From the *Department of Internal Medicine and †Division of Infectious Disease, Brown University Medical School, Memorial Hospital of Rhode Island, Pawtucket, Rhode Island
Reprint requests: Rosario Manalo, Department of Internal Medicine, Brown University Medical School, Memorial Hospital of Rhode Island, 111 Brewster Street, Pawtucket, RI 02860. E-mail: Rosario_Manalo@Brown.edu
Received for publication September 25, 2001,
revised December 18, 2001, and accepted December 26, 2001.
WE REPORT A CASE of Streptococcus pyogenes tuboovarian abscess and peritonitis in a previously healthy young woman. Tuboovarian abscesses occur as sequelae in 3% to 16% of women with acute salpingitis. 1 This condition predominantly involves a mixed flora of anaerobes and aerobic organisms that colonize the genitourinary tract. 1,2 The case described herein appears to be unusual in that it was caused solely by S pyogenes.
The patient, a 26-year-old Hispanic woman, gravida 2 para 2, presented to the emergency department with severe abdominal pain. The onset was approximately 3 weeks earlier, when intermittent low-grade fever, diaphoresis, and hypogastric pain developed. Physical examination in the emergency department showed that the patient was tachypneic and febrile; the white blood cell count was 21,000/mm3. Signs of peritonitis were prominent. The patient immediately underwent exploratory laparotomy, which revealed tuboovarian abscess on the right fallopian tube and left fallopian tube perforation. Bilateral salpingo-oophorectomy was performed.
The patient was admitted to the intensive care unit during the postoperative period and was treated with ciprofloxacin and piperacillin/tazobactam. However, signs of hemodynamic instability continued, and recurrent fever, arthralgias, and an intermittent lace-like rash on both thighs developed. Gram staining of the abscess and peritoneal fluid revealed gram-positive cocci only. Subsequent aerobic and anaerobic cultures yielded S pyogenes. No other organisms were isolated. Intravenous administration of penicillin and clindamycin was started, and the patient's condition improved clinically.
The patient's medical history included an episode of Chlamydia trachomatis cervicitis 8 years previously, which was treated with doxycycline. A cervical smear specimen was obtained after admission and proved positive in enzyme-linked immunosorbent assay for C trachomatis. Doxycycline was added to the antibiotic regimen during the patient's treatment in the intensive care unit.
The patient denied having any recent pharyngitis or skin infections. Her sex partner, however, had a mild upper respiratory tract infection approximately 1 month earlier. The couple reported engaging in oral sex shortly before the onset of the patient's symptoms. Culture of a throat specimen from the partner revealed S pyogenes. The patient's throat specimen culture was negative. Genomic DNA analysis was performed by a modification of the method of Anderson and McKay with use of a genomic DNA purification column (Nucleobond; Clontech, Palo Alto, CA). 3 Genomic analysis with restriction enzymes Sal I, Xba I, and Hind III showed that organisms isolated from the patient's peritoneal swab specimen and her partner's throat culture specimen had identical electrophoretic patterns. The patient's partner was treated with oral penicillin, and close follow-up was advised for both patient and partner.
Acute pelvic inflammatory disease is usually caused by organisms ascending from the vagina and cervix along the mucosa of the endometrium to the oviduct. They can produce one or more of the following inflammatory conditions: endometritis, salpingitis, tuboovarian abscess, and pelvic peritonitis. Approximately 85% of cases are spontaneous infections in sexually active females of the reproductive age group. 1 The other 15% occur after procedures that break the cervical mucus barrier, allowing the vaginal flora to colonize the upper genital tract. As noted above, acute pelvic inflammatory disease is usually polymicrobial, involving a mixture of aerobic and anaerobic bacteria and clinically apparent as single complex infection. 1
The occurrence of S pyogenes as the sole causative organism of tuboovarian abscess is distinctly unusual. The organism is not usually considered part of normal vaginal flora. In the literature there are scarce reports of recovery of S pyogenes from cervical and fallopian tubes, and each case was associated with instrumentation. 4S pyogenes is of epidemiologic significance in postpartum endometritis. Barham et al 5 reported a rare case of acute salpingitis caused by S pyogenes after endometrial biopsy. Although the organism has been known to cause vulvovaginitis in children, there are few reports on invasive pelvic inflammation in nonpregnant women. 4 Goepl et al 6 described a case of fatal sepsis in an elderly woman, in which S pyogenes was recovered from cultures of blood, peritoneal fluid, and cervical specimens. We found no reports of S pyogenes being transmitted through sexual activity.
The ability of S pyogenes to cause such a severe infection in a previously healthy young person is hardly surprising. Its capacity to cause explosive and life-threatening disease has been well documented in the past; the last major episode occurred in the early 20th century, just before the antibiotic era. Within the past 20 years, this “killer bug” or “flesh-eating bacterium” appears to have reacquired an enhanced virulence. 7 This is likely due to many factors, including the development of antibiotic resistance and, perhaps more important, its antigenic characteristics. S pyogenes has an array of defense mechanisms that allow invasion of host tissues and evasion of the neutrophil-mediated phagocytosis. 8 The bacterial cell wall structure components peptidoglycan and lipoteichoic acid are proinflammatory agents and play a major role in host activation. The capsule, composed of hyaluronic acid, is essential to the organism's invasiveness.
S pyogenes is also known to produce a family of superantigenic exotoxins capable of activating a large quantity of CD4+ lymphocytes. This mechanism results in massive cytokine release, leading to the induction of septic shock. 9 It is important to note that the organism's new-found virulence has been linked to these superantigens as well as the appearance of a new dominant streptococcal serotype. The M protein on the bacterial cell wall is responsible for the antiphagocytic activity and indirectly for the invasive capacity of the strain. 10–12 Antigenic differences on the M protein molecule determine streptococcal serotype. It has been postulated that the virulence of the organism is related to the total lack of antibodies to the new M protein molecule, in addition to the low capacity of the serum to neutralize the activity of superantigenic exotoxins. 11,12
At a time when S pyogenes has a newly reestablished virulence, it is reasonable to assume that the organism will not only cause an explosive presentation of invasive disease but also increasingly be transmitted through different portals of entry. On the basis of the culture results and genomic DNA analysis, we hypothesize that in the current case transmission of S pyogenes occurred between sex partners. There are several scenarios to consider. The occurrence of female-to-male contamination is possible yet not probable. Although we cannot confirm that the organism originated in either patient or partner, S pyogenes is a known colonizer of the oropharynx and a common agent of upper respiratory infections. It is highly likely that transfer of the organism occurred from the male to female. Transmission from mouth to hand to genitalia is a possibility. However, such ease of transmission does not correlate with the rare occurrence of group A tuboovarian abscesses in clinical medicine. Hence, on the basis of history, it is likely that the organism was transmitted by direct oral-genital contact. This then raises the question: Is S pyogenes tuboovarian abscess a potentially sexually transmitted disease?
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