Lactational Amenorrhea as a Risk Factor for Group A Streptococcal Vaginitis
- Reprints or correspondence: Dr. Jane R. Schwebke, University of Alabama at Birmingham, 1530 3rd Ave. S ZRB 239, Birmingham, AL 35294-0007 (schwebke{at}uab.edu).
Abstract
We report a case of Streptococcus pyogenes, β-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 vulvovaginitis 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 Alabama at Birmingham) during the winter with a profuse, 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 examination 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 amplification test results were negative for gonorrhea and chlamydia. Gram staining revealed abundant segmented WBCs, gram-positive cocci in pairs and chains, and a notable absence of Lactobacillus-like gram-positive 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 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.
Figure 1
A, Gram stain of vaginal fluid from a patient with group A streptococcal vaginitis. B, Gram stain of vaginal fluid with normal vaginal flora.
The patient had no recent history of dermal or respiratory infection, but her 3-year-old son had been treated for GAS pharyngitis 2 weeks before presentation. 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 patient'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 doctors and midwives and was most common during the fall and winter months [2, 3]. Since the advent of antisepsis, 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 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 respiratory infection due to GAS [4].
GAS genital infections are not only associated with household contact or autoinoculation with dermal and respiratory infections; 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 patients' 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 vaginitis. The most common findings are copious, yellow, seropurulent vaginal discharge, edema, and marked vulvar and vaginal 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 species. Typically, patients respond promptly to treatment. If improperly diagnosed and treated, the condition will persist and can sometimes spread rectally or even systemically.
Anatomic, hygienic, and—perhaps most importantly—physiologic factors predispose prepubescent girls to bacterial vulvovaginitis. The anestrogenic vaginal epithelium in prepubescent girls is thin and lacks cornification, and it is therefore subject to irritation and infection. It also lacks glycogen deposition and, consequently, lacks colonization with Lactobacillus 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 pathogenic bacteria [15].
Postmenopausal and postpartum women experience a similar regression to the immature, anestrogenic vaginal environment 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 [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 vaginal 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 attributable 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 environment found during menopause. Sobel [24] found that 6 of 51 patients with desquamative inflammatory vaginitis, a severe 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 Lactobacillus species and an abundance of a Streptococcus species, most frequently Streptococcus agalactiae, β-hemolytic Streptococcus, Lancefield group B, but there was 1 case of GAS infection. Permanent remission for some of the women who were postmenopausal and not receiving hormone replacement therapy 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 Human Services have all adopted policies that promote breast-feeding and advise extending its duration [25–28]. These policies should consider and provide for the potential consequences 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 treatment algorithms should be broadened to encompass infections and conditions that are normally associated with the hypoestrogenic states found in prepubescent girls and postmenopausal women.
Acknowledgments
Potential conflicts of interest. M.C.M. and J.R.S.: no conflicts.
- Received November 29, 2007.
- Revision received December 24, 2007.
- Accepted April 4, 2008.
- © 2008 Infectious Diseases Society of America
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