Thirty One

Question 1

What are five categories of STIs?

Answer 1

I. Vaginitis

II. Cervicitis

III. Genital lesions

A. Ulcerative

B. Non-ulcerative

IV. Pelvic Inflammatory Disease

Question 2

What are 3 types of vaginitis?

Answer 2

A. Vulvovaginal candidiasis

B. Bacterial vaginosis

C. Trichomoniasis

Question 3

What are two types of cervicitis?

Answer 3

A. Gonorrhea

B. Chlamydia

Question 4

What are 4 types of ulcerative genital lesions

Answer 4

1. Herpes
2. Syphilis
3. Chancroid
4. Lymphogranuloma venereum (LGV)

Question 5

What are 3 types of non-ulcerative genital lesions?

Answer 5

1. Genital warts
2. Molloscum contagiosum
3. Ectoparasites (scabies, crabs)

Question 6

What causes vulvovaginal candidiasis? What are the risk factors? What are the clinical features? How is the diagnosis made? What is the treatment?

Answer 6

Candida albicans (80-92%), rarely C. glabrata

Risk factors
 Antibiotics
 Oral contraceptives (especially high-dose estrogen)
 Contraceptive devices (sponges, diaphragms, IUD’s)
 Pregnancy
 Diabetes mellitus
 Immunosuppresion (HIV, chronic steroid use)

Clinical features
 Vulvar pruritis, dysuria, soreness, irritation, dyspareunia, thick white discharge
 Erythema of vulvar/vaginal mucosa, vulvar edema
 Discharge typically thick, adherent, and “cottage-cheese like” but may be absent (especially with C. glabrata)

Diagnosis
 Vaginal discharge
 pH 4.0-4.5 (normal vaginal pH)
 budding yeast and hyphae on KOH prep (70% sensitivity)
 culture

Treatment
 Indicated for relief of symptoms
 20% of asymptomatic patients may harbor C. albicans
 Azoles
 Topical: eg. Miconazole (Monistat)
 Oral: single dose of Fluconazole (Diflucan)

 C. glabrata
 50% resistant to azoles
 Boric acid vaginal suppository nightly x 2 weeks

Question 7

What is the pathogenesis of bacterial vaginosis? What are the risk factors? What are the clinical features? HOw is the diagnosis made? What are the indications for treatment? What treatments are available? What are some complications?

Answer 7

Bacterial Vaginosis

Most common cause of vaginitis

Pathogenesis

 Results from shift in vaginal flora
 reduction in lactobacilli
 Increase in Gardnerella vaginalis, Mobiluncus, Mycoplasma hominis, anaerobes (Prevotella, Porphyromonas, Atophobium vaginae, Bacteroides), and Peptostreptococcus

Risk factors

 Multiple or new sexual partners
 Early age of first coitus
 Douching
 Cigarette smoking
 Intrauterine device (IUD) 

Clinical features
 50-75% asymptomatic
 Discharge is grey, thin, homogenous, “fishy smelling”
 No pruritis, inflammation, dyspareunia, dysuria

Diagnosis
 3 of the following criteria must be met
 Homogenous grayish-white discharge
 Vaginal pH >4.5
 Positive whiff-amine test (fishy odor with addition of 10% KOH)
 Clue cells on saline wet mount (vaginal epithelial cells studded with adherent coccobacilli), minimal wbc’s unless another infection is present
 No role for vaginal culture
 Pap smears not reliable

Treatment

 Indications
 Symptomatic infection
 Asymptomatic infection prior to abortion or hysterectomy and in pregnant patients with history of preterm birth
 Not necessary to treat sexual partners
 Resolved in up to 30% of patients without treatment

 Metronidazole
 Oral regimens or vaginal preparation
 Side effects: metallic taste, nausea, neutropenia, disulfiram-like effect with alcohol, interaction with warfarin
 Allergy uncommon

 Clindamycin
 Less effective than Metronidazole
 May contribute to resistance

 Complications
 Increased risk of preterm delivery
 probably associated with chorioamnionitis
 May increase risk of endometritis, postpartum fever, post-hysterectomy vaginal-cuff cellulitis, and postabortal infection
 Risk factor for acquisition and transmission of HIV, HSV-2, gonorrhea, and chlamydia

Question 8

What causes trichomoniasis? Pathophys? Clinical features? Diagnosis? Treatment? Complications?

Answer 8

Trichomonas vaginalis

 flagellated protozoan found in the vagina, urethra, and paraurethral glands
 Sexually transmitted
 Carriage in men is self-limited and transient

Clinical features

 Asymptomatic carriage state can occur for prolonged period
 Purulent, malodorous, thin discharge
 Associated with burning, pruritis, dysuria, dyspareunia, postcoital bleeding

Diagnosis
 Erythema of the vulva and vaginal mucosa
 Green-yellow frothy discharge (10-20%)
 Punctate hemorrhages “strawberry cervix” (2%)
 pH 5.0-6.0
 Motile trichomonads on wet mount (70%) along with many wbc’s
 Rapid test using DNA probes
 Culture
 Pap smear (liquid-based)

Treatment

 Metronidazole, oral dosing only
 Treat sexual partners
 Desensitize if allergy

Complications
 Increased risk of post-hysterectomy cellulitis, tubal infertility, and cervical neoplasia
 May facilitate transmission of HIV

Question 9

What causes gonorrhea? What percent of women are asymptom.? Men? Clinical features? Diagnosis? Treatment?

Answer 9

Gonorrhea

 Caused by Neisseria gonorrhoeae
 50% of women asymptomatic, only 10% of men
 Humans are the only host

 Clinical features
 Cervicitis
 Vaginal pruritis, mucopurulent discharge
 Urethritis
 10% of dysuria in inner-city women
 Anorectal infection and proctitis
 Oropharyngeal infection

 Diagnosis

 Gram stain
 Intracellular Gram negative diplococci
 Sensitivity only 60% but may allow for immediate diagnosis

 Nucleic acid amplification
 Most sensitive and specific test available
 Non-invasive (may use urine or endocervical specimen)

 DNA probe
 Invasive (swab cervix or urethra)

 Culture
 Use modified Thayer-Martin media
 Gold-standard for diagnosis

 Treatment
 Ceftriaxone IM PLUS Doxycycline or Azithromycin
 Dual antibiotic therapy to delay resistance
 Resistance to fluoroquinolones
 Concurrent infection with Chlamydia in 40%
 Treat empirically unless documented negative

Question 10

What causes chlamydia? What is it like? How common is chlamydia? Why is this significant clinically? Treatment?

Answer 10

 Most common sexually transmitted infection
 Chlamydia.trachomatis
 small gram-negative bacterium
 obligate intracellular parasite
 can’t culture on artificial media – need tissue to culture

 Clinical features
 Cervicitis
 >50% asymptomatic
 Symptoms may include vaginal discharge and abdominal pain

 Urethritis
 Dysuria, frequency, abdominal pain
 “Sterile pyuria” – wbc’s on urinalysis but no organisms on Gram stain or culture

 Clinical features (cont.)
 Perihepatitis (Fitzhugh-Curtis syndrome)
 inflammation of the liver capsule and adjacent peritoneal surfaces

 Pelvic inflammatory disease (PID)
 30% of women with chlamydia infection will develop PID if left untreated
 PID caused by N. gonorrhoeae is more acutely symptomatic, PID due to C. trachomatisis associated with higher rates of subsequent infertility

 Pregnancy
 Increased risk of PPROM and low-birth weight
 If the mother is untreated, 20-50% of newborns develop conjunctivitis and 10-20% develop pneumonia.

 Diagnosis
 Culture – not routinely used

 Nucleic acid amplification
 Most sensitive and specific test available
 Non-invasive (may use urine or endocervical specimen)

 DNA probe
 Invasive (swab cervix or urethra)

 Treatment
 Tetracyclines, eg. doxycycline
 Macrolides, eg. azithromycin
 Test of cure not recommended unless symptoms persist or non-compliance suspected
 Wait 3 weeks to perform if needed
 Repeat screening in 3 months recommended

Question 11

What organisms cause herpes? Explain. What are the types of infection? What are the clinical features for the different types of infection? Treatment? Counseling? Pregnancy management?

Answer 11

Herpes

 Traditionally HSV-1 “fever blisters” and HSV-2 “genital lesions”
 HSV-2 causes most virologically confirmed genital herpes infections
 HSV-1 has emerged with increasing frequency in certain patient populations
 Over 50 million people in the U.S. have genital HSV infection

 Types of infection

 Primary
 No preexisting antibodies to HSV-1 or HSV-2

 Non-primary first episode
 Acquisition of genital HSV-1 in a patient with preexisting antibodies to HSV-2 or the acquisition of genital HSV-2 in a patient with preexisting antibodies to HSV-1

 Recurrent
 Reactivation of genital HSV in which the HSV type recovered in the lesion is the same type as antibodies in the serum
 Virus resides in the dorsal root ganglia

 Subclinical infection (asymptomatic viral shedding)
 More common with HSV-2 during first 12 months

 Clinical features
 Primary infection
 multiple, bilateral, ulcerating, painful, pustular lesions
 Systemic symptoms (fever, malaise, headache, myalgias)
 Tender lymphadenopathy

 Extragenital complications
 Aseptic meningitis
 Urinary retention (sacral autonomic nervous system dysfunction)
 Distant skin lesions

 Non-primary first episode
 Symptoms usually less severe than primary episode

 Clinical features
 Recurrent infection
 More common with HSV-2 than HSV-1
 Prodromal symptoms (local tingling, shooting pains to buttock, legs, hips)
 Fewer lesions, usually unilateral
 Subclinical infection (asymptomatic viral shedding)

 Diagnosis
 Virologic tests

 Viral culture
 Cytologic detection of cellular changes of HSV infection
 Unroof vesicle to sample vesicular fluid for culture
 50% sensitivity

 PCR
 More sensitive than culture, detect asymptomatic shedding
 Not FDA-approved for testing of genital specimens (spinal fluid only)

 Tzanck smear, pap smear
 Do not use (low sensitivity and specificity)

 Type-specific serologic tests
 IgM and IgG

 Treatment
 Acyclovir, famciclovir (prodrug for penciclovir), and valacylovir (prodrug for acyclovir) equivalent in efficacy

 Acyclovir least expensive

 Episodic therapy
 Initiate therapy within 24 hours of lesion onset or during prodrome

 Suppressive therapy
 Reduces recurrences by 70-80% in patients with ≥6 recurrences/year
 Offer to all
 Encourage if ≥6 recurrences/year, immunocompromised, or discordant couples

 Counseling
 Natural history of disease (recurrent episodes, asymptomatic viral shedding, risks of sexual transmission)
 Suppressive versus episodic treatment
 Inform current and future sexual partners
 Abstinence when lesions or prodromal symptoms present
 Risk of transmission in absence of symptoms
 Latex condoms may reduce risk of transmission – do not prevent
 Consider serology testing in partners to assess risk of transmission
 Risk of neonatal infection

 Pregnancy

 During pregnancy the major concern relates to the morbidity and mortality associated with neonatal infection
 Counseling
 Avoid intercourse during third trimester with partners with known or suspected genital herpes
 Avoid receptive oral sex during third trimester with partner known or suspected to have orolabial herpes

 Randomized trial of acyclovir after 36 weeks in women with recurrent genital herpes
 Significant decrease in clinical recurrences
 Reduction in the number of cesarean deliveries performed for active infections but not statistically significant
 Suppressive therapy generally recommended if history of genital herpes (not in seropositive women without a history of genital herpes)

 Cesarean delivery indicated if
 active genital lesions
 symptoms of vulvar pain or burning (may indicate impending outbreak)

Question 12

What organism causes syphillis? Pathophys? What is primary syphilis like? SEcondary? Latent? Tertiary? Diagnosis? Treatment? Management of syphillis? What is congenital syphilis like in the womb? In early infancy? Late infancy?

Answer 12

Syphilis

 Caused by bacterium Treponema pallidum

 Organism gains access to subcutaneous tissues via microscopic abrasions that occur during sexual intercourse

 Primary syphilis

 After 2-3 week incubation a chancre appears at the site of inoculation – painless, usually single ulcerative lesion
 May have associated inguinal lymphadenopathy
 Resolves spontaneously in 3-6 weeks

 Secondary syphilis
 Weeks to months later 25% of those with untreated infection develop secondary syphilis
 Rash
 symmetric papular eruption involving the entire trunk and extremities including the palms and soles
 Condyloma lata – large, raised, gray to white lesions, involving warm, moist areas such as mucous membranes in the mouth and perineum

 Systemic symptoms
 Fever, headache, malaise, anorexia, sore throat, myalgias, and weight loss
 These symptoms may prompt medical attention
 Diffuse lymphadenopathy
 Alopecia
 Moth-eaten appearance
 Acute manifestations may resolve without treatment
 Untreated patients may have episodes of relapsing secondary syphilis for up to five years after their initial episode

 Latent syphilis
 Patient is asymptomatic but infection demonstrated by serologic testing
 Early latent versus late latent
 Early latent – infection 1 year, no longer infectious

 Tertiary (late) syphilis
 May occur anytime from 1-30 years after primary infection
 May include
 Central nervous system involvement (neurosyphilis, particularly general paresis and tabes dorsalis)
 Cardiovascular syphilis (especially aortitis)
 Gummatous syphilis (granulomatous, nodular lesions which can occur in a variety of organs, most commonly skin and bones)

 40% of untreated syphilis may progress to tertiary
 6% develop neurosyphilis, 10% develop cardiovascular syphilis, 16% develop gummatous syphilis

 Diagnosis
 T. pallidum cannot be cultured in the laboratory
 Diagnosis from lesions (early syphilis)
 Darkfield microscopy
 Direct fluorescent antibody testing (DFA-TP)
 Sample from moist lesion
 Corkscrew-shaped organisms
 Don’t need to examine smears immediately
 Avoids misidentifying other spirochetes as T. pallidum

 Diagnosis by serologic testing
 Non-treponemal tests (screening, reported as titer)
 Treponemal tests (confirmatory, reported reactive or not)
 Venereal Disease Research Laboratory (VDRL)
 Rapid Plasma Reagin (RPR)
 Fluorescent treponemal antibody absorption (FTA-ABS) test
 Treponema pallidum particle agglutination assay (TP-PA)

 Treatment

 Benzathine penicillin G
 Give long-acting dose via IM route
 Dose differs depending on the stage of syphilis

 Penicillin allergy
 IV route associated with cardiopulmonary arrest and death
 Desensitize if possible
 Alternatives
 Azithromycin or doxycycline

 Jarisch-Herxheimer reaction
 acute febrile reaction accompanied by headache, myalgia, rash, and hypotension
 result from the release of large amounts of treponemal lipopolysaccharide from dying spirochetes
 begins within 1-2 hours of treatment, peaks at 8 hours, and resolves within 24-48 hours
 Occurs in up to 45% of pregnant women treated for syphilis
 Management is supportive care
 reaction may precipitate uterine contractions, preterm labor, and/or nonreassuring fetal heart rate tracings

 Follow-up
 RPR/VDRL titers checked at 1, 3, 6, 12, and 24 months following treatment
 Titers should decrease 4-fold by 6 months
 Titers become non-reactive at
 1 year for primary infection
 2 years for secondary infection
 5 years for late/tertiary infection
 If titers show a 4-fold rise or do not decrease appropriately, then treatment failure or re-
infection is likely  retreat

 Syphilis in pregnancy
 Screen at initial visit, repeat in 3rd trimester and after delivery in high-risk populations
 Must treat with PCN in pregnancy as it is the only drug that crosses the placenta and treats the fetus
 If allergic then desensitize

 Congenital syphilis
 Fetus
 Placental involvement and hepatic dysfunction –> amniotic fluid infection –>hematologic abnormalities –>ascites –> hydrops
 Intrauterine death in 25%

 Congenital syphilis

 Infant
 Early
 anemia
 snuffles
 cutaneous lesions
 hepatosplenomegaly
 jaundice

 Late
 frontal bossing
 short maxilla
 high palatal arch
 saddle nose
 perioral fissures
 Hutchinson triad: Hutchinson teeth (blunted upper incisors), interstitial keratitis, and eighth nerve deafness

Question 13

What causes chancroid? What is it like? Epidemiology? Diagnosis? Clinical features? Treatment?

Answer 13

Chancroid

 Uncommon infection in U.S. but more common in developing world (sub-Saharan Africa)
 Caused by Haemophilus ducreyi
 small, fastidious, gram-negative rod

 Diagnosis

 Gram stain
 Small Gram negative rods in a chain (“school of fish”)
 Poor sensitivity

 Culture
 Sensitivity pustule –>painful ulcer
 Multiple ulcers confined to genital area
 Base of ulcer covered by gray/yellow exudate
 Inguinal lymphadenitis (painful)
 Involved nodes may undergo liquefaction and become fluctuant (buboes)

 Treatment
 Azithromycin, ceftriaxone or cipro
 Examine and treat if sexual contact during the 10 days preceding the patient’s onset of symptoms

Question 14

What organisms cause lyphogranuloma venereum? Epidemiology? Clinical features? Diagnosis? Treatment?

Answer 14

Lymphogranuloma venereum (LGV)

 Caused by Chlamydia trachomatis serovars L1, L2, or L3
 Found in tropical areas (rare in U.S.)

 Clinical
 Self-limited genital ulcer at site of inoculation
 Tender inguinal lymphadenopathy, typically unilateral
 Rectal exposure causes proctocolitis
 Mucoid/hemorrhage rectal discharge, anal pain, constipation, fever, tenesmus
 If left untreated may lead to chronic colorectal fistulas and strictures

 Diagnosis
 Based on clinical suspicion and exclusion of other etiologies
 Genital and lymph node specimens may be tested for C. trachomatis by culture, direct immunofluorescent, or nucleic acid detection

 Treatment
 Doxycycline for 3 weeks (Erythromycin if pregnant)

Question 15

What causes condyloma acuminata? Explain. What is the incubation period? How is it spread? Clinical features?

Answer 15

Condyloma Acuminata (anogenital warts)

 Caused by human papilloma virus (HPV)
 Over 70 HPV subtypes
 35 subtypes specific for anogenital epithelium
 High-risk subtypes
 16 and 18
 Associated with squamous cell carcinoma

 Low-risk subtypes
 6 and 11
 Benign condylomas

 Incubation period 3 weeks to 8 months
 Most infections are transient and clear within 2 years

 Virus spread by
 Sexual activity
 Digital/anal contact
 Oral/anal contact
 Digital/vaginal contact

 Clinical features

 Symptoms vary depending on number, size, and location
 May include pruritus, bleeding, burning, tenderness, vaginal discharge, pain

 Diagnosis
 Visual inspection
 Skin-colored or pink
 Range from smooth flattened papules to a verrucous papilliform appearance
 Application of 5% acetic acid causes lesion to turn white

 Consider biopsy
 Uncertain diagnosis
 No response to therapy
 Prompt and frequent recurrences after therapy
 Immunocompromised
 Rapid growth
 Large lesions (>1 cm)
 Atypical features (pigmentation, ulceration, fixation to underlying tissue)

 Treatment

 Chemical or physical destruction

 Podophyllin
 Teratogenic

 Trichloroacetic acid
 Applied by clinician
 May use in pregnancy

 5-fluorouracil epinephrine cream
 Inject weekly for 6 weeks

 Immune modulation

 Imiquimod
 Apply 5% cream at night 3x/week for up to 16 weeks

 Surgical excision
 Cryotherapy
 Laser therapy
 Excisional procedures

Question 16

What causes molluscum contagiosum? Transmission? Clinical features? Diagnosis? Treatment?

Answer 16

Molluscum Contagiosum

 Poxvirus
 Humans are the only known host

 Transmission is by direct skin-to-skin contact
 Autoinoculation
 Contact sports
 Genital-to-genital contact (classified as STI)
 Bath sponges or towels via fomites

 Clinical features
 firm, dome shaped papules with an umbilicated center
 may appear anywhere except the palms and soles

 Diagnosis
 Usually made by characteristic appearance
 Histology or electron microscopy when necessary

 Treatment
 Usually self-limited and resolves spontaneously if immunocompetent
 Can get bacterial superinfection of the wart
 If needed may use curettage, cryo, or laser therapy

Question 17

What are the two examples of ectoparasites? What causes them? Transmission? Clinical features? Treatment?

Answer 17

 Scabies

 Infestation of the skin by the mite Sarcoptes scabiei
 Transmission by direct contact

CLINICAL FEATURES
 Symptom is itching (usually worse at night)
 Clinically see papules and elongated burrows

 Diagnosis
 Lesion seen clinically
 Scraping of lesion under microscope

 Treatment
 Permethrin cream or Lindane (not in pregnancy) – repeat in 1 week
 Treat close contacts
 Hot water/hot dryer of all clothes/bedding

 Pediculosis pubis
 Caused by Phthirus pubis (crab louse)
 Parasite 2-3 mm long, translucent and difficult to see unless filled with blood from a recent meal
 4 of its 6 legs end in crab-like claws to grasp pubic hairs

 Itching is primary symptom

 Treatment
 Permethrin cream or Lindane shampoo
 Treat all contact and wash bedding/clothing

Question 18

What is PID?

Answer 18

 Acute infection of the upper genital tract structures in women
 May involve the uterus, oviducts, and ovaries
 Community-acquired infection initiated by a sexually transmitted agent
 Different from pelvic infections caused by medical procedures, pregnancy, and other primary abdominal processes.

Question 19

What is the pathogenesis of PID?

Answer 19

 Vaginal flora includes a variety of potentially pathogenic bacteria

 Streptococci, Staphylococci, Enterobacteria (Klebsiella, E. coli, Proteus), anaerobes

 Endocervical canal functions as a barrier protecting the sterile upper genital tract from

vaginal flora

 Pathogens that disrupt this barrier include Neisseria gonorrhoeae and Chlamydia

trachomatis

 Disruption of the barrier gives vaginal flora access to the upper genital tract

Question 20

What are some risk factors?

Answer 20

 Risk factors

 New, multiple, or symptomatic sexual partners

 Age <25

 Young age at first sex

 History of PID

 African-American

 Non-barrier contraception
 OC’s – doubles prevalence of GC/CT but 50% reduction in clinical PID
 PID developed as frequently but less severe
 IUD’s – modern IUD’s have no increased risk of PID
 Tubal ligation – risk of PID unchanged

Question 21

What are some clinical features?

Answer 21

 Clinical features

 Lower abdominal pain

 Abnormal uterine bleeding (1/3)

 Fever/chills (1/2)

 RUQ pain (10%) indicating perihepatitis

 Purulent endocervical discharge

 Cervical motion tenderness

Question 22

What tests are used for diagnosis?

Answer 22

 Diagnostic tests

 Pregnancy test

 Wet mount of vaginal discharge

 CBC

 Tests for chlamydia and gonococcus

 Urinalysis

 Fecal occult blood test

 C-reactive protein (optional)

 Consider ultrasound

 Palpable mass

 Inpatient therapy planned

 Failure to respond to appropriate therapy

 Tenderness prevents adequate pelvic exam

 If high suspicion, empiric treatment is recommended if abdominal pain and at least one of

the following:

 Cervical motion tenderness or uterine/adnexal tenderness

 Temperature >101

 Leukocytosis

 Mucopurulent discharge from cervix

 WBC’s on wet mount of vaginal secretions

 Elevated erythrocyte sedimentation rate (ESR)

 Elevated C-reactive protein (CRP)

Question 23

How is a diagnosis confirmed?

Answer 23

 Diagnosis confirmed if pelvic pain and any one of the following:

 Endometritis or salpingitis by biopsy

 Positive N. gonorrhoeae or C.trachomatis

 Gross salpingitis by laparoscopy or laparotomy

 Isolation of the pathogenic bacteria from a clean specimen from the upper genital tract

 Inflammatory/purulent pelvic peritoneal fluid without another source

 Definitive diagnosis as defined by CDC requires presence of at least one of the following:

 Histologic evidence of endometritis in a biopsy

 CT or US revealing thickened fluid filled oviducts with or without free pelvic fluid or

tuboovarian complex

 Laparoscopic abnormalities consistent with PID

 tubal erythema, edema, adhesions

 purulent exudate or cul-de-sac fluid

 abnormal fimbriae

Question 24

How is PID treated?

Answer 24

 Treatment

 Most patients may be treated outpatient

 Multi-drug regimen like 2nd or 3rd generation cephalosporin plus doxycycline +/-

metronidazole

 Consider hospital admission if

 Possible surgical emergency

 Pregnant (PID in pregnancy is an extremely rare event)

 No response or unable to tolerate outpatient therapy

 At risk to be noncompliant with outpatient therapy

 Adolescents, unable to afford medications

 Severe clinical illness

 Pelvic abscess

 Immunodeficient

Question 25

What are some sequelae?

Answer 25

 Sequelae

 Infertility

 Frequency of tubal factor infertility after mild, moderate, and severe PID is 10%, 25%,

and 50%

 Each additional episode of PID decreases fertility further

 Ectopic pregnancy
 10-15% of conceptions are ectopic after mild/moderate PID
 50% after severe PID

 Chronic pelvic pain
 Seen in 30-50% of patients with symptomatic PID
 Due to adhesion formation

 Tuboovarian abscess
 Mixed polymicrobial infection with high prevalence of anaerobes
 Diagnosis by ultrasound
 Treatment
 Medical
 Hospitalize
 Must include coverage for anaerobes (i.e. Flagyl)
 Drainage (CT- or US-guided)
 Indicated if failure to respond to medical therapy

 Leave drain in place

 Surgical