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Gynecologic Infections

Genet Gebremedhin(MD)
Assistant Prof of gynecology & obstetrics
University of Gondar
March 4 2012
1
Gynecologic Infections
Gynecologic infections are frequent disorders
for which patients seek care from gynecologists
These infections can be seen as:
1. Pathogens Causing Genital Ulcer
2. Pathogens Causing Infectious Vaginitis
3. Pathogens Causing Suppurative Cervicitis
4. Pathogens Causing Mass Lesions
5. Pathogens Causing Pruritus

2
Normal Vaginal Flora

Vaginal flora of a normal asymptomatic reproductive-aged


woman includes multiple aerobic or facultative species as well as
obligate anaerobic species
Of these, anaerobes are predominant and outnumber aerobic
species approximately 10: 1
The function of and reason for bacterial colonization of the
vagina remains unknown.
Bacteria do exist in a symbiotic relationship with the host and are
alterable, depending on the microenvironment.
These organisms localize where their survival needs are met, and
have exemption from the infection-preventing destructive
capacity of the host.

3
Normal flora contd.
Aerobes Anaerobes
Gram-positive Gram-positive cocci Yeast
Lactobacillus spp Peptostreptococcus spp Candida albicans
Diphtheroids Clostridium spp
Staphylococcus aureus Gram-positive bacilli
Staphylococcus epidermidis Lactobacillus spp
Group B Streptococcus Propionibacterium spp
Enterococcus faecalis Eubacterium spp
Staphylococcus spp Bifidobacterium spp
Gram-negative Gram-negative
Escherichia coli Prevotella spp
Klebsiella spp Bacteroides spp
Proteus spp Bacteroides fragilis group
Enterobacter spp Fusobacterium spp
Acinetobacter spp Veillonella spp
Citrobacter spp
Pseudomonas spp

4
Normal Flora Contd.
Within this vaginal ecosystem, some microorganisms produce
substances such as lactic acid and hydrogen peroxide that inhibit
nonindigenous organisms.
Several other antibacterial compounds, termed bacteriocins,
provide a similar role and include peptides such as acidocin and
lactacin.
Some species have the ability to produce proteinaceous adhesions
and attach to vaginal epithelial cells.
For protection from many of these toxic substances, the vagina
secretes leukocyte protease inhibitor.
This protein protects local tissues against toxic inflammatory
products and infection

5
Normal Flora Contd.
Typically, the vaginal pH ranges between 4 and 4.5.
Although not completely understood, it is believed to result from
Lactobacillus species' production of lactic acid, fatty acids, and other
organic acids.
In addition, amino acid fermentation by anaerobic bacteria results in
organic acid production as does bacterial protein catabolism.
Glycogen present in healthy vaginal mucosa is believed to provide
nutrients for many species in the vaginal ecosystem.
Accordingly, as glycogen content within vaginal epithelial cells diminishes
after menopause, this decreased substrate for acid production leads to a
rise in vaginal pH
Changing any element of this ecology may alter the prevalence of
various species.

6
Normal Flora Contd.
Vaginal flora may be altered by
Menopause
Treatment with a broad-spectrum antibiotic
Menstruation
Total abdominal hysterectomy
Altered vaginal flora results in bacterial vaginosis(BV)
Is not sexually transmitted disease (STD), and
it is seen in women without previous sexual experience.
Successful prevention of BV is limited, but elimination or
diminished use of vaginal douches may be beneficial
7
Bacterial Vaginosis (BV)
BV reflects abnormal vaginal flora, and is poorly understood.
It has been variously named, and former terms include Haemophilus
vaginitis, Corynebacterium vaginitis, Gardnerella or anaerobic vaginitis,
and nonspecific vaginitis.
For unknown reasons, the vaginal flora's symbiotic relationship shifts to
one in which there is overgrowth of anaerobic species including
Gardnerella vaginalis, Ureaplasma urealyticum, Mobiluncus species,
Mycoplasma hominis, and Prevotella species.
Bacterial vaginosis (BV) is also associated with a significant reduction or
absence of the normal hydrogen peroxide-producing Lactobacillus
species.
Whether an altered ecosystem leads to lactobacilli disappearance or
whether its disappearance results in the changes observed with BV is
unknown.
8
Bacterial Vaginosis contd.
Risk Factors of Bacterial Vaginosis
Oral sex
Douching
Black race
Cigarette smoking
Sex during menses
Intrauterine device
Early age of sexual intercourse
New or multiple sexual partners
Sexual activity with other women

9
Bacterial Vaginosis contd.

10
Bacterial Vaginosis contd.
Diagnosis
Nonirritating, malodorous vaginal discharge is characteristic, but may not
always be present.
BV is associated with, vaginitis, endometritis, postabortal endometritis,
pelvic inflammatory disease unassociated with Neisseria gonorrhoeae or
Chlamydia trachomatis, and acute pelvic infections following pelvic surgery,
especially hysterectomy.
The vagina is usually not erythematous, and cervical examination reveals no
abnormalities.
Clinical diagnostic criteria were first proposed by Amsel and associates
(1983) and include:
Microscopic evaluation of a saline "wet prep" of vaginal secretions,
Determination of the vaginal PH, pH is >4.5
Release of volatile amines produced by anaerobic metabolism.
11
Bacterial Vaginosis contd.
Clue cells are epithelial cells contain many attached bacteria, which
create a poorly defined stippled cellular border.
Adding 10 percent potassium hydroxide (KOH) to a fresh sample of
vaginal secretions releases volatile amines that have a fishy odor.
whiff test.
Similarly, alkalinity of seminal fluid and blood are responsible for
odor complaints after intercourse and with menses.
The finding of both clue cells and a positive whiff test is
pathognomonic, even in asymptomatic patients.
Trichomonas vaginalis infection is also associated with anaerobic
overgrowth and resultant elaborated amines.
Women diagnosed with BV should have no microscopic evidence of
trichomoniasis.
12
Bacterial Vaginosis contd.
Treatment
Cure rates 80 to 90 percent at 1 week, but within 3 months,
30 percent of women have experienced a recurrence of
altered flora.
Treatment of male sexual partners does not benefit women
with this recurring condition and is not recommended.

13
Bacterial Vaginosis contd.

Recommended Treatment of Bacterial Vaginosis


Agent Dosage
Metronidazole 500 mg orally twice daily for 7 days
Metronidazole gel 0.75% 5 g (1 full applicator) intravaginally
once daily for 5 days
Clindamycin 300 mg, orally twice daily for 7 days
Clindamycin cream 2% 5 g (1 full applicator) intravaginally at
bedtime for 5 days

14
Pathogens Causing Genital Ulcer
Genital ulcer is complete loss of the epidermal covering with
invasion into the underlying dermis.
Erosion describes partial loss of the epidermis without dermal
penetration.
All are sexually transmitted and are associated with HIV infections
Sexual contacts require examination and treatment
The causes of genital ulcer include
Herpes simplex infection
Syphilis
Chancroid
Lymphogranuloma venereum
granuloma inguinale
15
Herpes Simplex Virus Infection
Genital herpes is the most prevalent genital ulcer disease and is a chronic
viral infection.
The virus enters sensory nerve endings and undergoes retrograde axonal
transport to the dorsal root ganglion, where the virus develops lifelong
latency.
Spontaneous reactivation by various events results in anterograde
transport of virus particles/protein to the surface.
Here virus is shed, with or without lesion formation.
Immune mechanisms control latency and reactivation.
There are two types of herpes simplex virus, HSV-1 and HSV-2.
Type 1 HSV is the most frequent cause of oral lesions.
Type 2 HSV is seen with genital lesions, although both types can cause
genital herpes.

16
Herpes Contd.
Clinical features
The mean incubation period is about 1 week.
Up to 90 percent of those who are symptomatic with their initial infection
will have another episode within a year.
Burning and severe pain accompany initial vesicular lesions, and urinary
symptoms such as frequency and/or dysuria may be present with those of
the vulva.
The virus infects viable epidermal cells, the response to which is erythema
and papule formation.
With cell death and cell wall lysis, blisters form.
The covering then disrupts, leaving a usually painful ulcer.
These lesions develop crusting and heal, but may become secondarily
infected.
17
Herpes Contd.
The three stages of lesions are:
1. Vesicle with or without pustule formation, which lasts about a
week;
2. Ulceration; and
3. Crusting.
Virus is predictably shed during the first two phases of an
infectious outbreak.
Herpetic lesions may involve the vagina, cervix, bladder,
and rectum.
Commonly, a woman may have other signs of viremia such
as a low-grade fever, malaise, and cephalalgia
18
Herpes Contd.
Viral load undoubtedly contributes to the numbers, size, and distribution of lesions.
Normal host defense mechanisms inhibit viral growth, and healing starts within 1 to 2
days.
Early treatment with an antiviral medication decreases the viral load.
For a previously uninfected patient, the vesicular, or initial stage, is longer. There is an
increased period of new lesion formation and a longer time to healing. Pain persists for
the first 7 to 10 days, and lesion healing requires 2 to 3 weeks.
If a patient has had prior exposure to HSV-2, the initial episode is significantly less severe,
with shorter pain and tenderness duration, and time to healing approximates 2 weeks.
Virus is shed usually only during the first week.
Recurrence following HSV-2 infection is common, and almost two thirds of patients have a
prodrome prior to lesion onset.
Heralding paresthesias are frequently described as pruritus or tingling in the area prior to
lesion formation.
prodrome symptoms may develop without actual lesion formation.

19
Herpes Contd.
Diagnosis
The gold standard for the diagnosis of a herpetic lesion(s) is
tissue culture.
Specificity is high, but sensitivity is low, and declines as lesions
heal.
In recurrent disease, less than 50 percent of cultures are positive.
Polymerase chain reaction (PCR) testing is 1.5 to 4 times more
sensitive than culture and will probably replace it.
Importantly, a negative culture result does not mean that there is
no herpetic infection.
The sensitivity of HSV-2 antibody testing ranges from 80 to 98
percent.
20
Herpes Contd.

21
Herpes Contd.
Treatment
Antiviral therapy (hasten healing and decrease symptoms, therapy
does not eradicate latent virus nor affect future history of
recurrent infections)
Analgesia with acetaminophen with codeine
Topical anesthetics such as lidocaine ointment may provide relief.
Local care to prevent secondary bacterial infection is important.
Patient education
See table on the next slide for treatment of herpes genitalis

22
Herpes Contd.
First Clinical Episode of Genital Herpes
Acyclovir 400 mg three times daily for 7 to 10 days or
Acyclovir 200 mg five times daily for 7 to 10 days or
Famciclovir 250 mg three times daily for 7 to 10 days or
Valacyclovir 1 g twice daily for 7 to 10 days
Episodic Therapy for Recurrent Disease
Acyclovir 400 mg three times daily for 5 days or
Acyclovir 800 mg twice daily for 5 days or
Oral Suppressive Therapy Options
Acyclovir 400 mg twice daily
Famciclovir 250 mg twice daily

23
Syphilis
Pathophysiology
Caused by the spirochete Treponema pallidum
The natural history of syphilis in untreated patients
can be divided into four stages.
1. Primary syphilis
2. Secondary syphilis
3. Latent syphilis
4. Tertiary syphilis

24
Syphilis Contd
Primary Syphilis
The median incubation period before clinical manifestations is 21 days
(range 3 to 90 days)
The incubation period is directly related to inoculum size. Without
treatment, these lesions spontaneously heal in up to 6 weeks
The hallmark lesion of this infection is termed a chancre, in which
spirochetes are abundant.
Classically, it is an isolated nontender ulcer with raised rounded borders
and an uninfected but integrated base.
However, it may become secondarily infected and painful.
Chancres are commonly found on the cervix, vagina, or vulva, but may
also form in the mouth or around the anus.

25
Syphilis Contd.

Chancre

26
Syphilis Contd.
Secondary Syphilis
This phase is associated with bacteremia and 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.
As is true for the chancre, this rash actively sheds spirochetes.
In warm, moist body areas, this rash may produce broad, pink or
gray-white, highly infectious plaques called condylomata lata.
Fever, malaise
The kidney, liver, joints, and central nervous system (CNS)
(meningitis) may be involved

27
Syphilis Contd.

Condylomata lata
maculopapular rash
28
Syphilis Contd.
Latent Syphilis
A. Early latent syphilis
Is first year following secondary syphilis without treatment secondary signs and symptoms
may recur.
Lesions associated with these outbreaks are not usually contagious.
B. Late latent syphilis is defined as a period greater than 1 year after the initial
infection.
Tertiary Syphilis
This phase of untreated syphilis may appear up to 20 years after latency. Gummas
During this phase, cardiovascular, CNS, and musculoskeletal involvement become
apparent.
cardiovascular and neurosyphilis are common in males

29
Syphilis Contd.
Diagnosis
Early syphilis is diagnosed by dark-field examination or
direct fluorescent antibody testing of lesion exudate.
In the absence of this positive diagnosis, presumptive
diagnosis may be reached with serologic tests that are
A. Nontreponemal
Venereal disease research laboratory (VDRL) or
Rapid plasma reagin (RPR) tests
B. Treponemal-specific tests may be selected:
Fluorescent treponemal antibody-absorption (FTA-ABS) or
Treponema pallidum particle agglutination (TP-PA) tests.
30
Syphilis Contd.
Treatment
Benzathine penicillin is the treatment of choice.
With treatment, Jarisch-Herxheimer reaction, may occur
After treatment follow up at 6-month intervals for clinical evaluation as well
as serologic retesting.
Following treatment, sequential nontreponemal tests should be performed.
A fourfold titer decrease (two dilutions) is required to define a clinically
significant decline.
During surveillance, the same type test should be used.
These tests usually become nonreactive after treatment and with time.
However, some women may have a persistent low rating, and these patients
are described as serofast.

31
Syphilis Contd.
Recommended Treatment of Syphilis
Primary, secondary, early latent (<1 year) syphilis
Recommended regimen:
Benzathine penicillin G, 2.4 million units IM once
Alternative oral regimens (penicillin-allergic, nonpregnant women):
Doxycycline 100 mg orally twice daily for 2 weeks or
Tetracycline 500 mg orally four times daily for 2 weeks
Late latent, tertiary, and cardiovascular syphilis
Recommended regimen:
Benzathine penicillin G, 2.4 million units IM weekly times 3 doses
Alternative oral regimen (penicillin-allergic, nonpregnant women):
Doxycycline 100 mg orally twice daily for 4 weeks

32
Chancroid
It is caused by a nonmotile, nonspore-forming, facultative, gram-
negative bacillus, Haemophilus ducreyi.
Incubation usually spans 3 to 10 days
Chancroid does not cause a systemic reaction,
Initially as an erythematous papule develops that becomes pustular
and within 48 hours, ulcerates.
Edges of these painful ulcers are usually irregular with erythematous
nonindurated margins.
The ulcer bases are usually red and granular,.
Lesions are frequently covered with purulent material
Fourchette, vestibule, clitoris, and labia are usual locations
Half of patients will develop unilateral or bilateral tender inguinal
lymphadenopathy. If large and fluctuant, they are termed buboes. 33
Chancroid Contd.
Diagnosis
Definitive diagnosis requires growth of H ducreyi on culture media.
A presumptive diagnosis can be made with identification of gram-
negative, nonmotile rods on a Gram stain of lesion contents.
Before obtaining either specimen, superficial pus or crusting should
be removed with sterile, saline-soaked gauze.
Treatment
Successful treatment will result in symptomatic improvement
within 3 days, and objective evidence of improvement within 1
week.
Lymphadenopathy resolves more slowly, and if fluctuant, incision
and drainage may be warranted.
34
Chancroid Contd.

Recommended Treatment of Chancroid


Azithromycin 1 g orally or

Ceftriaxone 250 mg intramuscularly or

Ciprofloxacin 500 mg orally twice daily for 3 days or

Erythromycin base 500 mg orally three times daily for 7 days

35
Granuloma Inguinale
Is also known as donovanosis
Caused by the intracellular gram-negative bacterium
Calymmatobacterium (Klebsiella) granulomatis.
This disease is only mildly contagious, requires repeated exposures, and
has a long incubation period of weeks to months.
Granuloma inguinale presents as painless inflammatory nodules that
progress to highly vascular, beefy red ulcers that bleed easily on contact.
If secondarily infected they may become painful.
These ulcers heal by fibrosis, which can result in scarring resembling
keloids.
Lymph nodes are usually uninvolved, but may become enlarged, and new
lesions may appear along these lymphatic drainage channels
Diagnosis is by identification of Donovan bodies during microscopic
evaluation of a specimen following Wright- Giemsa staining.
36
Granuloma Inguinale Contd.

Recommended Treatment of Granuloma Inguinale


Doxycycline 100 mg twice daily for a minimum of 3 weeks and until lesions
have completely healed or
Azithromycin 1 g orally once a week as above or

Ciprofloxacin 750 mg orally twice daily as above or

Erythromycin base 500 mg orally four time daily as above or

Trimethoprim-sulfamethoxazole DS orally twice daily as above

37
Lymphogranuloma Venereum (LGV)

This ulcerative genital disease is caused by Chlamydia trachomatis,


serotypes L1, L2, and L3.
The chlamydial life cycle is comprised of three stages.
Initially, infective particles (elementary bodies) penetrate a host cell.
Here they develop into metabolically active reticulate bodies.
Binary fission within the cell allows reticulate bodies to transform
themselves into multiple elementary bodies, which are released by
exocytosis.
This infection is commonly divided into three stages as follows:
Stage 1— Small vesicle or papule;
stage 2— Inguinal or femoral lymphadenopathy; and
stage 3— Anogenitorectal syndrome.

38
Lymphogranuloma Venereum Contd.

"groove" sign

39
Lymphogranuloma Venereum Contd.

Incubation for this infection ranges from 3 days to 2 weeks.


Initial papules heal quickly and without scarring.
They appear primarily on the fourchette and posterior vaginal wall up to
and including the cervix.
During the second stage, sometimes referred to as the inguinal syndrome,
progressive enlargement of inguinal and femoral lymph nodes is observed.
Enlarged painful nodes can mat together and create a characteristic
"groove sign", which appears in up to one fifth of infected women.
In addition, enlarging nodes may rupture through the skin, and chronically
draining sinuses may result.
LGV develop systemic infection with chlamydia and manifest malaise and
fever.
Pneumonitis, arthritis, and hepatitis have been reported

40
Lymphogranuloma Venereum Contd.

In the third stage of LGV, a patient develops rectal pruritus and a mucoid
discharge from rectal ulcers.
If these become infected, the discharge becomes purulent.
This is a result of lymphatic obstruction that follows lymphangitis and that
may result in elephantiasis of external genitalia initially and fibrosis of the
rectum.
Rectal bleeding, crampy, abdominal & distention, rectal pain occur .
Peritonitis may follow bowel perforation.
Stenosis of the urethra and the vagina has also been reported.
LGV is diagnosed by exclusion of other causes & positive chlamydial testing.
A serologic titer that is greater than 1:64 can support the diagnosis.
C trachomatis culture or PCR can be used for diagnosis.
Treatment: Doxycycline, 100 mg orally twice daily for 21 days.

41
Pathogens Causing Infectious Vaginitis

The term vaginitis is the diagnosis given to women


who present complaining of abnormal vaginal
discharge with vulvar burning, irritation, or itching.
The leading causes of symptomatic vaginal discharge
are bacterial vaginosis, candidiasis, & trichomoniasis.
Between 7 and 70 percent of women who have
vaginal discharge complaints will have no definitive
diagnosis.

42
Category Physiologic Bacterial Candidiasis Trichomoniasis Bacterial
(normal) Vaginosis (streptococcal,
staphylococcal,
E coli)
Chief None Bad odor, Itching, Frothy discharge, Thin, watery
complaint increased after burning, bad odor, dysuria, discharge,
intercourse discharge pruritis, spotting pruritis

Discharge White, clear Thin, gray or White "cottage Green-yellow, Purulent


white, adherent, cheese like" frothy, adherent,
often increased discharge increased

KOH "whiff Absent Present (fishy) Absent May be present Absent


test"
Vaginal pH 3.8–4.2 >4.5 <4.5 >4.5 >4.5

Microscopic N/A "Clue cells", Hyphae and Trichomonads Many WBCs


findings slight increase in buds in 10- (protozoa with 3-5
WBCs, clumps of percent KOH flagella) may be
bacteria (saline solution (wet seen moving on
wet mount) mount) saline wet mount

Table comparing vaginitis


43
Fungal Infection

Caused by Candida albicans


Candidiasis is seen more commonly in warmer climates and in obese
patients.
Additionally, immunosuppression, diabetes mellitus, pregnancy, and recent
broad-spectrum antibiotic use predispose women to clinical infection.
It can be sexually transmitted, and several studies have reported an
association between candidiasis and orogenital sex.
Symptoms of candidiasis include pruritus, pain, and swelling.
vulvar erythema and edema with excoriations are common findings.
The typical vaginal discharge is described as a cottage cheese-like
discharge. Vaginal pH is normal (less than 4.5) and microscopic examination
of vaginal discharge with saline and 10-percent KOH allows yeast
identification.

44
Fungal Infection Contd.
Diagnosis
Candida albicans is dimorphic with both yeast buds and hyphal forms.
It may be present in the vagina as a filamentous fungus (pseudohyphae) or
as germinated yeast with mycelia.
Vaginal candidal culture is not routinely recommended.
Women who have four or more candidal infections during a year are
classified as complicated (recurrent) disease, and cultures should be
obtained to confirm the diagnosis.
The treatment of patients with RVVC consists of fluconazole (150 mg
every 3 days for 3 doses).
Patients should then be maintained on a suppressive dose of this
agent (fluconazole, 150 mg weekly) for 6 months.
On this regimen, 90% of women with RVVC will remain in remission.
After
45
Fungal Infection Contd.

Candida vulvitis with more


papulous red areas.

Candida vaginitis with cottage cheese like


discharge and red vaginal walls. 46
Fungal Infection Contd.
Uncomplicated Complicated

Sporadic or infrequent Recurrent candidal infection

Mild to moderate Severe infection

Likely infecting agent is Candida albicans Non-albicans candidiasis (C tropicalis, C glabrata)

Non immunocompromised woman Uncontrolled diabetes, immunosuppression,


debilitation, pregnancy

47
Fungal Infection Contd.
Recommended Treatment of Vulvovaginal Candidal Infection
Intravaginal agents
Clotrimazole 1% cream, 5 g intravaginally 7 to 14 days or
100 mg tablet intravaginally for 7 days or
100 mg tablet intravaginally, 2 tablets for 3 days or
Miconazole 2% cream, 5 g intravaginally for 7 days
100 mg suppository intravaginally for 7 days
200 mg suppository intravaginally for 3 days
1200 mg suppository intravaginally once
Nystatin 100,000-unit tablet intravaginally for 14 days
Oral agent
Fluconazole 150 mg oral tablet once

48
Trichomoniasis
Trichomoniasis is more commonly diagnosed in women because most men
are asymptomatic.
This parasite is usually a marker of high-risk sexual behavior, and co-
infection with other sexually transmitted pathogens is common, especially
Neisseria gonorrhoeae.
Trichomonas vaginalis has predilection for squamous epithelium, and
lesions increase accessibility to other STIs.
Incubation with T vaginalis requires 3 days to 4 weeks, and the vagina,
urethra, endocervix, and bladder can be infected.
No symptoms may be noted in up to one-half of women with
trichomoniasis, and such colonization may persist for months or years in
some women.
vaginal discharge is typically described as foul, thin, and yellow or green.
Dysuria, dyspareunia, vulvar pruritus, and pain may be noted.
49
Trichomonas Contd.
At times, symptomatology and physical findings are identical
to those of acute pelvic inflammatory disease.
With trichomoniasis, the vulva may be erythematous,
edematous, and excoriated.
The vagina contains the above-described discharge, and
subepithelial hemorrhages or "strawberry spots" may be
seen on the vagina and cervix.
Diagnosed by microscopic identification of parasites in a
saline preparation of the discharge.
Trichomonads are anteriorly flagellated anaerobic protozoa.
Vaginal ph is often elevated
Culture in Diamond media is the most sensitive diagnosis.
50
Trichomonas Contd.

Trichomonas vaginitis Strawberry cervix Trichomonas vaginalis


Giemsa stain

51
Trichomonas Contd.

Recommended Treatment of Trichomoniasis


Primary therapy
Metronidazole single 1-g dose orally or
Tinidazole single 2-g dose orally
Alternative regimen
Metronidazole 500 mg orally twice daily for 7 days
Recurring infections
Tinidazole 500 mg orally three times daily for 7 days or four times daily for 14 days

52
Pathogens Causing Suppurative Cervicitis

The cause of cervical inflammation depends on the epithelium affected.


The ectocervical epithelium can become inflamed by the same micro-
organisms that arenresponsible for vaginitis.
Conversely, N. gonorrhoeae and C. trachomatis infect only the glandular
epithelium
Diagnosis
The diagnosis of cervicitis is based on the finding of a purulent endocervical
discharge, generally yellow or green in color and referred to as “mucopus”
Gram stain of mucopus shows increased number of neutrophils (30 per
high-power field).
Intracellular gram-negative diplococci, gonococcal endocervicitis,
Gram stain negative diagnosis is chlamydial
The microbial etiology of endocervicitis is unknown in about 50% of cases
in which neither gonococci nor chlamydia is detected.

53
Neisseria gonorrhoeae

Gonococcal infections among women are frequently asymptomatic.


Screening of high risk group is recommended
Risk factors for gonococcal carriage and potential upper
reproductive tract infection are:
Age less than 25 years
History of sexually transmitted infections
A history of previous gonococcal infection
New or multiple sexual partners
Lack of barrier protection
Drug use, and
Commercial sex work

54
Neisseria gonorrhoeae contd.
Symptoms include cervicitis.
Cervicitis commonly describe a profuse odorless,
nonirritating, and white-to-yellow vaginal discharge.
Gonococcus can also infect the Bartholin and Skene glands,
the urethra, and ascend into the endometrium and fallopian
tube to cause upper reproductive tract infection.
Neisseria gonorrhoeae is a gram-negative coccobacillus that
invades columnar and transitional epithelial cells, becoming
intracellular. For this reason, the vaginal epithelium is not
involved.
For gonococcal identification, NAATs are available, and ideal
specimens are recovered from the endocervix.
These tests have replaced culture in most laboratories.
55
Neisseria gonorrhoeae contd.

Recommended Single-Dose Treatment of Uncomplicated Gonococcal Infection


of the Cervix, Urethra, or Rectum
Ceftriaxone 125 mg IM or
Cefixime 400 mg orally or
Ciprofloxacin 500 mg orally or
Ofloxacin 400 mg orally or
Levofloxacin 250 mg orally

56
Chlamydia trachomatis
This obligate intracellular parasite is dependent on host cells for survival
It causes columnar epithelial infection.
Thus presenting symptoms reflect endocervical glandular infection,
with resultant mucopurulent discharge or endocervical secretions.
If infected, the endocervical tissue is commonly edematous and
hyperemic.
Urethritis is another lower genital tract infection that can develop, and
dysuria is prominent.
Diagnosis
Microscopic inspection of secretions following a saline preparation
typically reveals 20 or more leukocytes per high-power field.
More specifically, culture, NAAT, and enzyme-linked immunosorbent
assay (ELISA) are available for endocervical specimens.
57
Chlamydia trachomatis Contd.

Recommended Treatment of Chlamydial Infection


Primary treatment
Azithromycin 1 g orally once or
Doxycycline 100 mg orally twice daily for 7 days
Alternative regimens
Erythromycin base 500 mg orally four times daily for 7 days or
Ofloxacin 300 mg orally twice daily for 7 days or
Levofloxacin 500 mg orally daily for 7 days

58
Pathogens Causing Mass Lesions

External Genital Warts


These lesions are created from productive infection with the human
papillomavirus (HPV)
Genital warts have various morphologies, and appearances range from
flat papules to the classic verrucous, exophytic lesions, termed
condyloma acuminata .
Lesions are found on lower reproductive tract, urethra, anus, or mouth.
Diagnosed by clinical inspection, and biopsy is not required unless co-
existing neoplasia is suspected.
Condyloma acuminata may remain unchanged or spontaneously
resolve
Treatment: Podophyllin application/ Surgical removal

59
Mass Lesions contd.
Molluscum Contagiosum
The molluscum contagiosum pox virus.
It is transmitted by intimate contact.
The host response to viral invasion is papular with central umbilication,
giving a characteristic appearance.
It may be single or multiple and is commonly seen on the vulva, vagina,
thighs, and/or buttocks
Diagnosis usually clinical.
Giemsa, Gram, or Wright stains may demonstrate molluscum bodies, large
intracytoplasmic structures.
Most lesions spontaneously regress over 6 to 12 months.
If removal is preferred, lesions may be treated by cryotherapy,
electrosurgical needle coagulation, or sharp needle-tip curettage of a
lesion's umbilicated center.
60
Pathogens Causing Pruritus
Scabies
Sarcoptes scabiei infect skin and result in an intensely pruritic rash.
The mite causing this infection is crab-shaped, and the female digs into the skin and
remains there for approximately 30 days, elongating her burrow.
Several eggs are laid daily and begin hatching after 3 to 4 days.
The baby mites furrow their own burrows, becoming reproductive adults in
approximately 10 days.
Mites crawl at a rate of two and a half centimeters per minute, and sexual
transmission is the most likely cause of initial infection, although it can be seen in
household contacts
A delayed-type 4 hypersensitivity reaction to the mites, eggs, and feces develops and
results in erythematous papules, vesicles, or nodules in association with skin
burrows.
Definitive testing requires scraping across the burrow with a scalpel blade and mixing
these fragments in immersion oil on a microscope slide.
Identification of mites, eggs, egg fragments, or fecal pellets is diagnostic 61
Pruritus Contd.
Treatment
Once diagnosed, 1-percent lindane cream is a commonly used agent.
It is recommended that all family members be treated with the
exception of pregnant or lactating women and children younger than 2
years.
Treatment is effective within 4 hours.
Eight to 12 hours after application, a shower or bath should be taken
to remove the medication. Only one application is necessary, and bed
linens and recently worn clothing should be washed to prevent
reinfection.
5-percent permethrin cream (Elimite), which is effective after a single
application. It should be washed off in 8 to 12 hours and is safe in
children older than 2 months and in pregnant women.
62
Pruritus Contd.
Pediculosis
Lice are small ectoparasites that measure approximately one millimeter in length.
Three species infest humans and include the body louse (Pediculus humanus),
the crab louse (Phthirus pubis), and the head louse (Pediculus humanus capitis).
Lice attach to the base of human hair with claws, and it is this claw's diameter
that determines the infestation site.
For this reason, the crab louse is found on pubic hair and other hair of similar
diameter, such as axillary and facial hair, including eyelashes and eyebrows.
Lice depend on frequent human blood meals, and pubic lice may travel up to 10
centimeters in search of darkness and a new attachment site for blood. They
leave voluntarily if the victim becomes febrile, dies, or if there is close contact
with another human.
Accordingly, pubic lice usually are sexually transmitted, whereas head and body
lice may be transmitted by sharing personal objects such as combs, brushes, and
clothing.
63
Pruritus Contd.
The main symptom from louse attachment and biting is pruritus.
Patients may develop pyoderma and fever if secondarily
infected..
Each female adult pubic louse lays approximately four eggs a
day, which are glued to the base of hairs. Incubation is about 1
month.
Their attached eggs, termed nits, can be seen attached to the
hair shaft away from the skin line as hair growth progresses.
Pediculicides kill not only adult lice, but also the eggs. A single
application is usually effective, but a second application is
recommended within 7 to 10 days to kill new hatches.
Treatment : 1-percent lindane shampoo can also be used.

64
Sexually Transmitted Infections
The term "sexually transmitted diseases" is used to denote
disorders spread principally by intimate contact.
Although this usually means sexual intercourse, it also includes
close body contact, kissing, cunnilingus, anilingus, fellatio,
mouth–breast contact, and anal intercourse.
Caused by more than 20 micro organisms (some bacterial other
viral)
Most present like
Urethral discharge
Genital ulcer
Vaginal discharge
Swollen glands
65
STI Contd.

Produce Considerable morbidity and


mortality
High incidence and prevalence
High rate of complications
Bigger problem in women and young people
Facilitate HIV transmission

66
Management Objectives

Proper diagnosis
Proper treatment begins by
-Risk assessment
-Clinical evaluation
-Confirmation

67
STIs Management Approaches

I. Etiological/laboratory approach:-
Done by identifying the causative agent (s)
using lab. tests and giving treatment specific
to the pathogen identified.
II. Syndromic approach:-
Identification of clinical syndrome.

68
Etiologic Diagnosis

Ideal approach
Important for validation of treatment algorithm
Determine prevalence
The only way to diagnose asymptomatic STI
Expensive
Time consuming
Requires lab facility
Ranges from simple laboratory tests to complex
(Microscopy, culture, Immunological tests, DNA
amplification)
69
Syndromic Approach

A syndrome is a group of symptoms that patients


describe, combined with the signs that providers
observe during examination.
This approach entails identification of a clinical
syndrome and giving treatment targeting all the
locally known pathogens which can cause the
syndrome.
Syndromic approach focuses on common STIs such
as syphilis, chancroid, gonorrhea, chlamydial
infection, trichomoniasis and candidiasis.
70
Why Syndromic Approach?

STI sign and symptoms are rarely specific to a


particular causative agent;
Laboratories are either non-existent or non
functional due to lack of resources;
Dual infections are quite common and both clinician
and laboratory may miss one of them;
Waiting time for lab. results may discourage some
patients;
Failure of cure at first contact;
Shortage of STI specialists?

71
The Main Features of the Syndromic Approach

Grouping the main infectious agents according to the


clinical syndromes they cause,
Using flow-charts as tools,
Treating patients for all the important causes of a
syndrome,
Educating patients, promoting condoms and
emphasizing the importance of partner referral.

72
Identifying the Syndromes

The syndromes identified in Syndromic approach are:


1. Urethral discharge in men
2. Scrotal swelling
3. Vaginal discharge
4. Lower abdominal pain
5. Genital ulcer
6. Inguinal bubo
7. Neonatal conjunctivitis
73
Components of Syndromic Management
of STIs

Take proper history & physical examination


Treat for (the cause/causes)
Educate the patient
Counsel if needed
Promote/provide condoms
Partner management
Offer HIV counseling and testing
Advice to return if necessary

74
What do you need

Room with auditory privacy


Adequate light
Speculum
Glove
Slides and cotton swab
Others

75
Presenting complaint - vaginal discharge
or vulval itching/burning Vaginal Discharge
Take history, examine patient (external, speculum
(speculum & bimanual)
and bimanual) and assess risk

Educate
Abnormal discharge No Counsel
present? Promote and provide condoms
Depending on counselling capabilities offer
Yes HIV testing

Lower abdominal tenderness or Use flowchart for


cervical motion tenderness Lower Abdominal Pain
Yes

No
Treat for chlamydia trachomatis,
Risk assessment positive or gonococcal infection, bacterial
cervical mucopus vaginosis and trichomonas
Yes
No

Vulval oedema/curd like Treat for Candida


Yes
Treat for bacterial vaginosis discharge Albicans
and trichomonas Erythema, Excoriations
present?
No Educate
Counsel
: Needs adaptation to local epidemiological situation Promote and provide condoms
Depending on counselling capabilities
76
offer HIV testing
Figure 7
Patient complains of genital sore or ulcer

Take history &


examine •Educate on RR
Solitary non- No • Promote &
Vesicular recurrent No recurrent provide condoms
Ulcers or > three ulcers •Offer HIV testing
Non-vesicular ulcer,
Yes Yes
Treat syphilis, chancroid, HSV2
Treat HSV2

•Educate on risk reduction


•Promote & provide condoms
•Offer HIV testing & Partner management

ulcers healed No
ulcers improved Refer
Yes
•Educate & provide condoms
•Offer HIV testing Continue Rx 77
•Consider episodic Rx
complains of lower abdominal pain

Take history & examine (abdominal & vaginal)

cervical
excitation,
•Missed/overdue period, Any other
tenderness or
•Pregnancy lower abdominal No illness?
•Recent delivery/ No tenderness & VD
abortion /Miscarriage
• Abdominal guarding/ Yes Yes
rebound tenderness Manage
• Vaginal bleeding Treat for PID
•Abdominal mass & review in 3 days appropriately
•Vaginal bleeding

improved? No Refer
Yes patient for
Yes
• Refer patient for surgical • Continue treatment admission
or gynaecological • Educate on RR
assessment
• set up IV line • Offer HCT
• Condom use
• Resuscitate if measures 78
Figure 9
Pelvic inflammatory disease
Refers to acute infection of the upper genital tract of female
pelvis not related to pregnancy or surgery
Over 80% caused by STDs like gonorrhea and Chlamydia.
Lower abdominal pain is the cardinal presenting symptom
Recent onset of pain that worsens during coitus or with jarring
movement.
The onset of pain during or shortly after menses is particularly
suggestive
The abdominal pain is usually bilateral and rarely of more than
two weeks' duration
Uterus, tubes, ovaries, pelvic peritoneum are affected

79
PID Contd.
Perihepatitis 
 Perihepatitis (Fitz-Hugh Curtis Syndrome) was first associated with
gonococcal salpingitis in 1920 and subsequently with Chlamydia.
It consists of infection of the liver capsule and peritoneal surfaces of
the anterior right upper quadrant, with minimal stromal hepatic
involvement.
It manifests as a patchy purulent and fibrinous exudate in the acute
phase ("violin string" adhesions), most prominently affecting the
anterior surfaces of the liver (not the liver parenchyma)
Symptoms are typically the sudden onset of severe right upper
quadrant abdominal pain with a distinct pleuritic component,
sometimes referred to the right shoulder.
Aminotransferases are abnormal in approximately one-half of patients
Diagnosis is based on minimum & additional criteria 80
Perihepatitis 

"violin string" adhesions

81
PID Diagnostic Criteria

I. Minimum Diagnostic II. Additional Diagnostic


Criteria Criteria
Oral tem >38.3 C
Uterine tenderness
Elevated ESR
adnexal tenderness Elevated CRP
cervical motion Abnormal cervical or vaginal
tenderness mucopurulent discharge
Lower abdominal Presence of abundant
tenderness numbers of white blood cells
(WBCs) on saline microscopy
of vaginal secretions

82
Pelvic Inflammatory Disease

III. Definitive Diagnostic Criteria


Endometrial biopsy with histopathologic evidence of
endometritis
Transvaginal sonography or MRI showing thick fluid-
filled tubes
Laparoscopic abnormalities consistent with PID

83
Management of PID

Hospitalization is indicated if
Surgical emergencies not excluded
Pregnancy
Clinical failure of oral antimicrobials
Inability to follow or tolerate oral regimen
Severe illness, nausea/vomiting, high fever
Tubo -ovarian abscess

84
Management of PID Contd.

Parenteral Regimen A
Ceftriaxone 1- 2 g IV q 12 hours
or
Cefoxitin 2 g IV q 6 hours
PLUS
Doxycycline 100 mg orally/IV
q 12 hrs
WITH OR WITHOUT
Metronidazole 500 mg IV/po q 8 hours

85
Management of PID Contd.

Parenteral Regimen B
Clindamycin 900 mg IV q 8 hours
PLUS
Gentamicin loading dose IV/IM (2 mg/kg) followed
by maintenance dose (1.5 mg/kg) q 8 hours.
Single daily dosing may be substituted.

86
Management of PID Contd.

Alternative Parenteral Regimens


Ciprofloxacin 500 mg IV q 12 hours
or
Levofloxacin 500 mg IV once daily
WITH OR WITHOUT
Metronidazole 500 mg IV q 8 hours
or
Ampicillin/ Sulbactam 3 g IV q 6 hrs
PLUS
Doxycycline 100 mg orally/IV q 12 hrs
87
Management of PID Contd.
Oral Regimen A
Ciprofloxacin 500 mg single dose
Plus
Doxycycline 100 mg BID for 14 days
WITH OR WITHOUT
Metronidazole 500 mg twice daily for 14 days

88
Management of PID Contd.
Oral Regimen B
Ceftriaxone 250 mg IM in a single dose
or
Spectinomycin 2gm IM single dose
PLUS
Doxycycline 100 mg twice daily for 14 days
WITH or WITHOUT
Metronidazole 500 mg twice daily for 14 days

89
Management of Sex Partners

Male sex partners of women with PID should be


examined and treated for sexual contact 60 days
preceding pt’s onset of symptoms
Sex partners should be treated empirically with
regimens effective against CT and GC

90
Thank you

91

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