Sie sind auf Seite 1von 16

Diagnosis of Vaginitis

MARI E. EGAN, M.D., and MARTIN S. LIPSKY, M.D.


Northwestern University Medical School, Chicago, Illinois

Vaginitis is the most common gynecologic diagnosis in the primary care setting. In approximately
90 percent of affected women, this condition occurs secondary to bacterial vaginosis,
vulvovaginal candidiasis or trichomoniasis. Vaginitis develops when the vaginal flora has been
altered by introduction of a pathogen or by changes in the vaginal environment that allow
pathogens to proliferate. The evaluation of vaginitis requires a directed history and physical
examination, with focus on the site of involvement and the characteristics of the vaginal
discharge. The laboratory evaluation includes microscopic examination of a saline wet-mount
preparation and a potassium hydroxide preparation, a litmus test for the pH of vaginal secretions
and a "whiff" test. Metronidazole is the primary treatment for bacterial vaginosis and
trichomoniasis. Topical antifungal agents are the first-line treatments for candidal vaginitis. (Am
Fam Physician 2000;62:1095-104.)

Vaginitis is the most frequent gynecologic diagnosis encountered by physicians who


provide primary care to women.1-5 Accurate diagnosis can be elusive, complicating
treatment.6-9 Furthermore, the availability of over-the-counter medications increases the
likelihood of inappropriate or partial treatment of vaginitis.10

Epidemiology
The prevalence and causes of vaginitis are uncertain, in part because the condition is so
often self-diagnosed and self-treated. In addition, vaginitis is frequently asymptomatic or
has more than one cause. Most experts believe that up to 90 percent of vaginitis cases are
secondary to bacterial vaginosis, vulvovaginal candidiasis and trichomoniasis.4,8
Noninfectious causes include vaginal atrophy, allergies and chemical irritation.

Bacterial Vaginosis
The most common causes of
In the United States, bacterial vaginosis is currently vaginitis are bacterial
the most common cause of vaginitis, accounting for vaginosis, vulvovaginal
40 to 50 percent of cases in women of childbearing candidiasis, trichomoniasis,
age.11,12 This infection is believed to be caused by
vaginal atrophy, allergies and
proliferation of a number of organisms, including
chemical irritation.
Gardnerella vaginalis, Mobiluncus species,
Mycoplasma hominis and Peptostreptococcus
species.1,11
Determining the prevalence of bacterial vaginosis is difficult because one third to three
quarters of affected women are asymptomatic.2,12,13 In addition, reported prevalences vary
based on the population studied. Bacterial vaginosis has been found in 15 to 19 percent of

ambulatory gynecology patients, 10 to 30 percent of pregnant patients and 24 to 40


percent of patients in sexually transmitted disease clinics.8,11-15
Even though higher rates of bacterial vaginosis have been reported in sexually
transmitted disease clinics and in women with multiple sexual partners, the role of sexual
transmission is unclear. Studies indicate that treating the male sexual partner of a woman
with bacterial vaginosis is not beneficial and that even women who are not sexually
active can have the infection.12,16 Additional risk factors for bacterial vaginosis include the
use of intrauterine devices (IUDs), douching and pregnancy.1,11-13,17
Evidence suggests that bacterial vaginosis is a risk factor for premature rupture of
membranes and preterm labor. Treating the infection in pregnancy decreases this risk.8,18-21
Additional possible adverse outcomes include an increased frequency of abnormal
Papanicolaou (Pap) smears, pelvic inflammatory disease and endometritis.22-24 Vaginal
cuff cellulitis, pelvic inflammatory disease and endometritis can occur if invasive
gynecologic procedures or surgeries are performed when a patient has bacterial
vaginosis.1,8,11

Vulvovaginal Candidiasis
Vulvovaginal candidiasis is the second most common cause of vaginitis in the United
States and the most common cause in Europe.1 An estimated 75 percent of women have
vulvovaginal candidiasis at some time in life, and approximately 5 percent of women
have recurrent episodes.21,25-27 Candida albicans is the infecting agent in 80 to 90 percent
of patients.8,10 Recently, the frequency of non-albicans species (e.g., Candida glabrata)
has increased, possibly secondary to greater use of over-the-counter antifungal products.10
Risk factors for uncomplicated vulvovaginal candidiasis have been difficult to
determine.28 Studies have shown that the risk of this infection is increased in women who
use oral contraceptive pills, a diaphragm and spermicide, or an IUD.16,29,30 Other risk
factors include young age at first intercourse, intercourse more than four times per month
and receptive oral sex.25,27,28,31,32 The risk of vulvovaginal candidiasis is also increased in
some women who have diabetes, are pregnant or are taking antibiotics.25,28,33
Complications of vulvovaginal candidiasis are rare. Chorioamnionitis in pregnancy and
vulvar vestibulitis syndrome have been reported.34,35
Establishing Candida species as the cause of vaginitis can be difficult because as many as
50 percent of asymptomatic women have candidal organisms as part of their endogenous
vaginal flora.26 Candidal organisms are not transmitted sexually, and episodes of
vulvovaginal candidiasis do not appear to be related to the number of sexual partners.25,27,28
Treating the male partner is unnecessary unless he is uncircumcised or has inflammation
of the glans of the penis.36

Recurrent vulvovaginal candidiasis is defined as four or more episodes in a one-year


period. It is not clear whether recurrences are secondary to predisposing and/or
precipitating factors, sexual transmission, intestinal reservoir or vaginal persistence.37

Trichomoniasis
The protozoan Trichomonas vaginalis, a motile organism with four flagella,3 is the third
most common cause of vaginitis. It affects 180 million women worldwide and currently
accounts for 10 to 25 percent of vaginal infections.8 The incidence of trichomonal
vaginitis is decreasing in most industrialized countries.1
Trichomonads are transmitted sexually and may be identified in 30 to 80 percent of the
male sexual partners of infected women.8,38,39 Trichomoniasis is associated with and may
act as a vector for other venereal diseases.40,41 Studies indicate that this infection increases
the transmission rate of the human immunodeficiency virus.40
Risk factors for trichomoniasis include use of an IUD, cigarette smoking and multiple
sexual partners.16,17,42 From 20 to 50 percent of women with trichomoniasis are
asymptomatic.8,38 Trichomoniasis may be associated with premature rupture of
membranes and preterm delivery.41 Sexual partners should be treated and instructed to
avoid sexual intercourse until both partners are cured.36

Pathophysiology
The normal physiologic vaginal discharge comprises vaginal secretions, exfoliated cells
and cervical mucus. The frequency of vaginal discharge varies with age, menstrual cycle,
pregnancy and use of oral contraceptives.
The normal vaginal environment is characterized by a dynamic interrelationship between
Lactobacillus acidophilus and other endogenous flora, estrogen, glycogen, vaginal pH
and metabolic by-products of flora and pathogens. L. acidophilus produces hydrogen
peroxide, which is toxic to pathogens and keeps the healthy vaginal pH between 3.8 and
4.2. Vaginitis occurs because the vaginal flora has been altered by the introduction of
pathogens or changes in the vaginal environment that allow pathogens to proliferate.
Antibiotics, contraceptives, sexual intercourse, douching, stress and hormones can
change the vaginal environment and allow pathogens to grow.3,4 In bacterial vaginosis, it
is believed that some inciting event decreases the number of hydrogen peroxideproducing
L. acidophilus organisms.11 The resultant change in pH allows proliferation of organisms
that are normally suppressed, such as G. vaginalis, M. hominis and Mobiluncus
species.11,12 These organisms produce metabolic byproducts, such as amines, that further
increase the vaginal pH and cause exfoliation of vaginal epithelial cells. The amines are
also responsible for the characteristic malodorous discharge in bacterial vaginosis.
Similarly, changes in the vaginal environment, such as an increase in glycogen
production in pregnancy or altered estrogen and progesterone levels from the use of oral

contraceptives, enhance the adherence of C. albicans to vaginal epithelial cells and


facilitate the germination of yeast.26,28 These changes may transform asymptomatic
colonization into symptomatic infection. In patients with trichomoniasis, changes in
estrogen and progesterone levels, as well as elevations of vaginal pH and glycogen levels,
may enhance the growth and virulence of T. vaginalis.42

Evaluation
A patient who complains of vaginal discharge, itching, frequent urination and/or irritation
should be evaluated for vaginitis (Figure 1). The first step is to obtain a directed history.
The patient should be asked about specific symptoms and their duration, any previous
diagnosis and previous treatment and its effects. A general medical review, dermatologic
review, social history and contraceptive history can also be helpful.

Diagnosis of Vaginitis

FIGURE 1.Evaluation of patients with suspected vaginitis. (KOH = potassium hydroxide)

It is important to inquire about abdominal or pelvic pain, fever, recurrent or resistant


infections, urinary symptoms, menstrual history, pregnancy and sexual practices.43 The
nature of the discharge (i.e., amount, consistency, color, odor, accompanying pruritus)
may also provide important clues. Dysuria is a common symptom of vaginitis. It is
usually external and is defined as pain and burning when urine touches the vulva. In
contrast, internal dysuria, defined as pain inside the urethra, is usually a sign of cystitis.5

A physical examination can help to identify the anatomic site of involvement (vulva,
vagina or cervix). Inspection of the external genitalia for inflammation, lesions, masses,
atrophic tissue and enlarged lymph nodes is important. The physician should also assess
the patient for uterine or tubo-ovarian tenderness and perform a speculum examination to
detect erythema, edema or lesions. The pooled vaginal discharge should be assessed for
color, consistency, volume and adherence to the vaginal walls.
Because the diagnostic tests and treatments for cervicitis are different from those for
vaginitis, it is important to differentiate these conditions. Several clues can help to rule
out cervical infection as the cause of a vaginal discharge. Almost 90 percent of
symptomatic or asymptomatic women with chlamydial cervicitis meet at least two of the
following criteria: (1) younger than 24 years, (2) sexual intercourse with a new partner in
the previous two months, (3) presence of mucopurulent cervicitis, (4) cervical bleeding
induced by swabbing the endocervical mucosa and (5) no form of contraception.44 If
cervicitis is suspected, cultures for Chlamydia species and Neisseria gonorrhoeae should
be obtained.
If the findings of the history and/or physical
Wet-mount preparations have
examination suggest that the patient has vaginitis, a
low sensitivity but high
sample of the vaginal discharge should be obtained
specificity for bacterial
for gross and microscopic examination. Standard
vaginosis and trichomoniasis.
office examinations include a wet-mount
preparation using saline, a slide prepared with 10
percent potassium hydroxide (KOH), a "whiff" test to detect amines and a litmus test of
the pH level of vaginal fluid.
Wet-Mount Preparation
A wet-mount preparation is obtained by diluting the vaginal discharge with one or two
drops of 0.9 percent normal saline solution and placing it on a slide with a coverslip.
Alternatively, the vaginal discharge can be put into a 2-mL test tube containing saline
solution and then placed on a slide. The slide is examined microscopically using low
power (103) and high dry power (4003). The scanning of several fields for motile
trichomonads has a sensitivity of 60 percent and a specificity of up to 99 percent.45
Microscopic examination of a wet-mount preparation can also detect "clue cells," which
are vaginal epithelial cells that are coated with the coccobacilli. When a skilled examiner
performs the search for clue cells, examination of wet-mount preparations can have a
sensitivity of 60 percent and a specificity of up to 98 percent for the detection of bacterial
vaginosis.46-48 The examination may also detect fungal hyphae, increased numbers of
polymorphonuclear cells (seen in trichomoniasis) or round parabasal cells (seen in
atrophic vaginitis).
KOH Preparation and Whiff Test
A second specimen of the vaginal discharge should be placed on a slide with a 10 percent
KOH solution. A coverslip is placed on the slide and air- or flame-dried before
examination under a microscope using low power.43 This is useful for detecting candidal

hyphae, mycelial tangles and spores. The test is positive in 50 to 70 percent of women
with candidal infection.49
During preparation of the KOH slide, a whiff test can be performed. The whiff test is
positive if a "fishy" or amine odor is detected when KOH is added to the vaginal
discharge. The odor results from the liberation of amines and organic acids produced
from the alkalization of anaerobic bacteria. A positive whiff test is suggestive of bacterial
vaginosis.11
Litmus Testing for pH
The pH level can be determined by placing litmus paper in the pooled vaginal secretions
or against the lateral vaginal wall. The color is then compared to the colors and
corresponding pH values on a standard chart. A normal vaginal pH is between 3.8 and
4.2.
Blood and cervical mucus are alkaline and alter the pH of a vaginal sample. A pH greater
than 4.5 is found in 80 to 90 percent of patients with bacterial vaginosis and frequently in
patients with trichomoniasis.3,49 The pH level is also high in those with atrophic vaginitis.

Differential Diagnosis
The diagnosis of vaginitis is based on the patient's symptoms, the physical examination,
the findings of microscopic examination of the wet-mount and KOH preparations, and
the results of the pH litmus test. The features of bacterial vaginosis, vulvovaginal
candidiasis and trichomoniasis are presented in Table 1.3,8

TABLE 1
Features of the Most Common Causes of Vaginitis
Basis of diagnosis Bacterial vaginosis

Vulvovaginal
candidiasis

Signs and symptoms Thin, off-white discharge


Unpleasant "fishy" odor,
with odor increasing after
sexual intercourse

Thick, white
("cottage cheese")
discharge with no
odor

Trichomoniasis

Copious, malodorous,
yellow-green (or
discolored) discharge
Pruritus
Pruritus Vaginal irritation
Dysuria No symptoms in
20 to 50 percent of
affected women
Physical examination Usually, normal
Vulvar and vaginal Vulvar and vaginal
appearance of tissue;
erythema, edema edema and erythema
discolored discharge with and fissures
"Strawberry" cervix in up
abnormal odor,
Thick, white
to 25 percent of affected
homogeneous discharge discharge that
women

that adheres to vaginal


walls

adheres to vaginal Frothy, purulent


walls
discharge

Laboratory tests
Vaginal pH (normal Elevated (>4.5)
Normal
= <4.5)
Microscopic
"Clue cells" (vaginal
Pseudohyphae,
examination of wet- epithelial cells coated with mycelial tangles or
mount and KOH
coccobacilli)
budding yeast cells
preparations of
Few lactobacilli
vaginal discharge Occasional motile, curved
rods (Mobiluncus species)
"Whiff" test (normal Positive
Negative
= no odor)
Additional tests
Amsel's criteria (three of KOH microscopy
four criteria must be met): Gram stain
provides correct diagnosis Culture
in 90 percent of affected
women
Criteria of Nugent or
Spiegel for Gram stain to
diagnose bacterial
vaginosis
Other tests are
controversial.

Elevated (>4.5)
Motile trichomonads
Many
polymorphonuclear cells

Can be positive
DNA probe tests:
sensitivity of 90 percent
and specificity of 99.8
percent
Culture: sensitivity of 98
percent and specificity of
100 percent

KOH = potassium hydroxide.


Information derived from Carr PL, Felsenstein D, Friedman RH. Evaluation and management of vaginitis.
J Gen Intern Med 1998;13:335-46, and Sobel JD. Vaginitis. N Engl J Med 1997;337:1896-903.

Women with bacterial vaginosis have a broad


spectrum of clinical presentations. The classic
presentation is a vaginal discharge with its
characteristic odor and a clinical examination
that is otherwise normal.
Traditionally, bacterial vaginosis has been
diagnosed using Amsel's criteria, with three of
the four findings required to establish the
diagnosis (Table 2).46 Based on these criteria,
90 percent of women with bacterial vaginosis
can be diagnosed correctly.46,47,49
Other investigators have developed criteria to
diagnose bacterial vaginosis using a gramstained vaginal smear3,50-52 (Tables 350 and 451).
Evaluations of tests for bacterial vaginosis
have shown that the Gram stain is better than
gas-liquid chromatography, G. vaginalis
cultures or an assay for proline
aminopeptidase.48

TABLE 2
Amsel's Diagnostic Criteria for
Bacterial Vaginosis*
Thin, homogeneous discharge
Positive "whiff" test
"Clue cells" present on microscopy**
Vaginal pH >4.5

*--Three of four criteria must be met;


establishes accurate diagnosis of bacterial
vaginosis in 90 percent of affected women.
**--Highly significant criterion.
Information from Amsel R, Totten PA,
Spiegel CA, Chen KC, Eschenbach D,
Holmes KK. Nonspecific vaginitis.
Diagnostic criteria and microbial and
epidemiologic associations. Am J Med
1983;74:14-22.

Women with vulvovaginal candidiasis frequently complain of pruritus, vaginal irritation


and dysuria. Vulvovaginal itching generally is not a normal finding in healthy women; if
this symptom is present, other dermatologic conditions (e.g., lichen sclerosis and, rarely,
vulvar cancer) should also be considered, especially in the absence of candidal
infection.5,43
In vulvovaginal candidiasis, the discharge is usually white and thick, with no odor and a
normal pH. Women with candidiasis can have vulvar and vaginal erythema and,
occasionally, scaling and fissures of vulvar tissue.8,49 Microscopic examinations of wetmount and KOH preparations are positive in 50 to 70 percent of patients with candidal
infections.49 In patients with a negative microscopic examination but symptoms
compatible with yeast vaginitis, a Gram stain or a culture using Nickerson's medium or
Sabouraud's dextrose agar may be helpful.4,5,28 Other tests, such as the Pap smear or the
latex agglutination test, provide no advantage over microscopic techniques.21,26,53
Classic manifestations of vaginal trichomoniasis include a purulent, frothy, yellow
discharge with an abnormal odor, pruritus and dysuria. The physical examination may
reveal superficial vulvovaginal erythema, and the discharge usually has an elevated pH.5,49

TABLE 3
Nugent's Diagnostic Criteria for

TABLE 4
Spiegel's Diagnostic Criteria for

Bacterial Vaginosis

Bacterial Vaginosis

Scoring system (zero to 7+)* is a weighted


combination of the following bacterial
morphotypes:
A. Lactobacillus acidophilus (large
gram-positive rods)
B. Gardnerella vaginalis and
Bacteroides species (small gramvariable or gram-negative rods)
C. Mobiluncus species (curved gramvariable rods)

Normal: Gram stain shows a predominance


of Lactobacillus acidophilus (3+ or 4+), with
or without Gardnerella vaginalis.

The total score is the sum of the weighted


quantity of the three bacterial morphotypes.
Scoring for each of the above bacterial
morphotypes:
Zero = No morphotypes per oilimmersion field
1+ = Less than one morphotype per
oil-immersion field
2+ = One to four morphotypes per
oil-immersion field
3+ = Five to 30 morphotypes per oilimmersion field
4+ = More than 30 morphotypes per
oil-immersion field
*--For the combined score (A + B + C), zero to 3
represents normal flora, 4 to 6 represents
indeterminate, and 7 or higher is diagnostic of
bacterial vaginosis.

Bacterial vaginosis: Gram stain shows mixed


flora (gram-positive, gram-negative or gramvariable bacteria) and absent or decreased
L. acidophilus (zero to 2+).
A. L. acidophilus (large gram-positive
bacilli)
B. G. vaginalis (small gram-variable
rods)
Scoring for each of the above bacterial
morphotypes:
Zero = No morphotypes per oilimmersion field
1+ = Less than one morphotype per
oil-immersion field
2+ = One to five morphotypes per oilimmersion field
3+ = Six to 30 morphotypes per oilimmersion field
4+ = More than 30 morphotypes per
oil-immersion field

Information from Spiegel CA, Amsel R, Holmes


KK. Diagnosis of bacterial vaginosis by direct
Gram stain of vaginal fluid. J Clin Microbiol
1983;18:170-7.

Information from Nugent RP, Krohn MA, Hillier


SL. Reliability of diagnosing bacterial vaginosis
is improved by a standardized method of Gram
stain interpretation. J Clin Microbiol
1991;29:297-301.

For microscopic examination of the vaginal discharge, warming the slide and decreasing
the intensity of substage lighting are ways to increase sensitivity for trichomonads.43
Additional testing may include cultures using Diamond's medium, which has a sensitivity
of 95 percent for the diagnosis of trichomoniasis. Tests using DNA probes and
polymerase chain reaction tests have high sensitivity and specificity.54 Cultures or other
tests should be performed when the index of suspicion for trichomoniasis is high and
examination of the wet-mount preparation is negative.

The treatments of bacterial vaginosis, vulvovaginal candidiasis and trichomoniasis are


summarized in Table 5.36,55,56 Topical antifungal agents for the treatment of vaginitis are
listed in Table 6.57

TABLE 5
Treatments of the Most Common Causes of Vaginitis
Treatment
regimens
Acute
regimens

Bacterial vaginosis

Vulvovaginal
candidiasis

Metronidazole
Topical antifungal
(Flagyl), 500 mg orally agents** (see Table 6)
twice daily for seven Fluconazole (Diflucan),
days*
150 mg orally one time
Clindamycin
phosphate vaginal
cream 2 percent
(Cleocin Vaginal), one
full applicator (5 g)
intravaginally each
night for 7 days* (Note
that oil-based cream
may weaken condoms
and diaphragms.)
Metronidazole gel 0.75
percent (MetrogelVaginal), one full
applicator (5 g)
intravaginally twice
daily for 5 days*
Alternative Metronidazole, 2 g
Boric acid powder in
regimens
orally in a single dose size-0 gelatin capsules
Clindamycin (Cleocin), intravaginally once or
300 mg orally twice
twice daily for 2 weeks
daily for 7 days
Pregnancy
Metronidazole, 250 mg Only topical azole
orally three times daily agents intravaginally for
for 7 days
7 to 10 days
(recommended
regimen)||
Alternative Metronidazole, 2 g
regimens for orally in a single dose||
pregnancy
Clindamycin, 300 mg

Trichomoniasis
Metronidazole, 2 g
orally in a single
dose***

Metronidazole, 500
mg orally twice
daily for 7 days

Metronidazole, 2 g
orally in a single
dose (usually not
recommended in
first trimester)

orally twice daily for 7


days||
Metronidazole gel 0.75
percent, one full
applicator (5 g)
intravaginally twice
daily for 5 days
(acceptable only in
women who have not
had a previous
premature delivery)
Recurrence Retreat with an
For four or more
alternative regimen.
episodes of symptomatic
vulvovaginal candidiasis
annually: initial acute
intravaginal regimen for
10 to 14 days followed
immediately by
maintenance regimen for
at least 6 months (e.g.,
ketoconazole [Nizoral],
100 mg orally once
daily)

Metronidazole, 2 g
orally once daily for
3 to 5 days (Note
that treatment of
sexual partners
increases cure rate.)

*--Cure rates for these regimens for bacterial vaginosis range from 74 to 85 percent.
**--Cure rates for selected topical antifungal agents (e.g., polyenes, imidazoles) range from 75 to 90
percent.
***--Cure rate for acute therapy is 90 to 95 percent. Single-dose therapy is associated with better
compliance. Ensuring treatment of sexual partners will increase cure rate. Topical therapy secondary to
nontherapeutic levels in the urethra and perivaginal glands should not be used. Alcohol use should be
avoided during metronidazole therapy and for 24 hours after treatment.
--Although this treatment is not included in the recommendations from the Centers for Disease Control
and Prevention, a 98 percent cure rate has been reported for its use in patients who failed commonly used
treatments.56
||--Lower doses of medications are recommended during pregnancy; use in first trimester should be
avoided. Use of clindamycin phosphate vaginal cream is not recommended during pregnancy.
--All cases of recurrent vaginitis should be confirmed by culture before maintenance therapy is initiated.
Information from references 36, 55 and 56.

TABLE 6

Topical Antifungal Therapy for Vaginitis


Butoconazole 2 percent cream (Femstat 3, Mycelex-3), 5 g per day intravaginally for 3 days*
Clotrimazole 1 percent cream (Mycelex-7), 5 g per day intravaginally for 7 to 14 days*
Clotrimazole 100-mg vaginal tablet (Gyne-Lotrimen, Mycelex), one tablet per day intravaginally
for 7 days*
Clotrimazole 100-mg vaginal tablet, two tablets per day intravaginally for 3 days*
Clotrimazole 500-mg vaginal tablet (Mycelex-G), one tablet intravaginally in a single application*
Miconazole 2 percent cream (Monistat 7), 5 g per day intravaginally for 7 days*
Miconazole 200-mg vaginal suppository (Monistat 3), one suppository per day for 3 days*
Miconazole 100-mg vaginal suppository (Monistat 7), one suppository per day for 7 days*
Nystatin 100,000-unit vaginal tablet (Mycostatin), one tablet per day intravaginally for 14 days
Tioconazole 6.5 percent ointment (Vagistat-1), 5 g intravaginally in a single application*
Terconazole 0.4 percent cream (Terazol 7), 5 g per day intravaginally for 7 days*
Terconazole 0.8 percent cream (Terazol 3), 5 g per day intravaginally for 3 days*
Terconazole 80-mg vaginal suppository (Terazol 3), one suppository per day for 3 days*

*--These creams and suppositories are oil-based and might weaken latex condoms and diaphragms.
Additional information is available on condom product labelings.
--Over-the-counter preparations.
Adapted from 1998 guidelines for treatment of sexually transmitted diseases. Retrieved June 19, 2000,
from the World Wide Web: http://www.cdc.gov/nchstp/dstd/1998_STD_guidelines_for_the_treatment.htm.

The authors thank Mark Potter, M.D., Provident-Loyola Family Medicine Residency, Chicago, for
reviewing the manuscript, and Daved Shanks, Chicago, for assistance in preparing Figure 1.
Members of various family practice departments develop articles for "Problem-Oriented
Diagnosis." This article is one in a collaborative series coordinated by David R. Rudy, M.D.,
M.P.H., from the Department of Family Medicine at the Chicago Medical School of Finch
University of Health Sciences, and Martin S. Lipsky, M.D., from the Department of Family
Medicine at Northwestern University Medical School, Chicago.

The Authors
MARI E. EGAN, M.D.,
is instructor and preclinical coordinator in the Department of Family Medicine at
Northwestern University Medical School, Chicago. She received her medical degree from
Rush Medical College of Rush University, Chicago, and completed a residency at
Providence Family Medicine Residency, affiliated with the University of Washington,
Seattle. Dr. Egan is currently completing a master of medical education degree at the
University of Illinois, Chicago.
MARTIN S. LIPSKY, M.D.,
is professor and chair of the Department of Family Medicine at Northwestern University
Medical School and Evanston Northwestern Healthcare. Dr. Lipsky received his medical
degree from the Medical College of Pennsylvania, Philadelphia, and completed a family
medicine residency at the University of California, Irvine, College of Medicine.
Address correspondence to Mari E. Egan, M.D., Northwestern University Medical School,
Department of Family Medicine, 303 E. Chicago Ave., Chicago, IL 60611. Reprints are not
available from the authors.

REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.

Kent HL. Epidemiology of vaginitis. Am J Obstet Gynecol 1991;165:1168-76.


McCue JD. Evaluation and management of vaginitis. An update for primary care practitioners.
Arch Intern Med 1989;149:565-8.
Carr PL, Felsenstein D, Friedman RH. Evaluation and management of vaginitis. J Gen Intern Med
1998;13:335-46.
Sobel JD. Vulvovaginitis in healthy women. Compr Ther 1999;25:335-46.
Haefner HK. Current evaluation and management of vulvovaginitis. Clin Obstet Gynecol
1999;42:184-95.
Eschenbach DA, Hillier SL. Advances in diagnostic testing for vaginitis and cervicitis. J Reprod
Med 1989;34:555-64.
Schaaf VM, Perez-Stable EJ, Borchardt K. The limited value of symptoms and signs in the
diagnosis of vaginal infections. Arch Intern Med 1990;150:1929-33.
Sobel JD. Vaginitis. N Engl J Med 1997;337:1896-903.
Berg AO, Heidrich FE, Fihn SD, Bergman JJ, Wood RW, Stamm WE, et al. Establishing the cause
of genitourinary symptoms in women in a family practice. Comparison of clinical examination
and comprehensive microbiology. JAMA 1984;251:620-5.
Horowitz BJ, Giaquinta D, Ito S. Evolving pathogens in vulvovaginal candidiasis: implications for
patient care. J Clin Pharmacol 1992;32:248-55.
Hill GB. The microbiology of bacterial vaginosis. Am J Obstet Gynecol 1993;169:450-4.
Hay PE. Recurrent bacterial vaginosis. Dermatol Clin 1998;16:769-73,xii-xiii.
Sobel J. Bacterial vaginosis. Br J Clin Pract Infect 1990;71(suppl):65-9.
Hill LH, Ruparelia H, Embil JA. Nonspecific vaginitis and other genital infections in three clinic
populations. Sex Transm Dis 1983;10:114-8.
Bump RC, Buesching WJ 3d. Bacterial vaginosis in virginal and sexually active adolescent
females: evidence against exclusive sexual transmission. Am J Obstet Gynecol 1988;158:935-9.
Barbone F, Austin H, Louv WC, Alexander WJ. A follow-up study of methods of contraception,
sexual activity, and rates of trichomoniasis, candidiasis, and bacterial vaginosis. Am J Obstet
Gynecol 1990; 163:510-4.
Haukkamaa M, Stranden P, Jousimies-Somer H, Siitonen A. Bacterial flora of the cervix in women
using different methods of contraception. Am J Obstet Gynecol 1986;154:520-4.

18. Hay PE, Lamont RF, Taylor-Robinson D, Morgan DJ, Ison C, Pearson J. Abnormal bacterial
colonisation of the genital tract and subsequent preterm delivery and late miscarriage. BMJ
1994;308:295-8.
19. Hillier SL, Nugent RP, Eschenbach DA, Krohn MA, Gibbs RS, Martin DH, et al. Association
between bacterial vaginosis and preterm delivery of a low-birth-weight infant. The Vaginal
Infections and Prematurity Study Group. N Engl J Med 1995;333:1737-42.
20. Hauth JC, Goldenberg RL, Andrews WW, DuBard MB, Cooper RL. Reduced incidence of preterm
delivery with metronidazole and erythromycin in women with bacterial vaginosis. N Engl J Med
1995;333:1732-6.
21. Monif GR. Classification and pathogenesis of vulvovaginal candidiasis. Am J Obstet Gynecol
1985;152:935-9.
22. Eltabbakh GH, Eltabbakh GD, Broekhuizen FF, Griner BT. Value of wet mount and cervical
cultures at the time of cervical cytology in asymptomatic women. Obstet Gynecol 1995;85:499503.
23. Soper DE, Brockwell MJ, Dalton HP, Johnson D. Observations concerning the microbial etiology
of acute salpingitis. Am J Obstet Gynecol 1994;170: 1008-14.
24. Korn AP, Bolan G, Padian N, Ohm-Smith M, Schachter J, Landers DV. Plasma cell endometritis in
women with symptomatic bacterial vaginosis. Obstet Gynecol 1995;85:387-90.
25. Foxman B. The epidemiology of vulvovaginal candidiasis: risk factors. Am J Public Health
1990;80:329-31.
26. Sobel JD. Candidal vulvovaginitis. Clin Obstet Gynecol 1993;36:153-65.
27. Geiger AM, Foxman B. Risk factors for vulvovaginal candidiasis: a case-control study among
university students. Epidemiology 1996;7:182-7.
28. Sobel JD, Faro S, Force RW, Foxman B, Ledger WJ, Nyirjesy PR, et al. Vulvovaginal candidiasis:
epidemiologic, diagnostic, and therapeutic considerations. Am J Obstet Gynecol 1998;178:203-11.
29. Spinillo A, Capuzzo E, Nicola S, Baltaro F, Ferrari A, Monaco A. The impact of oral contraception
on vulvovaginal candidiasis. Contraception 1995;51:293-7.
30. Hooton TM, Roberts PL, Stamm WE. Effects of recent sexual activity and use of a diaphragm on
the vaginal microflora. Clin Infect Dis 1994;19:274-8.
31. Skinner CJ, Stokes J, Kirlew Y, Kavanagh J, Forster GE. A case-controlled study of the sexual
health needs of lesbians. Genitourin Med 1996;72:277-80.
32. Eckert LO, Hawes SE, Stevens CE, Koutsky LA, Eschenbach DA, Holmes KK. Vulvovaginal
candidiasis: clinical manifestations, risk factors, management algorithm. Obstet Gynecol
1998;92:757-65.
33. Spinillo A, Capuzzo E, Acciano S, De Santolo A, Zara F. Effect of antibiotic use on the prevalence
of symptomatic vulvovaginal candidiasis. Am J Obstet Gynecol 1999;180:14-7.
34. Cotch MF, Hillier SL, Gibbs RS, Eschenbach DA. Epidemiology and outcomes associated with
moderate to heavy Candida colonization during pregnancy. Vaginal Infections and Prematurity
Study Group. Am J Obstet Gynecol 1998;178:374-80.
35. Pagano R. Vulvar vestibulitis syndrome: an often unrecognized cause of dyspareunia. Aust N Z J
Obstet Gynaecol 1999;39:79-83.
36. 1998 guidelines for treatment of sexually transmitted diseases. Centers for Disease Control and
Prevention. MMWR Morb Mortal Wkly Rep 1998;47:1-111.
37. Sobel JD. Pathogenesis and treatment of recurrent vulvovaginal candidiasis. Clin Infect Dis 1992;
14(suppl 1):S148-53.
38. Lossick JG, Kent HL. Trichomoniasis: trends in diagnosis and management. Am J Obstet Gynecol
1991;165:1217-22.
39. Petrin D, Delgaty K, Bhatt R, Garber G. Clinical and microbiological aspects of Trichomonas
vaginalis. Clin Microbiol Rev 1998;11:300-17.
40. Laga M, Manoka AT, Kivuvu M, Malele B, Tuliza M, Nzila N, et al. Non-ulcerative sexually
transmitted diseases as risk factors for HIV-1 transmission in women: results from a cohort study.
AIDS 1993;7:95-102.
41. Cotch MF, Pastorek JG 2d, Nugent RP, Yerg DE, Martin DH, Eschenbach DA. Demographic and
behavioral predictors of Trichomonas vaginalis infection among pregnant women. The Vaginal
Infections and Prematurity Study Group. Obstet Gynecol 1991;78:1087-92.
42. Hammill HA. Trichomonas vaginalis. Obstet Gynecol Clin North Am 1989;16:531-40.

43. Reilly BM. Practical strategies in outpatient medicine. 2d ed. Philadelphia: Saunders, 1991:101646.
44. Handsfield HH, Jasman LL, Roberts PL, Hanson VW, Kothenbeutel RL, Stamm WE. Criteria for
selective screening for Chlamydia trachomatis infection in women attending family planning
clinics. JAMA 1986;255:1730-4.
45. Krieger JN, Tam MR, Stevens CE, Nielsen IO, Hale J, Kiviat NB, et al. Diagnosis of
trichomoniasis. Comparison of conventional wet-mount examination with cytologic studies,
cultures, and monoclonal antibody staining of direct specimens. JAMA 1988;259:1223-7.
46. Amsel R, Totten PA, Spiegel CA, Chen KC, Eschenbach D, Holmes KK. Nonspecific vaginitis.
Diagnostic criteria and microbial and epidemiologic associations. Am J Med 1983;74:14-22.
47. Thomason JL, Gelbart SM, Anderson RJ, Walt AK, Osypowski PJ, Broekhuizen FF. Statistical
evaluation of diagnostic criteria for bacterial vaginosis. Am J Obstet Gynecol 1990;162:155-60.
48. Krohn MA, Hillier SL, Eschenbach DA. Comparison of methods for diagnosing bacterial
vaginosis among pregnant women. J Clin Microbiol 1989;27:1266-71.
49. ACOG technical bulletin. Vaginitis. Number 226--July 1996 (replaces no. 221, March 1996).
Committee on Technical Bulletins of the American College of Obstetricians and Gynecologists. Int
J Gynaecol Obstet 1996;54:293-302.
50. Nugent RP, Krohn MA, Hillier SL. Reliability of diagnosing bacterial vaginosis is improved by a
standardized method of Gram stain interpretation. J Clin Microbiol 1991;29:297-301.
51. Spiegel CA, Amsel R, Holmes KK. Diagnosis of bacterial vaginosis by direct Gram stain of
vaginal fluid. J Clin Microbiol 1983;18:170-7.
52. Mazzulli T, Simor AE, Low DE. Reproducibility of interpretation of Gram-stained vaginal smears
for the diagnosis of bacterial vaginosis. J Clin Microbiol 1990;28:1506-8.
53. Sobel JD. Pathophysiology of vulvovaginal candidiasis. J Reprod Med 1989;34:572-9.
54. DeMeo LR, Draper DL, McGregor JA, Moore DF, Peter CR, Kapernick PS, et al. Evaluation of a
deoxyribonucleic acid probe for the detection of Trichomonas vaginalis in vaginal secretions. Am
J Obstet Gynecol 1996;174:1339-42.
55. Joesoef MR, Schmid GP, Hillier SL. Bacterial vaginosis: review of treatment options and potential
clinical indications for therapy. Clin Infect Dis 1999;28(suppl 1):S57-65.
56. Jovanovic R, Congema E, Nguyen HT. Antifungal agents vs. boric acid for treating chronic
mycotic vulvovaginitis. J Reprod Med 1991;36:593-7.
57. 1998 guidelines for treatment of sexually transmitted diseases. Retrieved June 19, 2000, from the
World Wide Web:
http://www.cdc.gov/nchstp/dstd/1998_STD_Guidlines/1998_guidelines_for_the_treatment.htm
Copyright 2000 by the American Academy of Family Physicians.
This content is owned by the AAFP. A person viewing it online may make one printout of the material and
may use that printout only for his or her personal, non-commercial reference. This material may not
otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now
known or later invented, except as authorized in writing by the AAFP. Contact afpserv@aafp.org for
copyright questions and/or permission requests.