Nosocomial Group A Streptococcal Infections Associated with Asymptomatic Health-Care Workers -- Maryland and California, 1997.
During July 1996-August 1997, seven patients with postpartum GAS infections were identified by hospital A. A case of GAS infection was defined as GAS isolated from any nonpharyngeal site in a patient whose symptoms began >12 hours after admission to hospital A during January 1996-September 1997. Review of the hospital's microbiology records for all nonpharyngitis GAS cultures during the study period identified two additional postpartum cases. No cases were identified on other wards. Of nine case-patients, seven had endometritis; two of these had sepsis; one developed hypotension and required admission to the intensive-care unit (ICU). One patient developed postcesarean delivery wound infection, and another had a urinary tract infection. No patients died.
Each of the nine case-patients was compared with five controls. Controls were selected randomly from patients on the obstetric ward during the study period. Exposure to one HCW (HCW A) was associated strongly with infection (odds ratio=25; 95% confidence interval=2.8-1200.O).
Swab specimens were collected and cultured from the throat, rectum, vagina, and skin of 198 HCWs who worked on the labor and delivery or postpartum wards during the outbreak period. GAS isolates from the HCWs and a patient isolate were typed by sequencing the variable portion of the M-protein gene (emm typing). Three HCWs had positive cultures for GAS. Only the rectal isolate from HCW A was identical to that of the case-patient (emm type 77). HCW A's wife, who was asymptomatic, had positive rectal and vaginal cultures for the same strain. HCW A and his wife were treated with oral vancomycin and rifampin Surveillance cultures of HCW A have remained negative, and hospital A has had no additional cases.
During December 23, 1996-January 1, 1997, three patients who had surgery at hospital B developed STSS. On December 23, a previously healthy 28-year-old woman underwent a parathyroidectomy performed by surgeon A. The day before surgery, surgeon B performed direct laryngoscopy on the patient. She developed chest pain and hypotension on December 24. On December 26, she was transferred to the ICU because of respiratory distress, then developed cardiopulmonary arrest. Cultures taken December 25 from the neck wound and pleural fluid grew GAS. She went into shock and developed renal failure, coagulopathy, and purpura and died on December 29.
On December 30, a previously healthy 56-year-old woman underwent a subtotal thyroidectomy performed by surgeon A with the assistance of surgeon B. She was discharged December 31. Later that day, she was found dead in her home. Post-mortem cultures of blood and tissue grew GAS. The cause of death was attributed to septicemia and GAS.
On December 30, a previously healthy 57-year-old woman underwent a subtotal thyroidectomy performed by surgeon A with surgeon B assisting. The next day she was discharged. On January 1, 1997, she sought care at the emergency department and was admitted to the ICU in shock, with acidosis, respiratory failure, renal impairment, and bilateral pleural effusions. Cultures from the surgical wound, pleural fluid, and blood grew GAS. After a hospital course including sepsis, global myocardial hypokinesis, and lower gastrointestinal bleeding, she was discharged on February 4.
Review of hospital B's microbiology records revealed no episodes of postoperative GAS infection during the 6 months before the outbreak. Surgeon A was the only HCW who had contact in the operating room with all three patients. Nasopharyngeal, throat, rectal, and vaginal cultures were obtained from the 41 staff members who worked in the operating room and the pre- or postoperative areas on the days of surgery for the patients. All cultures were negative except a throat culture from one orderly that grew GAS. Surgeon A received self-initiated penicillin on January 2, before adequate cultures were obtained. Rifampin was added following adequate culturing. Throat cultures from surgeon A's household contacts were negative.
GAS isolates from all three patients were emm type 1 and had indistinguishable restriction fragment length polymorphism patterns. The orderly's GAS isolate was emm type STNS5.
Surgeons A and B were restricted from patient care until each had completed a 10-day course of penicillin and rifampin. No further postoperative GAS infection has occurred In hospital B.
Reported by: T Aragon, MD, M Katz, MD, City and County of San Francisco Dept of Public Health; L Mintz, MD, Univ of California, San Francisco; D Vugia, MD, S Waterman, MD, State Epidemiologist, California Dept of Health Svcs. D Bradshaw, MD, T Lacey, M Sanders, PhD, D Dwyer, MD, State Epidemiologist, Maryland Dept of Health and Mental Hygiene. Respiratory Diseases Br, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases; Div of Applied Public Health Training, Epidemiology Program Office; and EIS officers, CDC.
Editorial Note: GAS is an unusual cause of surgical site or postpartum infections. The bacterium is isolated from <1% of surgical-site infections (2) and 3% of infections after vaginal delivery (CDC, unpublished data, 1986-1997). The most common site of asymptomatic carriage among HCWs is the anus (3-5), but vaginal (6,7), skin (2), and pharyngeal (8) carriage have been implicated. GAS carriers can shed the organism into the immediate environment despite proper gowning and gloving (2,3,5-7). The mode of transmission is presumed to be airborne.
Surgical and obstetric patients are particularly vulnerable to infection because broken cutaneous or mucosal barriers facilitate invasive infection after exposure. In Toronto, Ontario, Canada, three of eight investigations following an episode of nosocomial GAS on surgical or obstetric wards identified an asymptomatic HCW (9).
To prevent additional nosocomial GAS infections, enhanced surveillance and limited epidemiologic investigation are warranted following one episode of nosocomial GAS infection on a surgical or obstetric ward. After identification of a patient with postoperative or postpartum GAS, medical and laboratory records should be reviewed to identify other infections, and isolates from infected patients should be stored and surveillance heightened to identify additional episodes.
When an episode of postoperative or postpartum GAS is identified, limited HCW screening should be undertaken. Most nosocomial transmission is traced to carriers involved in direct patient care. For a postpartum GAS-infected patient, screening should include all HCWs present at the delivery and those who performed vaginal examinations before delivery. For a postoperative GAS-infected patient, screening should include all HCWs present in the operating room during the procedure and those who changed dressings on open wounds. Screening of HCWs should include culture of the nares, throat, vagina, rectum, and skin. HCWs may return to work pending culture results. Any HCW culture-positive for GAS should refrain from patient care for the first 24 hours of antimicrobial treatment. The regimen should be tailored to the carriage site; previous reports have indicated anal carriage may be difficult to eradicate (6). For example, appropriate treatment for a positive rectal culture may be van-comycin 250 mg orally four tim es a day and rifampin 600 mg orally twice a day for 10 days (3,5). For a positive throat, vaginal, or skin culture, appropriate treatment may be penicillin 500 mg four times a day for 10 days with rifampin 600 mg orally twice a day for the last 4 days of the 10-day course (10).
If surveillance identifies additional patients or HCWs with positive cultures for GAS, the isolates should be typed by emm, serologic, or other molecular methods to identify the strain. When the isolates are the same and a carrier has not been identified, screening should be expanded to include HCWs who had less direct patient care. CDC also recommends obtaining cultures from household contacts of implicated carriers to identify and treat potential reservoirs for reinfection. Because carriage may recur (4), implicated carriers should be monitored with periodic surveillance cultures for 1 year after treatment.
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2. Mastro TD, Farley TA, Elliot JA, et al. An outbreak of surgical-wound infections due to group A Streptococcus carried on the scalp. N Engl J Med 1990;323:968-72.
3. Schaffner W, Lefkowitz LB Jr. Goodman JS, Koenig MG. Hospital outbreak of infections with group A streptococci traced to an a symptomatic anal carrier. N Engl J Med 1969;280:1224-5.
4. Viglionese A, Nottebart VF, Bodman HA, Platt R. Recurrent group A streptococcal carriage in a health care worker associated with widely separated nosocomial outbreaks. Am J Med 1991;91:S329-S333.
5. McKee WM, DiCaprio JM, Roberts CE Jr, Sherris JC. Anal carriage as the probable source of a streptococcal epidemic. Lancet 1966;2:1007-9.
6. Stamm WE, Feeley JC, Facklam R. Wound infections due to group A Streptococcus traced to a vaginal carrier. J Infect Dis 1978;138:287-92.
7. Berkelmam RL, Martin D, Graham DR, et al. Streptococcal wound infections caused by a vaginal carrier. JAMA 1982;247:2680-2.
8. Paul SM, Genese C, Spitalny K. Postoperative group A beta-hemolytic Streptococcus outbreak with the pathogen traced to a member of the healthcare workers household. Infect Control Hosp Epidemiol 1990;11:643-6.
9. Green K, Low D, Schwartz B, Cann D, Wilson P, McGeer A. Prospective surveillance for nosecomial group A streptococcal infections in Ontario: do single cases warrant an investigation? [Abstract 1393]. In: 1993 Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC). New Orleans, Louisiana: American Society for Microbiology, 1993.
10. The Working Group on Prevention of Invasive Group A Streptococcal Infections. Prevention of invasive group A streptococcal disease among
household contacts of case-patients: is prophylaxis warranted? JAMA 1998;279:1206-10.
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|Publication:||Morbidity and Mortality Weekly Report|
|Date:||Mar 5, 1999|
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