You are on page 1of 5

British Journal of Obstetrics and Gynaecology

May 2001, Vol. 108, pp. 451±455

Vaginal microbiological ¯ora, and behavioural and clinical


®ndings in women with vulvar pain
Krasimira Tchoudomirova a, Per-Anders MaÊrdh b, Dan Hellberg c,*
Objective To study genital symptoms and signs in women with vulvar pain, and the association with potential
risk factors such as microbiological agents, sexual behaviour and genital hygiene.
Design Prospective cohort study of apparently healthy women attending for contraceptive advice.
Setting Two family planning clinics and one youth clinic in Sweden.
Population Out of 996 women recruited, 79 women (7.9%) had, on request, complaints of current burning and
smarting vulvar pain and/or super®cial dyspareunia (our de®nition of vulvar pain) while 917 women without
such symptoms served as controls.
Results Complaints of dysmenorrhoea, vaginal discharge, genito-anal pruritus, dysuria, and abdominal pain
were more frequent in the study group, than in the control group. In the women with vulvar pain, erythemas,
super®cial ulcerations, and ®ssures were found signi®cantly more frequently. Vaginal candidosis was the only
current genital infection that occurred more often in the study group, than among the controls. There were no
differences in the history of gonorrhoea, genital chlamydial infection, genital herpes, genital warts, and
candidosis between the two groups. The sexual debut of the women with vulvar pain occurred later in life,
compared with the control group. Control subjects were more likely to use tampons for menstrual sanitation,
than the women with vulvar pain.
Conclusions Neither infectious conditions caused by current known agents, with the exception of candidosis in
some cases, nor behavioural factors, such as sexual behaviour and genital hygiene habits could in this study
explain vulvar pain.

INTRODUCTION toses (e.g. lichen planus, bullous dermatoses, infectious


dermatoses, allergic dermatoses, autoimmune derma-
`Extensive sensitivity' or `hyperesthesia' of the vulva toses, and vulvar intraepithelial neoplasia) can cause
was described by Skene in 1889 1. The medical literature acute or chronic vulvar itching and pain. These diseases
did not mention vulvar pain until the early 1980s 2. The can cause complex differential diagnostic problems 9.
burning vulva syndrome is de®ned as chronic vulvar The aim of the present study was to register genital
discomfort, characterised by the patient's complaint of symptoms and signs among apparantly healthy women
burning, stinging, irritation or rawness 3. Vulvodynia is with current vulvar pain (i.e. burning and smarting pain
characterised by unexplained vulvar pain, sexual and/or super®cial dyspareunia) and to study the preva-
dysfunction, and psychological disability 4. Several lence of bacterial and viral genital infections and vaginal
subsets of vulvodynia have been recognised 5 (i.e. vulvar ¯ora changes. Finally, we tried to identify any possible
vestibulitis syndrome, cyclic vulvovaginitis, dysesthetic association between symptoms of vulvar pain and sexual
vulvodynia, and vulvar papillomatosis). Vulvodynia can behaviour and genital hygiene habits.
also be a combination of several of these subtypes. As
there are many de®nitions we chose only to use the term
vulvar pain in this study. METHODS
Other causes, such as cytolytic vaginitis 6, lactobacil-
losis 7, and desquamative in¯ammatory vaginitis 8 can The women were recruited at the family planning
mimic the symptoms of vulvodynia. Many vulvar derma- clinics at Eskilstuna Hospital, Eskilstuna and at Danderyd
Hospital, Stockholm, as well at the youth clinic in Eskil-
stuna, Sweden. Of the 1077 women, all attending for
a
Department of Venerology, University Hospital, Bulgaria contraceptive advice, who were asked, 1011 (93.9%)
b
Institute of Clinical Bacteriology, University Hospital, agreed to participate in the study. Due to incomplete
Sweden records, 15 women (1.5%) were excluded from the
c
Department of Obstetrics and Gynaecology, Falun analyses. Seventy-nine (7.9%) of the remaining 996
Hospital, Sweden women had burning and smarting pain and/or super®cial
dyspareunia, the majority of them for more than six
* Corresponding: Dr D. Hellberg, Department of Obstetrics and Gynae- months, and, on the basis of personal, structured inter-
cology, Falun Hospital, S-791 82 Falun, Sweden. views, were de®ned as suffering from vulvar pain. The
q RCOG 2001 British Journal of Obstetrics and Gynaecology
PII: S 0306-545 6(00)00114-5 www.bjog-elsevier.com
452 K. TCHOUDOMIROVA ET AL.

comparison group consisted of the remaining 917 women continuous variables. Logistic regression was used for
without such symptoms. multifactorial analyses (e.g. adjustment for age).
A structured in-depth interview included a history of
any sexually transmitted disease, other genital infections,
and current genital symptoms. Complaints of vaginal RESULTS
discharge, dysuria, dysmenorrhoea, hypermenorrhoea,
intermenstrual bleeding, and abdominal pain, including The mean age of the 79 women with vulvar pain and of
low-sited abdominal pain, were noted. A thorough gyne- the 917 controls differed signi®cantly: 23.5 and 26.1
cologic examination was performed where ®ndings of years, respectively [P ˆ 0.002; range 15-44 years].
erythema, ®ssures, super®cial vulvovaginal ulcerations, Therefore all comparisons were adjusted for age.
ectopies, and the character of the vaginal discharge, were With exception of candidosis, there was no signi®cant
noted. differences in the prevalence of any current sexually
Urethral and endocervical specimens were collected, transmitted disease or related conditions in the women
transported, and analysed for Chlamydia trachomatis and with vulvodynia, as compared with the controls (Table
Neisseria gonorrhoeae, while vaginal specimens were 1). Nor were there any difference in a history of pelvic
tested for Candida albicans, Mycoplasma hominis, lacto- in¯ammatory disease or any sexually transmitted
bacilli, and obligate and facultative anaerobic bacteria, as diseases, including gonorrhoea, genital chlamydial infec-
described in detail previously 10. tion, genital herpes, genital warts, and vaginal candidosis.
Wet smears of material collected from the vaginal Other vaginal ¯ora ®ndings, such as betahaemolytic
mucosa and from the posterior vaginal fornix were used streptococci group B, Escherichia coli, Staphylococcus
for detection of yeast blastospores and pseudohyphae, saprophyticus, G. vaginalis, lactobacilli species, Myco-
trichomonades, bacteria of mobiluncus morphotype, plasma hominis, Ureaplasma urealyticum, and obligate
and of clue cells. Vaginal secretion was also collected and facultative Gram-positive and Gram-negative cocci
for performing amine tests and pH-measurement. Genital and rods did not differ between the two groups of women.
candidosis was de®ned as a positive candida culture from Differences were noted between the study and the
the vagina and/or ®ndings of blastospores and pseudohy- comparison group concerning symptoms of dysmenor-
phae at wet smear microscopy as previously described 11. rhoea, vaginal discharge, genital and perianal pruritus,
Bacterial vaginosis was diagnosed in cases ful®lling at general abdominal pain, and lower abdominal pain
least three out of the following four criteria: a grey homo- (Table 2).
geneous vaginal discharge, clue cells (i.e. epithelial cells Among the women with vulvar pain, erythema, super-
covered by bacteria of Gardnerella vaginalis morpho- ®cial ulcerations, and ®ssures were signi®cantly more
type), a vaginal pH of $ 4.7, and a positive amine test. often observed at the examination as compared with
For detection and typing of human papillomavirus, the controls. Erythema was also associated with candi-
samples were collected from the ecto- and endocervix dosis in the study groupin that 11 of the 18 women
by means of a brush device (Cytobrush, Medscand, (38.9%) with candidosis had erythema, compared with
MalmoÈ, Sweden) and analysed by Southern blot as 8 of 61 (13.1%) without candidosis (P ˆ 0.02). The
described in detail elsewhere 10. corresponding ®gures for super®cial ulcerations were 5
The material was computerised and analysed with the of 13 (27.8%) and 3 of 66 (4.5%) (P ˆ 0.01), respec-
JMP statistical programme (SAS Institute Inc. JMP statis- tively. There was no signi®cant association between
tics for the Apple Macintosh, Cary, North Carolina USA, ®ssures and candidosis: 5.6% versus 6.6% (P ˆ 0.88).
1994). Differences were studied by using x 2 (Pearson and The women with vulvar pain less often used tampons
likelihood ratio) for nominal variables and t test for only for menstrual hygiene than the controls (11.4%

Table 1. Sexually transmitted diseases (STD), allied conditions, and urine cultures in women with (n ˆ 79) and without vulvar pain (n ˆ 917). Values are given
as n (%).

Vulvar pain

With (n ˆ 79) Without (n ˆ 917) P


n (%) n (%)

Genital chlamydial infection 9 (11.4) 76 (8.3) 0.55


Human papillomavirus infection 6 (7.6) 60 (6.6) 0.86
Genital warts 3 (3.8) 36 (3.9) 0.97
Vaginal candidosis 18 (22.8) 112 (12.4) 0.01
Bacterial vaginosis 7 (7.8) 124 (14.1) 0.33
Bacterial urine culture$ 10 5CFU/ml (colony forming units) 4 (5.1) 65 (7.1) 0.48

q RCOG 2001 Br J Obstet Gynaecol 108, pp. 451±455


POSSIBLE CAUSES OF VULVAR PAIN 453

Table 2. Gynaecological symptoms and signs in women with and without DISCUSSION
vulvar pain. Values are given as n (%).

Symptoms Vulvar pain One of the most interesting ®ndings in this study was
what we did not ®nd. Despite comprehensive cultures and
With (n ˆ 79) Without (n ˆ 917) P other diagnostic methods to detect all possible microor-
n (%) n (%)
ganisms that we could expect to ®nd, combined with a
Dysmenorrhoea 43 (54.4) 334 (36.4) 0.004 detailed history of previous genital infections, we only
Vaginal discharge 38 (48.1) 184 (20.1) 0.0001 found an increase of vulvovaginal candidosis among the
Genital pruritus 25 (31.7) 60 (6.5) 0.0001 women with vulvar pain compared with the control
Perianal pruritus 6 (7.6) 28 (3.1) 0.02 group. These cases of candidosis could only explain a
Dysuria 13 (16.5) 52 (5.7) 0.0003
General abdominal pain 38 (48.1) 277 (30.2) 0.0007
small minority of the cases of vulvar pain.
Lower abdominal pain 20 (27.0) 155 (17.7) 0.05 Although vulvodynia was described one hundred years
Signs ago, the aetiology remains obscure. Women may present
Abnormal discharge 21 (26.6) 217 (23.7) 0.37 with a variety of symptoms, but with few objective signs
Erythema 15 (19.0) 55 (6.0) 0.0001 of disease. A psychosomatic aetiology of this multisymp-
Super®cial ulcerations 8 (10.1) 12 (1.3) 0.0001
Fissures 5 (6.3) 19 (2.1) 0.03
tomatic condition has been assumed 12 along with various
Ectopy 34 (43.0) 399 (43.6) 0.53 infectious causes, such as candidosis 2,13±15, human papil-
lomavirus 16±18 and herpes virus infections 19. Also chronic
recurrent bacterial vaginosis 20, chronic alteration of the
versus 23.2%, P ˆ 0.02). No other signi®cant differ- vaginal pH 20 and the use of intimate hygiene products,
ences concerning genital hygiene such as other methods such as creams, soap, douches, and sprays, have all been
of menstrual sanitation, use of different kinds of washing considered as potential aetiological factors 21. Hormones
solutions, frequency of washing, vaginal douching and have also been regarded as possible causes for this condi-
the habit of taking hot baths, were observed between the tion 22,23. Furthermore, autoimmunity has been suggested
two groups of women studied. as an aetiological factor, because of the concordance of
No differences were observed between the study group the two in¯ammatory syndromes (interstitial cystitis and
and the controls concerning contraceptive use (i.e. for focal vulvitis) involving the bladder, the urethra and the
oral contraceptives, intrauterine device, condom, and vestibulum, all organs derived from the embryonic
for no contraceptive use at all). Sexual behaviour of the urogenital sinus 24.
women with vulvar pain, compared with the controls, The incidence and prevalence of vulvar pain is not
differed only for age at ®rst intercourse (which occurred known. However, vulvar pain is likely to be an under-
later among the women with vulvar pain), but not for diagnosed clinical syndrome. In one study 25 in a general
number of lifetime partners, more than one partner during gynaecological practice, the prevalence of vulvodynia
the last 6 months, the practise of casual sex, regular oral was 15% when it was actively looked for. In our study
or experience of anal sex, intercourse during menstrua- the prevalence of vulvodynia was 7.9% in a group of
tion and masturbation (Table 3). women who considered themselves gynaecologically
No age-adjusted differences were observed in having healthy.
had an induced or miscarriage. The controls had had The reported mean age of women with this condition
more pregnancies (1.0 versus 0.40) than the cases. has varied, with a range from 25 to 60 years of age 26. In
After adjustment for age and childbirths (0.65 versus this study the women with vulvar pain were younger than
0.30), the difference disappeared (P ˆ 0.25). the control group, with a mean age of 23.5 years.

Table 3. Sexual behaviour in women with and without vulvar pain. Values are given as n (%).

Variable Vulvar pain

With (n ˆ 79) Without (n ˆ 917) P


n (%) n (%)

Age of ®rst intercourse 16.7 16.1 0.0005


Number of lifetime partners 9.2 11.4 0.56
.1 partner last six months 17 (21.5) 188 (20.5) 0.55
Casual sex, ever 54 (68.4) 659 (72.3) 0.76
Masturbation .once/month 21 (26.6) 255 (24.5) 0.96
Oral sex .once /month 14 (17.7) 95 (10.4) 0.07
Anal sex, ever 19 (24.1) 199 (21.7) 0.30
Intercourse during menstruation 17 (21.5) 144 (15.7) 0.10

q RCOG 2001 Br J Obstet Gynaecol 108, pp. 451±455


454 K. TCHOUDOMIROVA ET AL.

The perception of one and the same pathological virus/or candida species may suggest an immune-
changes differ from woman to woman. In contrast to the mediated aetiology with sensitiisation to antigens causing
vivid ¯ora of symptoms reported by the women studied erythema and pain. Remission and exacerbation of symp-
(e.g. discharge, genital and anal pruritus, dysmenorrhoea, toms may occur when treatment for one condition affects
and abdominal pain) only erythema and super®cial ulcera- the development of another. For example, prompt treat-
tions and ®ssures could be found at gynaecological exam- ment for vulvovaginal candidosis or condylomata may
ination and these were mainly observed in those having prevent chronic in¯ammation contributing to vestibulitis.
candidosis. In 27% of the vulvodynia cases, an increased Fear of cancer or infection may lead to overcleaning and
discharge was observed on examination. This might give the use of potential allergens or irritants, which may
chronic irritation to the vulva. obscure an underlying dermatosis or vestibulitis. Long
Recent case±control studies have provided little support term topical application of corticosteroids may itself
for the hypothesis of a viral or bacterial infection being the induce vulvodynia as well as potentiating candidosis.
cause of vulvodynia 22. Studies have failed to identify It is important to investigate all potential aetiological
herpes simplex, N. gonorrhoeae, Staphylococcus aureus, factors in every patient with vulvodynia. The recognition
group B streptococci, C. trachomatis, Mycoplasma homi- of the multifactorial nature of vulvodynia is important for
nis, C. albicans, Trichomonas vaginalis, and human papil- appropriate diagnostic evaluation and management.
lomavirus as causes of vulvodynia 22,27±29. In one study a Patients who have experienced chronic pain are a manage-
history of recurrent candidosis, previous condyloma ment challenge, as they remain hypersensitive and fearful,
acuminata, or earlier oral contraceptive use was noted even after `successful' therapy. Vulvar pain usually
more often in patients with vulvodynia than in controls 28. improves in time, but resolution is typically slow. Patients
Our study, like others 22,26, did not ®nd any such associa- must be followed up regularly and encouraged as small
tions. increments of progress are made. One consequence of
Extensive washing with intimate hygiene products vulvar pain is that it may severely disturb relations with
might cause symptoms from the genital tract. However, partners. One of the major ®ndings of this study was that,
we could not ®nd any correlation between the genital despite extensive diagnostic procedures, we did not ®nd
washing habits of the women with vulvodynia concern- evidence of an infectious aetiology of vulvodynia, with the
ing low pH solutions, soap, water, taking hot baths or exception of some cases of candidosis. The pathogenicity
practising vaginal douching. The choice of menstrual of vulvodynia remains a scienti®c challenge.
sanitation method was related to vulvodynia, as these
women less often used tampons than the controls. This
may be due to pain at insertion of the tampon. References
Sexual partner factors, such as the number of lifetime
sexual partners, recent partner change, history of casual 1. Skene AJC. Treatise of the Diseases in Women. New York: D Appleton
and Company, 1889.
sex, and practise of anal and oral sex did not differ from 2. Friedrich EGJ. Vulvar vestibulitis syndrome. J Reprod Med
the comparison group. Age at ®rst intercourse differed 1987;32:110±114.
signi®cantly between the two groups of women studied, 3. The ISSVD task force. Burning vulva syndrome. J Reprod Med
but only by 0.6 years, due to a later sexual debut in the 1984;29:457±462.
women with vulvar pain, and would not seem likely to 4. Lynch PJ. Vulvodynia: a syndrome of unexplained vulvar pain,
psychologic disability and sexual disfunction. J Reprod Med
have any causal association to vulvodynia. However, oral 1986;31:773±780.
sex was practised by the women with vulvodynia almost 5. McKay M. Subsets of vulvodynia. J Reprod Med 1988;33:695±698.
twice as often as the controls: in 18% versus 10% 6. Cibley LJ, Cibley LJ. Cytolytic vaginosis. Am J Obstet Gynecol
(P ˆ 0.07). This might be explained by dyspareunia. 1991;165:1245±1249.
Bazin et al. 22 found no association of the occurrence of 7. Horowitz B, MaÊrdh P-A, Nagy E, Rank E. Vaginal lactobacillosis. Am
J Obstet Gynecol 1994;170:851±857.
the vestibulitis syndrome and the number of sexual part- 8. Oates J, Rowen D. Desquamative in¯ammatory vaginitis: a review.
ners, but reported that early age at ®rst intercourse was Genitourin Med 1990;6:275±279.
related to the development of vulvar vestibulitis. Bazin et 9. McKay M. Vulvitis and vulvovaginitis: cutaneous considerations. Am J
al. also found a greater parity rate was related to a Obstet Gynecol 1991;165:1176±11782.
decrease in the relative risk of vulvodynia. This was 10. Hellberg D, Borendal N, SikstroÈm B, Nilsson S, MaÊrdh P-A. Compar-
ison between women with cervical human papilloma virus infection
also the case in our study but after adjustment for age and genital warts. Some behaviour factors and clinical ®ndings. Geni-
the difference was not signi®cant between the study tourin Med 1995;71:88±91.
group and the control group. 11. Zdolsek B, Hellberg D, FroÈman G, Nilsson S, MaÊrdh P-A. Culture and
Vulvar pain continues to be a mystery as to its patho- wet smear microscopy in the diagnosis of low-symptomatic vulvova-
genesis. It is a complex multifactorial, multidisciplinary, ginal candidiasis. Eur J Obstet Gynecol Repro Biol 1995;58:47±51.
12. Dodson MG, Friedrich EGJ. Psychosomatic vulvovaginitis. Obstet
and underdiagnosed clinical syndrome. The interrelation- Gynecol 1978;51:23±25.
ship of factors in¯uencing vulvar pain is confusing. The 13. Hurley R, De Louvois J. Candida vaginitis. Postgrad Med
occurence of chronic infections with human papilloma- 1979;55:645±647.

q RCOG 2001 Br J Obstet Gynaecol 108, pp. 451±455


POSSIBLE CAUSES OF VULVAR PAIN 455

14. Marinoff SC, Turner MLC. Hyper sensitivity to vaginal candidiasis or 22. Bazin S, Bouchard C, Brisson J, Morin C, Meisels A, Fortier M. Vulvar
treatment vehicles in the pathogenesis of minor vestibular gland vestibulitis syndrome: an exploratory case control study. Obstet Gyne-
syndrome. J Reprod Med 1987;31:796±799. col 1994;83:47±50.
15. Pyka RE, Wilkinson EJJ, Friedrich EC, Croker BP. The histopathology 23. Pal T, Bhattacharyya AK. Structural changes in human cervical mucus.
of vulvar vestibulitis syndrome. Int J Gynecol Pathol 1988;7:249±257. Indian J Med Res 1989;90:44±50.
16. Di Paola GR, Rueda NG. Deceptive vulvar papilloma virus infection: 24. McCormack WM. Two urogenital sinus syndromes. Interstitial cystitis
A possible explanation for certain cases of vulvodynia. J Reprod Med and focal vulvitis. J Reprod Med 1990;35:873±876.
1986;10:790±966. 25. Goetsch MF. Prevalence and historic features in a general gynecologic
17. Turner MLC, Marinoff SC. Association of human papillomavirus with practice population. Am J Obstet Gynecol 1991;164:1609±1616.
vulvodynia and the vulvar vestibulitis syndrome. J Reprod Med 26. Paavonen J. Vulvodynia-a complex syndrome of vulvar pain. Acta
1988;33:533±537. Obstet Gynecol Scand 1995;74:243±247.
18. Umpierre SA, Kaufman RH, Adam E, Woods KV, Adler-Stoz K. 27. Eschenbach DA, Davick PR, Williams BL. Prevalence of hydrogen
Human papilloma virus DNA in tissue biopsy specimens of vulvar peroxide-producing Lactobacillus species in normal women and
vestibulitis patients treated with interferon. Obstet Gynecol women with bacterial vaginosis. J Clin Microbiol 1989;27:251±256.
1991;78:693±695. 28. Mann MS, Kaufman RH, Brown D, Adam E. Vulvar vestibulitis:
19. Chang TW, Fiumara NJ, Weinstein L. Genital herpes: some clinical signi®cant clinical variables and treatment outcome. Obstet Gynecol
and laboratory observations. JAMA 1974;229:544±545. 1992;79:122±125.
20. Marinoff SC, Turner ML. Vulvar vestibulitis syndrome: an overview. 29. Wilkinsson EJ, Guerrero E, Daniel R, et al. Vulvar vestibulitis is rarely
Am J Obstet Gynecol 1991;165:1228±1233. associated with human papilloma virus infection types 6, 11, 16, or 18.
21. Maibach HI, Mathias CT. Vulvar dermatitis and ®ssures-irritant Int J Gynecol Pathol 1993;12:344±349.
dermatitis from methyl benzethonium chloride. Contact Derm
1985;5:340±345. Accepted 21 November 2000

q RCOG 2001 Br J Obstet Gynaecol 108, pp. 451±455

You might also like