant concomitant inguinal, cervical, axillary
lymphadenopathy)
 Supportive laboratory testing (the appearance of
genital ulcers may vary and overlap)
 Tests for STD’s – C. trachomatis, N. gonorhoeae, HIV,
Hepatitis B, Hepatitis C
 Atypical presentation in the immunocompromised
host
 Follow-up
 To exclude non-infectious causes