GISSER, JONATHAN M. MD*; FIELDS, MADELINE C. MD*; PICK, NEORAH MD†; MOSES, ALLON E. MD‡; SRUGO, ISAAC MD†
From the *Technion Israel Institute of Technology Faculty of Medicine and
†Bnai Zion Medical Center, Haifa; and
‡Department of Clinical Microbiology and Infectious Diseases, Hebrew University–Hadassah Medical School, Jerusalem, Israel
Reprint requests: Isaac Srugo, MD, Director of clinical Microbiology, Bnai Zion Medical Center, P.O. Box 4940, Haifa, Israel 31048. E-mail: firstname.lastname@example.org
Received for publication August 16, 2001,
revised November 28, 2001, and accepted December 7, 2001.
Background: Peritonitis due to group A Streptococcus (GAS) and toxic shock syndrome occurred in a previously healthy 45-year-old woman with an intrauterine device. The intrauterine device was believed to be the portal of entry. In addition, her husband was found to be an asymptomatic carrier of GAS in his oropharynx.
Goal: The goal was to increase physicians’ awareness of oral sex as a risk factor for transmission of invasive GAS disease.
Study Design: This is a case report of the development of GAS peritonitis and toxic shock syndrome in a woman after acquisition of the organism through oral sex.
Results: The GAS strains isolated from the patient and her husband were identical in their M-type, T-type, and exotoxin gene pattern.
Conclusion: Because the couple practices oral sex, it was postulated that this was the mode of transmission of the GAS.
GROUP A STREPTOCOCCUS (GAS) is the cause of a variety of human illnesses, including severe invasive disease, which is associated with high morbidity and mortality rates. For many centuries it has been known to cause severe infection of the female genital tract, but it is associated mostly with puerperal infection. 1 In the past, the use of intrauterine devices (IUDs) has been associated with fatal invasive GAS disease. 2 Nevertheless, a search of the English-language literature revealed only two other cases of IUD-associated peritonitis in immunocompetent individuals. 2,3 In these articles, the source of infection is merely suggested.
Oral sex is a well-known means of transmission of various pathogenic organisms. 4 However, the transmission of GAS peritonitis via oral sex has never been described. We therefore report the following case of GAS peritonitis and toxic shock syndrome, which occurred in a previously healthy woman. The GAS was transmitted presumably by her husband, who was found to be an asymptomatic carrier of GAS in his pharynx.
A 45-year-old woman, gravida 3, para 3, was admitted to Bnai Zion Medical Center on March 21, 2000, because of nausea, vomiting, and diarrhea that had begun the night before. Her temperature was 37.8 °C; respiratory rate, 40 breaths/min; pulse, 140 beats/min; and blood pressure, 158/76 mm Hg. Physical examination in the emergency department revealed a fully conscious, toxic-appearing patient in respiratory distress. She was promptly transferred to the intensive care unit. There an abdominal examination revealed a macular–papular rash that gradually spread over her trunk and extremities (which subsequently desquamated after 7 days). Her abdomen was soft, with mild tenderness in both lower quadrants and no peritoneal signs.
Abdominal ultrasonography suggested peritonitis, and diagnostic paracentesis revealed purulent material. A Gram stain demonstrated chains of gram-positive cocci, which were later confirmed to be Streptococcus pyogenes by isolation on sheep blood agar and identification by a commercial latex agglutination immunoassay. GAS was also isolated in blood cultures. Because it was suspected that an IUD that had been inserted 1 year earlier was the source of infection, it was removed and sent for culture. Again, GAS was isolated. The patient was treated with clindamycin (600 mg three times per day), ceftriaxone (2 g four times per day), and intravenous immunoglobulin (150 mg/kg once per day for 5 days) for suspected GAS toxic shock syndrome.
GAS was subsequently isolated in a culture of a throat specimen from the patient's husband. Both of her daughters’ throat specimen cultures were negative. Serological M and T typing performed by the Israel Streptococcal Reference Laboratory revealed that the strains in the patient and her husband were identical (M type 2379 and T type 5/27/44). Polymerase chain reaction performed on DNA of the GSA strains showed that both were positive for SpeC (exotoxin C) and negative for SpeA (exotoxin A). 5
One day after admission the patient remained hemodynamically unstable and still had abdominal pain. She therefore underwent an exploratory laparotomy, which revealed fulminant necrotizing peritonitis and inflammation of the ovaries. A bilateral salpingectomy was performed. Despite surgery, the patient remained tachycardic and febrile. Her condition continued to deteriorate, and adult respiratory distress syndrome developed. Mechanical ventilation was started. Because she continued to have signs of uncontrolled infection, a relaparotomy was performed and exposed areas of uterine necrosis, necessitating a total abdominal hysterectomy. After the second operation the patient's condition stabilized, and in the following days she was weaned off the ventilator.
The pathology findings were histologically consistent with purulent salpingitis, endometritis, and peritonitis. Hemorrhagic necrosis of the ovarian cortices and microthrombi in the ovarian vasculature were noted.
One month later, the patient was transferred to the obstetrics and gynecology unit. Her condition was stable, but she had a low-grade fever. She began reporting pain in her right elbow, with limitation of motion. Findings from physical examination, technetium scanning, laboratory testing, and radiology supported a diagnosis of poststreptococcal reactive arthritis. Diagnostic arthrocentesis was not performed because of an insufficient amount of fluid. She began receiving treatment with steroids and nonsteroidal antiinflammatory drugs, as well as physical and occupational therapy. Her fever and elbow pain gradually decreased, and mobility of her elbow was restored.
Two months after admission the patient was discharged. Steroid therapy was discontinued at that time.
This is the third case of IUD-related invasive GAS described in the English-language literature. When the previous reports were published in 1973 and 1977, 2,3 GAS serotyping was not performed. Brosseau and Mazza 3 suggested sexual foreplay as a means of GAS transmission because the patient's spouse had been ill with GAS pharyngitis and cellulitis of the fingers; however, without the availability of serotyping, their hypothesis could not be confirmed. In the current case, identical GAS strains were isolated in the culture of a throat specimen from the patient's husband and of the patient's IUD.
Similarity between serotypes of the strain involved in index cases of invasive GAS infection and recovered from their family contacts ranges from 27%6 to 87%. 7 Because asymptomatic genital carriage of GAS is extremely rare and GAS is a rare cause of genital infection in nonpregnant women, in our case the association between the husband's asymptomatic colonization and the patient's infection is likely. Thus, we postulate that orogenital transmission of GAS occurred in association with minor endometrial trauma due to an IUD. Further inquiry revealed that the patient did indeed engage in cunnilingus with her husband.
Regardless of the source and route of infection, minor trauma to the skin or mucous membranes is probably necessary for dissemination of GAS. Various ports of entry have been implicated in invasive GAS disease and peritonitis. Direct intraperitoneal seeding during surgery, 8 seeding from transient bacteremia during dialysis, 9 and umbilical stump contamination in nurseries, 10 to name a few, have all been reported in the literature. In primary GAS peritonitis no route of entry or predisposing factors are found. 11 Invasive GAS is most commonly associated with infection by GAS strains that have M1 or M3 surface proteins as virulence factors. However, the host immunity factors involved in susceptibility to invasive GAS disease are not well understood. 12 Simply put, it is unknown why most GAS carriers do not develop invasive disease, whereas others may develop severe, sometimes fatal illness.
Placement of an IUD may be associated with a mild local transient bacterial infection at the time of insertion. 13 However, invasive infection at this time is rare. In contrast, if septic complications of IUD placement occur, it is usually later, after the endometrium has once again become sterile. 2 The current case illustrates this phenomenon. However, because GAS does not belong to the normal vaginal flora, it excludes the IUD as a primary source of the infection. Therefore, we postulate the minor trauma caused by the IUD facilitated passage of the bacteria across the endometrium. These bacteria must come from the vagina or uteral cervix. In our patient, oral sexual intercourse was the likely transport route for GAS.
Orogenital contact has been implicated as a route of transmission for a number of different organisms: viruses, bacteria, yeasts, and protozoa. 4 Organisms may be transmitted from the oropharynx to the genitals and vice versa. Depending on the organism, males may also acquire genital infection by fellatio. 4
Patients are generally not forthcoming about their sexual practices. 14 Moreover, physicians may not consider oral sex as a risk factor for an invasive disease that is typically not associated with sexual transmission. We therefore postulate that the incidence of orogenital transmission of invasive GAS is greater than presently estimated. Hence, primary invasive GAS may be transmitted orogenitally.
Currently, there are no specific recommendations for prophylactic measures for close contacts of patients. However, there does seem to be an increased risk of GAS carriage in the contacts of those with invasive disease, and because their risk of invasive disease is suspected to be increased up to 200-fold, some investigators have recommended the administration of prophylaxis to these contacts. 6,15
In summary, we have described a case of GAS peritonitis that developed in a nonpregnant woman with an IUD. We assume that her husband, who asymptomatically harbored GAS in his pharynx, transmitted the infection through oral sexual intercourse.
1. Anteby EY, Yagel S, Hanoch J, Shapiro M, Moses AE. Puerperal and intrapartum group A streptococcal infection. Infect Dis Obstet Gynecol 1999; 7: 276–282.
2. Marshall BR, Hepler JK, Jinguji MS. Fatal Streptococcus pyogenes
septicemia associated with an intrauterine device. Obstet Gynecol 1973; 41: 83–87.
3. Brosseau JD, Mazza JJ. Group A streptococcal sepsis and arthritis: origin from an intrauterine device. JAMA 1977; 238: 2178.
4. Edwards S, Carne C. Oral sex and the transmission of non-viral STI's. Sex Transm Infect 1998; 74: 95–100.
5. Tyler SD, Johnson WM, Huang JC, et al. Streptococcal erythrogenic toxin genes: Detection by polymerase chain reaction and association with disease in strains isolated in Canada from 1940 to 1991. J Clin Microbiol 1992; 30: 3127–3131.
6. Weiss K, Laverdiere M, Lovgren M, Delorme J, Poirier L, Béliveau C. Group A Streptococcus carriage among close contacts of patients with invasive infections. Am J Epidemiol 1999; 149: 863–868.
7. Moses AE, Goldberg S, Korenman Z, et al. Invasive group A streptococcal infection in Israel: a prospective population-based investigation. Emerg Infect Dis 2002; 8: 421–426.
8. Rutishauser J, Funke G, Lütticken R, Ruef C. Streptococcal toxic shock syndrome in two patients infected by a colonized surgeon. Infection 1999; 27: 259–260.
9. Cavalieri SJ, Allais JM, Schlievert PM, Dworzack DL, Clark RB. Group A streptococcal peritonitis in a patient undergoing continuous ambulatory peritoneal dialysis. Am J Med 1989; 86: 249–250.
10. Nelson JD, Dillon HC Jr, Howard JB. A prolonged nursery epidemic associated with a newly recognized type of group A streptococcus. J Pediatr 1976; 89: 792–796.
11. Graham JC, Moss PJ, McKendrick MW. Primary group A streptococcal peritonitis. Scand J Infect Dis 1995; 27: 171–172.
12. Efstratiou A. Group A streptococci in the 1990s. J Antimicrob Chemother 2000; 45 (Suppl): 3–12.
13. Mishell DR Jr, Moyer DL. Association of pelvic inflammatory disease with the intrauterine device. Clin Obstet Gynecol 1969; 12: 179–197.
14. Smith LB, Adler NE, Tschann JM. Underreporting sensitive behaviors: the case of young women's willingness to report abortion. Health Psychol 1999; 18: 37–43.
15. Davies HD, McGeer A, Schwartz B, et al. Invasive group A streptococcal infections in Ontario, Canada. N Engl J Med 1996; 335: 547–554.