Practical Guide to Diagnosing and Treating

Vaginitis
, MD, FACOG, US Naval Medical Center

Abstract and Introduction

Abstract

Bacterial vaginosis (BV), candidiasis, and trichomoniasis account for more than 90% of vaginal
infections. BV typically is associated with a decrease in commensal, protective lactobacilli and a
proliferation of other flora. Mobiluncus is pathognomonic but found in only 20% of cases.
Presence of 3 of 4 criteria indicates BV: a homogenous noninflammatory discharge (not many
WBCs); pH >4.5; clue cells (bacteria attached to borders of epithelial cells, > 20 % of epithelial
cells); and a positive whiff test. New intravaginal BV preparations cause less-adverse systemic
effects than oral regimens. Trichomonas vaginalis, a protozoan, appears to be sexually
transmitted and causes up to 25% of vaginitis cases. Diagnosis is made by observation of a foul,
frothy discharge; pH >4.5 (present in 70% of cases); punctate cervical microhemorrhages (25%
of cases); and motile trichomonads on wet mount (50%-75% of cases). Recommended treatment
is a single 2g dose of oral metronidazole. Treatment failure is usually due to nontreatment of the
male partner. Candidiasis typically presents as a thick, "curdled" white discharge or vulvar
pruritus, with a hyperemic vagina and an erythematous and/or excoriated vulva. Vaginal pH is
usually in the normal range of 3.8-4.2 in uncomplicated candidiasis. Microscopic examination of
the discharge reveals hyphae or budding yeast in 50%-70% of cases. While the most common
offender is Candida albicans, Candida tropicalis and Candida glabrata have become
increasingly prevalent. Approximately 15% of C albicans organisms are resistant to clotrimazole
and miconazole. Recurrent infections may be treated with fluconazole 150mg weekly for up to
12 consecutive weeks.

Introduction

Vaginal discharge and the associated vulvar itching are the most common reasons for a woman to
seek gynecological care. While these may seem minor complaints to the provider, the patient
may feel intensely anxious over the possibility of an underlying sexually transmitted disease
(STD) or even cancer. The initial episode provides the best opportunity for effective resolution of
symptoms. Hence, appropriate treatment needs to be based upon correct and complete diagnosis,
for which an understanding of the pathophysiology of the discharge is essential.

Not all vaginal discharges result from an infective etiology. Atrophic vaginitis, physiologic
leukorrhea, and local irritants cause a number of cases. Of the infective etiologies, bacterial

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vaginosis (BV) and yeast (candidiasis) are by far the most common. Add the occasional case of
trichomoniasis, and the list covers more than 90% of the cases of vaginal infections. [1] Not
infrequently, multiple etiologies exist.

Diagnosis and elimination of the cause of the problem rely heavily on an accurate and thorough
history and physical examination.[2] The history should investigate the patient's duration of
symptoms, her sexual activity, whether the discharge smells foul after intercourse, current
medical conditions, medications, contraceptive methods, prior similar episodes, and a history of
STDs.[3] In the search for a noninfective cause of the vaginosis, ask the woman if she has
changed detergents/fabric softeners or uses scented hygiene products or douches. Also ascertain
whether the woman has any signs of complications or systemic infection: abdominal or pelvic
pain suggesting pelvic inflammatory disease, dysuria suggesting urinary tract infection, and
fever.

Physical Exam
Using a good light source and a vaginal speculum, inspect the vulva, vaginal walls, and cervix
for the presence of lesions, erythema, and excoriations. The discharge should be observed for
color, consistency, odor, and whether it is vaginal or emanating from the cervix. Using either a
dipstick or paper roll, measure the pH of secretions from the vaginal sidewall (not from the
posterior fornix, which may be contaminated with cervical mucus). Separate slides of the
discharge should then be made with 10% KOH (potassium hydroxide) and with normal saline,
then secured with cover slips and examined for flagellated protozoa, hyphae or budding yeast, or
other organisms under the microscope. Slides should be wafted for the release of volatile amines
(a fishy or musty odor) upon adding the alkaline KOH solution, since this is a sign of bacterial
vaginosis.

Bacterial Vaginosis
BV is a polymicrobial, primarily anaerobic, infection associated with sometimes fishy-smelling
increased vaginal discharge (Fig. 1), but not accompanied by leukorrhea, vulvar burning, or
pruritis. Infection with BV can have significant sequelae, however. It has been associated with an
increased risk of septic abortion, premature rupture of amniotic membranes, preterm labor,
preterm delivery, post-Cesarean endomyometritis, and post-hysterectomy pelvic cellulitis.[4-11]

2
Figure 1. The characteristic milky or creamy vaginal discharge of bacterial
vaginosis is associated with a high vaginal pH and a fishy odor. Figure courtesy of
James A. McGregor, MD, University of Colorado Health Sciences Center.

Its presence represents a change in the vaginal ecosystem, specifically a decrease in lactobacilli,
which is part of the normal flora; a proliferation of pathogenic inhabitants of the vagina; and an
elevation of pH (>4.5). Despite exhaustive basic research, it is unclear whether the decline in
lactobacilli, proliferation of pathogens, or rise in pH initiates the cascade. While BV was
originally described by Curtis in 1911, it gained notoriety only in 1955 after Gardner and Dukes
described the offending organism as Haemophilus vaginalis; the organism has since been
renamed Gardnerella vaginalis in honor of its discoverer.[1] The current term, bacterial vaginosis,
rather than vaginitis, indicates lack of an inflammatory reaction (absence of WBCs in the
discharge) and is much more reflective of the true polymicrobial nature of this condition.

Although the majority of pathogens causing BV are derived from the endogenous flora, one
genus--Mobiluncus--is unique to patients with BV; it has never been found in patients without
vaginosis. Mobiluncus are comma-shaped, gram-variable or gram-negative, anaerobic rods with
tapered ends that utilize subpolar flagella for a tumbling motility. G vaginalis is found in nearly
100% of women with symptomatic BV.[12] In fact, G vaginalis may be the organism primarily
responsible for the premature rupture of membranes in women with BV. The organism has
phospholipase A2 activity, which initiates labor.[13] Other factors may also play a role in early
labor, however, as G vaginalis is also found in many normal women with uncomplicated
pregnancies.

Whether BV is sexually transmitted remains unsettled. The majority of observations, such as

those listed below, suggests that BV is probably not sexually transmitted.

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 1. Urethral colonization rates of Gardnerella and Mobiluncus species among male partners
of women with BV have been observed to be no higher than those for partners of normal
women.[14]

2. The incidence of BV has not been documented to rise with increasing number of lifetime
sexual partners.[14]

3. Cotreating the male partner has not been shown to reduce the recurrence risk in females
(hence the basis for the current recommendation not to cotreat the male partner).[14,15]

However, one contrary piece of evidence, suggesting a sexually transmitted aspect, is that
condom use is associated with a decreased incidence of BV among the female partners. Hence, if
a patient experiences recurrences of BV, there is some basis to treat the partner.[16]

Bacterial vaginosis identified on wet mount (Fig. 2) represents the most common vaginal
infection identified in women with inflammation or altered flora on Papanicolaou smear.[17]

Figure 2. On wet preparation of vaginal fluid, absence of WBCs and stippling of

epithelial cells support a diagnosis of bacterial vaginosis. From Infect Med 9(1):50,
1992. Copyright 1992, SCP Communications, Inc.

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Diagnosis. The diagnosis of BV requires the presence of at least 3 of the following 4 criteria
(Table I):[18]

1. A homogenous noninflammatory discharge (not many WBCs).

2. Vaginal pH >4.5.

3. Clue cells (bacteria attached to the borders of epithelial cells, >20 % of epithelial cells;
Fig. 3).

4. Whiff test positive for fishy or musty odor when alkaline KOH solution added to smear.

Figure 3. Pap smear showing clue cells consistent with bacterial vaginosis.
Courtesy of Abner P. Korn, MD. Copyright 1996, SCP Communications, Inc.

Applying these diagnostic criteria will result in correctly diagnosing BV more than 90% of the
time with a false-positive rate of less than 10%.[18,19] Note that neither Papanicolaou smear nor
culture are diagnostic in and of themselves. The Papanicolaou smear may indicate a
coccobacillary shift of flora, but this report should prompt patient evaluation for the formal
diagnostic criteria rather than empiric treatment. Culture is not helpful since the flora of BV are
largely derived from the normal commensal flora.

Treatment. For years, oral metronidazole has been the primary indicated regimen. While very
effective, this regimen is fraught with such serious side effects as convulsive seizures and
peripheral neuropathy, causing many patients to discontinue their treatment prior to completion
of the 7-day regimen. Other systemic options include oral clindamycin. More recently, the advent
of intravaginal preparations has afforded topical options that cause less-adverse systemic effects.
[20]
The amount of drug absorbed and delivered is also much less. For example, metronidazole
requires an oral dose of 500mg, while only 37.5mg of metronidazole intravaginal gel is needed

5
to achieve therapeutic vaginal tissue levels.[21,22] Similarly, oral and intravaginal preparations of
clindamycin achieve equal efficacy, although a lower dose is delivered intravaginally.[20,23]

While the regimens listed in Table II have been shown to provide 90% or better efficacy, the
single 2g dose of metronidazole affords only 70% efficacy and leads to more gastrointestinal
adverse effects than clindamycin.[24-27] The oral clindamycin regimen is associated with a higher
incidence of diarrhea than oral metronidazole.[28] A decade ago, ampicillin had traditionally been
endorsed as first-line therapy for BV in pregnancy; however, this finding was based more on
safety concerns than on efficacy. Given the more recent data suggesting that BV is associated
with worse obstetric outcomes,[4,9-11] more efficacious therapy is justified. Oral metronidazole
alone, or in combination with oral erythromycin, has been shown to reduce adverse obstetric
sequelae in high-risk patients with BV.[29,30] Clindamycin cream, while effectively treating the
BV, was associated by Amsel's criteria with worse obstetric outcomes.[31,32] This paradox may be
explained by clindamycin reducing the endogenous lactobacillus population or by the
overgrowth of Escherichia coli and Enterococcus.[23,33] Despite common opinion, exhaustive
studies have not shown metronidazole to be teratogenic. It is mutagenic in bacteria and
carcinogenic in rodents, but no human data have demonstrated adverse outcomes when subjected
to analytic scrutiny. However, several sources, albeit without evidence-based data, state that
metronidazole is contraindicated in the first trimester of pregnancy.[15,28]

Trichomonas vaginalis
The trichomonad parasite is a flagellated protozoan that causes up to 25% of vaginitis cases.
While trichomonas infection is asymptomatic up to 50% of the time, [34] when clinical signs are
present they include irritation and soreness of the vulva, perineum, and thighs, with dyspareunia
and dysuria. Typically, the trichomonas infection is accompanied by a copious, greenish-yellow
frothy discharge (Fig. 4a). Unlike bacterial vaginosis, it seems that trichomonas is primarily a
sexually transmitted infection.

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Figure 4a. Bubbly discharge of vaginal fluid growing the parasite Trichomonas
vaginalis. Figure courtesy of James A. McGregor, MD, University of Colorado Health
Sciences Center.

Diagnosis. The diagnosis is made by observation of the following features (Table I):

A foul-smelling frothy discharge (present in 35% of cases

Vaginal pH >4.5 (70% of cases)

Punctate cervical microhemorrhages (25%)[34]

Motile trichomonads on wet mount (50%-75%)[35]

Papanicolaou smear is quoted to be 70% sensitive in identifying trichomonads [28] (Fig. 4b). But
the resemblance of leukocytes to nonmotile parasites can lead to overdiagnosis of trichomonas
when a Pap smear is used to confirm a suspected infection. Cultures are not generally indicated
because wet mount and clinical diagnostic criteria are sufficiently accurate (except for
recalcitrant infections or when rare instances of metronidazole resistance are suspected).

Figure 4b. Pap smear is reported to be 70% sensitive in showing Trichomonas

vaginalis infection. Courtesy of Abner P. Korn, MD. Copyright 1996, SCP
Communications, Inc.

Treatment. The current primary treatment recommendation is a single 2g dose of oral

metronidazole (Table II). For those who cannot tolerate this single large dose, 500mg bid for 7
days is equally efficacious if the patient completes her regimen. The male partner(s) must also
receive treatment. The most common cause of treatment failure in a woman is failure to treat the
partner(s). Actual metronidazole resistance is decidedly rare. There is no consensus as to the best
treatment of this condition. Many authorities recommend high-dose (2g or more) metronidazole

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daily for several consecutive days.[15] This regimen may be supplemented with intravaginal
metronidazole suppositories (500mg bid). The 0.75% metronidazole gel is only 50% effective in
treating trichomoniasis. Alternatively, the patient may be admitted for intravenous metronidazole
500mg every 8 hours.[36,37] Clotrimazole, another nitro-imidazole compound similar to
metronidazole, has been reported to attain nearly a 50% cure rate when given as an intravaginal
cream.[38] Neither of these latter 2 regimens is endorsed by the US Food and Drug Administration
(FDA) for this indication.

While classically contraindicated in the first trimester of pregnancy, the 2g single dose of
metronidazole may be given thereafter in pregnancy. In the interim, clotrimazole has some
(approximately 50%) efficacy, although has not been approved by the FDA for this use.[38]

Candidiasis
Candida, a commensal organism, is found in small population densities in the vaginal
ecosystems of nearly one third of healthy women. Symptomatic infection arises, however, when
proliferation causes a shift from colonization to frank adherence and infection. The most
common offender is Calbicans; however, other species of Candida, such as tropicalis and
glabrata, have become increasingly prevalent, currently representing one third of isolates. [39]
Vaginal candidiasis occurs more commonly after antibiotic treatment and among women taking
oral contraceptives.[40-42] Yet unless a patient has a history of antibiotic-associated candidiasis, it
is not recommended to routinely prescribe antifungal therapy for every woman with candidiasis
preceded by a course of antibiotics.

Diagnosis. The patient typically presents with a thick, "curdled" white discharge or vulvar
pruritus (Table I). The vagina has no "itch" receptors, hence, pruritus ensues only after the fungus
has spread distally onto the vulva (Fig. 5). The discharge is usually neither malodorous nor off-
white unless a mixed infection is present. The vagina often appears hyperemic; the vulva can be
erythematous and/or excoriated. Vaginal pH is usually normal in cases of uncomplicated
candidiasis. Microscopy of the discharge with 10% KOH will often reveal hyphae or budding
yeast in 50%-70% of cases[43,44] (Fig. 6). C albicans organisms are easiest to identify, as they
have long hyphae with blastospores along their length and a terminal cluster of chlamydiaspores
(Fig. 7). The "atypical" species of yeast, however, may only have features of budding yeast
(resembling small snowmen), which are easily obscured within surrounding cellular debris.
Hence, if a patient presents with classic symptoms of candidiasis and her thorough evaluation is
otherwise negative (normal pH, no motile trichomonads, no clue cells, no excessive leukocytes),
it is not unreasonable to offer the patient an antifungal agent as a therapeutic trial. Fungal
cultures are not recommended initially.[39] The presence of fungal elements on Papanicolaou
smear is not necessarily indicative of infection; because it could simply represent colonization,
treatment is not recommended on the basis of this finding alone.[45]

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Figure 5. Vaginal mucosa can be covered with numerous white, thrushlike patches
in vulvovaginal candidiasis. From The AIDS Reader, 1(5):155, 1991, courtesy of
Jeffrey Laurence, MD. Reproduced from Kaufman RH: Common causes of vaginitis.
Hosp Med 22:23-44, 1986.

Figure 6. Pseudohyphae and blastoconidia (yeast cells) on wet mount (KOH

preparation) are consistent with Candida albicans. Copyright 1992, SCP
Communications, Inc.

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Figure 7. Both pseudohyphae and blastoconidia (yeast cells) stain purple on
Gram's stain preparation of clinical material from patient with candidiasis.
Copyright 1992, SCP Communications, Inc.

Patients often experience recurrent yeast infections. This complaint demands thorough attention.
It is important to assess for underlying hygiene issues, such as frequent douching and
constrictive synthetic undergarments that retain moisture in vaginal secretions. Also rule out
other conditions that have been closely associated with candidal infections (eg, diabetes and
immunocompromise). Finally, rule out other pathogens and mixed infections. Culture, to confirm
and speciate yeast, may play a role in this setting.

Treatment. In the treatment guidelines released in 1993 by the Centers for Disease Control and
Prevention, myriad imidazoles and triazoles were endorsed for treatment of vaginal candidiasis.
[15]
Notably, each regimen was an intravaginal preparation. In July 1994, the FDA approved oral
fluconazole for vaginal candidiasis (Table II). Most albicans species are susceptible to
commonly prescribed imidazoles (eg, clotrimazole, miconazole). However, approximately 15%
of albicans organisms are resistant; albicans strains are frequently more susceptible in vitro to
triazoles (eg, fluconazole, terconazole) than to imidazoles.[46] However, in comparing regimens, it
must be noted that in vitro susceptibility testing does not correlate well with clinical efficacy, and
study designs of various therapies are widely varied and hence not readily comparable. Another
cause of treatment failures, besides resistance, relates to the reservoir of yeast which 15% of
healthy women harbor in their gastrointestinal tract. [47] Obviously, intravaginal therapies fail to
target the source of infection in these individuals. Of orally available agents (fluconazole,
ketoconazole, and itraconazole), only fluconazole is currently approved by the FDA for this use.
Fluconazole has much less hepatotoxicity than ketoconazole. Recurrent infections may be treated
with weekly administration of fluconazole 150mg for up to 12 consecutive weeks. [47]
Alternatively, boric acid (600mg in #1 size gelatin capsules inserted bid per vagina for 10 days)

10
is quite effective against most strains of Candida.[39] While candidial vaginitis is not considered a
sexually transmitted disease, women may infect the glans penis of their partners. Cotreatment of
the male partner is usually not indicated, except in cases of fungal balanitis or in an
uncircumcised male who harbors a penile reservoir.

Miscellaneous Causes of Vaginitis

Still within the realm of infectious etiologies are other causes of vaginal discharge. One is termed
lactobacillosis or Dderlein cytolysis. This entity is characterized by an overgrowth of the
commensal lactobacilli (Fig. 8 shows lactobacilli from vaginal fluid of normal patient); hence, on
saline wet mount, one finds an excessive number of bacilli among the background flora. The pH
is typically low-normal. Treatment, therefore, is directed at correcting the disruption of the
vaginal ecosystem in order to limit the excessive proliferation of these protective organisms. [48]
Broad-spectrum antibiotics may lower the proliferation of the lactobacilli, and alkaline (sodium
bicarbonate) douches may raise the vaginal pH to restore the ecosystem.

Figure 8. On Gram's stain of vaginal fluid from normal patient, note predominance
of gram-positive forms with morphology consistent with lactobacilli, a microbe
essential to the ecological balance and health of the vagina. From Infect Med
9(1):50, 1992. Copyright 1992, SCP Communications, Inc.

Another entity, inflammatory vaginitis, features a vaginal pH above 4.2, large numbers of
leukocytes, and some parabasal and basal vaginal cells, with a paucity of superficial squamous
cells. Clinicians often find that patients are infected with group A or group B streptococcus (Fig.
9). Therefore, because infection is suspected to underlie the inflammation and desquamation,
treatments directed against bacterial vaginosis are recommended.[49]

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Figure 9. Honey-colored pus-like vaginal discharge characteristic of either group B
streptococcus or Staphylococcus aureus. Figure courtesy of James A. McGregor, MD,
University of Colorado Health Sciences Center.

Editorial Comment: Vaginitis Sequelae--Common, Serious, and Costly in

Women From Birth Through Menopause
As Dr. David Plourd points out in his well-written article on vaginitis, most vaginal complaints
are caused by local infections in women of childbearing age and if untreated can lead to preterm
birth and pelvic infection. But older women, children, and even babies also can be affected by
vaginitis, with direct care of vaginal infections in all groups costing billions of dollars annually.
Care of mothers and their babies who suffer preterm births costs billions of dollars more: Being
"born too soon" is the most common cause of cerebral palsy and mental retardation.

Causes of vaginitis vary widely, as the article describes, from pathogens transmitted during
contact with an infected partner, to vaginal flora-altering conditions (such as excess douching,
taking antibiotics, and immunity-impairing illnesses like AIDS or diabetes). Some patients may
not complain of symptoms despite the presence of florid inflammation or discharge; they may be
reticent to discuss sexual matters with their physicians or they may have become accustomed to
symptoms of chronic vaginitis.

Vaginitis in the newborn is most frequently caused by maternal vaginal microorganisms acquired
during birth; vaginitis in children is frequently caused by microbial pathogens including group A
and group B streptococcus. Less frequent culprits include E. coli, Haemophilus influenzae , and,
rarely, Enterobius vermicularis (pinworms).

Bacterial vaginitis in postmenopausal women is most frequently caused by overgrowth of

bacteria from the nearby gastrointestinal tract and/or bacterial vaginosis (BV)-associated

12
organisms. Evaluation of these infections commonly involves aerobic culture and specific
treatment along with systemic or topical estrogen treatment in women lacking estrogen.

The family physician frequently encounters patients with vaginitis: In one study, objective
evidence of vaginitis was found in fully 39% of nearly 400 female patients (Holmes). The
commonest causes of vaginal complaints in family medicine and student health care clinics are
bacterial vaginosis (BV), vaginal candidiasis, trichomoniasis and, less commonly, primary
genital herpes and infection with single organisms such as group B streptococcus, E. coli, and
Staphylococcus aureus. A number of less-understood entities also occur, including vestibulitis,
cytolytic vaginitis, and desquamative vaginitis. Mucopurulent endocervicitis (most commonly
caused by Chlamydia trachomatis, Neisseria gonorrhoeae, group B streptococcus, and genital
mycoplasmas) may also present as increased vaginal discharge and irritation.

Fully half of women with BV are asymptomatic. The sequelae of BV are increasingly recognized
as common and serious. The abundance of abnormal microflora and the virulence factors they
produce (endotoxins, phospholipases, proteases, sialidases, etc.) are associated with a scent and
establishment of BV microflora and inflammation in the endometrium and possibly fallopian
tubes. Multiple studies show that BV is associated with ascending reproductive tract infection
during pregnancy (preterm labor and birth, premature rupture of membranes, and intra-amniotic
fluid infection; and postpartum endometritis and post-cesarean infection). Among nonpregnant
women there are increased risks of pelvic inflammatory disease, post-termination endometritis,
and postoperative infections after hysterectomy. Controlled trials show that women should be
screened and treated during antenatal care and prior to any pelvic surgery. Some authorities
suggest that women should be screened for BV and treated as part of well-woman care.

BV is the commonest of vaginal infections found in reproductive age women (12%-25%). It also
can be found in children without any sexual exposure. Lower genital tract infections, including
bacterial vaginosis, are increasingly recognized causes of morbidity in health care expenditures
among newborns and children, and in post climacteric women.

The recognized key to vaginal health and prevention of vaginitis, as Dr. Plourde notes, is
presence of H2O2-producing strains of Lactobacillus species. These normally account for >95%
of vaginal microflora. Present understanding suggests that maintenance of healthy Lactobacillus
and low vaginal pH are mutually-reinforcing factors which reduce infection with various
sexually transmitted bacteria, protozoa, and viruses, including HIV-1.

James A. McGregor, MD, CM

Professor and Vice Chairman of Academic Affairs
University of Colorado Health Sciences Center
Denver, Colo.

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 Tables
Table 1. Vaginal Infections: Diagnostic Clues

Sexually
Discharge Vagina Transmitte
Clinical Signs Characteristics l pH Microbiology d?
Bacterial Vaginal discharge Color: off-white >4.5 Polymicrobial; Probably
Vaginosis NOT Consistency: mostly normal flora, not.
accompanied by creamy but can include
leukorrhea, vulvar Consistency: comma-shaped,
burning, or creamy gram-variable
pruritis. Odor: whiff test anaerobic
positive for fishy Mobiluncus rods ,
or musty odor Gardnerella
when alkaline vaginalis, or clue
KOH solution cells (> 20 % of the
added to smear. epithelial cells), but
few WBCs. Pap
smear may indicate
coccobacillary shift
of flora.
Trichomon Irritation and Color: greenish- > 4.5 Flagellated protozoa Yes
ads soreness of the yellow (70% visible on wet mount
vulva, perineum, Consistency: of (50%-75%); Pap
and thighs, with Frothy cases) smear sensitive for
dyspareunia and Odor: foul- trichomonads (70%).
dysuria. Punctate smelling
cervical
microhemorrhage
s visible in 25%
of cases.
Asymptomatic up
to 50% of the
time.
Candida Vulvar pruritus, Color: white; Norma Hyphae or budding Patients may
indicating spread off-white if l range yeast visible in 50%- infect the
of fungus distally mixed infection of 3.8- 70% of cases. Fungal glans penis
onto the vulva. present 4.2 elements on Pap of their
Hyperemic Consistency: smear could indicate partners.
vagina, "curdled" colonization, not
erythematous or Odor: not infection. Culture
excoriated vulva. malodorous can confirm and
unless a mixed speciate yeast.
infection is

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 present

Table 2. Current Treatment Recommendations for Bacterial Vaginosis, Trichomonas, and

Candida

Bacterial Vaginosis

o Metronidazole 500mg PO bid for 7 days

o Clindamycin 300mg PO bid for 7 days

o Metronidazole gel 0.75% bid per vagina for 5 days

o Clindamycin cream 2% per vagina for 7 nights

Trichomonas

o Metronidazole 2g PO, single dose

o Metronidazole 500mg PO for 7 days

o Metronidazole 2g or more daily for several consecutive days, supplemented with

intravaginal metronidazole suppositories (500mg bid)

o Metronidazole 500mg IV q8h*

o Clotrimazole,* single 500mg tablet or cream used once intravaginally at night

Candida**

o Intravaginal imidazoles and triazoles (eg, clotrimazole given as single 500mg

tablet or cream used once intravaginally at night, miconazole given as 200mg
suppository inserted intravaginally once daily at bedtime for 3 consecutive days)

o Fluconazole 150mg PO for up to 12 consecutive weeks for recurrent infections

o Boric acid 600mg in #1 gelatin capsule per vagina bid for 10 days

* Not endorsed by the US Food and Drug Administration for this indication.
** Cotreatment of the male partner usually not indicated, except in cases of fungal balanitis or in

15
an uncircumcised male with a penile reservoir.

16