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Genital Tract Infections - Dr. Julius King Kwedhi
1. GENITAL TRACT INFECTIONS AND
PELVIC INFLAMMATORY DISEASE
Julius M. Kwedhi
6th year, Medical Faculty, Sechenov University
Gynaecology Class
(29 November 2018)
2. Differential Diagnoses
⢠A 35 years old female, gravida
2, para 2, presents with a
history of severe midline lower
abdominal pain that started 2
days ago. Her menses started
at age 13.
⢠Question: What are the
differential diagnoses of acute
and chronic lower abdominal
pain?
5. Normal Vaginal Flora
⢠Normally, 5 to 15 different bacterial species (both
aerobic and anaerobic):
⢠Lactobacillus acidophilus
⢠group B streptococcus,
⢠Escherichia coli,
⢠Prevotella
⢠Etc.
6. Infection of the Vulva and Vagina
1.Non-sexually Transmitted Infections
2.Sexually Transmitted Infections
11. Introduction
⢠Pelvic inflammatory disease (PID) comprises a
spectrum of inflammatory diseases of the upper
genital tract of women. PID can involve infection
of the endometrium (endometritis), the oviducts
(salpingitis), the ovaries (oophoritis), the uterine
wall (myometritis), or portions of the parietal
peritoneum (peritonitis).
⢠PID is usually the result of a sexually transmitted
disease (STI) and less often results from
iatrogenic causes after instrumentation of the
female reproductive tract.
12. Definitions
⢠Acute PID refers to the acute symptoms accompanying
ascending infection from the cervix to the endometrium,
tubes, ovaries, and pelvic peritoneum.
⢠Chronic PID refers to chronic pelvic pain, often periodic in
exacerbation, which can follow an acute episode of PID, a
sequelae to the infl ammatory response to an acute infection
in the pelvis. Chronic pelvic infection can also be caused by
the more rare pelvic infection with tuberculosis (TB) and
actinomycosis.
⢠Silent PID refers to asymptomatic or mildly symptomatic
pelvic infection, which is usually diagnosed when the
sequelae of tubal damage is found at a later date.
13. Medical Sequelae
⢠Develop in one in four women with acute PID:
⢠Tubal obstruction that leads to infertility
⢠Ectopic pregnancy rate increases 6 to 10 fold
⢠Chronic pelvic pain in 20%
⢠Mortality as a result of ruptured tuboovarian
abscess that leads to septic shock and death
14. Risk Factors
⢠Frequent sexual activity
⢠Early onset of sexual activity
⢠Multiple sex partners
⢠Recent new sex partner
⢠Intrauterine devices (IUD
15. Prophylaxis
⢠Male & female condoms
⢠Oral contraceptives
⢠decrease menstrual flow,
⢠decrease ability of pathogenic bacteria to attache to
endometrial cells
⢠Progestin-induced changes in the cervical mucus that
retard the entrance of bacteria.
⢠Other barrier methods of contraception (e.g. the
diaphragm, sponge, contraceptive foam)
16. Bacteriology
⢠Acute PID is usually a polymicrobial infection caused by
normal flora of the cervix and vagina:
⢠Neisseria gonorrhoea (cervix & fallopian tubes)
⢠Chlamydia Trachomatis (cervix & fallopian tubes)
⢠Polymicrobial uterus and fallopian tubes infection by:
⢠Escherichia coli, Gardnerella vaginalis,Streptococcus
species, Proteus, Klebsiella, and Haemophilus
influenzae, Bacteroides, Peptostreptococcus, and
Peptococcus
⢠Actinomyces israelii (IUD-associated, unilateral
abscesses)
17. Pathophysiology
⢠When PID occurs, salpingo-oophoritis is usually preceded by cervical infection with gonorrhea and/or
chlamydia; infection ascends when an inciting event occurs that allows bacteria to ascend into the
uterus and then into the tubal lumen, usually bilaterally. Symptomatic ascending infection follows
10% to 40% of cervical infections with gonorrhea and chlamydia.
⢠Inciting Events:
1. Menstrual periods
2. Sexual intercourse
3. Bacterial vaginosis (BV) - Gardnerella vaginalis & Mycoplasma organisms
4. Iatrogenic events:
1.Elective abortion
2.Dilation and curettage and endometrial biopsy
3.IUD insertion or use
4.Hysterosalpingography
5.Chromopertubation at laparoscopy
18. Chronology of Salpingo-
oorphoritis
⢠Infection is usually bilateral, but unilateral infection is also possible,
especially in association with an IUD. The clinical course is as follows:
⢠Endosalpingitis develops initially with edema and ultimately proceeds to
destruction of luminal cells, cilia, and mucosal folds. Bacterial toxins are
most likely to be responsible.
⢠Infection spreads to the tubal muscularis and serosa. It also spreads by
direct extension to the abdominal cavity through the fi mbriated end of the
tube.
⢠Oophoritis develops over the surface of the ovaries, and microabscesses
may develop within the ovaries.
⢠Peritonitis may occur, and upper abdominal infection may result either by
direct extension of infection up the abdominal gutters laterally or by
lymphatic spread. Development of perihepatitis with adhesions and right
upper quadrant abdominal pain is known as FitzâHughâCurtis syndrome.
19. Sequelae of PID
⢠a. Pyosalpinges (tubal abscesses)
⢠b. Hydrosalpinges (fl uid-fi lled, dilated, thin-walled, destroyed tubes,
usually totally obstructed)
⢠c. Partial tubal obstruction and crypt formation
⢠d. Total tubal obstruction and infertility
⢠e. Tubo-ovarian abscesses
⢠f. Peritubal and ovarian adhesions
⢠g. Dense pelvic and abdominal adhesions
⢠h. Ruptured abscesses, resulting in sepsis and shock
⢠i. Chronic pelvic pain and dyspareunia
20. Minimum Diagnostic Criteria
⢠a. Lower abdominal tenderness
⢠b. Uterine or adnexal tenderness
⢠c. Cervical motion tenderness: lateral motion of
the cervix on examination causes pain by putting
tension on the adnexa
21. Additional Diagnostic Criteria
⢠For women with severe signs, these additional criteria are used to increase the specificity
of the diagnosis:
⢠a. Oral temperature higher than 100.9 ° F (38.3 ° C) present in less than one-third of
women diagnosed with PID
⢠b. Abnormal cervical or vaginal discharge. Mucopurulent cervical discharge with white
blood cells (WBCs) seen on wet mount is almost always seen in women with PID. If this
finding is not present, other diagnoses should be seriously entertained
⢠c. Elevated erythrocyte sedimentation rate (ESR)
⢠d. Elevated C-reactive protein
⢠e. Positive test for gonorrhea or chlamydia
⢠f. Tubo-ovarian abscess seen on ultrasound
⢠g. Evidence of endometritis on endometrial biopsy
⢠h. Laparoscopic evidence of PID
22. Diagnosis
⢠3. Other symptoms that may be seen in women
with PID include
⢠a. Abdominal pain
⢠b. Intermenstrual and/or postcoital bleeding
⢠c. Urinary frequency
⢠d. Nausea/vomiting
⢠e. Lower back pain
24. Diagnostic Techniques
⢠Cervical gram stain
⢠Serum Beta hCG
⢠Ultrasound
⢠CT Scan
⢠Laparoscopy
⢠Blood studies
⢠Leukocytosis is not a reliable indicator of acute PID
⢠ESR, although nonspecific, it is, nevertheless, elevated in 75% of laparoscopically
confirmed cases
⢠Follow up (48-72 hrs)
⢠Test for HIV and Pap smear creating
25. Treatment
⢠Individualized treatment
⢠Oral treatment regimens:
⢠Ceftriaxone 250 mg IM,
⢠Cefoxitin2 g IM with probenecid 1g orally at the
time of injection or other 3rd gen.
cephalosporin,
⢠Doxycycline 100 mg oral bd for 14 days,
⢠Metronidazole 500 mg bd for 15 days
26. Treatment
⢠Parenteral regimens:
⢠Regimen A:
⢠Cefotetan 2g IV every 12 hrs, or cefoxitin
2g IV every 6 hrs
⢠Plus Doxycycline 100 mg PO or IV every
12 hrs. Oral Clindamycin or metronidazole
may be added if abscess is suspected
27. Treatment
⢠Regimen B
⢠Clindamycin 900 mg IV every 8hrs +
Gentamicin 2mg/kg loading dose IV or IM
followed by 1.5 mg/kg maintenance dose
every 8 hrs
⢠When conversion to oral therapy takes place:
Doxycycline 100 mg bd or clindamycin 450
mg qd