Jpn. J. Infect. Dis., 53, 207-209, 2000

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Laboratory and Epidemiology Communications

Epidemiological Analysis of a Methicillin-Resistant Staphylococcus aureus Outbreak in Surgery Wards by Genomic DNA Polymorphisms

Aki Kaneko, Tomoko Fujino, Sosuke Kimura, Hirofumi Kuroki, Toshiko Suzuki, Mitsuharu Hasegawa, Tadatoshi Kuratsuji, Morito Sumiya, Koichiro Kudo, Oichirou Kobori, Yoshio Yazaki and Teruo Kirikae*

International Medical Center of Japan,
Toyama 1-21-1, Shinjuku-ku, Tokyo 162-8655

Communicated by Hiroshi Yoshikura

(Accepted November 2, 2000)

Hospital infection, especially postoperative infection, caused by methicillin-resistant Staphylococcus aureus (MRSA) is a serious problem in surgical wards (1). Analysis of restriction fragment length polymorphisms of genomic DNA using pulsed-field gel electrophoresis (PFGE) is an essential tool for epidemiology of MRSA infection.

In a cardiac surgery ward in a hospital in Tokyo, two patients, P1 and P2, successively contracted severe sepsis. In an orthopedic ward in that hospital, one patient, P3, simultaneously contracted acute arthritis at a left knee joint. MRSA was isolated from the blood or the affected region of each patient. The isolates and isolates from carriers in the same wards during that period were tested for chromosomal DNA typing by using a contour-clamped homogeneous electric field system (CHEF MapperTM: Bio-Rad Laboratories, Hercules, Calif., USA), antibiotic resistance (WalkAwayTM, Dade Behring, Deerfield, Ill., USA), enterotoxin serotyping (SET-RPLA: Denka Seiken Co., Tokyo), toxic shock syndrome toxin-1 (TSST-1) production (TST-RPLA: Denka Seiken), and coagulase serotyping (Denka Seiken).

Seven different PFGE patterns of SmaI DNA digests (Fig. 1A), six patterns of BglI digests (Fig. 1B), and eight patterns of BstX I digests (Fig. 1C) were detected. Sensitivity to antibiotics is shown in Table 1; three different patterns were observed. All isolates except No. 374 produced enterotoxin type C, TSST-1, and type II coagulase (Table 2). No. 374 produced neither enterotoxin nor TSST-1, but did produce type III coagulase (Table 2).

As summarized in Table 2, in patient P1, two different PFGE patterns of SmaI DNA digests were detected among twelve MRSA isolates obtained from different sources on different days. In patient P2, all eight MRSA isolates showed the same pattern (pattern A). Isolate No. 358 from patient P1, No. 357 from P2, and No. 379 from P3 showed the same PFGE pattern of SmaI DNA digests (pattern A), the same pattern of BglI digests (pattern A), the same pattern of BstX I digests (pattern ƒ¿), and the same spectrum of antibiotic susceptibility (pattern a). In an orthopedic surgery ward, another MRSA isolate was obtained from another patient (P4), in addition to P3. The PFGE patterns of the isolate (No. 382: patterns CBƒÃ) were different from those of No. 379 from P3 (patterns AAƒ¿). In a cardiac surgery ward, 17 doctors and 21 nurses were working during the outbreak. MRSA surveys of personnel were performed, and detected three carriers, including a doctor (M3) and two nurses (M1 and M2). Isolate No. 375 from M2 showed the same PFGE patterns as those of No. 356 from P1 (patterns BAƒÀ), though the antibiotic resistance pattern was slightly different. Isolate No. 374 was different from other MRSA isolates in PFGE pattern, antibiotic susceptibility, and other biological properties. From the end of July through August, four additional MRSA isolates were obtained from three patients (P5, P6, and P7) in the cardiac surgery ward. The PFGE patterns were different from those of isolates from patients P1, P2, and P3.

The above events could be summarized as follows. The infections of patients P1 and P2 in the cardiac surgery ward and possibly that of P3 in the orthopedic surgery ward were caused by the same or closely related MRSA, given that the isolates shared the same molecular markers. During the same period, three medical staff in the cardiac surgery ward were found to be MRSA carriers. The isolates were, however, different from one another and also different from the isolates from patients P1, P2, and P3. Later, three more patients in the same ward were infected by MRSA, though the strains were distinct from any of the previous isolates. This finding suggests that new MRSAs were constantly introduced into the ward.

REFERENCE

  1. Baltimore, R. S. (1998): Neonatal nosocomial infections. Semin. Perinatol., 22,25-32.


*Corresponding author: Fax: +81-3-3202-7364, E-mail: tkirikae@ri.imcj.go.jp


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