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 VAGINITIS

Differential Diagnosis and Management

 VAGINITIS
Differential Diagnosis and
Management

Sebastian Faro,MD, PhD

Clinical Professor
Department of Obstetrics, Gynecology, and
Reproductive Sciences
The University of Texas—Houston Health
Sciences Center
Attending Physician
The Woman’s Hospital of Texas
Houston, Texas

BOCA RATON LONDON NEW

YORK WASHINGTON, D.C
 Published in the USA by
The Parthenon Publishing Group
345 Park Avenue South
New York, NY 10010, USA

This edition published in the Taylor & Francis e-Library, 2005.

“To purchase your own copy of this or any of Taylor & Francis or Routledge’s collection of
thousands of eBooks please go to www.eBookstore.tandf.co.uk.”

Published in the UK by
The Parthenon Publishing Group
23–25 Blades Court
Deodar Road
London, SW15 2NU, UK

Copyright ©2004,The Parthenon Publishing Group

Library of Congress Cataloging-in-Publication Data

Faro, Sebastian.
Vaginitis: differential diagnosis and management/Sebastian Faro.
p.; cm.
Includes bibliographical references and index.
ISBN 1-84214-159-7 (alk. paper)
1. Vaginitis. 2. Vagina-Diseases. 3. Diagnosis, Differential. I. Title.
[DNLM: 1. Vaginitis-diagnosis. 2. Diagnosis, Differential. 3. Vaginitis-drug therapy.
WP 255 F237v 2003]
RG268.F37 2003
618.1’5–dc22
2003061739

British Library Cataloguing in Publication Data

Faro, Sebastian
Vaginitis: differential diagnosis and management
1. Vaginitis-Diagnosis 2. Vaginitis-Treatment
I. Title
618.1’5

ISBN 0-203-50011-3 Master e-book ISBN

ISBN 0-203-59625-0 (Adobe eReader Format)

ISBN 1-84214-159-7 (Print Edition)

No part of this book may be reproduced in any form without permission from the publishers
except for the quotation of brief passages for the purpose of review

Composition by The Parthenon Publishing Group, London, UK

 CONTENTS

Color illustrations v

1. Healthy vaginal ecosystem 1

2. Vulvitis 10
3. Bacterial vaginosis 14
4. Bacterial vaginitis 26
5. Vulvovaginal candidiasis 35
6. Trichomoniasis 58
7. Atrophic vaginitis 86
8. Desquamative vaginitis 92
9. Cytolytic vaginosis 96

Index 99
 COLOR ILLUSTRATIONS

Figures 1 and 2 Gram stains of vaginal fluid demonstrating well-

estrogenized squamous epithelial cells and large gram-positive bacilli
characteristic of Lactobacillus. Note the homogenous appearance of the
cytoplasm of the squamous cells, the distinct nucleus, and cell membrane.
There is a relative absence of other bacteria. Also note that there are no
bacteria adhering to the squamous cells
vi

Figure 4 Gram stain of vaginal fluid from a patient developing bacterial

vaginosis. Note adherent Gram-negative rods to cytoplasmic membranes of
the squamous epithelial cells. Bacteria in vaginal tend to occur in aggreagates;
this is typical of flora dominated by Gardnerella vaginalis

Figure 5 Gram stain of vaginal fluid from a patient with developing bacterial
vaginosis. Bacteria adhering to squamous epithelial cells. Note individual free-
floating bacteria in the vaginal fluid. The nucleus of the squamous epithelial
cells and cell membranes can be identified
 vii

Figure 6 Gram stain of vaginal fluid from a patient with bacterial vaginosis.
Note that the bacteria adhering to the squamous cells have obliterated the
nuclei and cell membrane. There are numerous free-floating bacteria in the
vaginal fluid. This microplutopaple is typical of the vaginal fluid from a
patient with bacterial vaginosis

Figure 7 Atrophic smear showing large number of intermediate and basal

cells. Reproduced with permission from Brown D. Atrophic and
postirradiation vaginitis. In Horowitz BJ, Mårdh P-A, eds. Vaginitisand
Vaginosis. New York: Wiley-Liss, 1991; 169–79
viii

Figure 8 Cytolytic vaginosis. Note large number of lactobacili and

dissolution of epithelial cells. Reproduced with permission from Cibley LJ,
Cibley LJ. Cytolytic vaginosis: a common cause of vaginitis. In Horowitz BJ,
Mårdh P-A, eds. Vaginitisand Vaginosis. New York: Wiley-Liss, 1991;181–87
 ix

Figure 9 Note erythema of the labia majora and labia minora. The labia
majora are swollen and there is a pustule in the right labia

Figure 10 Wet prep of vaginal discharge from a patient with candidiasis.

Note the hyphae among the squamous epithelial cells

Figure 11 Wet prep diluted with saline and viewed under phase contrast
microscopy. Note that the squamous cells are well estrogenized and the
x

relative absence of white blood cells. The hyphae are characteristic of Candida
ablicans

Figure 12 Wet prep from a patient with vaginal candidiasis. Note the
presence of budding yeast cells and the absence of hyphae. This patient had
Candida glabrata vaginitis

Figure 13 Gram stain of Trichomonas vaginalis. Note the elliptical shape and
flagella
 xi

Figure 14 Wet prep with vaginal fluid from a patient with Trichomonas
vaginalis vaginitis. T. vaginalis can assume a spherical shape that is larger than
white blood cells; note the variety of T. vaginalis shapes and absence of
lactobacilli

Figure 15 Phase contract microscopy of Trichomonasvaginalis vaginitis. One

trichomonad has an elliptical shape and another has assumed an amoeboid
characteristic
xii

Figure 16 Cytolytic vaginosis. White vaginal discharge mimicking candidal

infection (through colposcope, x6). Reproduced with permission from Cibley
LJ, Cibley LJ. Cytolytic vaginosis: a common cause of vaginitis. In Horowitz
BJ, Mårdh P-A, eds. Vaginitis andVaginosis. New York: Wiley-Liss, 1991; 181–
87

Figure 17 Cytolytic vaginosis. Excess lactobacilli with naked squamous cell

nuclei (Nomarski, x160). Reproduced with permission from Cibley LJ,
Cibley LJ. Cytolytic vaginosis: a common cause of vaginitis. In Horowitz BJ,
Mårdh P-A, eds. Vaginitis andVaginosis. New York: Wiley-Liss, 1991; 181–87
 1.
HEALTHY VAGINAL ECOSYSTEM

INTRODUCTION
The vaginal ecosystem is a complex biosphere, made up of a variety of
constituents existing in a delicate equilibrium. The ecosystem
contains many types of bacteria that are constantly secreting and
releasing metabolic products such as acids, carbohydrates, and proteins,
and cellular debris from the disruption of dying bacterial cells like
nucleic acids, fatty acids, and sugars. The host is also constantly
secreting metabolic products and cellular debris into this ecosystem.
This microflora consists of, among other organisms, Gram-positive
and Gram-negative aerobic, facultative and obligate anaerobic
bacteria. The most common bacterial species isolated from the vagina
are listed in Table 1. Both non-pathogenic and pathogenic bacteria are
among the numerous bacteria present. However, it is important to
understand that any bacterium, given the appropriate inoculum size
and proper environmental conditions, can become pathogenic and
cause disease. In a healthy vaginal ecosystem the microflora is
dominated by Lactobacillus spp. When the ecosystem becomes
disrupted or unbalanced, the pathogenic bacteria gain dominance and
pose a potential threat to the individual’s general health.
Although Table 1 represents the bacteria most commonly isolated
from the healthy vagina, it is by no means a complete list. Other
bacteria, such as Pseudomonas spp., Staphylococcus aureus and Haemophilus
influenzae, have also been isolated from the vagina of healthy
individuals.
2 VAGINITIS: DIFFERENTIAL DIAGNOSIS AND MANAGEMENT

Table 1 Bacteria Commonly isolated from a healthy vaginal ecosystem

THE VAGINAL ECOSYSTEM

The vagina is a potentially tubular organ lined by stratified squamous
epithelial cells. There are no mucus-secreting cells within the vaginal
epithelium; mucus is produced by the periurethral glands, Skene’s
glands, and the glands that exit from the medial inferior aspect of the
labia minora, known as Bartholin’s glands. The discharge found within
the vagina arises from a transudate secreted through the vaginal
epithelium and from the cervix. Therefore, the vaginal discharge is a
composite of fluid, cells, and cellular debris that is derived from the
vaginal transudate and cervical secretions, as well as fluid secreted
from the endometrium and fallopian tubes. The average amount of
vaginal discharge a woman of reproductive age not on hormonal
therapy produces on a daily basis is 1–3 g1.
The vaginal secretions contain a variety of compounds, including
proteins, carbohydrates, urea, and fatty acids. The carbohydrates are a
mixture of simple and complex sugars. Glucose, maltose,
maltotriose, maltotetraose, and free glycogen have all been isolated
from vaginal fluid2. The proteins in vaginal fluid are derived from a
transudate of serum proteins and proteins produced by the upper
genital tract and cervix. The major proteins found in vaginal fluid are
 HEALTHY VAGINAL ECOSYSTEM 3

albumin and immunoglobulins, and amino acids are also present3.

These constituents of the vaginal ecosystem provide an excellent
culture medium for the endogenous vaginal microflora (Table 1).
Since there are a tremendous number of genera and species of bacteria
and other microorganisms that constitute the endogenous flora, many
of which are pathogenic, a mechanism has evolved to regulate the
ratio of nonpathogenic to pathogenic bacteria, which allows the
ecosystem to be maintained in a healthy state. The microflora is in this
healthy state when the dominant bacterium is a non-pathogen and the
ratio of the non-pathogen to pathogen is approximately 200:1. The
balance is maintained by specific species of Lactobacillus and the
substances they produce that inhibit the growth of pathogenic bacteria.
A healthy vaginal ecosystem has definite characteristics (Table 2).
By using simple office techniques that do not require a significant
amount of time to perform the physician can easily recognize these
characteristics. It is important that each obstetrician/gynecologist
becomes very familiar with these characteristics.
Typically only one species of Lactobacillus resides in the vagina. In a
healthy state, the species of Lactobacillus that both resides and is
dominant in the vagina is a species that produces a significant amount
of organic acids, including lactic acid, and secretes hydrogen peroxide
(H2O2) and a bacteriocin frequently referred to as lactocin.
Lactobacillus has evolved as the dominant bacterium in a healthy
vaginal ecosystem because of its ability to grow at a relatively low pH:
less than 4.5 but greater than 3.8. However, not all species of
Lactobacillus can be considered ‘good’ species or capable of producing
the necessary compounds to maintain the vaginal ecosystem in a
balanced or healthy state. The most common species isolated from
women considered to have a healthy vaginal ecosystem are Lactobacillus
crispatus,L. gasseri, L. iners, and L. jensenii4.
The various bacterial constituents of the endogenous microflora
(Table 1) can be divided into two groups, the non-pathogenic and
pathogenic bacteria (Table 3). These designations are based on the
probability that a particular bacterium can initiate infection, and
accepting the premise that any bacterium can initiate infection if
presented with favorable environmental conditions. Lactobacillus can
cause infections such as chorioamnionitis and maternal and neonatal
4 VAGINITIS: DIFFERENTIAL DIAGNOSIS AND MANAGEMENT

Table 2 Characteristics of a healthy vaginal ecosystem

*wet prep (normal saline dilution of the vaginal discharge), wipe the lateral
vaginal wall with a cotton- or Dacrontipped applicator, immerse the
applicator in 2–3 ml of normal saline and shake vigorously. Remove the
applicator and press it to a glass slide to release 1–2 drops of the diluted
discharge, cover with a glass coverslip and view under 40x magnification;
WBC, white blood cells

bacteremia5. Gardnerella vaginalis has also been demonstrated to cause

chorioamnionitis as well as septic shock6. Bacteria and other
microorganisms can be introduced into the vaginal ecosystem from
the patient’s own fecal flora, for example Bacteriodes spp.
Microorganisms can also be introduced from the exogenous
environment through objects introduced into the vagina and by sexual
intercourse, for example Chlamydia trachomatis and Neisseria
 HEALTHY VAGINAL ECOSYSTEM 5

Table 3 Endogenous bacteria of the vaginal ecosystem

gonorrhoeae, as well as skin-to-skin contact during sexual activity, for

example human papillomavirus.
Other bacteria found in the vaginal ecosystem either do not grow
at a pH below 4.0, or grow poorly at pH values of 4.0–4.57–9.
Through the production of organic acids, especially lactic acid,
Lactobacillus provides an environment that can be considered hostile to
the growth of other bacteria. Lactobacillus grows very well at a pH ≥ 5
5 and, through the production of lactic acid, very quickly lowers the
pH to below 4.5. However, Lactobacillus does not compete well for
nutrients and yields to other bacteria when growing in their midst.
When appropriate environmental changes occur within the vagina, the
number of lactobacilli decrease, the other bacteria become dominant,
and an alteration in the vaginal microflora results. The alteration in
the vaginal microflora and ecosystem can cause the patient to become
symptomatic. With the symptoms depending on the condition that
has evolved, the patient can remain asymptomatic, as is seen with
bacterial vaginosis, or when group B Streptococcus or Escherichia coli
become dominant.
Lactobacillus appears to control the growth of other bacteria through
at least three mechanisms. Lactobacillus produces lactic acid, to
maintain the vaginal pH between 3.8 and 4.2, H2O2, and bacteriocin
or lactocin. Lactobacillus is not capable of breaking down H2O2 into
hydrogen and water because it lacks heme protein catalase and does
not use the cytochrome oxidase system. This results in the production
of large amounts of H2O2, which is secreted into the environment.
H2O2 has been shown to be toxic to some bacteria11–13. This
antibacterial activity is enhanced by the enzyme peroxidase in the
6 VAGINITIS: DIFFERENTIAL DIAGNOSIS AND MANAGEMENT

presence of the halide ion14. Peroxidase enzymes are found in many

cells and cellular products: for example, milk and saliva contain
lactoperoxidase, neutrophils and monocytes contain
myeloperoxidase, eosinophils contain eosinophil peroxidase, and
human cervical mucus contains peroxidase15−17. There is little doubt
that Lactobacillus plays a significant role in maintaining the balance of
the endogenous microflora. In addition to lactic acid, other organic
acids, and H2O2, Lactobacillus produces a bacteriocin that inhibits the
growth of bacteria12. This bacteriocin is of low molecular weight and
is active against a variety of bacteria, for example E. coli,S. agalactiae,
G. vaginalis, and Prevotella spp.7,18,19.
As long as Lactobacillus maintains dominance, the pathogenic
bacteria that constitute part of the endogenous vaginal microflora
remain suppressed. Thus, the vaginal ecosystem remains in a healthy
state and there is no potential threat to the health of the individual.
Garner and Dukes20 were the first to report the near absence of
Lactobacillus and its replacement by other endogenous vaginal bacteria.
They also reported that Lactobacillus was rarely observed in women
with Haemophilus vaginalis infection, now known as bacterial vaginosis.
The number of lactobacilli present in a healthy vaginal microflora is ≥
106 cfu/ml of vaginal fluid whereas other bacteria within the
endogenous microflora are present in a concentration ≤ 103 cfu/ml of
vaginal fluid. When viewing bacteria microscopically, the
concentration required to see the bacteria is ≤ 103 cfu/ml of fluid.
Therefore, it appears that lactobacilli play a key role in maintaining
the vaginal ecosystem and the microflora in a healthy state. Loss of
Lactobacillus dominance can result in bacterial vaginosis or bacterial
vaginitis. Once the pathogenic bacteria become dominant the health
of the patient becomes threatened, especially if the patient is
undergoing invasive procedures that are performed through the lower
genital tract.

PELVIC INFECTIONS
The majority of pelvic infections that occur in the gynecologic and
obstetric patient are derived from the patient’s own endogenous
vaginal microflora. In fact, excluding sexually transmitted organisms,
the incidence of pelvic infections caused by exogenous bacteria is low.
 HEALTHY VAGINAL ECOSYSTEM 7

The most frequent non-endogenous vaginal bacteria to cause pelvic

infections are Staphylococcus aureus and Listeriamonocytogenes, and these
bacteria are uncommon.
Antibiotic prophylaxis is frequently administered to patients
delivering by Cesarean section, especially if they have labored, and
women having a hysterectomy. The patient who has labored with
ruptured membranes for greater than 2 hours is at risk for the
development of postpartum endometritis. The patient scheduled to
have a hysterectomy, especially a vaginal hysterectomy, is at risk for
the development of a postoperative pelvic infection.
During labor, bacteria from the vagina ascend into the cervix and
colonize the endocervical epithelium. These bacteria eventually
advance to the decidua and the chorionic membranes and amniotic
fluid. Infection is established through reproduction, adherence to host
cells, and invasion into deeper tissue. Although antibiotic prophylaxis
is given, the amount of bacteria is excessive and they are not all in a
vulnerable state; therefore, the antibiotic is not effective. If the
patient has a Lactobacillus-dominant flora to begin with, then there is no
significant threat of infection and the antibiotic administered for
prophylaxis is effective.
Patients undergoing a vaginal hysterectomy are at risk for
developing a postoperative pelvic infection if they have an altered
vaginal microflora. There are several reasons why the vaginal
hysterectomy places the patient at risk for development of a
postoperative infection: (i) the procedure is performed through a
contaminated site, namely the vagina; (ii) if an altered vaginal
microflora is present the numbers of bacteria are high, i.e. there is a
large inoculum; (iii) the pelvic peritoneum is constantly abraded and
traumatized during the procedure; (iv) dead space is created; (v)
necrotic tissue is left behind; and (vi) a foreign body, a suture, is left
in the traumatized and necrotic tissue. These features, combined with
the presence of a high inoculum of virulent bacteria, create conditions
appropriate for infection. Again, administering an antibiotic
prophylactically will, in most cases, prove ineffective. The reasons for
this are: (i) the inoculum is too large; (ii) the bacteria are not all
vulnerable while the antibiotic concentration is high enough to be
effective; (iii) the presence of necrotic tissue and suture lowers the
required inoculum to initiate infection; and (iv) because of decreased
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