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Prof. Aboubakr Elnashar
Benha University Hospital, Egypt
ABOUBAKR ELNASHAR
INTRODUCTION
Common,
disturbing,
recurrent
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PHYSILOGICAL VAGINAL DISCHARGE
Contents:
Transudated fluid from vaginal wall:
Sq. epi. ,
Polymorph,
Bact. Flora
Secretion from:
endometrium & oviduct,
cervix,
vulva (Skene,s, Bartholin & seb. glands)
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Vaginal flora :
• Microbiological balance
• Includes:
Lactobacillous (most common),
streptoc.,
staphcoc.,
diphteroids,
G. vaginalis,
E.coli,
Anaerobic b.,
Candida,
mycoplasma.
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Characters:
• Color: clear
• Amount:
Variable
increase before ovulation, OCPs
• Smell:
• pH:
3.8-4.2 {lactic ac by lactobacilli on glycogen of
desquamated vag epi}
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DEFENSE MECHANISM AGAINST INFECTION
Vulva:
apposition
Fungicide from apocrine glands
Vagina:
apposition
S. Sq. epi is resistant.
flora
acidity
Cervix:
bactericide
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FACTORS DISTURBING THE DEFENSE
MECHANISM
1. Age:
childhood, Postmenopause {atrophic epi & increase
pH}
2. Menstruation:
increase pH & disappearance of cx mucous
3. Pregnancy
4. Puerperium:
trauma, contamination with bowel flora
5. OCPs:
increase pH, ectropion, increase cx secretion
6. F.B
7. Disease:
DM, immunosuppressive states, antibiotics
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VAGINITIS
Inflammation & irritation of the vagina
Types
A. Infectious
1. Bact: B.vaginosis,GBS
2. Fungal: Candidiasis
3. Parasitic: T.V.
4. Viral: HPV, HSV.
B. Noninfectious
1. Atrophic
2. Traumatic
3. Chemical
4. Vag. adenosis,VIN.
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Non-specific vaginitis: Haemophilus vaginalis
Gardnerella vaginitis: Gardnerella vaginalis
Anaerobic vaginosis: Gardnerella vaginalis &
anaerobic bacteria
Bacterial vaginosis:
polymicrobial alteration in vaginal flora causing an
increase in vaginal pH,
sometimes associated with an homogenous discharge,
but in the absence of a demonstrable inflammatory
response
(Eschenbach et al, 1988)
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BV is the most common cause of vaginal discharge
in young women of reproductive age.
Prevalence between 5% & 35% depends on method
of screening & the locality.
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Polymicrobial:
G. vaginalis (coccobacilli, surface pathogen),
Anaerobic bacteria (Bacteroids, Mobiluncus,
Prevotella) &
Mycoplasma hominis.
There is synergistic relationship between the
acquired organisms.
They replace lactobacilli
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Their metabolism produces volatile amines &
organic acids other than lactic acids leading to smell
& increase pH.
Mobiluncus produce trimethylamine giving the smell
of rotting fish.
Mobiluncus & Bacteroids produce succinate (Keto-
acid) which raises vaginal pH.
Absence of lactic acid & the production of succinate
blunt the chemotactic response of
polymorphnuclear leukocytes & reduce their killing
ability. This explains absence of cellular
inflammatory response.
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Gram stain
b= bacteroids, c= mobilincus, g= gardenerlla, p=peptostreptococci
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Electron micrograph of Mobiluncus
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1. Increase vaginal pH:
Semen,
after menstruation when estradiol levels increase.
2. Decrease lactobacilli:
Douching,
change of sexual partner (change of vaginal
environment),
episodes of candida
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3. Smoking: suppresses the immune system
facilitating infection.
4. IUCD:
5. Black ethnic groups
6. Lesbians
•It is not STD:
Treatment of the husband is not beneficial in
preventing recurrence of BV.
Detection of BV in 12% of virgins after menarche.
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The reason for the alteration in flora is unclear.
1.Hormonal changes:
mechanism is unclear
2.Enzymatic changes:
Mucinase & siallidase are elevated in vaginal
discharge of BV. Breaking down the mucosal
barrier
3.Bacteriophage (virus that infects bacteria)
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Up to half the women diagnosed with BV are
asymptomatic.
.Discharge: thin, homogenous, whitish-grey, frothy &
fishy. Absence of discharge does not imply the
absence of BV. It is not accepted as a reliable
indicator on its own as it is neither sensitive nor
specific to BV.(Deborah et al,2003)
.Seldom associated with mucosal inflammation or
irritation of the vagina or vulval itch.
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1.pH of discharge: 5.7
A low pH virtually excludes BV. An elevated pH is
the most sensitive but least specific as an increase
can also associated with menstruation, recent
sexual intercourse, or infection with T. vaginalis
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2.Whiff test (amine test).
Addition of 10% KOH to a sample of vaginal
discharge produces fishy odor.
It has a positive predictive value of 90% & specificity
of 70%
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3.Wet film (drop of vaginal secretion & drop of
saline):
clue cells (epithelial cells covered by coccobacilli,
borders are indistinct), No WBC.
It is the single most sensitive & specific criterion for
BV. , but it is operator dependent. Debris &
degenerated cells may be mistaken for clue cells &
lactobacilli may adhere to epithelial cells in low
numbers.
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4. Gram stain:
90% sensitivity, highly sensitive & specific (Gr.
Variable c.bacilli, no WBC, no lactobacilli).
Scoring systems which weight numbers of lactobacilli
& numbers of G vaginalis & Mobiluncus.
It is simple & objective method. However the cost &
need for microscopist.
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5.Rapid tests:
.Diamine test: rapid, sensitive & specific
.Proline aminopeptidase test (Pip Activity test Card)
.A card test for detection of elevated pH &
trimethylamine (FemExam test card)
.DNA probe based test for high concentration of G.
vaginalis (Affirm VP III) may have clinical utility.
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. Pap. smear: clue cells. Limited clinical utility
because of low sensitivity
.Culture: It is not recommended as a diagnostic tools
because it is not specific.
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Amsel’s criteria
3 of the following:
.Homogenous discharge.
.pH> 4.5.
. Amine test.
.Clue cells.
Gram stain alone corresponds well to Amsel’s
criteria & to the presence of the associated
bacteria.
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Gynecological
1. Psychological disturbance
2. PID:
The microorganisms of BV & PID are similar. There is
10 fold-increased risk of PID in females with BV.
3. Tubal infertility: 1/3 of women with tubal factor
infertility had BV compared to 16% of male factor
infertility (Wilson et al, 2000).
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4. Post-hysterectomy vaginal cuff infection.
5. Uretheral syndrome.
6. HIV susceptibility infection.
The presence of BV increases susceptibility to HIV
infection
BV is not associated with CIN
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Obstetric
1. Miscarriage:
Women with BV had a higher rate of first trimester
miscarriage than those with normal vaginal flora.
Recurrent first trimester miscarriage has not been
associated with BV.
The incidence of late miscarriage (13-23 w) is higher
in women with BV.
2. Postabortal sepsis.
The use of antibiotic prophylaxis before surgical
termination of pregnancy demonstrates a protective
effect.
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3.Preterm labour.
The earlier in pregnancy that BV is detected the
greater the risk of PTL. Treatment of high risk, BV
positive pregnant women has resulted in reduction of
PTL by 40-50%.
4.Bactraemia after instrumental delivery
6.Chorioamnionitis.
7.Postpartum endometritis, post cesarean wound
infection
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A. Non pregnant
Benefits of treatment:
. relieve vaginal symptoms & signs of infection.
. Reduce the risk for infectious complications after
hysterectomy or abortion.
. Reduction of other infectious complications e.g.,
HIV, STD
Indications
1. Symptomatic women (Grade A recommendation).
2. Women undergoing some surgical
procedures(Grade A recommendation).
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Recommended regimens (CDC,2002)
Metronidazole 500 mg orally twice a day for 7 days,
OR
Metronidazole gel 0.75%, one full applicator (5g)
intravaginally, once a day for 5 days OR
Clindamycin cream 2%, one full applicator (5g)
intravaginally at bed time for 7 days.
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Alternative regimens (CDC,2002)
Metronidazole 2 g orally in a single dose, OR
Clindamycin 300 mg orally twice a day for 7 days,
OR
Clindamycin ovules 100 mg intravaginally once at
bedtime for 3 days.
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Notes:
•The recommended metronidazole regimens are
equally effective. Metronidazole gel is more
expensive than tablets
•The vaginal clindamycin is less effective than the
metronidazole regimens.
•The alternative regimens have lower efficacy for
BV.
•No data support the use of non-vaginal lactobacilli
or douching for treatment of BV.
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•Clindamycin cream or oral is preferred in case of
allergy or intolerance to metronidazole.
•Theoretically, Metronidazole has an advantage
because it is less active against lactobacilli than
clindamycin.
•Conversely, clindamycin is more active than
metronidazole against most of the bacteria
associated with bacterial vaginosis
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.Follow up
Follow-up visits are unnecessary if symptoms
resolve.
Another recommended treatment regimen may be
used to treat recurrent disease.
Management of husband is not recommended
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B. Pregnant
Natural history:
•BV is present in up to 20% of pregnant women
depending on how often the population is screened.
•The majority is asymptomatic.
•It may spontaneously resolve without treatment,
although the majority is likely to have persistent
infection later in pregnancy.
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Recommended regimen
Metronidazole 250 mg orally three times a day for 7
days, OR
Clindamycin 300 mg orally twice a day for 7 days
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Notes:
•Existing data do not support the use of topical
agents during pregnancy. Evidence from three trials
suggests an increase in adverse events (e.g.
prematurity & neonatal infection), particularly in
newborns, after use of clindamycin cream
(McGregor et al,1994; Joesoef et al,1995; Vermeulen et al,1999).
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•Multiple studies & meta-analysis have not
demonstrated a consistent association between
metronidazole during pregnancy & teratogenic or
mutagenic effects in newborns
(Caro-Paton et al,1997).
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Indications
1. All symptomatic pregnant women should be tested
& treated.
2. Asymptomatic pregnant women at high risk for
PTL (previous history), should be screened early in
pregnancy & treated
(Cochrane library,2002)
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3. Asymptomatic pregnant females at low risk for
PTL:
Data are conflicting whether treatment reduces
adverse outcomes of pregnancy.
One trial, using oral clindamycin demonstrated a
reduction in PTL & postpartum infectious
complications
(Hay et al, 2001).
Oral clindamycin early in the second trimester
significantly reduced the rate of late miscarriage &
PTL in general obstetric population
(Ugwumadu et al, 2003).
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How to screen for BV ?
(Gierdingen et al, 2000)
Ask about symptoms & pH of the vagina is
determined frequently during pregnancy.
If pH > 4.5 ( BV or TV in 84%), do wet mount.
Follow-up of pregnant women
One month after treatment to evaluate whether
therapy was effective is recommended.
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C. lactation
•Metronidazole enters breast milk & may affect its
taste. The manufacturer recommend avoiding high
doses if breast feeding.
•Small amounts of clindamycin enter breast milk.
•It is prudent therefore to use an intravaginal
treatment for lactating women
(Grade C recommendation)
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Recurrent BV:
European (IUSTI/WHO) Guideline, 2011
Most patients will have recurrences within 3 to 12
months, whatever treatment has been used.
Suppressive regimens
Metronidazole jell (Metrojell)
weekly during 16 weeks
Adjuvant regimen
lactobacilli
daily intravaginal for 6 months
Acidifying gel
ABOUBAKR ELNASHAR
Benha University Hospital, Egypt
ABOUBAKR ELNASHAR
BENHA UNIVERSITY HOSPITAL, EGYPT
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Prevalence of fungal infection:
37%.
dramatic decrease after menopause
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There are 150 candida species
C albicans is by far the most common, it accounts for
80-90%
C glabrata is the second most common, it accounts
for 5-15%
C tropicalis (5%)
Other species eg C krusei, C guilliermondi are rarely
isolated
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In recent years, there is significant increase in non-
albicans species, particularly C glabrata & C
tropicalis, especially in recurrent cases.
At present non candidal account for 20% of cases &
30% of recurrent cases.
1.Widespread & inappropriate use of antimycotic
treatments (self medication, long term treatment,
repeated treatments). Shorter courses of imidazole
for c. albicans may lead to an overgrowth of c
glabrata
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2.Eradication of C albicans causes a selection of
species (such as C glabrata) that are resistant to
commonly used drugs.
Eradication of intestinal C with medication is not
successful
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Candida is found in 2 different states:
1.Blastopores or spores are the phenotype for
extension, dissemination & transmission. They are
also a resistance form of the fungus, that can be
associated with a symptomless colonization.
2.Mycelia are germinative forms; this phenotype can
invade tissues & cause symptoms.
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1. Vagina: 35% of healthy females,2ndry opportunistic
pathogen
2. GIT: anogenital transfer
3. Husband: 25% STD.
VVC is not usually acquired through sexual intercourse
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1. Compromised immunity:
broad spectrum antibiotic, other vag. Infection, trauma
(SI), allergen causing skin sensitization, late
pregnancy, immuno-suppression.
2. Endocrine disorders:
DM, thyroid, parathyroid & adrenal.
3. Menstrual cycle: late luteal phase
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4. Drugs:
OCPs, corticosteroids, immunosuppressive,
antibiotics, antitrichomonal
5. Clothing:
occlusive tights.
Pregnancy:
High estrogen levels cause an increased glycogen
load in epithelium, which is a nutritional source for C
growth & germination. Estrogen promotes fungal
adhesion & germination, fungi are more capable to
penetrate vaginal wall
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OCP:
containing high estrogen,the mechanism is same as
in pregnancy. No synergic action has ever been
shown for low estrogen OCP regarding C growth
IUCD:
is associated with recurrence because the thread
acts as a C reservoir
DM:
Metabolic disturbance predispose to clinical vaginitis
Antibiotics:
suppress lactobacilli flora, C are free to grow,
adhere & germinate. However several studies failed
to show this
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To be invasive, C follow 3 stage mechanism
1.Adhesion
2.Blastopore germination, mycelium or hyphae
development
3.Epithelium invasion
Defense factors against C in the vagina:
1. Lactobacilli
2. Humoral immunity, antibodies
3. Cellular immunity
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Symptomatic vaginitis development
Transformation of vaginal colonization into vaginitis
is a critical step in the pathogenic mechanism of C
vaginitis.
During colonization stage, C are present basically in
blastopore forms, & their number is not very high.
There is a balance between C organisms & vaginal
defense factors controlling & limiting fungal growth.
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Vaginitis appear because of:
1.An increased number or an enhanced virulence
of C organisms.or
2. Decreased vaginal defense mechanisms. When
this occurs, blastopores adhere to vaginal
epithelium & germinate; mycelium develops &
finally invades mucous membrane producing
vaginitis.
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.
Vulval itch (cardinal symptom): increase with warmth
& at night
. Discharge: ranging from scanty, thick, whitish,
adherent to vagina to a thin watery liquid,pH:4-5.
. Burning: Vulval & vaginaL is not dominant, but gets
worse with micturition or coitus
. dysparunia , dysuria.
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PH of discharge:4-5
. Wet mount: saline
Koh 10%: can ifentify pseudohyphae & blastospores
in 70%
. Gram stain.
. Pap. Smear:
50%. It is not performed for this condition
. Culture:
Nickerson, Sabourad, Only when microscopy is not
diagnostic
. Kits:
slide agglutination test is rapid diagnostic test.ABOUBAKR ELNASHAR
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.Colonization
.Uncomplicated VVC:
1.Sporadic or infrequent VVC
2.Mild or moderate VVC
3.Likely to be C. albicans
4.Non-immunocompromized
.
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.Complicated VVC:
1.Recurrent VVC
2.Severe VVC: extensive vulvar erythema, oedema,
and excoriation, fissure formation. Symptoms are
correlated with the amount of yeast in the vagina
(Odds,1988)
3.Non-albicans VVC
4.Women with uncontrolled , DM, debilitation,
immunosuppression or those who are pregnant
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1. other causes of vaginal discharge.
Infection with Herpes genitals, TV, bacterial vaginosis,
&
2. Vulval disease, especially vulval eczema, dermatitis,
lichen sclerosis & vulval vestibulitis.
Ask the patient to identify the itchy area. If there are
symptoms of dysparunia, the Q-tip test for the vulval
vestibulitis syndrome should be performed
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1.Wiping from front to back
2.Avoiding tight underwear especially synthetics
3.Avoidance of excessive washing, use of bubble baths &
perfumed soaps
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Asymptomatic female should not be
treated even if the culture is positive
Uncomplicated:
. Local (topical, intravaginal) antifungal:
Polyene: nystatin.
Azoles: clotrimazole, miconazole, econazole,
butoconazole, ticonazole, terconazole.
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•Both azoles & nystatin are fungistatic rather than
fungicidal.
•Nystatin (Nysert, Mycostatin and Nystan) less
effective than azole treatment. It needs to be given
for 14 days, but is indicated if there is a possibility of
non-albicans yeast infection.
•Azoles resulted in higher rates of clinical &
mycologic cure (80-95%) than nystatin (&0-90%) in
non pregnant acute VVC.
•Short course (single dose & regimens of 1-3
days)effectively treat uncomplicated VVC.
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2. Oral antifungal:
more effective against non-albican species.
. Ketoconazole
(Nizoral ,200mg)
Dose: 1X2X5
. Itraconazole
(Sporanox, 100 mg ) Dose: 2X2X1
. Fluconazole
(Diflucan, Alkanazol,150 mg)
Dose : 1 tab single dose
•
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Oral or vaginal antifungal
(Cochrane libarary, 2001)
.No differences in effectiveness (mycological &
clinical cure ) for uncomplicated candidiasis. (Both
routes had clinical cure 80%)
.The oral route is the preferred route by the patient.
The decision to prescribe oral or vaginal depends on
safety, cost, effectiveness, & patient preference. Oral
preparation is more expensive & associated with
more systemic side effects than vaginal route.
Vaginal route is first line of therapy
(Reef, 1993)
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Follow-up:
Patients should be instructed to return for follow-up
visits only if symptoms persist or recur within 2
months of onset of initial symptoms
T.T of the husband with oral antifungal did not
influence either cure rate or recurrence rate
(Shihadeh & Nawafleh,2000)
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Causes of clinical failure:
1.Vaginitis due to other causes.
2.Undiagnosed urogenital infection.
3.Chemical irritants: perfumed products, detergents
4.Physical damage: sexual intercourse, tampons
Causes of therapeutic failure:
1.Resistance to the antifungal
2.Presence of species out side the spectrum of the
antifungal. Non albicans C are associated with
vaginitis & are more resistant to conventional
antifungal therapy.
These is evidence that C glabrata & C Krusei are
resistant to fluconazole & itraconazole
(Rex,2000)ABOUBAKR ELNASHAR
Complicated VVC
Recurrent VVC
Define:
4 or more episodes/Y. Reappearance of C in the
vagina of a patient, who was cured, & may be either
Relapse, (due to re-growth of a previously
undetected residual population of C.) or
Re-infection (the vagina is re-inoculated from some
extravaginal source).
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Prevalence:
5% in family planning clinic & 10% in antenatal
clinic. No apparent predisposing or underlying
conditions in most cases.
Pathogenesis:
Non-albicans are found in 30% of cases
Source:
1.Vaginal inoculation: most common
Intestinal reservoir theory
Sexual transmission
2.Vaginal recurrence
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Although iron deficiency anaemia has been
suggested as a cause of recurrent VVC, there is no
evidence to support this.
DM is rarely newly diagnosed.
Allergic rhinitis/hayfever may be immunologically
linked with RVVC.
Mechanisms:
1.Increased C virulence
2.Host factors
Decreased secretory local immunity
IgE mediated hypersensitivity reaction
Loss of lactobacilli protective effect
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Treatment:
.Vaginal culture should be obtained to confirm clinical
diagnosis & to identify unusual species, including
non-albicans species, particularly C glabrata (not
form hyphae).
1. Longer duration of initial therapy
a.7-14 days of topical therapy or
b. 150-mg, oral dose of fluconazole repeated 3 days
later to achieve mycologic remission before initiating
a maintenance therapy.
In contrast to severe VVC, increasing the length of
therapy by up to 1 week, for example by adding a
second dose of fluconazole, does not improve
response
(Sobel et al, 2001)
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2. Maintenance (Suppressive) therapy for 6 months:
Clotrimazole (500-mg dose vaginal sup once weekly)
Ketoconazole (100 mg once daily)
Fluconazole (100-150 mg once weekly)
Itraconazole (400 mg once monthly or 100 mg once
daily)
The frequency of therapy depend on frequency of
attacks (White & Vanthuyne,2002):
> 1/month: weekly doses, 1/month: monthly doses.
Twice-monthly doses are usually adequate: D8 & D
18 of the cycle just before the hormonal peaks
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Treatment of the husband: controversial
Treatment of the predisposing factors:
Nitrofurantoin & nalidixic acid are recommended for
UTI since they give low tissue levels.
Psychosexual problems are common in RVVC, use
of vaginal lubricants is important
Relapse: 40% of women, the cycle of suppressive
therapy can be continued indefinitely
(Sobel et al,1992)
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Side effects of oral azoles: are few
(Inman et al,1993)
1.Gastrointestinal symptoms
2.Headache
3.Interactions with other drugs: astemizole, calcium
channel antagonists, cisapride, coumadin,
cyclosporin A, oral hypoglycemic agents, phenytoin,
theophylline, rifampicin.
.If there is poor response: typing to exclude C
glabrata: Itraconazol 200 mg daily for a month
combined with Nystatin 500 iu qds orally & nystatin
pessaries one bd for 3-4 months
(Emens, 1998).
Monitoring of liver function is mandatory
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Severe VVC:
Response to short course of topical or oral therapy is
poor
Topical azole 7-10 days or
Fluconazole in 2 sequential doses (second dose 72
hrs after initial dose)
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Non-albicans VVC
1.First line therapy: Longer duration therapy with a
non-fluconazole azole is recommended i.e; Nstatin
pessaries once or twice nightly for 14 days.
2.2nd line treatment (If recurrence occurs) 600 mg of
boric acid in gelatin capsule vaginally once daily for 2
weeks.
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3.The final resort: Topical 4% flucytosine, the only
fungicidal agent, & amphotericin B (Fungizone)in
lubricating gjelly for 14 nights
4.If non-albicans VVC continues to recur, a
maintenance regimen of 100,000 units of nstatin
delivered vaginally.
5. Intravaginal painting with gentian violet & oral
progesterone ( little information is available)
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Compromised host:
1.Correction of the condition
2.Prolonged conventional treatment course (7-10
days)
Pregnancy:
Only topical azole therapies applied for 7 days are
recommended
(CDC, 2002)
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VVC During pregnancy
VVC is more common during pregnancy
Cochrane library,( 2002):
•There is no evidence that VVC is harmful to the baby
•Azole drugs are more effective than nystatin.
•Treatment for 7 days is necessary. Treatment for >
1w confer no extra benefit. 4-day course will cure half
of infections & 7 day course cures over 90%.
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•There is no evidence that any one azole is any more
effective than another.
•Oral antifungal is not known to be effective or safe
in pregnancy.
•Benjamin et al (2000) reported that
•itraconazole is safe during pregnancy. It is
teratogenic in rat through affecting the adrenal gland.
These adrenal effects do not occur in human being.
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Incidence
decreased
Etiology
T.V (actively mobile with 4 unipolar flagellae)
Mode of transmission
STD
Vertical (urethra)
Non sexual (bath water, swimming pool,
toilets)
Reservoir: urethral & periurethral glands.
Incubation period: 3 to 28 days
ABOUBAKR ELNASHAR
Clinical picture
Vag. discharge:
foul, frothy, greenish, excessive (during or
immediately after menses)
Itching, vulval soreness (TV & candidiasis cause
90% of P. vulvae)
Dysparunia, dysuria
• Common symptoms:
vaginal discharge (50% to 75%), vaginal itching and
pain during intercourse
 Pelvic exam:
frothy vaginal discharge, vaginal erythema and
“strawberry” cervix
ABOUBAKR ELNASHAR
Purulent Vaginal Discharge in
Trichomonal Vaginitis
McGraw-Hill
ABOUBAKR ELNASHAR
Diagnosis
Wet mount:
motile, pear shaped, size of polymorph. 60%
sensitivity
Pap. smear:
50 % sensitivity
pH of discharge: 5-7 alkaline
Culture:
Feinberg, Whittington (>95%)
Colposcopy:
focal vaginitis, red punctate vaginitis, Y shaped
vessels.
ABOUBAKR ELNASHAR
Saline wet mount of vaginal secretions in trichomonal vaginitis,
showing two T. vaginalis (arrows), leukocytes and a normal
vaginal epithelial cell
McGraw-Hill
ABOUBAKR ELNASHAR
Pap smear: 70% sensitive in showing TV.
Wet mount: TV
ABOUBAKR ELNASHAR
ABOUBAKR ELNASHAR
Treatment
TT of the husband: In 1/3 the organism is found in
male urethra
Metronidazole: drug of choice
Recommended regimen: 2gm single dose
Alternative regimen: 250 mg1x3x7 or 500 mg twice
a day for 7 days
2. Metronidazole gel:
3. Tinidazole (Fasigen) 4 t single dose
During pregnancy:
1. Clotrimazole: eradicate TV in 50% & symptoms in
75 %
2. Metronidazole gel:
ABOUBAKR ELNASHAR
*
Failure of the treatment:
rare
Cause:
1.Degradation of metronidazole by other
bacteria
2.failure of absorption of metronidazole
TT:
1. Metronidazole:2-4 gm/ d in divided doses
2. Metronidazole + broad spectrum antibiotics
ABOUBAKR ELNASHAR
ABOUBAKR ELNASHAR
Etiology
Estrogen deficiency: childhood,
postmenopause
Clinical picture
1.Vag. dryness, itching, dysparunia
Vag. bleeding
Dysuria, frequency, urgency (atrohy of the
lower urinary tract).
Vagina: pale, thin, peticheal he
(superimposed infection).
ABOUBAKR ELNASHAR
DIAGNOSIS
1.Pap. smear
2.Colposcopy
D & C
Hysteroscopy
TREATMENT
Estrogen : oral
vag cream intravaginally every other
day.
ABOUBAKR ELNASHAR
ABOUBAKR ELNASHAR
G B STREPTOCOCCUS
Purulent vag discharge
Diagnosis:
10 WBC/HPF
HVS
Treatment:
penicillin or erythromycin
ABOUBAKR ELNASHAR
ABOUBAKR ELNASHAR

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Vaginitis

  • 1. Prof. Aboubakr Elnashar Benha University Hospital, Egypt ABOUBAKR ELNASHAR
  • 3. PHYSILOGICAL VAGINAL DISCHARGE Contents: Transudated fluid from vaginal wall: Sq. epi. , Polymorph, Bact. Flora Secretion from: endometrium & oviduct, cervix, vulva (Skene,s, Bartholin & seb. glands) ABOUBAKR ELNASHAR
  • 4. Vaginal flora : • Microbiological balance • Includes: Lactobacillous (most common), streptoc., staphcoc., diphteroids, G. vaginalis, E.coli, Anaerobic b., Candida, mycoplasma. ABOUBAKR ELNASHAR
  • 5. Characters: • Color: clear • Amount: Variable increase before ovulation, OCPs • Smell: • pH: 3.8-4.2 {lactic ac by lactobacilli on glycogen of desquamated vag epi} ABOUBAKR ELNASHAR
  • 6. DEFENSE MECHANISM AGAINST INFECTION Vulva: apposition Fungicide from apocrine glands Vagina: apposition S. Sq. epi is resistant. flora acidity Cervix: bactericide ABOUBAKR ELNASHAR
  • 7. FACTORS DISTURBING THE DEFENSE MECHANISM 1. Age: childhood, Postmenopause {atrophic epi & increase pH} 2. Menstruation: increase pH & disappearance of cx mucous 3. Pregnancy 4. Puerperium: trauma, contamination with bowel flora 5. OCPs: increase pH, ectropion, increase cx secretion 6. F.B 7. Disease: DM, immunosuppressive states, antibiotics ABOUBAKR ELNASHAR
  • 8. VAGINITIS Inflammation & irritation of the vagina Types A. Infectious 1. Bact: B.vaginosis,GBS 2. Fungal: Candidiasis 3. Parasitic: T.V. 4. Viral: HPV, HSV. B. Noninfectious 1. Atrophic 2. Traumatic 3. Chemical 4. Vag. adenosis,VIN. ABOUBAKR ELNASHAR
  • 10. Non-specific vaginitis: Haemophilus vaginalis Gardnerella vaginitis: Gardnerella vaginalis Anaerobic vaginosis: Gardnerella vaginalis & anaerobic bacteria Bacterial vaginosis: polymicrobial alteration in vaginal flora causing an increase in vaginal pH, sometimes associated with an homogenous discharge, but in the absence of a demonstrable inflammatory response (Eschenbach et al, 1988) ABOUBAKR ELNASHAR
  • 11. BV is the most common cause of vaginal discharge in young women of reproductive age. Prevalence between 5% & 35% depends on method of screening & the locality. ABOUBAKR ELNASHAR
  • 12. Polymicrobial: G. vaginalis (coccobacilli, surface pathogen), Anaerobic bacteria (Bacteroids, Mobiluncus, Prevotella) & Mycoplasma hominis. There is synergistic relationship between the acquired organisms. They replace lactobacilli ABOUBAKR ELNASHAR
  • 13. Their metabolism produces volatile amines & organic acids other than lactic acids leading to smell & increase pH. Mobiluncus produce trimethylamine giving the smell of rotting fish. Mobiluncus & Bacteroids produce succinate (Keto- acid) which raises vaginal pH. Absence of lactic acid & the production of succinate blunt the chemotactic response of polymorphnuclear leukocytes & reduce their killing ability. This explains absence of cellular inflammatory response. ABOUBAKR ELNASHAR
  • 14. Gram stain b= bacteroids, c= mobilincus, g= gardenerlla, p=peptostreptococci ABOUBAKR ELNASHAR
  • 15. Electron micrograph of Mobiluncus ABOUBAKR ELNASHAR
  • 16. 1. Increase vaginal pH: Semen, after menstruation when estradiol levels increase. 2. Decrease lactobacilli: Douching, change of sexual partner (change of vaginal environment), episodes of candida ABOUBAKR ELNASHAR
  • 17. 3. Smoking: suppresses the immune system facilitating infection. 4. IUCD: 5. Black ethnic groups 6. Lesbians •It is not STD: Treatment of the husband is not beneficial in preventing recurrence of BV. Detection of BV in 12% of virgins after menarche. ABOUBAKR ELNASHAR
  • 18. The reason for the alteration in flora is unclear. 1.Hormonal changes: mechanism is unclear 2.Enzymatic changes: Mucinase & siallidase are elevated in vaginal discharge of BV. Breaking down the mucosal barrier 3.Bacteriophage (virus that infects bacteria) ABOUBAKR ELNASHAR
  • 19. Up to half the women diagnosed with BV are asymptomatic. .Discharge: thin, homogenous, whitish-grey, frothy & fishy. Absence of discharge does not imply the absence of BV. It is not accepted as a reliable indicator on its own as it is neither sensitive nor specific to BV.(Deborah et al,2003) .Seldom associated with mucosal inflammation or irritation of the vagina or vulval itch. ABOUBAKR ELNASHAR
  • 20. 1.pH of discharge: 5.7 A low pH virtually excludes BV. An elevated pH is the most sensitive but least specific as an increase can also associated with menstruation, recent sexual intercourse, or infection with T. vaginalis ABOUBAKR ELNASHAR
  • 21. 2.Whiff test (amine test). Addition of 10% KOH to a sample of vaginal discharge produces fishy odor. It has a positive predictive value of 90% & specificity of 70% ABOUBAKR ELNASHAR
  • 22. 3.Wet film (drop of vaginal secretion & drop of saline): clue cells (epithelial cells covered by coccobacilli, borders are indistinct), No WBC. It is the single most sensitive & specific criterion for BV. , but it is operator dependent. Debris & degenerated cells may be mistaken for clue cells & lactobacilli may adhere to epithelial cells in low numbers. ABOUBAKR ELNASHAR
  • 23. 4. Gram stain: 90% sensitivity, highly sensitive & specific (Gr. Variable c.bacilli, no WBC, no lactobacilli). Scoring systems which weight numbers of lactobacilli & numbers of G vaginalis & Mobiluncus. It is simple & objective method. However the cost & need for microscopist. ABOUBAKR ELNASHAR
  • 24. 5.Rapid tests: .Diamine test: rapid, sensitive & specific .Proline aminopeptidase test (Pip Activity test Card) .A card test for detection of elevated pH & trimethylamine (FemExam test card) .DNA probe based test for high concentration of G. vaginalis (Affirm VP III) may have clinical utility. ABOUBAKR ELNASHAR
  • 25. . Pap. smear: clue cells. Limited clinical utility because of low sensitivity .Culture: It is not recommended as a diagnostic tools because it is not specific. ABOUBAKR ELNASHAR
  • 26. Amsel’s criteria 3 of the following: .Homogenous discharge. .pH> 4.5. . Amine test. .Clue cells. Gram stain alone corresponds well to Amsel’s criteria & to the presence of the associated bacteria. ABOUBAKR ELNASHAR
  • 27. Gynecological 1. Psychological disturbance 2. PID: The microorganisms of BV & PID are similar. There is 10 fold-increased risk of PID in females with BV. 3. Tubal infertility: 1/3 of women with tubal factor infertility had BV compared to 16% of male factor infertility (Wilson et al, 2000). ABOUBAKR ELNASHAR
  • 28. 4. Post-hysterectomy vaginal cuff infection. 5. Uretheral syndrome. 6. HIV susceptibility infection. The presence of BV increases susceptibility to HIV infection BV is not associated with CIN ABOUBAKR ELNASHAR
  • 29. Obstetric 1. Miscarriage: Women with BV had a higher rate of first trimester miscarriage than those with normal vaginal flora. Recurrent first trimester miscarriage has not been associated with BV. The incidence of late miscarriage (13-23 w) is higher in women with BV. 2. Postabortal sepsis. The use of antibiotic prophylaxis before surgical termination of pregnancy demonstrates a protective effect. ABOUBAKR ELNASHAR
  • 30. 3.Preterm labour. The earlier in pregnancy that BV is detected the greater the risk of PTL. Treatment of high risk, BV positive pregnant women has resulted in reduction of PTL by 40-50%. 4.Bactraemia after instrumental delivery 6.Chorioamnionitis. 7.Postpartum endometritis, post cesarean wound infection ABOUBAKR ELNASHAR
  • 31. A. Non pregnant Benefits of treatment: . relieve vaginal symptoms & signs of infection. . Reduce the risk for infectious complications after hysterectomy or abortion. . Reduction of other infectious complications e.g., HIV, STD Indications 1. Symptomatic women (Grade A recommendation). 2. Women undergoing some surgical procedures(Grade A recommendation). ABOUBAKR ELNASHAR
  • 32. Recommended regimens (CDC,2002) Metronidazole 500 mg orally twice a day for 7 days, OR Metronidazole gel 0.75%, one full applicator (5g) intravaginally, once a day for 5 days OR Clindamycin cream 2%, one full applicator (5g) intravaginally at bed time for 7 days. ABOUBAKR ELNASHAR
  • 33. Alternative regimens (CDC,2002) Metronidazole 2 g orally in a single dose, OR Clindamycin 300 mg orally twice a day for 7 days, OR Clindamycin ovules 100 mg intravaginally once at bedtime for 3 days. ABOUBAKR ELNASHAR
  • 34. Notes: •The recommended metronidazole regimens are equally effective. Metronidazole gel is more expensive than tablets •The vaginal clindamycin is less effective than the metronidazole regimens. •The alternative regimens have lower efficacy for BV. •No data support the use of non-vaginal lactobacilli or douching for treatment of BV. ABOUBAKR ELNASHAR
  • 35. •Clindamycin cream or oral is preferred in case of allergy or intolerance to metronidazole. •Theoretically, Metronidazole has an advantage because it is less active against lactobacilli than clindamycin. •Conversely, clindamycin is more active than metronidazole against most of the bacteria associated with bacterial vaginosis ABOUBAKR ELNASHAR
  • 36. .Follow up Follow-up visits are unnecessary if symptoms resolve. Another recommended treatment regimen may be used to treat recurrent disease. Management of husband is not recommended ABOUBAKR ELNASHAR
  • 37. B. Pregnant Natural history: •BV is present in up to 20% of pregnant women depending on how often the population is screened. •The majority is asymptomatic. •It may spontaneously resolve without treatment, although the majority is likely to have persistent infection later in pregnancy. ABOUBAKR ELNASHAR
  • 38. Recommended regimen Metronidazole 250 mg orally three times a day for 7 days, OR Clindamycin 300 mg orally twice a day for 7 days ABOUBAKR ELNASHAR
  • 39. Notes: •Existing data do not support the use of topical agents during pregnancy. Evidence from three trials suggests an increase in adverse events (e.g. prematurity & neonatal infection), particularly in newborns, after use of clindamycin cream (McGregor et al,1994; Joesoef et al,1995; Vermeulen et al,1999). ABOUBAKR ELNASHAR
  • 40. •Multiple studies & meta-analysis have not demonstrated a consistent association between metronidazole during pregnancy & teratogenic or mutagenic effects in newborns (Caro-Paton et al,1997). ABOUBAKR ELNASHAR
  • 41. Indications 1. All symptomatic pregnant women should be tested & treated. 2. Asymptomatic pregnant women at high risk for PTL (previous history), should be screened early in pregnancy & treated (Cochrane library,2002) ABOUBAKR ELNASHAR
  • 42. 3. Asymptomatic pregnant females at low risk for PTL: Data are conflicting whether treatment reduces adverse outcomes of pregnancy. One trial, using oral clindamycin demonstrated a reduction in PTL & postpartum infectious complications (Hay et al, 2001). Oral clindamycin early in the second trimester significantly reduced the rate of late miscarriage & PTL in general obstetric population (Ugwumadu et al, 2003). ABOUBAKR ELNASHAR
  • 43. How to screen for BV ? (Gierdingen et al, 2000) Ask about symptoms & pH of the vagina is determined frequently during pregnancy. If pH > 4.5 ( BV or TV in 84%), do wet mount. Follow-up of pregnant women One month after treatment to evaluate whether therapy was effective is recommended. ABOUBAKR ELNASHAR
  • 44. C. lactation •Metronidazole enters breast milk & may affect its taste. The manufacturer recommend avoiding high doses if breast feeding. •Small amounts of clindamycin enter breast milk. •It is prudent therefore to use an intravaginal treatment for lactating women (Grade C recommendation) ABOUBAKR ELNASHAR
  • 45. Recurrent BV: European (IUSTI/WHO) Guideline, 2011 Most patients will have recurrences within 3 to 12 months, whatever treatment has been used. Suppressive regimens Metronidazole jell (Metrojell) weekly during 16 weeks Adjuvant regimen lactobacilli daily intravaginal for 6 months Acidifying gel ABOUBAKR ELNASHAR
  • 46. Benha University Hospital, Egypt ABOUBAKR ELNASHAR
  • 47. BENHA UNIVERSITY HOSPITAL, EGYPT ABOUBAKR ELNASHAR
  • 48. Prevalence of fungal infection: 37%. dramatic decrease after menopause ABOUBAKR ELNASHAR
  • 49. There are 150 candida species C albicans is by far the most common, it accounts for 80-90% C glabrata is the second most common, it accounts for 5-15% C tropicalis (5%) Other species eg C krusei, C guilliermondi are rarely isolated ABOUBAKR ELNASHAR
  • 50. In recent years, there is significant increase in non- albicans species, particularly C glabrata & C tropicalis, especially in recurrent cases. At present non candidal account for 20% of cases & 30% of recurrent cases. 1.Widespread & inappropriate use of antimycotic treatments (self medication, long term treatment, repeated treatments). Shorter courses of imidazole for c. albicans may lead to an overgrowth of c glabrata ABOUBAKR ELNASHAR
  • 51. 2.Eradication of C albicans causes a selection of species (such as C glabrata) that are resistant to commonly used drugs. Eradication of intestinal C with medication is not successful ABOUBAKR ELNASHAR
  • 52. Candida is found in 2 different states: 1.Blastopores or spores are the phenotype for extension, dissemination & transmission. They are also a resistance form of the fungus, that can be associated with a symptomless colonization. 2.Mycelia are germinative forms; this phenotype can invade tissues & cause symptoms. ABOUBAKR ELNASHAR
  • 53. 1. Vagina: 35% of healthy females,2ndry opportunistic pathogen 2. GIT: anogenital transfer 3. Husband: 25% STD. VVC is not usually acquired through sexual intercourse ABOUBAKR ELNASHAR
  • 54. 1. Compromised immunity: broad spectrum antibiotic, other vag. Infection, trauma (SI), allergen causing skin sensitization, late pregnancy, immuno-suppression. 2. Endocrine disorders: DM, thyroid, parathyroid & adrenal. 3. Menstrual cycle: late luteal phase ABOUBAKR ELNASHAR
  • 55. 4. Drugs: OCPs, corticosteroids, immunosuppressive, antibiotics, antitrichomonal 5. Clothing: occlusive tights. Pregnancy: High estrogen levels cause an increased glycogen load in epithelium, which is a nutritional source for C growth & germination. Estrogen promotes fungal adhesion & germination, fungi are more capable to penetrate vaginal wall ABOUBAKR ELNASHAR
  • 56. OCP: containing high estrogen,the mechanism is same as in pregnancy. No synergic action has ever been shown for low estrogen OCP regarding C growth IUCD: is associated with recurrence because the thread acts as a C reservoir DM: Metabolic disturbance predispose to clinical vaginitis Antibiotics: suppress lactobacilli flora, C are free to grow, adhere & germinate. However several studies failed to show this ABOUBAKR ELNASHAR
  • 57. To be invasive, C follow 3 stage mechanism 1.Adhesion 2.Blastopore germination, mycelium or hyphae development 3.Epithelium invasion Defense factors against C in the vagina: 1. Lactobacilli 2. Humoral immunity, antibodies 3. Cellular immunity ABOUBAKR ELNASHAR
  • 58. Symptomatic vaginitis development Transformation of vaginal colonization into vaginitis is a critical step in the pathogenic mechanism of C vaginitis. During colonization stage, C are present basically in blastopore forms, & their number is not very high. There is a balance between C organisms & vaginal defense factors controlling & limiting fungal growth. ABOUBAKR ELNASHAR
  • 59. Vaginitis appear because of: 1.An increased number or an enhanced virulence of C organisms.or 2. Decreased vaginal defense mechanisms. When this occurs, blastopores adhere to vaginal epithelium & germinate; mycelium develops & finally invades mucous membrane producing vaginitis. ABOUBAKR ELNASHAR
  • 60. . Vulval itch (cardinal symptom): increase with warmth & at night . Discharge: ranging from scanty, thick, whitish, adherent to vagina to a thin watery liquid,pH:4-5. . Burning: Vulval & vaginaL is not dominant, but gets worse with micturition or coitus . dysparunia , dysuria. ABOUBAKR ELNASHAR
  • 62. PH of discharge:4-5 . Wet mount: saline Koh 10%: can ifentify pseudohyphae & blastospores in 70% . Gram stain. . Pap. Smear: 50%. It is not performed for this condition . Culture: Nickerson, Sabourad, Only when microscopy is not diagnostic . Kits: slide agglutination test is rapid diagnostic test.ABOUBAKR ELNASHAR
  • 64. .Colonization .Uncomplicated VVC: 1.Sporadic or infrequent VVC 2.Mild or moderate VVC 3.Likely to be C. albicans 4.Non-immunocompromized . ABOUBAKR ELNASHAR
  • 65. .Complicated VVC: 1.Recurrent VVC 2.Severe VVC: extensive vulvar erythema, oedema, and excoriation, fissure formation. Symptoms are correlated with the amount of yeast in the vagina (Odds,1988) 3.Non-albicans VVC 4.Women with uncontrolled , DM, debilitation, immunosuppression or those who are pregnant ABOUBAKR ELNASHAR
  • 66. 1. other causes of vaginal discharge. Infection with Herpes genitals, TV, bacterial vaginosis, & 2. Vulval disease, especially vulval eczema, dermatitis, lichen sclerosis & vulval vestibulitis. Ask the patient to identify the itchy area. If there are symptoms of dysparunia, the Q-tip test for the vulval vestibulitis syndrome should be performed ABOUBAKR ELNASHAR
  • 67. 1.Wiping from front to back 2.Avoiding tight underwear especially synthetics 3.Avoidance of excessive washing, use of bubble baths & perfumed soaps ABOUBAKR ELNASHAR
  • 68. Asymptomatic female should not be treated even if the culture is positive Uncomplicated: . Local (topical, intravaginal) antifungal: Polyene: nystatin. Azoles: clotrimazole, miconazole, econazole, butoconazole, ticonazole, terconazole. ABOUBAKR ELNASHAR
  • 69. •Both azoles & nystatin are fungistatic rather than fungicidal. •Nystatin (Nysert, Mycostatin and Nystan) less effective than azole treatment. It needs to be given for 14 days, but is indicated if there is a possibility of non-albicans yeast infection. •Azoles resulted in higher rates of clinical & mycologic cure (80-95%) than nystatin (&0-90%) in non pregnant acute VVC. •Short course (single dose & regimens of 1-3 days)effectively treat uncomplicated VVC. ABOUBAKR ELNASHAR
  • 70. 2. Oral antifungal: more effective against non-albican species. . Ketoconazole (Nizoral ,200mg) Dose: 1X2X5 . Itraconazole (Sporanox, 100 mg ) Dose: 2X2X1 . Fluconazole (Diflucan, Alkanazol,150 mg) Dose : 1 tab single dose • ABOUBAKR ELNASHAR
  • 71. Oral or vaginal antifungal (Cochrane libarary, 2001) .No differences in effectiveness (mycological & clinical cure ) for uncomplicated candidiasis. (Both routes had clinical cure 80%) .The oral route is the preferred route by the patient. The decision to prescribe oral or vaginal depends on safety, cost, effectiveness, & patient preference. Oral preparation is more expensive & associated with more systemic side effects than vaginal route. Vaginal route is first line of therapy (Reef, 1993) ABOUBAKR ELNASHAR
  • 72. Follow-up: Patients should be instructed to return for follow-up visits only if symptoms persist or recur within 2 months of onset of initial symptoms T.T of the husband with oral antifungal did not influence either cure rate or recurrence rate (Shihadeh & Nawafleh,2000) ABOUBAKR ELNASHAR
  • 73. Causes of clinical failure: 1.Vaginitis due to other causes. 2.Undiagnosed urogenital infection. 3.Chemical irritants: perfumed products, detergents 4.Physical damage: sexual intercourse, tampons Causes of therapeutic failure: 1.Resistance to the antifungal 2.Presence of species out side the spectrum of the antifungal. Non albicans C are associated with vaginitis & are more resistant to conventional antifungal therapy. These is evidence that C glabrata & C Krusei are resistant to fluconazole & itraconazole (Rex,2000)ABOUBAKR ELNASHAR
  • 74. Complicated VVC Recurrent VVC Define: 4 or more episodes/Y. Reappearance of C in the vagina of a patient, who was cured, & may be either Relapse, (due to re-growth of a previously undetected residual population of C.) or Re-infection (the vagina is re-inoculated from some extravaginal source). ABOUBAKR ELNASHAR
  • 75. Prevalence: 5% in family planning clinic & 10% in antenatal clinic. No apparent predisposing or underlying conditions in most cases. Pathogenesis: Non-albicans are found in 30% of cases Source: 1.Vaginal inoculation: most common Intestinal reservoir theory Sexual transmission 2.Vaginal recurrence ABOUBAKR ELNASHAR
  • 76. Although iron deficiency anaemia has been suggested as a cause of recurrent VVC, there is no evidence to support this. DM is rarely newly diagnosed. Allergic rhinitis/hayfever may be immunologically linked with RVVC. Mechanisms: 1.Increased C virulence 2.Host factors Decreased secretory local immunity IgE mediated hypersensitivity reaction Loss of lactobacilli protective effect ABOUBAKR ELNASHAR
  • 77. Treatment: .Vaginal culture should be obtained to confirm clinical diagnosis & to identify unusual species, including non-albicans species, particularly C glabrata (not form hyphae). 1. Longer duration of initial therapy a.7-14 days of topical therapy or b. 150-mg, oral dose of fluconazole repeated 3 days later to achieve mycologic remission before initiating a maintenance therapy. In contrast to severe VVC, increasing the length of therapy by up to 1 week, for example by adding a second dose of fluconazole, does not improve response (Sobel et al, 2001) ABOUBAKR ELNASHAR
  • 78. 2. Maintenance (Suppressive) therapy for 6 months: Clotrimazole (500-mg dose vaginal sup once weekly) Ketoconazole (100 mg once daily) Fluconazole (100-150 mg once weekly) Itraconazole (400 mg once monthly or 100 mg once daily) The frequency of therapy depend on frequency of attacks (White & Vanthuyne,2002): > 1/month: weekly doses, 1/month: monthly doses. Twice-monthly doses are usually adequate: D8 & D 18 of the cycle just before the hormonal peaks ABOUBAKR ELNASHAR
  • 79. Treatment of the husband: controversial Treatment of the predisposing factors: Nitrofurantoin & nalidixic acid are recommended for UTI since they give low tissue levels. Psychosexual problems are common in RVVC, use of vaginal lubricants is important Relapse: 40% of women, the cycle of suppressive therapy can be continued indefinitely (Sobel et al,1992) ABOUBAKR ELNASHAR
  • 80. Side effects of oral azoles: are few (Inman et al,1993) 1.Gastrointestinal symptoms 2.Headache 3.Interactions with other drugs: astemizole, calcium channel antagonists, cisapride, coumadin, cyclosporin A, oral hypoglycemic agents, phenytoin, theophylline, rifampicin. .If there is poor response: typing to exclude C glabrata: Itraconazol 200 mg daily for a month combined with Nystatin 500 iu qds orally & nystatin pessaries one bd for 3-4 months (Emens, 1998). Monitoring of liver function is mandatory ABOUBAKR ELNASHAR
  • 81. Severe VVC: Response to short course of topical or oral therapy is poor Topical azole 7-10 days or Fluconazole in 2 sequential doses (second dose 72 hrs after initial dose) ABOUBAKR ELNASHAR
  • 82. Non-albicans VVC 1.First line therapy: Longer duration therapy with a non-fluconazole azole is recommended i.e; Nstatin pessaries once or twice nightly for 14 days. 2.2nd line treatment (If recurrence occurs) 600 mg of boric acid in gelatin capsule vaginally once daily for 2 weeks. ABOUBAKR ELNASHAR
  • 83. 3.The final resort: Topical 4% flucytosine, the only fungicidal agent, & amphotericin B (Fungizone)in lubricating gjelly for 14 nights 4.If non-albicans VVC continues to recur, a maintenance regimen of 100,000 units of nstatin delivered vaginally. 5. Intravaginal painting with gentian violet & oral progesterone ( little information is available) ABOUBAKR ELNASHAR
  • 84. Compromised host: 1.Correction of the condition 2.Prolonged conventional treatment course (7-10 days) Pregnancy: Only topical azole therapies applied for 7 days are recommended (CDC, 2002) ABOUBAKR ELNASHAR
  • 85. VVC During pregnancy VVC is more common during pregnancy Cochrane library,( 2002): •There is no evidence that VVC is harmful to the baby •Azole drugs are more effective than nystatin. •Treatment for 7 days is necessary. Treatment for > 1w confer no extra benefit. 4-day course will cure half of infections & 7 day course cures over 90%. ABOUBAKR ELNASHAR
  • 86. •There is no evidence that any one azole is any more effective than another. •Oral antifungal is not known to be effective or safe in pregnancy. •Benjamin et al (2000) reported that •itraconazole is safe during pregnancy. It is teratogenic in rat through affecting the adrenal gland. These adrenal effects do not occur in human being. ABOUBAKR ELNASHAR
  • 88. Incidence decreased Etiology T.V (actively mobile with 4 unipolar flagellae) Mode of transmission STD Vertical (urethra) Non sexual (bath water, swimming pool, toilets) Reservoir: urethral & periurethral glands. Incubation period: 3 to 28 days ABOUBAKR ELNASHAR
  • 89. Clinical picture Vag. discharge: foul, frothy, greenish, excessive (during or immediately after menses) Itching, vulval soreness (TV & candidiasis cause 90% of P. vulvae) Dysparunia, dysuria • Common symptoms: vaginal discharge (50% to 75%), vaginal itching and pain during intercourse  Pelvic exam: frothy vaginal discharge, vaginal erythema and “strawberry” cervix ABOUBAKR ELNASHAR
  • 90. Purulent Vaginal Discharge in Trichomonal Vaginitis McGraw-Hill ABOUBAKR ELNASHAR
  • 91. Diagnosis Wet mount: motile, pear shaped, size of polymorph. 60% sensitivity Pap. smear: 50 % sensitivity pH of discharge: 5-7 alkaline Culture: Feinberg, Whittington (>95%) Colposcopy: focal vaginitis, red punctate vaginitis, Y shaped vessels. ABOUBAKR ELNASHAR
  • 92. Saline wet mount of vaginal secretions in trichomonal vaginitis, showing two T. vaginalis (arrows), leukocytes and a normal vaginal epithelial cell McGraw-Hill ABOUBAKR ELNASHAR
  • 93. Pap smear: 70% sensitive in showing TV. Wet mount: TV ABOUBAKR ELNASHAR
  • 95. Treatment TT of the husband: In 1/3 the organism is found in male urethra Metronidazole: drug of choice Recommended regimen: 2gm single dose Alternative regimen: 250 mg1x3x7 or 500 mg twice a day for 7 days 2. Metronidazole gel: 3. Tinidazole (Fasigen) 4 t single dose During pregnancy: 1. Clotrimazole: eradicate TV in 50% & symptoms in 75 % 2. Metronidazole gel: ABOUBAKR ELNASHAR
  • 96. * Failure of the treatment: rare Cause: 1.Degradation of metronidazole by other bacteria 2.failure of absorption of metronidazole TT: 1. Metronidazole:2-4 gm/ d in divided doses 2. Metronidazole + broad spectrum antibiotics ABOUBAKR ELNASHAR
  • 98. Etiology Estrogen deficiency: childhood, postmenopause Clinical picture 1.Vag. dryness, itching, dysparunia Vag. bleeding Dysuria, frequency, urgency (atrohy of the lower urinary tract). Vagina: pale, thin, peticheal he (superimposed infection). ABOUBAKR ELNASHAR
  • 99. DIAGNOSIS 1.Pap. smear 2.Colposcopy D & C Hysteroscopy TREATMENT Estrogen : oral vag cream intravaginally every other day. ABOUBAKR ELNASHAR
  • 101. G B STREPTOCOCCUS Purulent vag discharge Diagnosis: 10 WBC/HPF HVS Treatment: penicillin or erythromycin ABOUBAKR ELNASHAR