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Sexually transmitted infections
and pelvic inflammatory disease
PREPARED BY: EYOB HABTAMU (MD/009/2015)
MODERATOR: DOCTOR MEKONEN
1
OUTLINE
• Introduction to the normal vaginal flora
• Bacterial vaginosis
• Genital ulcers
• Infectious vaginitis
• Supparative cervicitis
• Pelvic inflammatory disease
• Syndromic management of STIs
2
INTRODUCTION
 The vaginal flora of a normal, asymptomatic reproductive-aged woman includes multiple
aerobic, facultative anaerobic, and obligate anaerobic species.
 These bacteria exist in a symbiotic relationship with the host and are alterable, depending on
the microenvironment.
 Certain bacterial species normally found in vaginal flora have access to the upper reproductive
tract.
 Typically, the vaginal pH ranges between 4 and 4.5.
 Some conditions predispose to the altering of the vaginal flora: post menopausal state,
menstruation, treatment with broad spectrum antibiotics.
3
Source: WHO HIV/AIDS/STI Initiative4
1- Bacterial vaginosis
• This common, and poorly understood clinical syndrome reflects abnormal vaginal flora.
• The vaginal flora’s symbiotic relationship shifts or unknown reasons to one in which anaerobic
species overgrow and include Gardnerella vaginalis, Ureaplasma urealyticum, Mobiluncus
species, Mycoplasma hominis, and Prevotella species.
• Not considered an STI even if BV is associated with sexual contact with multiple and new male
and female partners, and condom use lowers the risk.
5
Bacterial vaginosis (clinical picture)
• Bacterial vaginosis is the most common cause of vaginal discharge among reproductive-aged
women.
• A nonirritating, malodorous vaginal discharge is characteristic, but may not always be present.
• The vagina is usually not erythematous, and cervical examination reveals no abnormalities.
• Clinical diagnostic criteria [Amsel (1983)]:
(1) microscopic evaluation of a vaginal-secretion saline preparation,
(2) release of volatile amines produced by anaerobic metabolism,
(3) determination of the vaginal pH.
6
Bacterial vaginosis (clinical picture)
• A wet preparation may show clue cells (95% positive predictive value).
• The “whiff test” uses 10% KOH to release a fishy odor.
• The finding of both clue cells and a positive whiff test result is pathognomonic, even in
asymptomatic patients.
• Nugent Score: scores based on assessing bacteria staining and morphology.
7
BV (adverse effects and management)
 Vaginitis,
 Endometritis,
 Postabortal endometritis,
 Pelvic inflammatory disease (PID) unassociated with N gonorrhoeae or Chlamydia trachomatis,
 Acute pelvic infections following pelvic surgery, (esp. hysterectomy)
 Elevated risk o preterm delivery
8
2- Genital ulcer infections
• Ulceration defines complete loss of the epidermal covering with invasion into the underlying
dermis.
• Erosion describes partial loss of the epidermis without dermal penetration.
• Cause of genital ulcers include; HSV, syphilis, LGV, chancroid, granuloma inguinale
• All are essentially sexually transmitted therefore partners should be involved in management .
• High association with HIV transmission (Co-testing advised)
9
A- Herpes simplex infection
• Is the most common cause for genital ulcers (developed nations).
• Undergoes retrograde axonal transport to the dorsal root ganglion, where the virus develops
lifelong latency.
• Most women who have been infected with HSV-2 lack this diagnosis because of mild or
unrecognized infections.
• Infected patients can shed infectious virus while asymptomatic,
• Most infections are transmitted sexually by patients who are unaware of their infection.
10
Herpes simplex infection
• Symptoms at initial presentation will depend primarily on whether or not a patient during the
current episode has antibody rom previous exposure.
• The three stages o lesions are:
(1) vesicle with or without pustule formation, which lasts approximately a week;
(2) ulceration;
(3) crusting.
• Virus is predictably shed during the first two phases of an infectious outbreak.
• In addition dysuria, vulvar swelling causing urethral obstruction, vaginal, cervical, bladder, anal and
rectal lesions can be present.
• Other signs of viremia such as a low-grade ever, headache, malaise, and myalgia are usually
present .
• Hepatitis, encephalitis, or pneumonia infrequently develop, and disseminated disease is rare.
11
Herpes simplex infection (course)
 For a previously uninfected patient,
• The vesicular stage is longer.
• The vesicular stage, period of new lesion formation and time to healing are both longer.
• Pain persists for the first 7 to 10 days, and lesion healing requires 2 to 3 weeks.
 Prior exposure to HSV-2,
• Episode is significantly less severe, with shorter pain and tenderness duration,
• Time to healing approximates 2 weeks.
• Virus is shed usually only during the first week.
12
Herpes simplex infection (management)
• Antiviral therapy
• Analgesia
• Prevention of secondary infection
• Patient education
• Suppressive therapy if indicated
13
HSV in pregnancy
• Virus poses a disproportionately higher risk to the newborn than to the mother.
• The virus can be passed to the fetus/neonate by three routes:
(1) peripartum in 85 percent,
(2) postnatal in 10 percent,
(3) intrauterine in 5 percent (James, 2015).
• For a primary outbreak during pregnancy, women may be given antiviral therapy to attenuate
and decrease the duration of symptoms and viral shedding
• Women with HIV co-infection may require a longer duration of treatment.
• For intense discomfort, oral analgesics and topical anesthetics may provide some relief, and
comorbid urinary retention is treated with an indwelling bladder catheter.
14
HSV in pregnancy
• Cesarean delivery is indicated for women with active genital lesions or prodromal symptoms.
• An active lesion in a nongenital area is not an indication for cesarean delivery. occlusive
dressing is placed, and vaginal delivery is allowed.
• In cases of prematurely ruptured membranes with active lesions there is not an absolute
duration of membrane rupture beyond which the fetus would not benefit from cesarean
delivery.
• Viral therapy at or beyond 36 weeks for women who had primary genital herpes infection or
active recurrent genital herpes during pregnancy.
• Women with active HSV may breastfeed if there are no active breast lesions.
• Acyclovir is safe during breast feeding.
15
B- Syphilis
• Caused by the spirochete Treponema pallidum,
• Women at highest risk are those from lower socioeconomic groups, adolescents, those with early
onset o sexual activity, and those with a large number of life time sexual partners.
• Divided into four stages:
• Primary syphilis, the hallmark lesion is the chancre, in which spirochetes are abundant.
• Secondary syphilis, bacteremia develops 6 weeks to 6 months after a chancre appears. Its hallmark
is a maculopapular rash that may involve the entire body and includes the palms, soles, and mucous
membranes.
• Early latent syphilis during the first year following secondary syphilis without treatment, secondary
signs and symptoms may recur. However, lesions associated with these outbreaks are not usually
contagious.
• Tertiary syphilis is the phase of untreated syphilis that may appear up to 20 years after latency.
16
Syphilis (diagnosis)
Non- Treponemal tests:
(1) Venereal Disease Research Laboratory (VDRL)
(2) rapid plasma reagin (RPR) tests.
Treponemal tests:
(1) fluorescent treponemal antibody-absorption (FTA-ABS)
(2) Treponema pallidum particle agglutination ( TP-PA) tests
• For population screening, RPR or VDRL testing is appropriate.
• A positive test result in a woman who has not been treated previously or syphilis or a four fold titer (two
dilutions) increase in a woman previously treated or syphilis should prompt confirmation with treponemal
specific tests.
• A four fold titer decrease is required by 6 months after therapy for primary or secondary syphilis or within 12
to 24 months for those with latent syphilis or women with initially high titers (> 1:32) to document cure.
17
Syphilis (management)
• Penicillin is the first-line therapeutic agent or this infection, and benzathine penicillin is
primarily chosen.
• Patients with penicillin allergy who cannot be surveilled post therapy or whose compliance is
questioned; skin testing, desensitization, and treatment with IM benzathine penicillin.
• After initial treatment, women are seen at 6-month intervals or clinical evaluation and
serologic retesting.
18
Syphilis and pregnancy
• Maternal syphilis can cause fetal infection by several routes.
• Transplacental transmission is the most common route, but neonatal infection may follow after
contact with spirochetes through lesions at delivery or across the placental membranes.
• Without screening and treatment, approximately 70 percent of infected women will have an
adverse pregnancy outcome, such as; preterm labor, fetal death, fetal growth restriction, or
fetal infection.
• The newborn may have jaundice with petechiae or purpuric skin lesions, lymphadenopathy,
rhinitis, pneumonia, myocarditis, nephrosis, or long-bone involvement
19
Syphilis and pregnancy
• Following maternal diagnosis, sonographic evaluation is performed for fetuses >20 weeks’ gestation
to search for signs of congenital syphilis.
• 31 percent of infected women diagnosed at ≥18 weeks’ gestation had abnormal fetal sonographic
findings.
• Hepatomegaly, placental thickening, hydramnios, ascites, hydrops fetalis, and elevated middle
cerebral artery Doppler velocimetry measurements are indicative of fetal infection.
• For fetuses of viable age with sonographic findings, antepartum fetal heart rate monitoring prior to
treatment is recommended
20
C- Chancroid
• Caused by a nonmotile, non-spore- forming, facultative, gram-negative bacillus, Haemophilus
ducreyi.
• Chancroid lacks a systemic reaction and prodrome. Infection presents initially with an erythematous
papule that becomes pustular and ulcerates within 48 hours.
• The most common locations in women include the fourchette, vestibule, clitoris, and labia.
• Recommended regimens for non-pregnant women include single doses o oral azithromycin (1 g) or
IM ceftriaxone (250 mg).
• Multiple-dose options are ciprofloxacin 500 mg orally twice daily or 3 days or erythromycin 500 mg
orally three times daily or 7 days.
• Successful treatment leads to symptomatic improvement within 3 days, and objective evidence of
improvement within 1 week.
• Treatment failure is more common in RVI patients.
21
D- Granuloma inguinale
• Also known as donovanosis, and is caused by Calymmatobacterium (Klebsiella) granulomatis
• Disease is only mildly contagious, requires repeated exposures, and has a long incubation
period of weeks to months.
• Presents as a painless inflammatory nodule that progress to highly vascular, beefy red ulcers
that bleed easily on contact. (painful if secondarily infected)
• Diagnosis is by identification of Donovan bodies during microscopic evaluation of a specimen
following Wright-Giemsa staining.
• If successfully treated, improvement will be evident within the first few treatment days. But
relapses can occur as much as 18 months post therapy.
22
E- Lymphogranuloma venerum
• Is an ulcerative genital disease is caused by trachomatis serotypes L1, L2, and L3.
• Usually found in lower socioeconomic groups among persons with multiple sexual partners.
• Clinical course is divided into three stages:
(1) small vesicle or papule,
(2) inguinal or femoral lymphadenopathy,
(3) anogenitorectal syndrome.
• LGV may be diagnosed following clinical evaluation with exclusion of other etiologies and positive
chlamydial testing.
• CDC-recommended regimen is Doxycycline, 100 mg orally twice daily or 21 days or alternatively
Erythromycin 500 mg orally four times daily for the same duration.
• Sexual contacts within the prior 60 days are tested or urethral or cervical infection and treated.
23
Infectious vaginitis
• Symptomatic vaginal discharge most o ten reflects BV, candidiasis, or trichomoniasis.
• In contrast, if abnormal discharge is associated with vulvar burning, irritation, or itching, then
vaginitis is diagnosed.
• During evaluation a concise sexual and menstrual history Is taken.
• A thorough physical examination of the vulva, vagina, and cervix is also performed.
• Wet preps, KOH test and acidity testing can be performed on the vaginal fluid.
24
A- Fungal infection
• Candida albicans, can be found in the vagina of asymptomatic patients and is a commensal of
the mouth, rectum, and vagina.
• Warmer climates, obesity, immunosuppression, diabetes mellitus, pregnancy, and recent
broadspectrum antibiotic use predispose women to clinical infection.
• Pruritus, pain, vulvar erythema, and edema with excoriations are frequent findings
• The typical vaginal discharge is described as curdy or cottage cheese-like. KOH prep can
visualize the fungus.
• 10 to 20 percent of women have complicated candidiasis, which implies greater symptom
severity, perhaps involvement o non-albicans species, affected patients with relative
immunosuppression, or recurrent disease (four of more episodes per year).
25
Fungal infection (management)
• For uncomplicated infection, azoles are extremely effective, and women warrant specific follow-up
only if therapy is unsuccessful.
• For women in these complicated candidiasis categories, cultures are obtained to direct care, and
longer therapy may be needed to achieve clinical cure (local intravaginal therapy or 7 to 14 days).
• For recurrent disease, local intravaginal therapy or 7 to 14 days or oral fluconazole in 100-mg, 150-
mg, or 200-mg doses once every third day or a total of three doses (day 1, 4, and 7) are options.
• Suppressive maintenance regimen or recurrence prevention is oral fluconazole, 100 to 200 mg
weekly for 6 months.
• Non-albicans candida species are not as responsive to topical azole therapy (locsl boric acid is an
option)
**** Oral fluconazole is generally not considered teratogenic, but in 2016, the FDA released a safety
alert regarding a possible link with miscarriage.
26
B- Trichomoniasis
• Is a protozoan infection be trichomonas vaginalis.
• 70 percent of male partners of women with vaginal trichomoniasis will have trichomonads in
their urinary tract.
• Parasite is usually a marker of high-risk sexual behavior, and co-infection with other sexually
transmitted pathogens is common, especially N gonorrhoeae.
• The vagina, urethra, endocervix, and bladder can be infected.
• Vertical transmission during birth is possible and may persist or a year.
• 50% are asymptomatic and may stay so for years.
• vaginal discharge is typically described as foul, thin, and yellow or green.
• Additionally, dysuria, dyspareunia, vulvar pruritus, vaginal spotting, and pain may be noted.
27
Trichomoniasis
• At times, clinical findings are identical to those o acute PID.
• With trichomoniasis, the vulva may be erythematous, edematous, and excoriated.
• The vagina contains the discharge just described, and subepithelial hemorrhages or
“strawberry spots” dot the vagina and cervix.
• Microscopic identification of motile parasites in a saline preparation o the discharge is
diagnostic (60-80% sensitivity).
• Women with trichomoniasis are tested or other STDs.
• Additionally, sexual contact(s) are evaluated or re erred or evaluation.
28
Trichomoniasis (management)
• Oral regimens are either metronidazole 2g once or tinidazole 2 g once.
• Oral metronidazole 500 mg BID for 7 days may be more effective in compliant patients.
• Affected women are retested within 3 months o treatment. Recurrence occurs in
approximately 30 percent of patients.
• Patients are reminded to abstain rom sex until they and their partners are cured. Condom use
may be protective.
• Resistant organisms are sensitive to tinidazole.
• Metronidazole is not teratogenic, but best avoided in the first trimester.
29
30
Suppurative cervicitis
Can be due to:
A.Neisseria gonorrhea
B. Chlamydia tracomatis
C. Mycoplasma genitalium
31
A- Gonorrhea
• N gonorrhoeae is a gram-negative coccobacillus that invades columnar and transitional
epithelial cells, becoming intracellular.
• Symptomatic lower female reproductive tract gonorrhea may present as vaginitis or cervicitis.
• Those with cervicitis commonly describe a profuse odorless, nonirritating, and white-to
yellow vaginal discharge.
• Patients may report intermenstrual or postcoital vaginal bleeding, or gentle passage of a
cotton swab into the cervical os often produces endocervical bleeding.
• Gonococcus can also infects the Bartholin and Skene glands, the urethra, and ascend into the
endometrium and fallopian tube to cause upper reproductive tract infection
32
Gonorrhea
• Many women with cervical N gonorrhoeae are asymptomatic. For this reason, women at risk
are screened periodically.
• Risk actors or gonococcal carriage that merit screening are:
 age ≤ 24 years,
 prior or current STDs,
 new or multiple sexual partners,
 a partner with other concurrent partners,
 a partner with an STD,
 lack of barrier protection in those without a monogamous relationship,
 and commercial sex work
33
Gonorrhea
• Sexual contacts from the preceding 60 days are evaluated and treated or referred for this.
• Abstinence is practiced until therapy is completed and until they and their treated sexual
partners have symptom resolution.
• In cases of cephalosporin allergy, single doses of gentamicin 240 mg IM plus oral azithromycin
2 g.
• Untreated gonococcal cervicitis is associated with septic abortion, infection after voluntary
abortion, Preterm delivery, prematurely ruptured membranes, chorioamnionitis, and
postpartum infection.
• Repeat testing is recommended in the third trimester for any woman treated for gonorrhea in
the first trimester and for any uninfected woman who is at high risk for gonococcal infection (
34
B- Chlamydia
• Is caused by an obligate intracellular organism; Chlamydia Tracomatis
• It infects columnar epithelial cells, and endocervical glandular infection leads to mucopurulent
discharge or endocervical secretions.(can also cause uretritis)
• Diagnosis can be confirmed by microscopy, or NAAT of endocervical/vaginal swab samples.
• If C trachomatis is diagnosed or suspected, then screening or other S Ds is indicated.
• It is disputed whether untreated cervical infection increases the risk of preterm delivery,
preterm ruptured membranes, low birthweight, or perinatal mortality.
• Known to cause delayed postpartum metritis characterized by vaginal bleeding or discharge,
low-grade fever, and uterine tenderness.
• Neonatal conjunctivitis and pneumonia are also associated with chlamydial infection.
35
C- Mycoplasma genitalium
• Role in female lower reproductive tract pathology is poorly defined.
• Most women carriers are asymptomatic, but it has been linked in some studies to urethritis,
cervicitis, PID, and later to tubal- actor infertility.
• Azithromycin 1 g orally once is recommended.
• moxifloxacin 400 mg once orally or 7 to 14 days in women with PID who fail to respond to
other treatment and mycoplasma is detected.
36
Pelvic inflammatory
disease
37
Introduction
• Is an infection o the upper female reproductive tract organs (yet the organ of importance is the fallopian tube).
• Classified as silent, acute and chronic PIDs.
• Low threshold for diagnosis is necessary due to its known complications;
 Ectopic pregnancy
 Tubal infertility
 Chronic pelvic pain
• Risk factors;
Douching Single status Substance abuse Multiple sexual partners
Lower socioeconomic status Recent new sexual partner(s) Younger age (10 to 19 years)
Other STI Sexual partner with STI Previous diagnosis of PID Not using l contraceptive barriers
38
Microbiology
• Classic salpingitis is associated with and secondary to N gonorrhoeae infection, and C
trachomatis is also commonly recovered.
• Upper tract infection is believed to be caused by bacteria that ascend rom the lower
reproductive tract.
• Women with pulmonary tuberculosis can develop salpingitis and endometritis.
• The fallopian tubes also can be infected by direct extension from inflammatory GI disease.
39
Silent PID
• Silent PID is not a clinical diagnosis. Rather, it is an ultimate diagnosis given to women with
tubal- actor infertility who lack a history compatible with upper tract infection.
• is thought to follow multiple or continuous low-grade infection in asymptomatic women.
• Grossly the fallopian tubes are normal (may have adhesions though)
• Internally, however, tubes show flattened mucosal olds, extensive deciliation of the
epithelium, and secretory epithelial cell degeneration.
• Alternatively hydrospalphinx may be found on sonography or gross inspection.
• Adhesions between the liver and anterior abdominal wall can also be considered as evidence
for prior infection.
40
Acute PID
• Represents a spectrum of clinical disease, from mild, vague pelvic symptoms to tubo-ovarian abscess
and, rarely, fatal intra-abdominal sepsis.
• is characterized by the acute onset of lower abdominal or pelvic pain, pelvic organ tenderness, and
evidence of inflammation of the genital tract.
• PID is diagnosed clinically if uterine tenderness, adnexal tenderness, or cervical motion tenderness
is present.
One or more of the following enhances diagnostic specificity:
• (1) oral temperature > 38.3°C (101.6°F),
• (2) mucopurulent cervical discharge or cervical friability,
• (3) abundant WBCs on saline microscopy of cervical secretions,
• (4) elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP),
• (5) presence of cervical N gonorrhoeae or C trachomatis.
41
Criteria
Based on laparoscopic studies fulfillment of ceratin criteria increased the chances of PID
presence;
(1) single status,
(2) adnexal mass,
(3) age < 25 years,
(4) temperature > 38°C,
(5) cervical N gonorrhoeae, (6) purulent vaginal discharge, and
(7) ESR ≥ 15 mm/hr
- 97-percent accurate if a woman meets all seven criteria,
42
Acute PID
• With acute PID, symptoms characteristically develop during or soon following menstruation.
• These include abdominal and/or pelvic pain, yellow vaginal discharge, heavy menstrual
bleeding, ever, chills, anorexia, nausea, vomiting, diarrhea, dysmenorrhea, dyspareunia and
signs consistent with a urinary tract infection.
• leucorrhea or mucopurulent endocervicitis is common and is diagnosed visually and
microscopically
• During bimanual pelvic examination, affected women will usually have pelvic organ
tenderness.
• RUQ abdominal pain and other signs may suggest perihepatits.
• During examination, if all abdominal quadrants are involved, suspicion or a ruptured
tuboovarian abscess ( OA) is heightened.
43
Differential diagnosis
44
Investigations in Acute PID
In women with lower abdominal pain, tests directed at diagnosing PID or excluding other pain
sources are selected.
LAB: CBC, urinalysis, Beta-Hcg, LFT, saline preparation of cervical discharge, testing for other STIs
Sonography: in acute tubal inflammation the sonographic appearance inclides
(1) distended, ovoid-shaped tube filled with anechoic or echogenic fluid,
(2) fallopian tube wall thickening,
(3) incomplete internal septa,
(4) a “cogwheel” appearance when inflamed tubes are imaged in cross section.
In women with right upper quadrant pain suggestive o perihepatitis, chest radiography or upper
abdominal sonography may be needed to exclude other pathology.
45
Tubo-ovarian abscess
• With infection, the inflamed and suppurative fallopian tube can adhere to the ovary.
• “tuboovarian complex” - both tube and ovary are recognizable,
• “tuboovarian abscess” - tissue planes and distinction between the two is lost
• Tuboovarian abscesses are typically unilateral and may also involve adjacent structures that include
bowel, bladder, and contralateral adnexa.
• Microorganisms frequently cultured include E coli, Bacteroides spp, Peptostreptococcus spp, and
aerobic Streptococcus spp.
• Most will respond to intravenous (IV) antibiotic therapy alone and avoid the need or drainage.
• Parenteral antimicrobial therapy is continued until the patient has been afebrile or at least 24
hours, preferably 48 to 72 hours.
46
Management of PID
• The primary therapy goal is to eradicate bacteria, relieve symptoms, and prevent sequelae.
• In women with a mild to moderate clinical presentation, outpatient treatment and inpatient
therapy yield similar results.
• If patients are treated as outpatients, an initial parenteral dose may be beneficial.
• Women treated as outpatients are reevaluated in approximately 72 hours.
• If not responding to oral therapy within 72 hours, parenteral therapy is initiated.(assuming
• diagnosis is confirmed at reevaluation)
• IUDs must be removed in severe disease or if patient fails to resolve in 48-72 hours.
47
Prognosis
 The most successful patient outcomes follow early diagnosis and prompt, appropriate therapy.
 Infertility is a major concern with rates following one episode approximate 15 percent; two
episodes, 35 percent; and three or more episodes, 75 percent
 Yet even in cases of bilateral tubo-ovarian abcess formation there still remains a 25% chance for
future pregnancy.
 Ectopic pregnancy risk is increased 6 to 10 fold and may reach a 10-percent risk or those who
conceive.
Other complications include;
•chronic pelvic pain (15 to 20 percent),
• recurrent infection (20 to 25 percent),
•abscess formation (5 to 15 percent)
48
Syndromic management
of STI
49
Approaches to STI Case
Management
Etiologic
Clinical
Syndromic
50
Etiologic Approach
ADVANTAGES
• Avoids over treatment
• Satisfies patients who feel not properly
attended to
• Can be used to screen asymptomatic patients
LIMITATIONS
• Requires skilled personnel and sophisticated
Lab equipment
• Lab tests are expensive, time consuming and
results may not be reliable
• Delay in treatment
• Mixed infections often overlooked
51
Clinical Approach
ADVANTAGES
• Saves time for patients
• Reduces Lab expenses
LIMITATIONS
• Requires high clinical skill
• Mixed infections often overlooked
• Doesn’t identify asymptomatic STIs
52
Syndromic approach
ADVANTAGES
• Complete STI care offered at first visit
• Simple, rapid and inexpensive
• Patients treated for possible mixed infections
• Curtails unnecessary referral to hospitals
LIMITATIONS
• Risk of over- treatment
• Asymptomatic infections are missed
• Requires prior research to determine the
common causes of particular syndromes
53
Components of the syndromic approach
Classification by Syndrome:
Classifying the main causal pathogens by the syndromes they produce
Use of Algorithms:
Using flowcharts to guide the management of a given syndrome
Treatment and Counseling:
Using often more than one treatment that addresses all the pathogens with potential to cause a given syndrome
Treatment of Partners:
Promoting treatment of sex partners
54
The STI syndromes
 Urethral discharge in men
 Genital ulcer
 Vaginal discharge
 Lower abdominal pain in women
 Inguinal bubo
 Scrotal swelling
 Neonatal conjunctivitis
55
Urethral discharge
56
RECURRENT/PERSISTENT URETHRAL
DISCHARGE SYNDROME
57
Genital Ulcer syndrome
58
Vaginal discharge syndrome
59
LOWER ABDOMINAL PAIN/PELVIC
INFLAMMATORY DISEASE (PID)
60
Scrotal swelling syndrome
61
Inguinal Bubo syndrome
62
Neonatal conjunctivitis
63
References
• Williams gynecology 3rd edition
• Williams obstetrics 25th edition
• FDRE. MOH. NATIONAL GUIDELINES FOR THE MANAGEMENT OF SEXUALLY TRANSMITTED
INFECTIONS USING SYNDROMIC APPROACH, 2015
• WHO GUIDELINE ON Syphilis screening and treatment for pregnant women 2017
• UP-TO-DATE 2018
64

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Sexually transmitted infections and pelvic inflammatory disease

  • 1. Sexually transmitted infections and pelvic inflammatory disease PREPARED BY: EYOB HABTAMU (MD/009/2015) MODERATOR: DOCTOR MEKONEN 1
  • 2. OUTLINE • Introduction to the normal vaginal flora • Bacterial vaginosis • Genital ulcers • Infectious vaginitis • Supparative cervicitis • Pelvic inflammatory disease • Syndromic management of STIs 2
  • 3. INTRODUCTION  The vaginal flora of a normal, asymptomatic reproductive-aged woman includes multiple aerobic, facultative anaerobic, and obligate anaerobic species.  These bacteria exist in a symbiotic relationship with the host and are alterable, depending on the microenvironment.  Certain bacterial species normally found in vaginal flora have access to the upper reproductive tract.  Typically, the vaginal pH ranges between 4 and 4.5.  Some conditions predispose to the altering of the vaginal flora: post menopausal state, menstruation, treatment with broad spectrum antibiotics. 3
  • 5. 1- Bacterial vaginosis • This common, and poorly understood clinical syndrome reflects abnormal vaginal flora. • The vaginal flora’s symbiotic relationship shifts or unknown reasons to one in which anaerobic species overgrow and include Gardnerella vaginalis, Ureaplasma urealyticum, Mobiluncus species, Mycoplasma hominis, and Prevotella species. • Not considered an STI even if BV is associated with sexual contact with multiple and new male and female partners, and condom use lowers the risk. 5
  • 6. Bacterial vaginosis (clinical picture) • Bacterial vaginosis is the most common cause of vaginal discharge among reproductive-aged women. • A nonirritating, malodorous vaginal discharge is characteristic, but may not always be present. • The vagina is usually not erythematous, and cervical examination reveals no abnormalities. • Clinical diagnostic criteria [Amsel (1983)]: (1) microscopic evaluation of a vaginal-secretion saline preparation, (2) release of volatile amines produced by anaerobic metabolism, (3) determination of the vaginal pH. 6
  • 7. Bacterial vaginosis (clinical picture) • A wet preparation may show clue cells (95% positive predictive value). • The “whiff test” uses 10% KOH to release a fishy odor. • The finding of both clue cells and a positive whiff test result is pathognomonic, even in asymptomatic patients. • Nugent Score: scores based on assessing bacteria staining and morphology. 7
  • 8. BV (adverse effects and management)  Vaginitis,  Endometritis,  Postabortal endometritis,  Pelvic inflammatory disease (PID) unassociated with N gonorrhoeae or Chlamydia trachomatis,  Acute pelvic infections following pelvic surgery, (esp. hysterectomy)  Elevated risk o preterm delivery 8
  • 9. 2- Genital ulcer infections • Ulceration defines complete loss of the epidermal covering with invasion into the underlying dermis. • Erosion describes partial loss of the epidermis without dermal penetration. • Cause of genital ulcers include; HSV, syphilis, LGV, chancroid, granuloma inguinale • All are essentially sexually transmitted therefore partners should be involved in management . • High association with HIV transmission (Co-testing advised) 9
  • 10. A- Herpes simplex infection • Is the most common cause for genital ulcers (developed nations). • Undergoes retrograde axonal transport to the dorsal root ganglion, where the virus develops lifelong latency. • Most women who have been infected with HSV-2 lack this diagnosis because of mild or unrecognized infections. • Infected patients can shed infectious virus while asymptomatic, • Most infections are transmitted sexually by patients who are unaware of their infection. 10
  • 11. Herpes simplex infection • Symptoms at initial presentation will depend primarily on whether or not a patient during the current episode has antibody rom previous exposure. • The three stages o lesions are: (1) vesicle with or without pustule formation, which lasts approximately a week; (2) ulceration; (3) crusting. • Virus is predictably shed during the first two phases of an infectious outbreak. • In addition dysuria, vulvar swelling causing urethral obstruction, vaginal, cervical, bladder, anal and rectal lesions can be present. • Other signs of viremia such as a low-grade ever, headache, malaise, and myalgia are usually present . • Hepatitis, encephalitis, or pneumonia infrequently develop, and disseminated disease is rare. 11
  • 12. Herpes simplex infection (course)  For a previously uninfected patient, • The vesicular stage is longer. • The vesicular stage, period of new lesion formation and time to healing are both longer. • Pain persists for the first 7 to 10 days, and lesion healing requires 2 to 3 weeks.  Prior exposure to HSV-2, • Episode is significantly less severe, with shorter pain and tenderness duration, • Time to healing approximates 2 weeks. • Virus is shed usually only during the first week. 12
  • 13. Herpes simplex infection (management) • Antiviral therapy • Analgesia • Prevention of secondary infection • Patient education • Suppressive therapy if indicated 13
  • 14. HSV in pregnancy • Virus poses a disproportionately higher risk to the newborn than to the mother. • The virus can be passed to the fetus/neonate by three routes: (1) peripartum in 85 percent, (2) postnatal in 10 percent, (3) intrauterine in 5 percent (James, 2015). • For a primary outbreak during pregnancy, women may be given antiviral therapy to attenuate and decrease the duration of symptoms and viral shedding • Women with HIV co-infection may require a longer duration of treatment. • For intense discomfort, oral analgesics and topical anesthetics may provide some relief, and comorbid urinary retention is treated with an indwelling bladder catheter. 14
  • 15. HSV in pregnancy • Cesarean delivery is indicated for women with active genital lesions or prodromal symptoms. • An active lesion in a nongenital area is not an indication for cesarean delivery. occlusive dressing is placed, and vaginal delivery is allowed. • In cases of prematurely ruptured membranes with active lesions there is not an absolute duration of membrane rupture beyond which the fetus would not benefit from cesarean delivery. • Viral therapy at or beyond 36 weeks for women who had primary genital herpes infection or active recurrent genital herpes during pregnancy. • Women with active HSV may breastfeed if there are no active breast lesions. • Acyclovir is safe during breast feeding. 15
  • 16. B- Syphilis • Caused by the spirochete Treponema pallidum, • Women at highest risk are those from lower socioeconomic groups, adolescents, those with early onset o sexual activity, and those with a large number of life time sexual partners. • Divided into four stages: • Primary syphilis, the hallmark lesion is the chancre, in which spirochetes are abundant. • Secondary syphilis, bacteremia develops 6 weeks to 6 months after a chancre appears. Its hallmark is a maculopapular rash that may involve the entire body and includes the palms, soles, and mucous membranes. • Early latent syphilis during the first year following secondary syphilis without treatment, secondary signs and symptoms may recur. However, lesions associated with these outbreaks are not usually contagious. • Tertiary syphilis is the phase of untreated syphilis that may appear up to 20 years after latency. 16
  • 17. Syphilis (diagnosis) Non- Treponemal tests: (1) Venereal Disease Research Laboratory (VDRL) (2) rapid plasma reagin (RPR) tests. Treponemal tests: (1) fluorescent treponemal antibody-absorption (FTA-ABS) (2) Treponema pallidum particle agglutination ( TP-PA) tests • For population screening, RPR or VDRL testing is appropriate. • A positive test result in a woman who has not been treated previously or syphilis or a four fold titer (two dilutions) increase in a woman previously treated or syphilis should prompt confirmation with treponemal specific tests. • A four fold titer decrease is required by 6 months after therapy for primary or secondary syphilis or within 12 to 24 months for those with latent syphilis or women with initially high titers (> 1:32) to document cure. 17
  • 18. Syphilis (management) • Penicillin is the first-line therapeutic agent or this infection, and benzathine penicillin is primarily chosen. • Patients with penicillin allergy who cannot be surveilled post therapy or whose compliance is questioned; skin testing, desensitization, and treatment with IM benzathine penicillin. • After initial treatment, women are seen at 6-month intervals or clinical evaluation and serologic retesting. 18
  • 19. Syphilis and pregnancy • Maternal syphilis can cause fetal infection by several routes. • Transplacental transmission is the most common route, but neonatal infection may follow after contact with spirochetes through lesions at delivery or across the placental membranes. • Without screening and treatment, approximately 70 percent of infected women will have an adverse pregnancy outcome, such as; preterm labor, fetal death, fetal growth restriction, or fetal infection. • The newborn may have jaundice with petechiae or purpuric skin lesions, lymphadenopathy, rhinitis, pneumonia, myocarditis, nephrosis, or long-bone involvement 19
  • 20. Syphilis and pregnancy • Following maternal diagnosis, sonographic evaluation is performed for fetuses >20 weeks’ gestation to search for signs of congenital syphilis. • 31 percent of infected women diagnosed at ≥18 weeks’ gestation had abnormal fetal sonographic findings. • Hepatomegaly, placental thickening, hydramnios, ascites, hydrops fetalis, and elevated middle cerebral artery Doppler velocimetry measurements are indicative of fetal infection. • For fetuses of viable age with sonographic findings, antepartum fetal heart rate monitoring prior to treatment is recommended 20
  • 21. C- Chancroid • Caused by a nonmotile, non-spore- forming, facultative, gram-negative bacillus, Haemophilus ducreyi. • Chancroid lacks a systemic reaction and prodrome. Infection presents initially with an erythematous papule that becomes pustular and ulcerates within 48 hours. • The most common locations in women include the fourchette, vestibule, clitoris, and labia. • Recommended regimens for non-pregnant women include single doses o oral azithromycin (1 g) or IM ceftriaxone (250 mg). • Multiple-dose options are ciprofloxacin 500 mg orally twice daily or 3 days or erythromycin 500 mg orally three times daily or 7 days. • Successful treatment leads to symptomatic improvement within 3 days, and objective evidence of improvement within 1 week. • Treatment failure is more common in RVI patients. 21
  • 22. D- Granuloma inguinale • Also known as donovanosis, and is caused by Calymmatobacterium (Klebsiella) granulomatis • Disease is only mildly contagious, requires repeated exposures, and has a long incubation period of weeks to months. • Presents as a painless inflammatory nodule that progress to highly vascular, beefy red ulcers that bleed easily on contact. (painful if secondarily infected) • Diagnosis is by identification of Donovan bodies during microscopic evaluation of a specimen following Wright-Giemsa staining. • If successfully treated, improvement will be evident within the first few treatment days. But relapses can occur as much as 18 months post therapy. 22
  • 23. E- Lymphogranuloma venerum • Is an ulcerative genital disease is caused by trachomatis serotypes L1, L2, and L3. • Usually found in lower socioeconomic groups among persons with multiple sexual partners. • Clinical course is divided into three stages: (1) small vesicle or papule, (2) inguinal or femoral lymphadenopathy, (3) anogenitorectal syndrome. • LGV may be diagnosed following clinical evaluation with exclusion of other etiologies and positive chlamydial testing. • CDC-recommended regimen is Doxycycline, 100 mg orally twice daily or 21 days or alternatively Erythromycin 500 mg orally four times daily for the same duration. • Sexual contacts within the prior 60 days are tested or urethral or cervical infection and treated. 23
  • 24. Infectious vaginitis • Symptomatic vaginal discharge most o ten reflects BV, candidiasis, or trichomoniasis. • In contrast, if abnormal discharge is associated with vulvar burning, irritation, or itching, then vaginitis is diagnosed. • During evaluation a concise sexual and menstrual history Is taken. • A thorough physical examination of the vulva, vagina, and cervix is also performed. • Wet preps, KOH test and acidity testing can be performed on the vaginal fluid. 24
  • 25. A- Fungal infection • Candida albicans, can be found in the vagina of asymptomatic patients and is a commensal of the mouth, rectum, and vagina. • Warmer climates, obesity, immunosuppression, diabetes mellitus, pregnancy, and recent broadspectrum antibiotic use predispose women to clinical infection. • Pruritus, pain, vulvar erythema, and edema with excoriations are frequent findings • The typical vaginal discharge is described as curdy or cottage cheese-like. KOH prep can visualize the fungus. • 10 to 20 percent of women have complicated candidiasis, which implies greater symptom severity, perhaps involvement o non-albicans species, affected patients with relative immunosuppression, or recurrent disease (four of more episodes per year). 25
  • 26. Fungal infection (management) • For uncomplicated infection, azoles are extremely effective, and women warrant specific follow-up only if therapy is unsuccessful. • For women in these complicated candidiasis categories, cultures are obtained to direct care, and longer therapy may be needed to achieve clinical cure (local intravaginal therapy or 7 to 14 days). • For recurrent disease, local intravaginal therapy or 7 to 14 days or oral fluconazole in 100-mg, 150- mg, or 200-mg doses once every third day or a total of three doses (day 1, 4, and 7) are options. • Suppressive maintenance regimen or recurrence prevention is oral fluconazole, 100 to 200 mg weekly for 6 months. • Non-albicans candida species are not as responsive to topical azole therapy (locsl boric acid is an option) **** Oral fluconazole is generally not considered teratogenic, but in 2016, the FDA released a safety alert regarding a possible link with miscarriage. 26
  • 27. B- Trichomoniasis • Is a protozoan infection be trichomonas vaginalis. • 70 percent of male partners of women with vaginal trichomoniasis will have trichomonads in their urinary tract. • Parasite is usually a marker of high-risk sexual behavior, and co-infection with other sexually transmitted pathogens is common, especially N gonorrhoeae. • The vagina, urethra, endocervix, and bladder can be infected. • Vertical transmission during birth is possible and may persist or a year. • 50% are asymptomatic and may stay so for years. • vaginal discharge is typically described as foul, thin, and yellow or green. • Additionally, dysuria, dyspareunia, vulvar pruritus, vaginal spotting, and pain may be noted. 27
  • 28. Trichomoniasis • At times, clinical findings are identical to those o acute PID. • With trichomoniasis, the vulva may be erythematous, edematous, and excoriated. • The vagina contains the discharge just described, and subepithelial hemorrhages or “strawberry spots” dot the vagina and cervix. • Microscopic identification of motile parasites in a saline preparation o the discharge is diagnostic (60-80% sensitivity). • Women with trichomoniasis are tested or other STDs. • Additionally, sexual contact(s) are evaluated or re erred or evaluation. 28
  • 29. Trichomoniasis (management) • Oral regimens are either metronidazole 2g once or tinidazole 2 g once. • Oral metronidazole 500 mg BID for 7 days may be more effective in compliant patients. • Affected women are retested within 3 months o treatment. Recurrence occurs in approximately 30 percent of patients. • Patients are reminded to abstain rom sex until they and their partners are cured. Condom use may be protective. • Resistant organisms are sensitive to tinidazole. • Metronidazole is not teratogenic, but best avoided in the first trimester. 29
  • 30. 30
  • 31. Suppurative cervicitis Can be due to: A.Neisseria gonorrhea B. Chlamydia tracomatis C. Mycoplasma genitalium 31
  • 32. A- Gonorrhea • N gonorrhoeae is a gram-negative coccobacillus that invades columnar and transitional epithelial cells, becoming intracellular. • Symptomatic lower female reproductive tract gonorrhea may present as vaginitis or cervicitis. • Those with cervicitis commonly describe a profuse odorless, nonirritating, and white-to yellow vaginal discharge. • Patients may report intermenstrual or postcoital vaginal bleeding, or gentle passage of a cotton swab into the cervical os often produces endocervical bleeding. • Gonococcus can also infects the Bartholin and Skene glands, the urethra, and ascend into the endometrium and fallopian tube to cause upper reproductive tract infection 32
  • 33. Gonorrhea • Many women with cervical N gonorrhoeae are asymptomatic. For this reason, women at risk are screened periodically. • Risk actors or gonococcal carriage that merit screening are:  age ≤ 24 years,  prior or current STDs,  new or multiple sexual partners,  a partner with other concurrent partners,  a partner with an STD,  lack of barrier protection in those without a monogamous relationship,  and commercial sex work 33
  • 34. Gonorrhea • Sexual contacts from the preceding 60 days are evaluated and treated or referred for this. • Abstinence is practiced until therapy is completed and until they and their treated sexual partners have symptom resolution. • In cases of cephalosporin allergy, single doses of gentamicin 240 mg IM plus oral azithromycin 2 g. • Untreated gonococcal cervicitis is associated with septic abortion, infection after voluntary abortion, Preterm delivery, prematurely ruptured membranes, chorioamnionitis, and postpartum infection. • Repeat testing is recommended in the third trimester for any woman treated for gonorrhea in the first trimester and for any uninfected woman who is at high risk for gonococcal infection ( 34
  • 35. B- Chlamydia • Is caused by an obligate intracellular organism; Chlamydia Tracomatis • It infects columnar epithelial cells, and endocervical glandular infection leads to mucopurulent discharge or endocervical secretions.(can also cause uretritis) • Diagnosis can be confirmed by microscopy, or NAAT of endocervical/vaginal swab samples. • If C trachomatis is diagnosed or suspected, then screening or other S Ds is indicated. • It is disputed whether untreated cervical infection increases the risk of preterm delivery, preterm ruptured membranes, low birthweight, or perinatal mortality. • Known to cause delayed postpartum metritis characterized by vaginal bleeding or discharge, low-grade fever, and uterine tenderness. • Neonatal conjunctivitis and pneumonia are also associated with chlamydial infection. 35
  • 36. C- Mycoplasma genitalium • Role in female lower reproductive tract pathology is poorly defined. • Most women carriers are asymptomatic, but it has been linked in some studies to urethritis, cervicitis, PID, and later to tubal- actor infertility. • Azithromycin 1 g orally once is recommended. • moxifloxacin 400 mg once orally or 7 to 14 days in women with PID who fail to respond to other treatment and mycoplasma is detected. 36
  • 38. Introduction • Is an infection o the upper female reproductive tract organs (yet the organ of importance is the fallopian tube). • Classified as silent, acute and chronic PIDs. • Low threshold for diagnosis is necessary due to its known complications;  Ectopic pregnancy  Tubal infertility  Chronic pelvic pain • Risk factors; Douching Single status Substance abuse Multiple sexual partners Lower socioeconomic status Recent new sexual partner(s) Younger age (10 to 19 years) Other STI Sexual partner with STI Previous diagnosis of PID Not using l contraceptive barriers 38
  • 39. Microbiology • Classic salpingitis is associated with and secondary to N gonorrhoeae infection, and C trachomatis is also commonly recovered. • Upper tract infection is believed to be caused by bacteria that ascend rom the lower reproductive tract. • Women with pulmonary tuberculosis can develop salpingitis and endometritis. • The fallopian tubes also can be infected by direct extension from inflammatory GI disease. 39
  • 40. Silent PID • Silent PID is not a clinical diagnosis. Rather, it is an ultimate diagnosis given to women with tubal- actor infertility who lack a history compatible with upper tract infection. • is thought to follow multiple or continuous low-grade infection in asymptomatic women. • Grossly the fallopian tubes are normal (may have adhesions though) • Internally, however, tubes show flattened mucosal olds, extensive deciliation of the epithelium, and secretory epithelial cell degeneration. • Alternatively hydrospalphinx may be found on sonography or gross inspection. • Adhesions between the liver and anterior abdominal wall can also be considered as evidence for prior infection. 40
  • 41. Acute PID • Represents a spectrum of clinical disease, from mild, vague pelvic symptoms to tubo-ovarian abscess and, rarely, fatal intra-abdominal sepsis. • is characterized by the acute onset of lower abdominal or pelvic pain, pelvic organ tenderness, and evidence of inflammation of the genital tract. • PID is diagnosed clinically if uterine tenderness, adnexal tenderness, or cervical motion tenderness is present. One or more of the following enhances diagnostic specificity: • (1) oral temperature > 38.3°C (101.6°F), • (2) mucopurulent cervical discharge or cervical friability, • (3) abundant WBCs on saline microscopy of cervical secretions, • (4) elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP), • (5) presence of cervical N gonorrhoeae or C trachomatis. 41
  • 42. Criteria Based on laparoscopic studies fulfillment of ceratin criteria increased the chances of PID presence; (1) single status, (2) adnexal mass, (3) age < 25 years, (4) temperature > 38°C, (5) cervical N gonorrhoeae, (6) purulent vaginal discharge, and (7) ESR ≥ 15 mm/hr - 97-percent accurate if a woman meets all seven criteria, 42
  • 43. Acute PID • With acute PID, symptoms characteristically develop during or soon following menstruation. • These include abdominal and/or pelvic pain, yellow vaginal discharge, heavy menstrual bleeding, ever, chills, anorexia, nausea, vomiting, diarrhea, dysmenorrhea, dyspareunia and signs consistent with a urinary tract infection. • leucorrhea or mucopurulent endocervicitis is common and is diagnosed visually and microscopically • During bimanual pelvic examination, affected women will usually have pelvic organ tenderness. • RUQ abdominal pain and other signs may suggest perihepatits. • During examination, if all abdominal quadrants are involved, suspicion or a ruptured tuboovarian abscess ( OA) is heightened. 43
  • 45. Investigations in Acute PID In women with lower abdominal pain, tests directed at diagnosing PID or excluding other pain sources are selected. LAB: CBC, urinalysis, Beta-Hcg, LFT, saline preparation of cervical discharge, testing for other STIs Sonography: in acute tubal inflammation the sonographic appearance inclides (1) distended, ovoid-shaped tube filled with anechoic or echogenic fluid, (2) fallopian tube wall thickening, (3) incomplete internal septa, (4) a “cogwheel” appearance when inflamed tubes are imaged in cross section. In women with right upper quadrant pain suggestive o perihepatitis, chest radiography or upper abdominal sonography may be needed to exclude other pathology. 45
  • 46. Tubo-ovarian abscess • With infection, the inflamed and suppurative fallopian tube can adhere to the ovary. • “tuboovarian complex” - both tube and ovary are recognizable, • “tuboovarian abscess” - tissue planes and distinction between the two is lost • Tuboovarian abscesses are typically unilateral and may also involve adjacent structures that include bowel, bladder, and contralateral adnexa. • Microorganisms frequently cultured include E coli, Bacteroides spp, Peptostreptococcus spp, and aerobic Streptococcus spp. • Most will respond to intravenous (IV) antibiotic therapy alone and avoid the need or drainage. • Parenteral antimicrobial therapy is continued until the patient has been afebrile or at least 24 hours, preferably 48 to 72 hours. 46
  • 47. Management of PID • The primary therapy goal is to eradicate bacteria, relieve symptoms, and prevent sequelae. • In women with a mild to moderate clinical presentation, outpatient treatment and inpatient therapy yield similar results. • If patients are treated as outpatients, an initial parenteral dose may be beneficial. • Women treated as outpatients are reevaluated in approximately 72 hours. • If not responding to oral therapy within 72 hours, parenteral therapy is initiated.(assuming • diagnosis is confirmed at reevaluation) • IUDs must be removed in severe disease or if patient fails to resolve in 48-72 hours. 47
  • 48. Prognosis  The most successful patient outcomes follow early diagnosis and prompt, appropriate therapy.  Infertility is a major concern with rates following one episode approximate 15 percent; two episodes, 35 percent; and three or more episodes, 75 percent  Yet even in cases of bilateral tubo-ovarian abcess formation there still remains a 25% chance for future pregnancy.  Ectopic pregnancy risk is increased 6 to 10 fold and may reach a 10-percent risk or those who conceive. Other complications include; •chronic pelvic pain (15 to 20 percent), • recurrent infection (20 to 25 percent), •abscess formation (5 to 15 percent) 48
  • 50. Approaches to STI Case Management Etiologic Clinical Syndromic 50
  • 51. Etiologic Approach ADVANTAGES • Avoids over treatment • Satisfies patients who feel not properly attended to • Can be used to screen asymptomatic patients LIMITATIONS • Requires skilled personnel and sophisticated Lab equipment • Lab tests are expensive, time consuming and results may not be reliable • Delay in treatment • Mixed infections often overlooked 51
  • 52. Clinical Approach ADVANTAGES • Saves time for patients • Reduces Lab expenses LIMITATIONS • Requires high clinical skill • Mixed infections often overlooked • Doesn’t identify asymptomatic STIs 52
  • 53. Syndromic approach ADVANTAGES • Complete STI care offered at first visit • Simple, rapid and inexpensive • Patients treated for possible mixed infections • Curtails unnecessary referral to hospitals LIMITATIONS • Risk of over- treatment • Asymptomatic infections are missed • Requires prior research to determine the common causes of particular syndromes 53
  • 54. Components of the syndromic approach Classification by Syndrome: Classifying the main causal pathogens by the syndromes they produce Use of Algorithms: Using flowcharts to guide the management of a given syndrome Treatment and Counseling: Using often more than one treatment that addresses all the pathogens with potential to cause a given syndrome Treatment of Partners: Promoting treatment of sex partners 54
  • 55. The STI syndromes  Urethral discharge in men  Genital ulcer  Vaginal discharge  Lower abdominal pain in women  Inguinal bubo  Scrotal swelling  Neonatal conjunctivitis 55
  • 64. References • Williams gynecology 3rd edition • Williams obstetrics 25th edition • FDRE. MOH. NATIONAL GUIDELINES FOR THE MANAGEMENT OF SEXUALLY TRANSMITTED INFECTIONS USING SYNDROMIC APPROACH, 2015 • WHO GUIDELINE ON Syphilis screening and treatment for pregnant women 2017 • UP-TO-DATE 2018 64

Hinweis der Redaktion

  1. anaerobes predominate and outnumber aerobic species approximately 10 to 1. Within this vaginal ecosystem, some microorganisms produce substances such as lactic acid and hydrogen peroxide that inhibit nonindigenous organisms (Marrazzo, 2006). Several other antibacterial compounds, termed bacteriocins, play a similar role. For protection rom many o these toxic substances, a secretory leukocyte protease inhibitor is ound in the vagina. T is protein protects local tissues against toxic in ammatory products and in ection. --- Lactobacillus species contribute by production o lactic acid, atty acids, and other organic acids. Other bacteria can also add organic acids rom protein catabolism, and anaerobic bacteria donate by amino acid ermentation. Glycogen, which is present in healthy vaginal mucosa, provides nutrients or many vaginal ecosystem species and is metabolized to lactic acid (Boskey, 2001). Accordingly, as glycogen content within vaginal epithelial cells diminishes a ter menopause, this decreased substrate or acid production leads to a rise in vaginal pH. Speci cally, i no pH-altering pathogens are present, a vaginal pH o 6.0 to 7.5 is strongly suggestive o menopause (Caillouette, 1997).
  2. Bacterial vaginosis (BV) is also associated with a signi cant reduction or absence o normal hydrogen peroxideproducing Lactobacillus species. -- Whether an altered ecosystem leads to lactobacilli disappearance or whether its disappearance results in the changes observed with BV is unclear.
  3. PH is greater than 4.5 in BV.
  4. At least 20 percent o the e.pithelial cells should be clue cells Similarly, Trichomonas vaginalis in ection is also associated with anaerobic overgrowth and resultant elaborated amines. T us, women diagnosed with BV should have no microscopic evidence o trichomoniasis.
  5. 80-90% cure rates in one week. 30% recurrent abnormal growth in 3 months.
  6. Asymptomatic viral shedding is defined by the absence of clinical findings. Most infected women shed virus intermittently over time, and most HSV transmission to a partner occurs during these periods of asymptomatic viral shedding.
  7. -If a patient has no antibody, the attack rate in an exposed person approaches 70 percent. T e mean incubation period is approximately 1 week. Up to 90 percent o those who are symptomatic with their initial infection will have another episode within a year.
  8. Diagnosis T e gold standard or the diagnosis o genital herpes is tissue culture. Speci city is high, but sensitivity is low and declines as lesions heal. In recurrent disease, less than 50 percent o cultures are positive. Polymerase chain reaction (PCR) testing o exudate swabbed rom the ulcer is many times more sensitive than culture and will probably replace it. Importantly, a negative culture result does not mean that there is no herpetic in ection. Serologic testing may also add clarity. T e herpes simplex virus is surrounded by envelope glycoproteins, and o these, glycoprotein G is the antigen o interest or antibody screening. Serologic assays can detect antibodies speci c to the HSV type-speci c glycoprotein G2 (HSV-2) and glycoprotein G1 (HSV-1). Assay speci city is ≥ 96 percent, and the sensitivity o HSV-2 antibody testing ranges rom 80 to 98 percent. Importantly, with serologic screening, only IgG antibody assays are ordered. IgM testing can lead to ambiguous results as the IgM assays are not type-speci c and also may be positive during a recurrent outbreak. Although these tests may be used to con rm herpes simplex in ection, seroconversion ollowing initial HSV-2 in ection takes approximately 3 weeks (Ashley- Morrow, 2003). T us, in clinically obvious cases, immediate treatment and additional S D screening can be initiated ollowing physical examination alone. In general, S D screening or a woman ound to have any S D typically includes testing directed to identi y syphilis, gonorrhea, trichomoniasis, and HIV, chlamydial, and hepatitis B in ections. Serologic screening or HSV in the general population is not recommended. However, HSV serologic testing can be considered or HIV-in ected individuals or or women presenting or an S D evaluation, especially or those with multiple partners and or those in demographics with high prevalence (Centers or Disease Control and Prevention, 2015). It can also add management in ormation or couples thought but not con rmed to be discordant or in ection (American College o Obstetricians and Gynecologists, 2014b).
  9. -Patient education is mandatory, and speci c topics include the natural history o the disease, its sexual transmission, methods to reduce transmission, and obstetric consequences. --Women with genital herpes should re rain rom sexual activity with unin ected partners when prodrome symptoms or lesions are present. --Episodic therapy or recurrent disease is ideally initiated at least within 1 day o lesion outbreak or during the prodrome, i it exists. --I episodes recur at requent intervals, a woman may elect daily suppressive therapy, which reduces recurrences by 70 to 80 percent. Suppressive therapy may eliminate recurrences and decreases sexual transmission o virus by approximately 50 percent (Corey, 2004). Once-daily dosing may result in enhanced compliance and decreased cost.
  10. Peripartum transmission is by far the more frequent route of infection, and the fetus is exposed to virus shed from the cervix or lower genital tract. HSV-1 or -2 invades the uterus following membrane rupture or is transmitted by contact at delivery. The newborn is mainly infected, but rare cases of maternal endometritis have been described (Hollier, 1997; McGill, 2012). Neonatal manifestations vary. First, infection may be localized to the skin, eye, or mouth—SEM disease—in approximately 40 percent of cases. Second, central nervous system disease with encephalitis is seen in 30 percent. Last, disseminated disease with involvement of multiple major organs is found in 32 percent. Localized infection is usually associated with a good outcome. Conversely, even with acyclovir treatment, disseminated infection has a mortality rate of nearly 30 percent (Corey, 2009; Kimberlin, 2011). Of disseminated or cerebral infection survivors, serious developmental and central nervous system morbidity is seen in 20 to 50 percent. The neonatal infection rate is 0.5 to 1 per 10,000 births in the United States (Flagg, 2011; Mahnert, 2007). Most infected newborns are born to mothers with no reported history of HSV infection (Gardella, 2010). The risk of neonatal infection correlates with the presence of HSV in the genital tract, the HSV type, invasive obstetrical procedures, and stage of maternal infection (Brown, 2005, 2007). For example, neonates born to women who acquire genital HSV near the time of delivery have a 30- to 50-percent risk of infection. This is attributed to higher viral loads and the lack of transplacental protective antibodies (Brown, 1997, 2000). Women with recurrent HSV have less than a 1-percent risk of neonatal infection (Pasternak, 2010; Prober, 1987). Postpartum transmission is uncommon and passed to the newborn by contact with an infected mother, family member, or health-care worker. The clinical presentation mirrors that with peripartum transmission. In utero transmission of HSV-1 or HSV-2 is rare and is part of the TORCH (toxoplasmosis, other, rubella, cytomegalovirus, herpes virus) collection of infections. Intrauterine HSV infection classically leads to disease involving the skin (blisters, scarring), the central nervous system (hydranencephaly, microcephaly, intracranial calcification), or the eyes (chorioretinitis, microphthalmia) (Hutto, 1987). Bone and viscera can be involved (Marquez, 2011). If seen sonographically, findings should prompt viral serological testing as described next. PCR analysis of an amniocentesis sample is another potential tool (Diguet, 2006). ----Those with severe or disseminated HSV are given IV acyclovir, 5 to 10 mg/kg every 8 hours for 2 to 7 days until clinically improved. This is followed by oral antiviral drugs to complete at least 10 days of total therapy
  11. With primary syphilis, the hallmark lesion is the chancre, in which spirochetes are abundant. Classically, it is an isolated nontender ulcer with raised rounded borders and an unin ected base (Fig. 3-3). However, it may become secondarily in ected and pain ul. Chancres are o ten ound on the cervix, vagina, or vulva but may also orm in the mouth or around the anus. T is lesion can develop 10 days to 12 weeks a ter exposure, with a mean incubation period o 3 weeks. T e incubation period is directly related to inoculum size. Without treatment, these lesions spontaneously heal in up to 6 weeks. --With secondary syphilis, bacteremia develops 6 weeks to 6 months a ter a chancre appears. Its hallmark is a maculopapular rash that may involve the entire body and includes the palms, soles, and mucous membranes (Fig. 3-4). As is true or the chancre, this rash actively sheds spirochetes. In warm, moist body areas, this rash may produce broad, pink or gray-white,
  12. However, some women may have a persistent low titer, and these patients are described as sero ast. Moreover, women with a reactive treponemal-speci c test will more than likely have a positive test or the remainder o their lives, but up to 25 percent may revert to a negative result a ter several yea
  13. Fetal infection develops in >50 percent of untreated early syphilis cases and in 10 percent of late latent disease. Because of immune incompetence prior to midpregnancy, the fetus generally does not manifest the immunological inflammatory response characteristic of clinical disease before this time (Silverstein, 1962). Once fetal syphilis develops, however, it manifests as a continuum. Fetal hepatic abnormalities are followed by anemia and thrombocytopenia, then ascites and hydrops (Hollier, 2001). Stillbirth remains a major complication (Lawn, 2016; Su, 2016). The newborn may have jaundice with petechiae or purpuric skin lesions, lymphadenopathy, rhinitis, pneumonia, myocarditis, nephrosis, or long-bone involvement
  14. Before 20 weeks, treatment is highly successful, and sonographic findings are rare. --- For fetuses of viable age with sonographic findings, antepartum fetal heart rate monitoring prior to treatment is recommended. Spontaneous late decelerations or a nonreactive tracing likely reflects an extremely ill fetus that may poorly tolerate a Jarisch-Herxheimer reaction, described next. In this extreme case, consultation with a neonatologist regarding a plan of delaying treatment, pursuing delivery, and then treating in the nursery is a consideration (Wendel, 2002).
  15. -- Edges o these pain ul ulcers are usually irregular with erythematous nonindurated margins. T e ulcer bases are usually red and granular and, in contrast to a syphilitic chancre, are typically so t. Lesions are requently covered with purulent material and may become secondarily in ected. -- Ulcers on the cervix or vagina may be nontender ---Success ul treatment leads to symptomatic improvement within 3 days, and objective evidence o improvement within 1 week. Lymphadenopathy resolves more slowly, and i uctuant, incision and drainage may be warranted.
  16. Lymph nodes are usually uninvolved but can become enlarged, and new lesions can appear along these lymphatic drainage channels
  17. -----Initial papules appear primarily on the ourchette and posterior vaginal wall up to and including the cervix. Repeated inoculation may result in lesions at multiple sites. hese primary lesions heal quickly and without scarring. -------During the second stage, sometimes re erred to as the inguinal syndrome, inguinal and emoral lymph nodes progressively enlarge. Pain ul nodes can mat together on either side o the inguinal ligament and create a characteristic “groove sign,” which appears in up to one th o in ected women (Fig. 3-5). Moreover, enlarging nodes may rupture through the skin and lead to chronically draining sinuses. Women with lymphogranuloma venereum (LGV) commonly develop systemic in ection, mani est by malaise and ever. Additionally, pneumonitis, arthritis, and hepatitis have been reported. -------In the third stage o LGV, a patient develops rectal pruritus and a mucoid discharge rom rectal ulcers. I these become in ected, the discharge turns purulent. T is presentation stems rom lymphatic obstruction that ollows lymphangitis and that may result in elephantiasis o external genitalia initially and brosis o the rectum. Stenosis o the urethra and the vagina has also been reported. Rectal bleeding is common, and a woman may complain o crampy, abdominal pain with abdominal distention, rectal pain, and ever. Peritonitis may ollow bowel per oration. ---------
  18. Between 7 and 70 percent o women who have vaginal discharge complaints will have no de nitive diagnosis ===For those in whom identi able in ection is absent, an in ammatory diagnosis and treatment or in ection should not be given. In such instances, a woman may seek reassurance, having concern about a recent sexual exposure, and S D screening may alleviate this.
  19. It can be sexually transmitted, and several studies have reported an association between candidiasis and orogenital sex (Bradshaw
  20. Oral azole therapy has been associated with serum liver enzyme elevation. T us, prolonged oral therapy may not be easible or that reason or because o interactions with other patient medications such as calcium-channel blockers, war arin, protease inhibitors, trimetrexate, ter enadine, cyclosporine A, phenytoin, and ri ampin. In these cases, local intravaginal therapy once or twice weekly may give a similar clinical response
  21. Trichomonas vaginalis has predilection or squamous epithelium, and lesions may increase accessibility to other sexually transmitted species.
  22. However, trichomonads are less motile with cooling, and slides ideally are examined within 20 minutes.
  23. Patients are instructed to abstain from sexual intercourse for 7 days after they and their sexual partners have completed treatment. ----Gonococcal bacteremia may cause disseminated infections that manifest as petechial or pustular skin lesions, arthralgias, or septic arthritis. For treatment of septic arthritis, the CDC recommends ceftriaxone, 1 g intramuscularly or intravenously (IV) every 24 hours plus a single 1-g oral dose of azithromycin (Workowski, 2015). Treatment is continued for 24 to 48 hours after clinical improvement, and therapy is then changed to an oral agent to complete 1 week of therapy. Prompt recognition and antimicrobial treatment will usually yield favorable outcomes in pregnancy (Bleich, 2012). Meningitis and endocarditis rarely complicate pregnancy, but they may be fatal (Bataskov, 1991; Burgis, 2006). For gonococcal endocarditis, ceftriaxone 1 to 2 g IV every 12 hours should be continued for at least 4 weeks, and for meningitis, 10 to 14 days. A single 1-g oral dose of azithromycin is also provided for chlamydial co-infection (Workowski, 2015).
  24. Delaye metritis -2-3 weeks post delivery. -- Chlamydial testing is repeated 3 to 4 weeks after therapy completion and again 3 months after treatment. In high-risk individuals, third-trimester rescreening is recommended
  25. It has a much more established role in male urethritis
  26. Another species requently ound is T vaginalis. ---In contrast, intracellular C trachomatis does not cause an acute in ammatory response, and little direct permanent damage results rom chlamydial tubal involvement (Patton, 1983). However, cell-mediated immune mechanisms may be responsible or subsequent tissue injury. Speci cally, persistent chlamydial antigens can trigger a delayed hypersensitivity reaction with continued tubal scarring and destruction ( oth, 2000).
  27. Many o these patients have antibodies to C trachomatis and/or N gonorrhoeae
  28. ---Parenteral antimicrobial therapy is continued until the patient has been a ebrile or at least 24 hours, pre erably 48 to 72 hours. In transitioning to oral therapy, doxycycline 100 mg twice daily is combined with either metronidazole 500 mg twice daily or clindamycin 450 mg our times daily to complete a 14-day course. ------For those not improved within 2 to 3 days o treatment, prior to attempts at abscess drainage, antimicrobial regimen modi cation is indicated. Drainage plus antibiotic therapy can be considered as initial treatment or larger abscesses (≥ 8 cm). -----In ection con ned within one organ, such as a pyosalpinx, responds more avorably to antimicrobial therapy because o adequate blood and lymphatic supply. T is is true even i attached to an adjacent ovary. A cul-de-sac or interloop abscess is more likely to require drainage, however, because o poor blood and lymphatic supply and a less prompt response to antimicrobial therapy.
  29. Clinical treatment with oral therapy is also appropriate or women with HIV in ection and PID. T ese women have the same species recovered compared with non-HIV-in ected patients, and their response to therapy is similar. --------women treated as outpatients took 70 percent o prescribed doses, and or less than 50 percent o their outpatient treatment days. --------Another potential clinical decision involves management o a coexistent IUD. During the rst 3 weeks a ter device insertion, patients have an increased IUD-associated PID risk. A ter this time, other PID risks are considered causative. With PID, theoretical concerns are that a coexistent IUD might worsen the in ection or delay resolution. Although a provider may choose to remove the device, evidence supports leaving an IUD during treatment in those hospitalized with mild or moderate PID (Centers or Disease Control and Prevention, 2015; epper, 2013). Severe disease warrants IUD removal. With or without an IUD, women are treated with similar antibiotic regimens. But, i a patient ails to improve within 48 to 72 hours, the device is removed.