An outbreak of M serotype 1 group A Streptococcus in a neonatal intensive care unit.

OBJECTIVE

To describe the investigation and control of an outbreak of M serotype 1, Streptococcus pyogenes (group A Streptococcus, GAS) infections in a neonatal intensive care unit (NICU).

STUDY DESIGN

The study was conducted in an NICU in a large urban university-affiliated hospital. Retrospective review was performed of all infants and health care workers in the NICU, especially those either colonized or infected with GAS during the outbreak and the prospective surveillance period (July through September 1994). Prospective epidemiologic investigation, including cultures of throat, umbilicus, and anorectum (infants), or throat and anus (NICU personnel), identified a possible common source of the disease in case infants. Antimicrobial susceptibility testing and serotyping of all GAS strains were performed; M serotype 1 isolates were examined by DNA analysis with restriction fragment length polymorphism. The M-1 GAS isolates were tested for streptococcal pyrogenic exotoxin (SPE) A and SPE B production. A retrospective chart review and analysis of infants with GAS infection or colonization was conducted.

RESULTS

During a 1-week period, two very low birth weight infants more than 3 weeks of age had GAS septicemia and focal infection. Two additional very low birth weight infants with asymptomatic throat colonization were identified during the first week of surveillance. Benzathine penicillin G was administered to all NICU infants, but failed to eradicate throat colonization in the four case subjects. Seven days after completing parenteral antibiotic therapy, the index patient had a recurrence of GAS septicemia that was fatal. Eradication of throat colonization in the remaining three infants was achieved with a 10-day course of intravenous clindamycin therapy. Among 103 NICU personnel, five (4.9%) had asymptomatic GAS colonization with strains that were uniformly susceptible to penicillin. Each colonized adult was successfully treated with oral clindamycin therapy. Serotyping revealed that five isolates of GAS from four infants and one NICU respiratory therapist were M-1 isolates; DNA analysis confirmed that these were the same strain. The five M-1 isolates produced both SPE A and SPE B.

CONCLUSIONS

The previously documented increase in prevalence of M-1 strains of GAS in the United States is likely to be associated with their introduction into closed populations including NICUs. Control of such outbreaks may be achieved by isolation, cohorting of case subjects and possible carriers, and successful eradication of colonization in case subjects and carriers. Although GAS organisms are uniformly susceptible to penicillin G, eradication may require agents other than penicillin.