VAGINAL CANDIDIASIS

Prevalence of fungal infection:

37%.
dramatic decrease after menopause
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
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
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
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.
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
1. Compromised immunity:
broad spectrum antibiotic,Infection,
late pregnancy, immuno-suppression.

2. Endocrine disorders:
DM, thyroid, parathyroid & adrenal.

3. Menstrual cycle: late luteal phase

4. Drugs:
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
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
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
 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

blastospore forms, & their number is not very high.
There is a balance between C organisms & vaginal
defense factors controlling & limiting fungal growth.
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.
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.
 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.
.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
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
1.Wiping from front to back
2.Avoiding tight underwear especially synthetics
3.Avoidance of excessive washing, use of bubble baths &
perfumed soaps
 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.
•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.
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
•
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)
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