Amenorrea come fattore di rischio per vaginite da streptococco
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Amenorrea come fattore di rischio per vaginite da streptococco

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Amenorrea come fattore di rischio per vaginite da streptococco Amenorrea come fattore di rischio per vaginite da streptococco Document Transcript

  • REVIEW ARTICLE Lactational Amenorrhea as a Risk Factor for Group A Streptococcal Vaginitis Micelle C. Meltzer and Jane R. Schwebke Department 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 Downloaded from cid.oxfordjournals.org at GlaxoSmithKline on January 27, 2011 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 treated with 500 mg of amoxicillin 3 times per day for months postpartum and was experiencing lactational 7 days. Follow-up via telephone confirmed that the amenorrhea, presented to our clinic (University of Al- patient’s condition rapidly improved. abama at Birmingham) during the winter with a pro- The patient had no recent history of dermal or re- fuse, watery, yellow vaginal discharge. The discharge spiratory infection, but her 3-year-old son had been was accompanied by moderate-to-severe vulvar pain treated for GAS pharyngitis 2 weeks before presenta- and pruritus. The onset, which occurred 4 days before tion. The patient’s husband had been ill with an upper presentation, was acute and occurred !24 h after having respiratory tract infection at the time of sexual contact. unprotected vaginal sex with her husband. She denied After learning about his wife’s culture results, the pa- having oral sex or digital penetration. A physical ex- tient’s husband (who was still ill) went to see his health amination showed a yellow, watery discharge. The wet care practitioner. A nasopharyngeal culture sample was mount preparation revealed numerous WBCs and was collected, and it was positive for GAS. negative for Trichomonas vaginalis, clue cells, and yeast. Discussion. GAS vulvovaginitis in menarchal Vaginal pH was not determined. Nucleic acid ampli- women is rare. In a study involving 3430 women and fication test results were negative for gonorrhea and children with vulvovaginitis, the isolation rate in women was just over 1% [1]. Historically, GAS was a chlamydia. Gram staining revealed abundant seg- common and often fatal cause of postpartum infection. mented WBCs, gram-positive cocci in pairs and chains, In the United Kingdom, from 1880 through 1930, there and a notable absence of Lactobacillus-like gram-posi- were 2000 deaths annually attributed to puerperal sepsis tive rods (figure 1). A vaginal swab sample was sent to [2]. GAS infection was spread between patients by doc- the laboratory for culture. The patient’s culture grew tors and midwives and was most common during the abundant group A streptococci (GAS). The patient was fall and winter months [2, 3]. Since the advent of an- tisepsis, better hygiene, and antibiotics, there has been Received 29 November 2007; accepted 24 December 2007; electronically a sharp decrease in the incidence of puerperal infection published 4 April 2008. caused by GAS. There are, however, anecdotal reports Reprints or correspondence: Dr. Jane R. Schwebke, University of Alabama at of current cases of GAS puerperal sepsis and an increase Birmingham, 1530 3rd Ave. S ZRB 239, Birmingham, AL 35294-0007 (schwebke@uab.edu). in the rate of GAS isolated from high vaginal swab Clinical Infectious Diseases 2008; 46:e112–5 samples obtained from menarchal women with vaginal 2008 by the Infectious Diseases Society of America. All rights reserved. 1058-4838/2008/4610-00E3$15.00 discharge [2]. DOI: 10.1086/587748 In contrast, GAS vulvovaginitis is not uncommon ine112 • CID 2008:46 (15 May) • Meltzer and Schwebke
  • Downloaded from cid.oxfordjournals.org at GlaxoSmithKline on January 27, 2011Figure 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 pruritus, and dyspareunia. There is often no odor, but if therecomplaint among prepubescent girls. Its most frequent cause is, it is foul, not fishy like the odor associated with bacterialis idiopathic (in 64% of cases), but it is sometimes associated vaginosis. Wet mount preparations reveal abundant WBCs,with a specific bacterial pathogen [4]. GAS may be isolated in Gram staining often reveals gram-positive cocci in pairs andas many as 59% of these cases [4]. GAS is most often isolated chains and few or no Lactobacillus species, and the pH is usuallyfrom school-aged children with respiratory infections during quite elevated. Vaginal cultures often grow abundant GAS withthe fall and winter [3]. This seasonal preponderance is reflected few or no other organisms isolated [4, 8–13]. It should be notedin the rate of GAS isolation from patients with vulvovaginitis, that the rate of vaginal carriage of GAS in healthy women andas well [1]. Most cases of GAS vulvovaginitis in children have children ranges from 0% to slightly over 1% [8, 11]. Thus, ifhad either a household or personal history of dermal or re- a patient is symptomatic and has culture results that are positivespiratory infection due to GAS [4]. for GAS, this result should not be ignored, and the patient GAS genital infections are not only associated with household should be treated with agents active against Streptococcus spe-contact or autoinoculation with dermal and respiratory infec- cies. Typically, patients respond promptly to treatment. If im-tions; they are also transmitted sexually. Fisk and Riley [5] properly diagnosed and treated, the condition will persist andreport a case in which a husband and wife both had GAS genital can sometimes spread rectally or even systemically.infections after engaging in both oral and vaginal sex while the Anatomic, hygienic, and—perhaps most importantly—phys-wife had pharyngitis. Wakatsuki [6] reports 47 cases of GAS iologic factors predispose prepubescent girls to bacterial vul-balanoposthitis in which the route of infection was thought to vovaginitis. The anestrogenic vaginal epithelium in prepubes-be sexual contact, especially through fellatio with commercial cent girls is thin and lacks cornification, and it is thereforesex workers. Manalo et al. [7] describe a female patient with subject to irritation and infection. It also lacks glycogen de-GAS tuboovarian abscess and peritonitis thought to be caused position and, consequently, lacks colonization with Lactobacil-by engaging in receptive oral sex with a partner who had an lus species and vaginal acidification [4, 10, 12, 14]. It is knownupper respiratory tract GAS infection. Bray and Morgan [8] that healthy, Lactobacillus species–dominant, vaginal microflorareport 2 cases of GAS vulvovaginitis thought to be transmitted provide protection against the overgrowth of potentially path-after vaginal intercourse only (i.e., oral sex was not believed to ogenic bacteria [15].have occurred). Sobel et al. [9] report 2 cases of recurrent GAS Postmenopausal and postpartum women experience a sim-vulvovaginitis in which the gastrointestinal tracts of the pa- ilar regression to the immature, anestrogenic vaginal environ-tients’ husbands were colonized with GAS. ment found in prepubescent girls. The condition is called senile The signs and symptoms of GAS vulvovaginitis are acute and vaginal atrophy in postmenopausal women and postpartumtypically more severe than those caused by other types of vag- vaginal atrophy in postpartum women. Both conditions areinitis. The most common findings are copious, yellow, sero- characterized by dyspareunia, vaginal stinging and tightness,purulent vaginal discharge, edema, and marked vulvar and vag- dysuria, vaginal color change, an increase in parabasal cells, ainal erythema. The patient usually complains of vulvar pain, decrease in Lactobacillus species, and an increase in vaginal pH GAS Vaginitis • CID 2008:46 (15 May) • e113
  • [16–20]. The association of breast-feeding with vaginal atrophy Referencesand the resultant absence of Lactobacillus species, along with 1. Morris C. Seasonal variations in streptococcal vulvo-vaginitis in anits potential risks, may be underappreciated. Postpartum vag- urban community. J Clin Pathol 1971; 24:805–7.inal atrophy has a 17% prevalence rate, is strongly associated 2. Cartwright K. Group A streptococcal infections in humans. Soc Appl Bacteriol Symp Ser 1997; 26:52S–61S.with breast-feeding, and responds well to topical estrogen [20]. 3. Boycott J. Seasonal variations in streptococcal infections. Lancet 1966;1:Goetsch [21] described a similar condition but focused on the 706–7.dyspareunia experienced by 39% of postpartum patients and 4. Stricker T, Navratil F, Sennhauser F. Vulvovaginitis in prepubertal girls.also found a strong correlation with breast-feeding. Palmer and Arch Dis Child 2003; 88:324–6. 5. Fisk P, Riley V. Fellatio in the sexual transmission of lancefield groupLikis [22] report a case of lactational atrophic vaginitis attrib- A b-hemolytic streptococcus. Int J STD AIDS 1995; 6:458.utable to protracted breast-feeding. The clinical characteristics 6. Wakatsuki A. Clinical experience of streptococcal balanoposthitis in 47of this patient were nearly identical to those associated with health adult males [in Japanese]. Hinyokika Kiyo 2005; 51:737–40. 7. Manalo R, Mirza H, Opal S. Streptococcus pyogenes tuboovarian abscess:advanced senile vaginal atrophy, and she complained of severe a potential sexually transmitted disease? Sex Transm Dis 2002; 29:dyspareunia. Her symptoms were alleviated with topical 606–7.estrogen. 8. Bray S, Morgan J. Two cases of group A streptococcal vulvovaginitis in premenopausal adults in a sexual health setting. Sex Health 2006; The vaginal physiology of these women is analogous to that 3:187–8.of prepubescent girls, and they are, therefore, also at risk of Downloaded from cid.oxfordjournals.org at GlaxoSmithKline on January 27, 2011 9. Sobel J, Funaro D, Kaplan EL. Recurrent group A streptococcal vul-infectious vulvovaginitis. Paraskevaides and Wilson [23] report vovaginitis in adult women: family epidemiology. Clin Infect Disa case of fatal disseminated intravascular coagulation secondary 2007; 44:e43–5. 10. Figueroa-Colon R, Grunow JE, Torres-Pinedo R, Rettig PJ. Group Ato GAS cervicitis in a 57-year-old woman with no apparent streptococcal proctitis and vulvovaginitis in a prepubertal girl. Pediatrpredisposing factors other than the change in the vaginal en- Infect Dis 1984; 3:439–42.vironment found during menopause. Sobel [24] found that 6 11. Jaquiery A, Stylianopoulos A, Hogg G, Grover S. Vulvovaginitis: clinical features, aetiology, and microbiology of the genital tract. Arch Dis Childof 51 patients with desquamative inflammatory vaginitis, a se- 1999; 81:64–7.vere form of purulent vaginitis, were postpartum and lactating; 12. Straumanis JP, Bocchini JA Jr. Group A beta-hemolytic streptococcal31 of the 51 women were perimenopausal, menopausal, or had vulvovaginitis in prepubertal girls: a case report and review of the past twenty years. Pediatr Infect Dis J 1990; 9:845–8.received antiestrogen therapy. These women often had no Lac- 13. Tonkovic-Capin V, Fleming MG, Kleven-Kranz K, Lund MR. Vulvo-tobacillus species and an abundance of a Streptococcus species, vaginitis and perineal cellulitis due to group A streptococcus in anmost frequently Streptococcus agalactiae, b-hemolytic Strepto- adult woman. Arch Dermatol 2005; 141:790–2. 14. Boskey E, Telsch KM, Whaley KJ, Moench TR, Cone RA. Acid pro-coccus, Lancefield group B, but there was 1 case of GAS infec- duction by vaginal flora in vitro is consistent with the rate and extenttion. Permanent remission for some of the women who were of vaginal acidification. Infect Immun 1999; 67:5170–5.postmenopausal and not receiving hormone replacement ther- 15. Martin H, Richardson BA, Nyange PM, et al. Vaginal lactobacilli, mi-apy was not attained until antibiotic treatment was paired with crobial flora, and risk of human immunodeficiency virus type 1 and sexually transmitted disease acquisition. J Infect Dis 1999; 180:1863–8.estrogen therapy. 16. Molander U, Milsom I, Ekelund P, Mellstrom D, Eriksson O. Effect The American College of Obstetricians and Gynecologists, of oral oestriol on vaginal flora and cytology and urogenital symptomsthe American Academy of Pediatrics, the American Academy in the post-menopause. Maturitas 1990; 12:113–20. 17. Blum M, Elian I. The vaginal flora after natural or surgical menopause.of Family Physicians, and the Department of Health and Hu- J Am Geriatr Soc 1979; 27:395–7.man Services have all adopted policies that promote breast- 18. Caillouette J, Sharp CF, Zimmerman GJ, Roy S. Vaginal pH as a markerfeeding and advise extending its duration [25–28]. These pol- for bacterial pathogens and menopausal status. Am J Obstet Gynecol 1997; 176:1270–5.icies should consider and provide for the potential conse- 19. Hillier SL, Lau RJ. Vaginal microflora in postmenopausal women whoquences that breast-feeding may have on the mother’s sexual have not received estrogen replacement therapy. Clin Infect Dishealth and function, in addition to the numerous reported 1997; 25(Suppl 2):S123–6. 20. Wisniewski P, Wilkinson EJ. Postpartum vaginal atrophy. Am J Obstetbenefits of breast-feeding to mother and baby. Women who Gynecol 1991; 165:1249–54.choose to breast-feed should be counseled about protecting 21. Goetsch M. Postpartum dyspareunia: an unexplored problem. J Reprodthemselves from infection, and when lactating women present Med 1999; 44:963–8.with vaginal complaints, the differential diagnosis and treat- 22. Palmer A, Likis FE. Lactational atrophic vaginitis. J Midwifery Womens Health 2003; 48:282–4.ment algorithms should be broadened to encompass infections 23. Paraskevaides E, Wilson MC. Fatal disseminated intravascular coag-and conditions that are normally associated with the hypoes- ulation secondary to streptococcal cervicitis. Eur J Obstet Gynecoltrogenic states found in prepubescent girls and postmenopausal Reprod Biol 1988; 29:39–40. 24. Sobel J. Desquamative inflammatory vaginitis: a new subgroup of pu-women. rulent vaginitis responsive to topical 2% clindamycin therapy. Am J Obstet Gynecol 1994; 171:1215–20.Acknowledgments 25. Gartner L, Eidelman AI. Breastfeeding and the use of human milk. Pediatrics 2005; 115:496–506. Potential conflicts of interest. M.C.M. and J.R.S.: no conflicts. 26. US Department of Health and Human Services. Healthy people 2010:e114 • CID 2008:46 (15 May) • Meltzer and Schwebke
  • understanding and improving health and objectives for improving 28 American Academy of Family Physicians Web page. Available at: health, 2nd ed. Washington, DC: US Government Printing Office, 2000. http://www.aafp.org/online/en/home/policy/policies/b/breastfeeding27. American College of Obstetricians and Gynecologists Web page. Avail- positionpaper.html. Accessed 27 March 2008. able at: http://www.acog.org/from_home/publications/press_releases/ nr01-25-06.cfm. Accessed 27 March 2008. Downloaded from cid.oxfordjournals.org at GlaxoSmithKline on January 27, 2011 GAS Vaginitis • CID 2008:46 (15 May) • e115