Vulvovaginal candidiasis

1. ABOUBAKR ELNASHAR
BENHA UNIVERSITY HOSPITAL, EGYPT

2. Prevalence of fungal infection:
37%.
dramatic decrease after menopause
ABOUBAKR ELNASHAR

3. 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

4. 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

5. 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

6. 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

7. 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

8. 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

9. 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

10. 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

11. 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

12. 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

13. 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

14. .
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

15. ABOUBAKR ELNASHAR

16. 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

17. ABOUBAKR ELNASHAR

18. .Colonization
.Uncomplicated VVC:
1.Sporadic or infrequent VVC
2.Mild or moderate VVC
3.Likely to be C. albicans
4.Non-immunocompromized
.
ABOUBAKR ELNASHAR

19. .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

20. 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

21. 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

22. 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

23. •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

24. 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

25. 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

26. 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

27. 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

28. 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

29. 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

30. 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

31. 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

32. 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

33. 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

34. 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

35. 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

36. 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

37. 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

38. Non-C. albicans-related disease is less likely to respond to
azole therapy (184).
Vaginal boric acid, administered in a gelatin capsule at a
dosage of 600 mg daily for 14 days, cures up to 70% of C.
glabrata infections (238).
Treatment with AmB suppositories (50 mg nightly for 14 days)
is another option with minimal side effects that has shown to
be successful in 70% of women with non-C. albicans VVC,
mostly due to C. glabrata, that did not respond to azole
treatment (197). Other alternatives include topical 17%
flucytosine cream alone or in combination with 3% AmB cream
administered daily for 14 days,albeit at considerable expense
due to the high cost of flucytosine (189). Of note is that all the
treatment options for non-C. albicans VVC need to be
compounded.
ABOUBAKR ELNASHAR

39. 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

40. 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

41. •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

42. ABOUBAKR ELNASHAR