General Medical Information

Bacterial Vulvitis

Wilberto Nieves-Neira
Bhagirath Majmudar
Ira R. Horowitz

Bacterial vulvitis (and vulvovaginitis) is caused most commonly by group A b-hemolytic streptococcus. Vulvar infection can result from autoinoculation from pharyngitis, cutaneous infections, or the gastrointestinal tract, although no recent association with upper respiratory tract infections, tonsillitis, or nasopharyngitis is common. Presentation is acute in most cases, with an evolution of several days only. The most common symptoms are dysuria, vaginal discharge, and vulvar pain. On examination, erythema of the vulva or a fiery-red rash resembling cellulitis and vaginal discharge are the most frequent findings. The vaginal discharge is serosanguinous in about half the patients presenting with this finding. Other findings include edema, local excoriation, and tenderness. Final diagnosis is made by cultures, which should include proper medium to support the growth of hemolytic streptococcus (5% sheep blood agar with a bacitracin disk). Treatment with penicillin, a cephalosporin, or erythromycin is effective and a response usually is obtained within 24 hours.

Group A b-hemolytic streptococcal vulvovaginitis is a well-recognized complication of scarlet fever. Nowadays scarlet fever is sporadic in nature. A case of coexisting group A streptococcal proctitis and vulvovaginitis, which required 21 days of erythromycin for treatment, was reported. Other streptococcal infections may result in significant vulvar disease. Streptococcus pneumoniae has been associated with vulvar and intragluteal abscesses. Pneumococcus may be isolated from the pharynx and the vagina simultaneously in symptomatic as well as asymptomatic girls. Impetigo is a common childhood skin condition caused by staphylococcal or streptococcal organisms. Sources include the mother, other children, or a nosocomial infection. Lesions develop as 1- to 2-mm vesicles that, after eroding, develop a crust and then form vesicles and bullae on the face, extremities, and “diaper area.” Treatment includes systemic antibiotics to cover streptococcal and staphylococcal organisms.

Other bacterial pathogens have manifested symptoms of vulvovaginitis. Shigella vaginitis may occur alone or may be associated with shigella gastroenteritis. The most common presentation is a bloody vaginal discharge and vulvar irritation with inflammation and/or erosion. Chronic vulvovaginitis has been associated with Shigella flexneri. In areas where shigellosis is endemic, 6% of girls presenting with vulvovaginitis have positive cultures for S. flexneri. Interestingly, a low prevalence of shigella in the rectum of patients with shigella vulvovaginitis was found. Ampicillin and trimethoprim-sulfamethoxazole are effective antibiotics. Patients with resistant isolates to these antibiotics respond well to nalidixic acid 50 mg/kg/day for 7 days. A case of Yersinia enterocolitica vulvovaginitis that responded well to trimethoprim-sulfamethoxazole was reported. A labial abscess associated with Yersinia infection in household dogs also was reported . Escherichia coli may be a frequent isolate in girls with vulvovaginitis, suggesting that hygiene and contamination with bowel flora are important factors in the development of the condition. It usually presents with a purulent vaginal discharge.

Haemophilus influenzae type B has been associated with purulent vulvovaginitis. In some populations, H. influenzae is the second most common organism identified in girls with vulvovaginitis. Autoinoculation is probably an important mode of transmission. Amoxicillin is adequate treatment, with few recurrences. Mycoplasma sp have been found to be a cause of vulvovaginitis in children. In 1897, Williams reported a case of diphtheria of the vulva, although in his own discussion he acknowledged that the “diphtheritic membrane” was not a justifiable reason to believe that the infection was true diphtheria. In the last 30 years, two cases of vulvar diphtheria have been reported.