Vulvovaginal Candidiasis as a

Chronic Disease: Diagnostic

Criteria and Definition
Esther Hong, BSc, MBBS,1 Shreya Dixit, B Med Sci, MBBS(Hons),2
Paul L. Fidel, PhD,3 Jennifer Bradford, MBBS, FRANZCOG,4
and Gayle Fischer, MBBS(Hons), FACD1
1

Northern Clinical School, University of Sydney; 2Department of Dermatology,

Royal North Shore Hospital, St Leonards, NSW, Australia; 3Louisiana State University
Health Sciences Center School of Dentistry, New Orleans, LA;
and 4University of Western Sydney, NSW, Australia

h Abstract
Although recurrent vulvovaginal candidiasis
is defined as 4 or more discrete attacks of vulvovaginal
candidiasis per year, there is no diagnostic nomenclature or
definition for the many women who are chronically symptomatic. This study aims to establish and propose a definition and a set of diagnostic criteria, which would enable
clinicians to promptly identify and treat women with chronic
vulvovaginal candidiasis (CVVC).
Design. Prospective cohort study.
Setting. Public and private vulvar dermatology outpatient clinics in Sydney, Australia.
Participants. Data were obtained prospectively from
50 women with presumptive CVVC and 42 controls. Historical
and clinical features of CVVC identified by expert consensus
were compared between the 2 groups. Diagnostic criteria
were then prospectively applied to a further 163 patients to
verify their accuracy.
Outcome Measures. Signs and symptoms diagnostic
of CVVC.
Results. The following characteristics were found to be
significantly more common in women with CVVC compared
to controls (p e .001): a history of positive vaginal Candida
swab, discharge, dyspareunia, soreness, swelling, cyclicity,
and exacerbation of symptoms with antibiotics.
Objective.

Reprint requests to: Shreya Dixit, B Med Sci, MBBS(Hons), Department

of Dermatology, Royal North Shore Hospital, Reserve Rd, St Leonards, NSW
2065, Australia. E-mail: sdixit177@gmail.com
The authors have declared they have no conflicts of interest.

2013, American Society for Colposcopy and Cervical Pathology

Journal of Lower Genital Tract Disease, Volume 18, Number 1, 2014, 31Y38

Conclusions. We propose that CVVC can be confidently

diagnosed using the major criteria of a chronic nonspecific
and nonerosive vulvovaginitis that includes at least 5 or
more properties from the following criteria: soreness,
dyspareunia, positive vaginal swab either at presentation or
in the past, previous response to antifungal medication,
exacerbation with antibiotics, cyclicity, swelling, and discharge. This condition responds reliably to oral antifungal
medication. h
Key Words: vulvovaginal, candidiasis, chronic, diagnosis,
definition

e have frequently observed a subtype of VVC,

common in vulvar disease clinics, in which
patients symptoms are continuous rather than discretely
episodic. In a vulvar clinic situation, acute and even recurrent VVC is rarely encountered and we, therefore,
presume it is being successfully managed in primary
care. In contrast to recurrent vulvovaginal candidiasis
(RVVC) where patients are asymptomatic between discrete attacks, this third group has an as-yet undefined and
uncharacterized condition that we have termed chronic
vulvovaginal candidiasis (CVVC). In this condition, patients present with chronic, continuous symptoms, which
improve during menses and remit with antifungal therapy, often recurring when this is ceased, particularly after
short course therapy. We have also observed that vaginal
swabs do not invariably demonstrate Candida at presentation even in the presence of intense symptoms and
obvious signs and that insisting on this as a diagnostic

Copyright 2013 American Society for Colposcopy and Cervical Pathology. Unauthorized reproduction of this article is prohibited.

32

&

HONG ET AL.

criterion would limit our ability to identify and correctly

treat this condition.
Vulvovaginal candidiasis (VVC) is defined as vulvovaginitis causally related to vaginal carriage of Candida
species and is a common problem associated with a high
level of morbidity. The burden of cost to the community
is significant and has been estimated at $1.8 billion per
year in the United States [1, 2]. Topical and oral antifungal medications are readily available over the counter.
Many women self-medicate, generating extra costs in
medication use and false-negatives when medication has
been used before microbiologic confirmation.
There are 2 well-described subtypes of VVC that relate to the duration and frequency of disease: acute and
recurrent. In acute VVC, women experience signs and
symptoms of acute vaginitis with a heavy white discharge
sporadically. Candida is readily cultured from the vagina.
Acute VVC is common, estimated to affect up to 75% of
women during their lives and is usually easily diagnosed
and treated [1]. Recurrent VVC is defined as 4 or more
culture-proven episodes per year and is estimated to occur
in 5% of women. It is, however, difficult to know accurately the true incidence of VVC because of widespread
self-diagnosis and self-treatment with over-the-counter
preparations [3].
The pathogenic mechanisms of recurrent VVC are
still not fully understood, and there is no simple and reliable diagnostic test. Self-medication may result in falsepositives in patients with clinical candidiasis, while, on
the other hand, we know that Candida is a commensal in
the genital tract, and a positive vaginal swab in the absence of signs and symptoms is without significance. As
a result, diagnosis can be surprisingly difficult. Cyclical
vulvovaginal itch, discharge, swelling, and pain are typical
features that have been previously identified [4]. VVC,
like many vulvar diseases, has the potential to cause great
psychologic distress and negatively impact a patients
quality of life (QoL) [5, 6].
This clinical syndrome is the focus of this article in
which we propose a definition and diagnostic criteria.

members of the Australia and New Zealand Vulvovaginal

Society including dermatologists and gynecologists specializing in the treatment of vulvovaginal conditions.
Survey participants were asked to choose and rank those
clinical and historical features they considered most important in diagnosing candidiasis. There was a 72% response to the survey. Results are shown in Table 1 and
were used to define the selection criteria for the study
cohort. Patients with a minimum of 5 of 8 clinical characteristics considered characteristic of candidiasis were
included in the study. Although a positive vaginal swab
for Candida was found in most patients, this was not
considered an essential criterion.

METHODS

Table 1. Diagnostic Features in CVVC by Expert Consensus

The study was granted approval by the ethics committee

of the Northern Sydney Central Coast Area Health Service and was conducted in 3 stages.
Stage 1: Expert Consensus to Establish Inclusion
Criteria
An online survey (Survey Monkey 2010) was sent to 18
experienced Australian vulvologists, all of whom were

Stage 2: Cohort Study

Between January and August 2010, patients were recruited
from a vulvar dermatology disease clinic in a tertiary
hospital and a private tertiary referral dermogynecology
practice in Sydney, Australia. All patients presenting
were screened for eligibility to participate in the study.
Inclusion criteria were women aged at least 18 years with
nonerosive vulval erythema and a minimum 3-month
history of chronic vulvar symptoms including a minimum of 5 historical features as established by consensus.
A control group was chosen from patients with vulvar
erythema due to dermatitis or psoriasis, the appearance
of which closely resembles candidiasis on examination
and is easily confused clinically with CVVC. We were not
able to compare our CVVC patients to those with either
acute or recurrent VVC as we rarely encounter these
patients in a vulvar clinic situation. A total of 92 patients
were included in the study: 50 patients in the study group
and 42 patients in the control group.

Stage 3: Forward Testing of Diagnostic Criteria

Between October 2010 and July 2011, the diagnostic
criteria established from the initial study group were
then applied prospectively to a further 163 patients to

Sign/symptom
Itch
History of improvement with antifungal treatment
Dyspareunia
Previous positive vaginal swab
Soreness
Cyclicity
Exacerbation with antibiotics
Discharge

Concordance, %
90
90
88
86
82
62
60
40

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Vulvovaginal Candidiasis as a Chronic Disease

determine their accuracy. All patients identified using the

criteria were fully responsive to oral antifungal therapy.
CVVC Questionnaire
A 61-item CVVC questionnaire was devised to allow
investigators to compare between the study cohort and
control groups, clinical features for diagnostic evaluation,
demographic data for comparing baseline characteristics,
as well as behavioral and QoL data. The QoL questions
were modified from the Dermatology Life Quality Index
(DLQI), a validated tool used widely in assessing the impact of skin diseases such as psoriasis on a patients QoL
[7]. QoL data are not presented in this article.
Study Protocol
At the first visit, all patients completed the CVVC
Questionnaire. History and vulvar examination findings
at baseline were recorded, and a low vaginal swab for
Candida was also collected. Patients in the study group
were commenced on treatment with a 3-month course of
oral antifungal therapy, either fluconazole 50 to 100 mg
daily or itraconazole 100 mg daily. Patients in the control group were treated with topical corticosteroid alone
as appropriate to their condition. A follow-up visit was
conducted for all patients after 3 months where history,
questionnaire, and physical examination findings were
again recorded, as well as specific treatment type used and
clinical response to therapy. The target outcome desired
was complete resolution of objective signs and self-reported
symptoms. A complete response to the oral antifungal
treatment regimen, defined as resolution of symptoms and
resolution of objective inflammation, was used as confirmation of the provisional diagnosis of CVVC.
Statistical Analysis
Clinical and historical characteristics for the study cohort
and the control group were compared to determine significant differences, sensitivity, specificity, and positive

&

33

and negative predictive values. Statistical analyses were

performed using SPSS v17. For univariate analysis, W2 test
and 2-tailed Fisher exact test were used, where values of
p G .05 were considered significant and p G .01 were
considered highly significant. Multivariable logistic regression and receiver operating characteristic curve analyses
were used to determine diagnostic criteria for CVVC.

RESULTS
The following items relating to signs and symptoms were
all significantly more common in the CVVC study cohort
compared to the control group (with p e .001): soreness,
dyspareunia, cyclicity, vulvovaginal swelling vaginal discharge, and positive vaginal swab for Candida. The following historical features were all significantly more
likely in the CVVC group (p G .001): history of previous
positive Candida vaginal swab while symptomatic, exacerbation of symptoms with oral antibiotics, and history
of improvement with any antifungal treatment even if
brief. At the follow-up visit, response to 3 months of oral
antifungal therapy was measured. All women with CVVC
had complete resolution of signs and symptoms with
prolonged daily oral antifungal treatment (p G .001). It
should be especially noted that 68% of the study group
and 7% of the control group had a positive swab at presentation. This is a significant difference; however, there
still remained 32% of patients who were fully responsive
to oral antifungal therapy who had a negative swab.
Eight clinical and historical features were identified as
being significantly more common in the CVVC group
(with high statistical significance, p e .001). Table 2
highlights odds ratios (ORs) associated with these features. Patients in the CVVC group were 79 times more
likely to have had a previous positive Candida swab than
women in the control group. Exacerbation with oral
antibiotics and vaginal discharge were more than
25 times more likely in patients with CVVC. Cyclicity of
symptoms and dyspareunia were 17 and 9 times more
likely in CVVC, respectively, whereas soreness and

Table 2. Statistical Analysis of Criteria V Control Versus CVVC

Total no.
a) Previous response to antifungals
b) Previous or current positive swab
c) Exacerbation with antibiotics
d) Discharge
e) Cyclicity
f) Dyspareunia
g) Soreness
h) Swelling

92
92
86
92
88
92
92
92

Cases (n = 50), n (%)

50
43
30
42
30
43
44
31

(100)
(86.0)
(68.2)
(84.0)
(65.2)
(86.0)
(88.0)
(62.0)

Controls (n = 42), n (%)

3
3
3
7
4
16
24
10

(7.1)
(7.1)
(7.1)
(16.7)
(9.5)
(38.1)
(57.1)
(23.8)

OR (95% CI)

79.86
27.86
26.25
17.81
9.98
5.50
5.22

n/a
(19.30Y330.5)
(7.33Y105.8)
(8.66Y79.58)
(5.39Y58.88)
(3.63Y27.49)
(1.93Y15.71)
(2.10Y12.99)

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34

&

HONG ET AL.

Figure 1. Hormonal influence on symptoms.

swelling were 5 times more likely to be found in the

CVVC group compared to controls.
Vulvovaginal itch was not a significant distinguishing
feature of CVVC in our study group as it was present in
88% of the control group also. A history of atopy was
associated more frequently with the control group
(71% vs 50%, p G .05), and more women in the CVVC

group reported an improvement of their vulvovaginal

symptoms during pregnancy (53% vs 20%, p G .05).
However, neither atopic history nor improvement during
pregnancy significantly differed between the 2 groups.
Qualitative data on suspected risk factors for CVVC
were collected and analyzed using a 5-point Likert scale,
where 1 = strongly disagree, 2 = disagree, 3 = neither
agree or disagree, 4 = agree, and 5 = strongly agree. Mean
scores for each item were used to compare the 2 patient
groups. Figure 1 summarizes the findings. A mean score
less than 3 was represented as a negative value or disagreeing with a statement. Mean scores greater than
3 (agreeing with a statement) were represented as positive
values. A mean score equal to 3 was interpreted as being
neutral and assigned a value of zero.
Of the 34 patients in the CVVC group that had positive Candida swabs taken at the start of the study, only
1 swab was identified as Candida glabrata, the rest were
Candida albicans. A history of a positive Candida swab
during the course of their disease was reported in 86% of
women in the CVVC group.

Figure 2. Number of criteria met (CVVC vs control).

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Vulvovaginal Candidiasis as a Chronic Disease

A selected multivariable logistic regression analysis of

8 significant features for the identification of CVVC
demonstrated 4 criteria (positive swab, cyclicity, soreness,
and discharge) to have excellent predictive validity as
diagnostic criteria. The corresponding area under the
receiver operating characteristic curve was 0.969 (95%
confidence interval [CI] = 0.935Y1.00). According to
these analyses, patients with any 2 of the 4 aforementioned criteria (except soreness with discharge only)
may be accurately classified as having CVVC in this
study. The proposed diagnostic criteria gave a sensitivity of 0.90 (95% CI = 0.77Y0.96), specificity of 0.98 (95%
CI = 0.86Y1.00), positive predictive value of 0.98 (95% CI =
0.87Y1.00), negative predictive value of 0.89 (95% CI =
0.76Y0.96), and positive likelihood ratio of 37.8 (95%
CI = 5.44Y262.7).
The 8 historical and clinical features found to be significant discriminators for CVVC were analyzed further
to determine how many features were present for each
patient across both groups. Results are summarized in
Figure 2. In the CVVC group, no women had fewer than
3 of the 8 criteria. Most CVVC women (88%) fulfilled 4
to 8 of 8 criteria. In the control group, no patients met
more than 4 of 8 criteria, whereas 95% of control patients met 0 to 3 criteria only. Table 3 outlines the diagnostic criteria.
These criteria were prospectively applied to a further
163 patients to determine their accuracy. Of these
patients, 86.5% fulfilled 1 major and 5 or more minor
criteria, and the remainder had a presumptive diagnosis
with 3 to 4 minor criteria. All patients (100%) with a
definite diagnosis responded to oral antifungal therapy
within 3 months.
Table 4 compares the percentage of prospectively
studied patients with the control group. In both the orig-

Table 3. Diagnostic Criteria for Chronic Vulvovaginal

Candidiasis
& Diagnostic: One major + 5 minor criteria
& Presumptive: One major + 3Y4 minor criteria
Major Criterion:
& Chronic nonerosive, nonspecific vulvovaginitis
Minor Criteria: Q5
& Positive vaginal swab either on presentation or in the past
& Soreness
& Cyclicity
& Dyspareunia
& Previous response to antifungal therapy even if incomplete
& Exacerbation with antibiotics
& Swelling
& Discharge

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35

Table 4. Results From the Prospective Group Compared

to the Control Group
Prospective
(n = 163),
n (%)

Diagnostic criteria
Previous response to antifungals
Previous or current positive swab
Exacerbation with antibiotics
Discharge
Cyclicity
Dyspareunia
Soreness
Swelling

139
133
126
102
131
153
146
103

(85.3)
(81.6)
(77.3)
(62.6)
(80.4)
(93.9)
(89.6)
(63.2)

Controls
(n = 42),
n (%)
3
3
3
7
4
16
24
10

(7.1)
(7.1)
(7.1)
(16.7)
(9.5)
(38.1)
(57.1)
(23.8)

p
G.0001
G.0001
G.0001
G.0001
G.0001
G.0001
G.0001
G.0001

inal study group and the prospective group, the criteria

were found to be highly significant compared to controls.

DISCUSSION
CVVC seems to exist on a spectrum with acute and recurrent variants of VVC but presents as a different entity.
We propose that it be defined as a chronic nonerosive
vulvovaginitis causally related to Candida. These patients
symptoms are not recurrent but chronic and continuous,
remitting only during treatment with antifungal medication and frequently recurring rapidly on cessation. Our
results show that CVVC may be diagnosed using the
criteria set out in Table 3. This in turn results in the
ability to predict which patients will reliably benefit from
oral antifungal treatment.
Positive vaginal swabs were found in 68% of women
in the original study group and 81.6% of women in the
prospective group at the initial visit. Women with CVVC
in our study were found to have very low rates of positive
microscopy examinations for their swabs, and indeed, the
majority had completely normal microscopy. There are a
number of possible explanations for these results. The
ready availability of over-the-counter antifungal agents
used by patients who self-diagnose their CVVC may be
responsible. There are no data on how long antifungals
should be ceased for before a culture can become positive
again, and even if this were available, there is likely to be
a wide range between individuals. Women with CVVC
may also have lower Candida counts in the vaginal
epithelium that trigger symptoms compared to women
with more acute forms of VVC. Another possible but less
likely explanation is that the Candida strains found in
CVVC may differ to those implicit in more acute VVC
and may be more fastidious and difficult to culture. In
future studies of CVVC, it may be useful to use various
media other than CHROMagar for swab cultures and
polymerase chain reaction, which has not yet been shown
to be more sensitive than culture for Candida detection

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36

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HONG ET AL.

[8]. Our own experience with Candida polymerase chain

reaction reflects this, and we have not found it to be
positive unless there is also a positive culture. It is not
a routinely available test in Australia and was not performed on our study cohort.
Sobel [5] reported that low microscopy counts correlated with low culture numbers, which, in turn, was associated with asymptomatic carriage of Candida and that
high counts correlated with greater severity of signs and
symptoms. The patients in our study had highly symptomatic disease despite low microscopy counts, which
may suggest a hypersensitivity to Candida by these genetically susceptible women in producing symptomatic
CVVC. Importantly, a positive culture on presentation is
not essential for the diagnosis of CVVC provided there
are sufficient other diagnostic features present. This is a
significant difference from acute and recurrent VVC,
which both, by definition, require a positive culture for
diagnosis and may support the notion that CVVC is a
hypersensitivity reaction, which continues in the absence
of detectable Candida in the vagina. There is a possibility
that Candida in the bowel may be the antigenic stimulus
for a vaginal, estrogen-mediated hypersensitivity response.
This could explain why oral antifungal medication is so
much more effective than topical vaginal antifungals in
treating CVVC. Further investigation is required to explain the possibility of this phenomenon.
The pathogenic mechanisms that explain how a normal commensal organism of the genital tract can cause
severe chronic symptoms in otherwise healthy women,
even in the absence of a positive vaginal swab, remain
unknown, and further studies are required to elucidate
this. In acute VVC and recurrent VVC (which, by definition, is simply frequent attacks of acute VVC), an intermittent increase in vaginal Candida colonization,
associated with typical signs of acute inflammation (itch,
soreness, sudden onset of intense vaginal erythema, typical white cheesy discharge, polymorphonuclear leukocytes [PMNs] on vaginal swab, and positive culture for
Candida) occurs. A short course of topical or oral antifungal medication is usually effective. In CVVC, the
clinical picture is quite different. Inflammation, although
at times intense, is variable or even absent, particularly
during menses. Discharge is frequent but inoffensive and
mucoid, lacking in PMNs and usually normal to microscopy. Symptoms (itch, soreness, dyspareunia) are complex
and continuous, flaring premenstrually. Short-course topical and oral antifungals afford brief and incomplete relief.
It would seem that high estrogen states, which have
been highlighted in previous publications as a risk factor,

are important [9Y12]. The control group did not report

any cyclical change in symptoms, whereas it is characteristic of the CVVC groups symptoms to worsen during
the premenstrual phase and improve markedly during
menstruation. In addition, CVVC is not seen in prepubertal children or postmenopausal women unless the latter
are on hormone replacement therapy [13, 14].
Immunodeficiency has been postulated as a factor;
however, in this study, all patients were systemically well,
were not immunosuppressed, and had no oral involvement. A study by Fidel et al. [15] using a live intravaginal
Candida challenge showed that patients with candidiasis
in fact mount an exaggerated inflammatory response to
the organism and also that these patients have a history
of previous susceptibility. A lack of inflammation is
attributed to protection from symptoms. These data, together with our finding in this study that the presence of
a discharge that is not characterized by the presence of
polymorphs, may suggest that Candida is behaving as an
antigen producing an inflammatory response in genetically susceptible individuals. The difference between this
effect in patients with acute or recurrent VVC and CVVC
may simply be one of degree; however, this has not been
demonstrated. It is possible that there is a threshold beyond which patients react to Candida in a maladaptive
way and that it is lowest in CVVC. Our empirical observation has been that CVVC patients have often, historically, evolved from RVVC to CVVC, and we postulate
that a diminishing threshold is associated with a progressive increase in intolerance of the organism and symptoms. Prolonged antifungal therapy may be effective in
reducing this threshold.
The idea that CVVC is a maladaptive inflammatory
response rather than an immune deficiency explains paradoxes that have so far confounded investigators, including lack of local or systemic immune deficiency, the
fact that it is no more common in HIV-infected patients
than healthy patients, the lack of oral involvement, and
irrelevance of infection by the male partner. Candida
antigen interaction with specific estrogen receptors present
in vulvovaginal tissue may explain why there is almost
never oral involvement, why symptoms cycle, why
CVVC is not seen in low estrogen states, and why patients
may improve in pregnancy when estrogen receptors are
downregulated.
Itch was one of the most common presenting complaints in both the study (92%) and control (88%)
groups, and although it is characteristic, it is nonspecific
for VVC. Itch has been used as a diagnostic feature in
previous studies of acute and recurrent VVC but was not

Copyright 2013 American Society for Colposcopy and Cervical Pathology. Unauthorized reproduction of this article is prohibited.

Vulvovaginal Candidiasis as a Chronic Disease

a sensitive marker useful in the diagnosis of CVVC in this

study (p 9 .05) [16]. Patients complaining of vaginal itch
in the absence of other features should not be assumed to
have VVC. We believe this is an important point, as this
is a very common assumption.
The treatment of chronic and recurrent VVC requires
long-term continuous suppressive therapy, often for more
than 6 months. Given the lengthy duration of treatment
necessary to achieve control of CVVC, oral antifungals
are a more attractive option over topicals, less likely to
cause irritant reactions, and not significantly more expensive than an equivalent number of antifungal pessaries.
Itraconazole and fluconazole are associated with a better
liver safety profile compared to ketoconazole (100 mg
daily in previous studies), and none of our patients experienced any adverse effects. We have previously empirically observed that daily dosing is more reliable than
the widely published treatment regimen of weekly 150 mg
of fluconazole, which we have often observed to fail.
Thus, women were initially treated with daily itraconazole
100 mg or fluconazole 50 mg, until symptom resolution was achieved, usually approximately 1 to 3 months.
Thereafter, a maintenance dose was reached by tapering
the dose. The time needed for symptom resolution varied
between individuals, but many women were able to
maintain symptom control with once- or twice-weekly 50to 100-mg doses. Women were also instructed to take
rescue doses during oral antibiotic treatment, especially
if this was a known previous precipitant of flares. Concomitant antifungal therapy may prevent the flare experienced by some women with CVVC during antibiotic
therapy for other infections. Boric acid vaginal suppositories (600 mg used twice daily) have been shown to be
effective in some treatment-resistant cases of VVC, for
example, with C. glabrata colonization, and were used to
treat our single patient with C. glabrata on vaginal swab
[17]. Given the very large cost burden of treatment of
all forms of VVC, it is important to correctly identify
patients who will genuinely benefit from treatment.
Despite the absence of a placebo control group, the rates
of response were much higher than one would expect
from placebo effect in correctly selected patients.
Donders et al. [18] have called for RVVC to be
regarded as a chronic condition. We agree that this is a
worthy idea based on the need for prolonged treatment;
however, we believe that a condition that behaves chronically should be called a chronic condition.
There is still a great deal of research that is required to
explain both RVVC and CVVC, which may indeed exist
on a spectrum.

&

37

CONCLUSIONS
Patients presenting with chronic, erythematous nonerosive vulvovaginitis who answered yes to at least 5 of
the 8 criteria, which we identified as most characteristic
of this condition (Table 3), responded to a 3-month
course of oral antifungal medication with complete resolution of symptoms and signs in 100% of patients.
These criteria were subsequently verified in a further
group of 163 patients. This included patients with a
negative vaginal swab for Candida at presentation. We
propose that these diagnostic criteria may be useful in
correctly identifying patients who will be genuinely responsive to oral antifungal therapy and that CVVC
may be defined as a chronic nonerosive vulvovaginitis
causally associated with the antigenic effects of Candida.

REFERENCES
1. Foxman B, Barlow R, DArcy H, Gillespie B, Sobel JD.
Candida vaginitis: self-reported incidence and associated costs.
Sex Transmit Dis 2000;27:230Y5.
2. Sobel JD. Vulvovaginal candidiasis. Lancet 2007;369:
1961Y71.
3. Irving G, Miller D, Robinsons A, Reynolds S, Copas AJ.
Psychological factors associated with recurrent vaginal candidiasis: a preliminary study. Sex Transm Infect 1998;74:334Y8.
4. Sobel JD. Pathogenesis and treatment of recurrent
vulvovaginal candidiasis. Clin Infect Dis 1992;14(suppl 1):
S148Y53.
5. Sobel JD. Candidal vulvovaginitis. Clin Obstet Gynecol
1993;36:153Y65.
6. Powell K. Vaginal thrush: quality of life and treatments.
Br J Nurs 2010;19:1106Y11.
7. Finlay AY, Khan GK. Dermatology Life Quality Index.
1991. Available at: http://www.dermatology.org.uk. Accessed
June 2010.
8. Mardh PA, Novikova N, Witkin SS, Korneeva I,
Rodriques AR. Detection of Candida by polymerase chain
reaction vs microscopy and culture in women diagnosed as
recurrent vulvovaginal cases. Int J STD AIDS 2003;14:753Y6.
9. Hamad M, Abu-Elteen KH, Ghaleb M. Estrogendependent induction of persistent vaginal candidosis in naBve
mice. Mycoses 2004;47:304Y309.
10. 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;178:203Y11.
11. Geiger AM, Foxman B. Risk factors for vulvovaginal
candidiasis: a case-control study among university students.
Epidemiology 1996;7:182Y7.
12. Calderon L, Williams R, Martinez M, Clemons KV,
Stevens DA. Genetic susceptibility to vaginal candidiasis. Med
Mycol 2003;41:143Y7.

Copyright 2013 American Society for Colposcopy and Cervical Pathology. Unauthorized reproduction of this article is prohibited.

38

&

HONG ET AL.

13. Fischer G, Bradford J. Vulvovaginal candidiasis in

postmenopausal women: the role of hormone replacement
therapy. J Low Genit Tract Dis 2011;15:263Y7.
14. Dennerstein GJ, Ellis DH. Oestrogen, glycogen and vaginal candidiasis. Aust N Z J Obstet Gynaecol 2001;41:326Y8.
15. Fidel PL Jr, Barousse M, Espinosa T, Ficarra M,
Sturtevant J, Martin DH, et al. An intravaginal live Candida
challenge in humans lead to new hypotheses for the immunopathogenesis of vulvovaginal candidiasis. Infect Immun 2004;
72:2939Y46.

16. Nyirjesy P, Peyton C, Weitz MV, Mathew L,

Culhane JF. Causes of chronic vaginitis: analysis of a prospective database of affected women. Obstet Gynecol 2006;
108:1185Y91.
17. Redondo-Lopez V, Lynch M, Schmitt CA. Torulopsis
glabrata vaginitis: clinical aspects and susceptibility to antifungal agents. Obstet Gynecol 1990;76:651Y5.
18. Donders GG, Bellen G, Mendling W. Management of
recurrent vulvo-vaginal candidosis as a chronic illness. Gynecol
Obstet Invest 2010;70:306Y21.

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