Infectious Diseases in Obstetrics and Gynecology 7:206-209 (1999) (C) 1999 Wiley-Liss, Inc.

Can Group B Streptococci Cause Symptomatic ?

E. Honig, 1. J.W. Mouton,2 and W.I. van der Meijden 1 1Department of Dermatology and Venereo/ogy, Erasmus Medical Centre, Rotterdam, Netherlands eDepartment of Clinical Microbiology, Erasmus Medical Centre, Rotterdam, Netaerlands

ABSTRACT

Background: Maternal cervicovaginal colonization with Lancefield group B streptococci (GBS) is an important risk factor for neonatal morbidity and mortality. About 15% of women are carriers of GBS. Usually, they are asymptomatic. Cases: We describe two patients with symptomatic vaginitis for which no apparent cause was found. Both patients were heavily colonizedwith GBS. After antibiotic treatment, both became asymptomatic and culture negative, but after recolonization with GBS, symptoms resumed. This phenomenon was repeatedly observed. After emergence of resistance to antibiotics, local applica- tion of chlorhexidine appeared to be the only useful treatment. Conclusion: We hypothesize that GBS-vaginitis may be a possible disease entity. Although at present it is not clear why some patients become symptomatic, we speculate that the immunologic response is somehow selectively hampered in such patients. Infect. Dis. Obstet. Gynecol. 7:206-209, 1999. (C) 1999 Wiley-Liss, Inc.

KEY WORDS ; vulvar maceration; chlorhexidine

ancefield group B beta-hemolytic streptococci vaginitis presumably caused by GBS, a condition (group B streptococci [GBS] or Streptococcus aga- that, to our knowledge, has not been reported be- lactiae) play an important role in the development fore. of neonatal morbidity and mortality. that occur before the seventh day of lifemsocalled CASE REPORTS early onset infectionsmare usually caused by ver- Case tical transmission. Between five percent and 40% A 39-year-old woman, mother of five children, re- of women carry GBS. Carriers of cervicovaginal ported , , and excessive GBS are usually asymptomatic. However, one vaginal discharge. She was first examined by a gy- study showed that in patients with purulent vaginal necologist, who diagnosed and treated discharge the prevalence of GBS was increased. her with cefuroxime, , and erythro- Colonization with GBS seems to be more prevalent mycin. Although her symptoms disappeared ini- in patients with excessive vaginal discharge, z A cor- tially, the vaginal discharge reappeared after a few relation has also been demonstrated between the days. She was then referred to our clinic. Excessive diagnosis of vaginitis and colonization with GBS. 3 vaginal discharge and dyspareunia had been pre- However, in the papers noted, there was no state- sent for several months. Her medical history had ment about GBS being the cause of the vaginitis or been uneventful apart from , for just a cofactor. We here describe two patients with which she was treated with , causing

*Correspondence to: E. Honig, MD, Department of Dermatology and Venereology, Erasmus Medical Centre, Dr. Mole- waterplein 40, 3015 GD Rotterdam, Netherlands. Received 19 October 1998 Gynecological Case Report Accepted II February 1999 GROUP B STREPTOCOCCUS AND VAGINITIS HONIG ET AL.

Fig. I. Clinical picture of patient I: abundant white/yellow discharge and erythema of vaginal walls. . Childbirth had been uncomplicated Laboratory examination included direct smears each time, and she had had no cesarean deliveries. and cultures for , Trichomonas She had been married for a long time and .had no vaginalis, and Candida species, all of which were other sexual contacts. In the preceding year, her negative. A culture for trachomatis was husband had been hospitalized three times with also negative. All of these tests were performed periods of for which no explanation could be more than once, at different times. The Gram stain found. A culture from his was positive for GBS. of vaginal discharge showed many gram-positive Gynecological examination showed redness and cocci and leukocytes (4+) (Fig. 2). Neither lactoba- maceration of vaginal introitus and perianal area cilli, clue cells, nor basal or parabasal cells were (probably because of excessive vaginal discharge). seen. An aerobic culture of vaginal discharge There was abundant, watery, white/yellow, odor- showed abundant growth of GBS. An anaerobic less vaginal discharge and erythema of vaginal walls culture showed no growth of bacteria. Urinanalysis, (Fig. 1). hematology, biochemistry, and serologic tests for

Fig. 2. Gram stain of vaginal fluid: streptococci and leukocytes.

INFECTIOUS DISEASES IN OBSTETRICS AND GYNECOLOGY 207 GROUP B STREPTOCOCCUS AND VAGINITIS HONIG ET AL. syphilis and hepatitis B showed no abnormalities. A eases was not done. A presumed diagnosis of GBS- presumed diagnosis of GBS-vaginitis was made. vaginitis was made. The patient together with her partner received Local and oral antibiotic treatment (i.e., clinda- several courses of antibiotic treatment (for ex- mycin cream and oral co-trimoxazole) resulted, as ample, clindamycin and co-trimoxazole). These in Case 1, only in a temporary absence of symp- treatments only provided temporary relief from toms. During the symptom-free period, cultures symptoms. During symptom-free periods, cultures from the did not show GBS. When symp- were negative for GBS. When symptoms resumed, toms resumed, cultures were again GBS-positive. cultures were again GBS-positive. Antibiotic susceptibility tests showed that the After several antibiotic treatments, antibiotic patient's GBS had become resistant to clindamy- susceptibility tests showed that the patient's GBS cin. Treatment with chlorhexidine gel was then had become resistant to clindamycin. It was then started. As in Case 1, this caused considerable re- decided to start treatment with chlorhexidine, 0.5% duction of symptoms. However, symptoms quickly gel. This antiseptic caused considerable symptom- reappeared after discontinuation of treatment. atic relief but did not offer a permanent solution. DISCUSSION Case 2 A 19-year-old woman was referred to our clinic by In contrast with group A streptococcus, it is gener- a gynecologist because of persistent vaginal dis- ally thought that GBS is not capable of causing charge, from which GBS was cultured at several vaginitis.4 Our findings seem to suggest otherwise. occasions. Discharge had been present for about Both patients described showed excessive white/ one year and was accompanied by vulvar and peri- yellow, odorless vaginal discharge, as well as vulvar anal . She had already been treated with and perianal maceration. This clinical picture, in several antibiotics (e.g., penicillin) and antimy- combination with abundant presence of gram- cotics. All antibiotic treatments only caused tem- positive cocci in the Gram stain and abundant porary symptomatic relief. growth of GBS in cultures, led to the hypothesis of A few weeks before she first visited our clinic, GBS-vaginitis. This hypothesis is supported by the she had been hospitalized because of an episode of exclusion of other usual causes of vaginitis. erythema nodosum for which no explanation was It is also supported by the occurrence of symp- found. Otherwise, her medical history had been tom-free and culture-negative periods after antibi- uneventful. The patient had never had sexual in- otic treatment and the fact that reappearance of tercourse. symptoms was associated with vaginal recoloniza- Gynecological examination showed maceration tion with GBS. Although the source of recoloniza- and linear erosions on the and majora tion is not clear, it could be explained by the gas- and the perianal region. There was white/yellow, trointestinal tract functioning as a reservoir of GBS. odorless discharge in the introitus. Examination by In the first case, reinfection from the partner is also speculum was not performed. a possibility, since he also was a carrier of GBS. For the laboratory examination, material was In the second case, it could be speculated that collected from the vagina with a cotton swab for the patient had become colonized at birth, since direct smears and cultures. Direct smears did not her mother is also a carrier of GBS. At any rate, show clue cells, pseudohyphae, or trichomonads. A since GBS colonization occurs in about 15-25% of Gram stain of vaginal discharge showed gram- the Dutch female population,6 the most interesting positive cocci and leukocytes (2+); neither lactoba- question is not how our patients acquired GBS, but cilli nor basal or parabasal cells were seen. A vaginal why they had symptoms, while most women do not. culture for Candida species was negative. An aero- One of the reasons might be that the immunologic bic culture showed abundant growth of GBS. Rec- response is somehow selectively hampered in these tal culture also showed GBS. An anaerobic culture patients. This phenomenon has been described in of vaginal fluid showed no growth. relation to nonresponders in vaccination programs. The patient's mother was also colonized with It is also frequently observed in patients with a GBS. Routine testing for sexually transmitted dis- selective deficiency of immunoglobulin G2 who

208 INFECTIOUS DISEASES IN OBSTETRICS AND GYNECOLOGY GROUP B STREPTOCOCCUS AND VAGINITIS HONIG ET AL. have recurrent infections with capsulated bacteria, REFERENCES 7 such as meningococci. It would be interesting to 1. Regan JA, Klebanoff MA, Nugent RP. The epidemiol- determine whether patients with symptoms of ogy of group B streptococcal colonization in . GBS-vaginitis have such deficiencies. Obstet Gynecol 1991;77:604-610. Treatment of GBS vaginitis appears to be a 2. Farrag OA, Gawad AA, Antar S. Group B-beta haemo- lytic streptococcal colonization in women using intra- problem. Current literature only addresses at- uterine contraceptive devices. Contraception 1985;31: tempts to decrease the rate of vaginal colonization 595-602. 8 in order to reduce vertical transmission. Complete 3. Jensen NE, Andersen BL. The prevalence of group B eradication of GBS-carriership is usually not a goal. streptococci in human urogenital secretions. $cand J In- Antibiotic treatment of GBS-vaginitis is probably fect Dis 1979; 11:199-202. hampered by the fact that recolonization is so easily 4. Ginsburg CM. Group A streptococcal vaginitis in chil- dren. Pediatr Infect Dis 1982;1:36-37. established. The with our two patients experience 5. Dillon HC, Gray E, Pass MA, Gray BM. Anorectal and seems to suggest that oral as well as local antibiotic vaginal carriage of group B streptococci during preg- treatment only has a temporary effect and might nancy. J Infect Dis 1982;145:794-799. possibly lead to resistance against certain antibiot- 6. van Oppen AC, Gerards LJ, Fleer A, Feldman RG, Bru- ics. Local chlorhexidine application a treatment inse HW. Diagnosis and chemoprophylaxis of perinatal infections caused by beta-hemolytic streptococci from that is also used to prevent neonatal transmission of Group B. Ned Tijdschr Geneeskd 1993;137:583-587. to so GBS- seems be the only useful alternative 7. Umetsu DT, Ambrosino DM, Quinti I, Siber GR, Geha far. RS. Recurrent sinopulmonary and impaired In conclusion, our report seems to provide cir- antibody response to bacterial capsular polysaccharide cumstantial evidence that GBS can cause symp- antigen in children with selective IgG-subclass defi- tomatic vaginitis in some women, although causa- ciency. N Engl J Med 1985;313:1247-1251. 8. Adriaanse AH, Koll6e LAA, Muytjens HL, Nijhuis JG, tion can not be definitively ascribed. Given the de Haan AFJ, Eskes TKAB. Randomized study of vagi- chronicity of the condition and the absence of ef- nal chlorhexidine disinfection during labor to prevent fective treatment (at least so far), further study of vertical transmission of group B streptococci. Eur J Ob- the subject seems appropriate. stet Gynaecol Reprod Biol 1995;61:135-141.

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