For 3 patients, household member investigations were performed. One husband demonstrated negative anal and throat swabs. One patient had 2 children who underwent antibiotic treatment for pharyngitis before the patient's first symptoms; her asymptomatic husband demonstrated GAS-positive penile specimens. The third patient's asymptomatic husband had a GAS-positive throat swab.
Patients were treated with β-lactam antibiotics (16), pristinamycin (2), or quinolone (1) for 7 to 15 days (see Table 1). Fourteen patients had a complete regression of symptoms (pain, pruritus) and coexisting signs (erythema, fissures, edema, oozing, discharge). Five patients had a recurrence within 1 to 2 weeks after completion of the treatment. No recurrence was reported after a second line of antibiotics (see Table 1).
In this study, the main symptoms of vulvar GAS infections were pain and pruritus, consistent with the published literature,5–7 and the main signs were bilateral erythema, oozing, edema, and fissures. In all but 2 cases, GAS were also found in the vagina, regardless of whether they caused symptoms. The perianal area was infected in almost half of the patients, and an association with psoriasis was found in almost one third of the patients.
Eleven of our 19 patients were postmenopausal. Previous studies have indicated that postmenopausal estrogen deficiency is frequently associated with the absence of protective lactobacilli4,5 and may, thus, be a risk factor for GAS vulvovaginitis.
In all but one case, GAS vulvitis was associated with another infected site, typically the vagina (17/19 cases). However, vaginal discharge, the most common vaginal symptom1,2,6 in girls and adult women, was reported by only 10 of our 17 patients with GAS-positive vaginal specimens. The relatively low rate of reported vaginal discharge may be explained by asymptomatic GAS carriage or by underreporting due to the absence of systematic questions about vaginal discharge.
The main physical sign of GAS vulvitis was bilateral erythema of the labia minora and inner labia majora. Edema (see Figures 1, 2) was present in 6 patients, also reported by Verkaeren et al.7 Erythema, fissures, and edema have also been described in childhood perianal GAS infections.1,2,8 In adults, these signs may initially be interpreted as candidiasis, psoriasis, or contact dermatitis. Oozing has not been previously reported as a sign of GAS vulvitis or anitis and might be a more specific sign of GAS vulvitis.
Almost half of our 19 patients with GAS vulvitis had an associated dermatological condition, most commonly psoriasis (6 cases). In 5 of those cases, the psoriasis was only recognized at the time of the GAS vulvitis diagnoses. The association of guttate psoriasis with GAS pharyngitis, vulvovaginitis, or perineal infections is well documented9,10; the association of perianal or vulvar GAS infections, with psoriasis at the infection sites, has not been previously reported. We hypothesize that this association is not just a coincidence. Group A streptococci might have triggered infection site psoriatic lesions via immune reactions leading to T-cell stimulation and cytokine activation.10 Alternatively, GAS infections may have induced isomorphic responses, similar to those after trauma (Koebner phenomenon). Preexistent vulvar psoriasis might have also facilitated concurrent GAS infections.
The epidemiology of vulvovaginal GAS infections is poorly understood. In this study, GAS were found in the throats of two of the patients' husbands (and on the penis of one), suggesting the possibility of sexual transmission. Verkaeren et al7 suggested oral sex as a mode of transmission. Two cases of asymptomatic rectal carriage have been reported in the husbands of patients and interpreted to be the source of recurrent GAS vulvovaginitis.11 Group A streptococcal vulvovaginitis in adult women may also result from transmission from a patient's child, if the child has pharyngeal, perineal, or cutaneous infection or colonization.6,12 Thus, systematic investigations (pharynx and anus in both children and adults; penis, anus, vulva, vagina in adults) for sexual or nonsexual sources of transmission seem worthwhile, particularly in cases of recurrent vaginitis.11
This study describes the clinical features of an uncommon, underrecognized, vulvar infection. In this study, clinical signs were precisely analyzed from photographs available for 15 patients. The results suggest a relationship between GAS infections and psoriasis and emphasize the need for bacterial investigations of the patient's household members and sexual partners.
However, this study does not provide enough accurate information regarding the vaginal and anal clinical features coexisting with GAS vulvitis. The association with psoriasis also needs to be more fully investigated using systematic family histories; examinations of the whole skin, scalp, and nails; and vulvar re-examination of the patient after the cure of the GAS infection.
Group A streptococcal vulvitis should be suspected in patients with painful, itchy, vulvar, or anovulvar bilateral erythema, particularly when associated with fissures, edema, or oozing. In most cases, a coexisting vaginal infection or colonization is identified. An association with dermatological conditions, such as psoriasis, does not seem coincidental; it may result from the GAS infection or from a superinfection from a vaginal GAS source. Bacteriological investigations of household members and sexual partners are worthwhile as antibiotic treatment of these GAS carriers might prevent recurrence of the infection.
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Keywords:Copyright © 2019 by the American Society for Colposcopy and Cervical Pathology
vulvovaginitis; vulvitis; Group A streptococcus; vulva; vagina; psoriasis