PELVIC INFECTIONS AND SEXUALLY TRANSMITTED DISEASES Dr Dora Milman Kaplan Medical Center Rehovot

The Normal Vagina Vulvar secretions from sebaceous, sweat, Bartholin, Skene glands Transudate from vaginal wall Exfoliated vaginal & cervical cells Cervical mucus Endometrial & oviductal fluids Micro-organisms and their metabolic products

The Normal vagina 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 Normal Vagina 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 NormaVagina 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

The Normal Vagina 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)

Bacterial Vaginosis - BV 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 – 100- 1,000 times higher than in normal women The possible triggers: repeated alkalinization of the vagina (frequent sexual intercourse or use of douches)

Bacterial vaginosis - BV 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

BV - diagnosis 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)

BV – Clue cells

BV - Treatment 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)

Trichomonas Vaginalis

Trichomonas Vaginitis 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)

Trichomonas Vaginitis - Diagnosis Local immune factors and inoculum size influence the 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

Trichomonas Vaginitis 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

Trichomonas vaginitis - Treatment 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

VVC – Candida albicans

Vulvovaginal Candidiasis - VVC 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

VVC - Diagnosis Vulvar pruritus, vaginal discharge – “cottage cheese” 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

VVC - Treatment 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

Recurrent VVC 4 or more episodes in a year – a small number of 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

Atrophic Vaginitis In Menopause – naturally or secondary to 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

Cervicitis

Cervicitis 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

Cervicitis - Diagnosis A purulent endocervical discharge, yellow or green – “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

Cervicitis - Treatment 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

PID

Pelvic Inflammatory Disease - PID Acute infection of the upper female genital tract – 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

PID – Long-term complications 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 laparoscopically- confirmed PID versus 1.3% without PID at laparoscopy.

PID - Diagnosis Lower abdominal pain– may be subtle, worsens 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 PID - diagnosis There is NO single diagnostic gold standard

PID – Risk factors 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

PID - diagnosis 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?)

PID - Diagnosis Leukocytosis Elevated CRP or ESR Positive test for Gonorrhea or Chlamydia Ultrasound documenting tubo-ovarian abscess Laparoscopy visually confirming salpingitis

Tubo-ovarian abscess Sonographic image

Fitz-Hugh-Curtis Perihepatitis

PID - Treatment Empirical, broad-spectrum coverage of likely pathogens, including N. Gonorrhoeae C. Trachomatis M. Genitalium Gram-negative facultative bacteria Anaerobes Streptococci

PID - treatment 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

Tubo-ovarian abscess 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)

Genital Ulcer Disease 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

Genital Ulcer disease Noninfectious: Fixed drug reactions Behchet’s disease Neoplasms Trauma

Genital Ulcer - infectious 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

Genital ulcer - infectious Syphilis: Ulcer – usually a single, indurated, with smooth firm borders Usually painless Inguinal lymphadenopathy

Genital ulcer - infectious 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

Genital ulcer - infectious 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

Genital ulcer – infectious 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”

Genital ulcer - summary 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)

Genital ulcer - summary 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