e112 • CID 2008:46 (15 May) • Meltzer and Schwebke

R E V I E W A R T I C L E

Lactational Amenorrhea as a Risk Factor for GroupA Streptococcal Vaginitis

Micelle C. Meltzer and Jane R. SchwebkeDepartment of Medicine, University of Alabama at Birmingham, Birmingham

We report a case of Streptococcus pyogenes, b-hemolytic Streptococcus, Lancefield group A vulvovaginitis in

an otherwise healthy adult female patient experiencing lactational amenorrhea. Group A streptococcal infection

is the infective cause of vulvovaginitis in 21% of prepubescent girls, but it is an uncommon cause of vulvo-

vaginitis in adults. Group A streptococcal vulvovaginitis is frequently associated with households that have

had a recent outbreak of respiratory or dermal infection. The case described here appears to be unusual in

that it was sexually transmitted, and the lack of estrogen associated with anovualtion may have been a

predisposing factor for this unusual sexually transmitted disease.

The patient, a 32-year-old white woman who was 6

months postpartum and was experiencing lactational

amenorrhea, presented to our clinic (University of Al-

abama at Birmingham) during the winter with a pro-

fuse, watery, yellow vaginal discharge. The discharge

was accompanied by moderate-to-severe vulvar pain

and pruritus. The onset, which occurred 4 days before

presentation, was acute and occurred !24 h after having

unprotected vaginal sex with her husband. She denied

having oral sex or digital penetration. A physical ex-

amination showed a yellow, watery discharge. The wet

mount preparation revealed numerous WBCs and was

negative for Trichomonas vaginalis, clue cells, and yeast.

Vaginal pH was not determined. Nucleic acid ampli-

fication test results were negative for gonorrhea and

chlamydia. Gram staining revealed abundant seg-

mented WBCs, gram-positive cocci in pairs and chains,

and a notable absence of Lactobacillus-like gram-posi-

tive rods (figure 1). A vaginal swab sample was sent to

the laboratory for culture. The patient’s culture grew

abundant group A streptococci (GAS). The patient was

Received 29 November 2007; accepted 24 December 2007; electronicallypublished 4 April 2008.

Reprints or correspondence: Dr. Jane R. Schwebke, University of Alabama atBirmingham, 1530 3rd Ave. S ZRB 239, Birmingham, AL 35294-0007(schwebke@uab.edu).

Clinical Infectious Diseases 2008; 46:e112–5� 2008 by the Infectious Diseases Society of America. All rights reserved.1058-4838/2008/4610-00E3$15.00DOI: 10.1086/587748

treated with 500 mg of amoxicillin 3 times per day for

7 days. Follow-up via telephone confirmed that the

patient’s condition rapidly improved.

The patient had no recent history of dermal or re-

spiratory infection, but her 3-year-old son had been

treated for GAS pharyngitis 2 weeks before presenta-

tion. The patient’s husband had been ill with an upper

respiratory tract infection at the time of sexual contact.

After learning about his wife’s culture results, the pa-

tient’s husband (who was still ill) went to see his health

care practitioner. A nasopharyngeal culture sample was

collected, and it was positive for GAS.

Discussion. GAS vulvovaginitis in menarchal

women is rare. In a study involving 3430 women and

children with vulvovaginitis, the isolation rate in

women was just over 1% [1]. Historically, GAS was a

common and often fatal cause of postpartum infection.

In the United Kingdom, from 1880 through 1930, there

were 2000 deaths annually attributed to puerperal sepsis

[2]. GAS infection was spread between patients by doc-

tors and midwives and was most common during the

fall and winter months [2, 3]. Since the advent of an-

tisepsis, better hygiene, and antibiotics, there has been

a sharp decrease in the incidence of puerperal infection

caused by GAS. There are, however, anecdotal reports

of current cases of GAS puerperal sepsis and an increase

in the rate of GAS isolated from high vaginal swab

samples obtained from menarchal women with vaginal

discharge [2].

In contrast, GAS vulvovaginitis is not uncommon in

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GAS Vaginitis • CID 2008:46 (15 May) • e113

Figure 1. A, Gram stain of vaginal fluid from a patient with group A streptococcal vaginitis. B, Gram stain of vaginal fluid with normal vaginalflora.

young girls. Vulvovaginitis is the most common gynecological

complaint among prepubescent girls. Its most frequent cause

is idiopathic (in 64% of cases), but it is sometimes associated

with a specific bacterial pathogen [4]. GAS may be isolated in

as many as 59% of these cases [4]. GAS is most often isolated

from school-aged children with respiratory infections during

the fall and winter [3]. This seasonal preponderance is reflected

in the rate of GAS isolation from patients with vulvovaginitis,

as well [1]. Most cases of GAS vulvovaginitis in children have

had either a household or personal history of dermal or re-

spiratory infection due to GAS [4].

GAS genital infections are not only associated with household

contact or autoinoculation with dermal and respiratory infec-

tions; they are also transmitted sexually. Fisk and Riley [5]

report a case in which a husband and wife both had GAS genital

infections after engaging in both oral and vaginal sex while the

wife had pharyngitis. Wakatsuki [6] reports 47 cases of GAS

balanoposthitis in which the route of infection was thought to

be sexual contact, especially through fellatio with commercial

sex workers. Manalo et al. [7] describe a female patient with

GAS tuboovarian abscess and peritonitis thought to be caused

by engaging in receptive oral sex with a partner who had an

upper respiratory tract GAS infection. Bray and Morgan [8]

report 2 cases of GAS vulvovaginitis thought to be transmitted

after vaginal intercourse only (i.e., oral sex was not believed to

have occurred). Sobel et al. [9] report 2 cases of recurrent GAS

vulvovaginitis in which the gastrointestinal tracts of the pa-

tients’ husbands were colonized with GAS.

The signs and symptoms of GAS vulvovaginitis are acute and

typically more severe than those caused by other types of vag-

initis. The most common findings are copious, yellow, sero-

purulent vaginal discharge, edema, and marked vulvar and vag-

inal erythema. The patient usually complains of vulvar pain,

pruritus, and dyspareunia. There is often no odor, but if there

is, it is foul, not fishy like the odor associated with bacterial

vaginosis. Wet mount preparations reveal abundant WBCs,

Gram staining often reveals gram-positive cocci in pairs and

chains and few or no Lactobacillus species, and the pH is usually

quite elevated. Vaginal cultures often grow abundant GAS with

few or no other organisms isolated [4, 8–13]. It should be noted

that the rate of vaginal carriage of GAS in healthy women and

children ranges from 0% to slightly over 1% [8, 11]. Thus, if

a patient is symptomatic and has culture results that are positive

for GAS, this result should not be ignored, and the patient

should be treated with agents active against Streptococcus spe-

cies. Typically, patients respond promptly to treatment. If im-

properly diagnosed and treated, the condition will persist and

can sometimes spread rectally or even systemically.

Anatomic, hygienic, and—perhaps most importantly—phys-

iologic factors predispose prepubescent girls to bacterial vul-

vovaginitis. The anestrogenic vaginal epithelium in prepubes-

cent girls is thin and lacks cornification, and it is therefore

subject to irritation and infection. It also lacks glycogen de-

position and, consequently, lacks colonization with Lactobacil-

lus species and vaginal acidification [4, 10, 12, 14]. It is known

that healthy, Lactobacillus species–dominant, vaginal microflora

provide protection against the overgrowth of potentially path-

ogenic bacteria [15].

Postmenopausal and postpartum women experience a sim-

ilar regression to the immature, anestrogenic vaginal environ-

ment found in prepubescent girls. The condition is called senile

vaginal atrophy in postmenopausal women and postpartum

vaginal atrophy in postpartum women. Both conditions are

characterized by dyspareunia, vaginal stinging and tightness,

dysuria, vaginal color change, an increase in parabasal cells, a

decrease in Lactobacillus species, and an increase in vaginal pH

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[16–20]. The association of breast-feeding with vaginal atrophy

and the resultant absence of Lactobacillus species, along with

its potential risks, may be underappreciated. Postpartum vag-

inal atrophy has a 17% prevalence rate, is strongly associated

with breast-feeding, and responds well to topical estrogen [20].

Goetsch [21] described a similar condition but focused on the

dyspareunia experienced by 39% of postpartum patients and

also found a strong correlation with breast-feeding. Palmer and

Likis [22] report a case of lactational atrophic vaginitis attrib-

utable to protracted breast-feeding. The clinical characteristics

of this patient were nearly identical to those associated with

advanced senile vaginal atrophy, and she complained of severe

dyspareunia. Her symptoms were alleviated with topical

estrogen.

The vaginal physiology of these women is analogous to that

of prepubescent girls, and they are, therefore, also at risk of

infectious vulvovaginitis. Paraskevaides and Wilson [23] report

a case of fatal disseminated intravascular coagulation secondary

to GAS cervicitis in a 57-year-old woman with no apparent

predisposing factors other than the change in the vaginal en-

vironment found during menopause. Sobel [24] found that 6

of 51 patients with desquamative inflammatory vaginitis, a se-

vere form of purulent vaginitis, were postpartum and lactating;

31 of the 51 women were perimenopausal, menopausal, or had

received antiestrogen therapy. These women often had no Lac-

tobacillus species and an abundance of a Streptococcus species,

most frequently Streptococcus agalactiae, b-hemolytic Strepto-

coccus, Lancefield group B, but there was 1 case of GAS infec-

tion. Permanent remission for some of the women who were

postmenopausal and not receiving hormone replacement ther-

apy was not attained until antibiotic treatment was paired with

estrogen therapy.

The American College of Obstetricians and Gynecologists,

the American Academy of Pediatrics, the American Academy

of Family Physicians, and the Department of Health and Hu-

man Services have all adopted policies that promote breast-

feeding and advise extending its duration [25–28]. These pol-

icies should consider and provide for the potential conse-

quences that breast-feeding may have on the mother’s sexual

health and function, in addition to the numerous reported

benefits of breast-feeding to mother and baby. Women who

choose to breast-feed should be counseled about protecting

themselves from infection, and when lactating women present

with vaginal complaints, the differential diagnosis and treat-

ment algorithms should be broadened to encompass infections

and conditions that are normally associated with the hypoes-

trogenic states found in prepubescent girls and postmenopausal

women.

Acknowledgments

Potential conflicts of interest. M.C.M. and J.R.S.: no conflicts.

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