                    
~ Candidal Vaginal Infections ~
§ Epidemiology:
° Candida species
reside in the yeast form as commensals in human being. It is
estimated that up to 40% of normal women with no evidence
of active
disease harbor Candida species in their vaginas.
° 75% of all women will
develop a vaginal fungal (yeast) infection at some
time in their lives.
° Additional 40% to 50% of
these women will have recurrent infections of a
similar nature.
§ Risk factors:
j Diabetes:
– Increased amount of
glucose in their vaginal secretions, which predisposing the yeast
organism to overgrowth, resulting in infection.
– Hyperglycemia,
which enhances yeast adhesion and alters phagocytosis
k HIV infections
l Broad-spectrum
antimicrobial agents:
– Tetracycline, impairing
the host immune response by altering phagocytosis and
decreasing the numbers of bacteria in the normal vaginal
flora, thereby reducing the
number of organisms competing with the yeast for the food
supply.
m Pregnancy:
– Increased glycogen
stores in the vaginal mucosal cells
– Alteration of
carbohydrate metabolism and the generation of sugar substrates that
enhance yeast attachment to epithelial cells
– Suppression of T-cell
immunity, which lowers natural defenses and can lead to
proliferation of the organisms.
n Oral contraceptives:
– Increased glycogen
stores in the vaginal mucosal cells
– Alteration of
carbohydrate metabolism and the generation of sugar substrates that
enhance yeast attachment to epithelial cells
– Suppression of T-cell
immunity, which lowers natural defenses and can lead to
proliferation of the organisms.
– Proliferation is related
to hormone levels.
o Intrauterine contraceptive
devices
§ Pathophysiology and etiology:
° Candida species
truly are opportunistic pathogens. They usually do not cause
disease unless a disturbance in the status quo causes a
rapid increase in their
numbers.
° Once the events that lead
to disease occur, however, these organisms take on
the invasive hyphae or pseudohyphae form. The one exception
to this rule is
C glabrata, which does not have a mycelial
phase.
° The species most commonly
associated with candidal vaginal infections:
C albicans, C glabrata, C tropicalis,
C krusei, C guilliermondii, and C pseudotropicalis.
§ Diagnosis:
° The major problem in
making a diagnosis and determining the frequency of
fungal infections in women is that these conditions are
often mimicked by
other physiologic phenomena, for example, physiologic
discharge at
midcycle.
° The diagnosis usually is
based on symptoms, clinical signs, and confirmatory
microscopy. Rarely are cultures or more sophisticated
diagnostic techniques
required.
° The prime symptom of a
true infection: pruritus
° Clinical signs:
– Erythema
rarely presented
– Edema with
a physiologic
– Tenderness discharge
at midcycle
– Discharge:
å The discharge of a
true yeast infection may take many forms. It may be absent or
unremarkable in appearance, or it may be thick, white,
and curdy, with attendant
plaques on the vaginal wall.
° Microscopic examination of
vaginal secretions (with either a normal saline or
strong base wet preparation):
– The presence of a
psedohyphae or mycelial phase is diagnostic of fungal
infection, as opposed to fungal colonization.
– If only the yeast form
is seen, the patient either is not infected and
carrying a commensal or is infectied with C glabrata.
° Culture and speciation of
the organism:
– Maybe helpful for those
patients harboring organisms that do not respond
to treatment and in those instances when there is a
question of
antimicrobial resistance.
– Uniform methods for
fungal antimicrobial sensitivity have not been
established.
° Other tools:
– Gram’s stain of vaginal
secretions
– Pap smears of cervical
and vaginal secretions
– latex fixation for C
albicans
§ Treatment:
° There are numerous
therapeutic options with a wide range of topical and
systemic agents at varying prices available to patients.
These therapies
appear to be equally effective, with 80% to 95% cure rates.
° The selection of one
method of therapy over another depends on the patient’s
preference.
° The development of
resistance to the current therapeutic agents has not been a
significant clinical problem.
° Types of treatment:
| |
Topical Preparations |
Systemic Formula |
|
Polyenes |
P Nystatin (MycostatinR)
(100000 IU) |
P Amphotericin B (FungizoneR):
¾ Intravenous
infusion.
¾ Reserved for
deep-seated,
serious infection because of
its high toxicity |
|
Azoles |
P Butoconazole
P Clotrimazole (CanestenR)
P Miconazole (Antifungal
VTR)
P Terconazole
P Tioconazole
ø Currently most
commonly
used topical agents
ø Mode of
action:
inhibition of ergosterol synthesis. |
P Ketoconazole (NizoralR):
¾ Requiring more
doses
P Fluconazole (DiflucanR):
¾ Single-dose
P Itraconazole (SporanoxR):
¾ Single-dose
ø Orally
administration |
|
Nonazole |
P Boric acid:
¾ 600 mg VT qd
for 14 days
¾ effective in
eradicating most of
the more aggressive and more
difficult to treat vaginal fungal
infections |
|
|
註 |
ø Available
preparation:
creams, suppositories, vaginal tablets |
|
° CDC-recommended regimens
for candidal vaginal infections:
|
Agent |
Dosage |
|
Intravaginal |
|
|
Butoconazole |
2% cream, 5g qd for 3 days |
|
Clotrimazole (CanestenR) (1%, 20g/T)) |
1% cream, 5g qd for 7-14 days |
|
Clotrimazole (CanestenR) (100mg) |
1# qd for 7 days |
|
Clotrimazole (CanestenR) (100mg) |
2# qd for 3 days |
|
Clotrimazole (CanestenR) |
One 500mg tablet in a single application |
|
Miconazole (AntifungalR) |
2% cream, 5g qd for 7 days |
|
Miconazole (Antifungal VTR) (100mg) |
1# qd for 7 days |
|
Miconazole (Antifungal VTR) |
One 200mg suppository qd for 3 days |
|
Nystatin (MycostatinR) (100000 IU) |
1# qd for 14 days |
|
Terconazole |
0.4% cream, 5g qd for 7 days |
|
Terconazole |
0.8% cream, 5g qd for 3 days |
|
Terconazole |
One 80mg suppository qd for 3 days |
|
Tioconazole |
6.5% ointment, 5g in a single application |
|
Oral |
|
|
Fluconazole (DiflucanR) (50mg) |
3# in a single dose |
§ Complications:
j Balanitis in the male
partner resulting from sexual transmission
k Chronic persistence or
recurrence of the infection due to difficulty in
eradicating the fungus
ø It has been found
that C tropicalis and C glabrata tend to be more hardy and more
difficult
to treat than C albicans.
l Chorioamnionitis caused by
ascending infection
§ References:
1). Candidal vaginal infections: diagnosis and treatment.
Michael R. Spence, MD, MPH.
Contemporary OB/GYN April 2000: 15-23
Filename: Candidal Vaginal Infections
| 
