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Change in the molecular epidemiology of methicillin-resistant Staphylococcus aureus bloodstream infections in Taiwan
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Diagnostic Microbiology and Infectious Disease 65 (2009) 199 – 201 www.elsevier.com/locate/diagmicrobio
Change in the molecular epidemiology of methicillin-resistant Staphylococcus aureus bloodstream infections in Taiwan☆ Chih-Jung Chena,c , Po-Ren Hsuehe , Lin-Hui Sub,d , Cheng-Hsun Chiua,d , Tzou-Yien Lina,d , Yhu-Chering Huanga,d,⁎ a
Divisions of Pediatric Infectious Diseases, Department of Pediatrics, Chang Gung Children's Hospital, 333, Taoyuan, Taiwan b Department of Clinical Pathology, Chang Gung Memorial Hospital, Taoyuan, Taiwan c Graduate Institute of Clinical Medical Science, College of Medicine, Chang Gung University, 333, Taoyuan, Taiwan d Pediatric Research Center, Chang Gung Memorial Hospital, Taoyuan, 333, Taiwan e Department of Laboratory Medicine, National Taiwan University Hospital, 100, Taipei, Taiwan Received 1 February 2009; accepted 29 May 2009
Abstract A multiresistant community-associated methicillin-resistant Staphylococcus aureus clone (sequence type 59) established itself as a significant cause of nosocomial bloodstream infections soon after emergence in the communities. Multiresistance might be one of the characteristics that could have contributed to its quick adaptation to hospital environments. © 2009 Elsevier Inc. All rights reserved. Keywords: Methicillin-resistant Staphylococcus aureus; Community-associated infections; Bloodstream infections; Taiwan
Methicillin-resistant Staphylococcus aureus (MRSA) that met the epidemiologic definition for community-associated (CA) infection was first documented in Taiwan in 1997 and identified in 9.8% to 36% of all childhood CA S. aureus infections between 1997 and 2001 (Chen et al., 2005a; Wang et al., 2004). The rate rapidly increased to 56% during 2004 and 2005 (Huang et al., 2008). Genotypic analysis demonstrated that a clone (ST59, defined by multilocus sequence typing [MLST]) carrying a SCCmec IV or VT element and expressing multiresistance to non–β-lactams (including erythromycin and clindamycin) was responsible for the major outbreaks of CA-MRSA infections in this island (Lo et al., 2006; Wang et al., 2004). Further, the ST59 clone caused a substantial proportion of health care-associated (HA)-MRSA infections in a children's hospital during 2000 and 2001 (Chen et al., 2005a, 2005b). The finding suggested ☆ The study was supported by a grant from Chang Gung Memorial Hospital (CMRPG450122). ⁎ Corresponding author. Division of Pediatric Infectious diseases, Department of Pediatrics, Chang Gung Memorial Hospital, Taoyuan 333, Taiwan. Tel.: +886-3-3281200; fax: +886-3-3288957. E-mail address: [email protected] (Y.-C. Huang).
0732-8893/$ – see front matter © 2009 Elsevier Inc. All rights reserved. doi:10.1016/j.diagmicrobio.2009.05.020
that the multiresistant CA-MRSA clone might have spread into the hospitals soon after its emergence in the communities. To better understand the change in epidemiology of MRSA infections in the health care facilities and estimate the magnitude of the multiresistant CA-MRSA clone in causing serous nosocomial infections in Taiwan, we conducted a longitudinal study by comparing the antibiograms and molecular features of 257 MRSA blood isolates collected from 1995 to 2006 in the National Taiwan University Hospital, Taipei, Taiwan. The 257 isolates comprised the first 10% of consecutive and nonduplicate MRSA bloodstream infections (BSIs) isolates in each year of the study. Community-onset MRSA was defined as isolates from bloodstreams obtained within 48 h of admission, whereas HA-MRSA was defined as those from bloodstreams obtained beyond that time. Susceptibilities to various antibiotics (Table 2) were determined with disc diffusion methods according to the guidelines set forth by Clinical and Laboratory Standards Institute. The pulsed-field gel electrophoresis (PFGE) of SmaI digests of chromosomal DNAs and SCCmec typing was according to previously described methods (Huang et al., 2004). MLST was performed for representative strains of each major PFGE type according to
200
C.-J. Chen et al. / Diagnostic Microbiology and Infectious Disease 65 (2009) 199–201
Table 1 Distributions of SCCmec elements, presence of PVL genes, and MLST among 257 MRSA blood isolates according to PFGE types No. of subtypes
SCCmec types II III IV VT Nontypeable PVL genes Present Absent MLST type(s)a
Overall no. (%)
PFGE patterns, no. (%) A (n = 167)
B (n = 18)
C (n = 26)
D (n = 19)
E (n = 4)
F (n = 11)
90
37
7
16
12
2
4
12 (4.7) 182 (70.8) 31 (12.1) 17 (6.6) 15 (5.8)
0 164 (98.2) 0 0 3 (1.8)
0 13 (72.2) 0 0 5 (27.8)
0 0 26 (100) 0 0
0 0 1 (5.3) 16 (84.2) 2 (10.5)
0 4 (100) 0 0 0
11 (100) 0 0 0 0
1 (8.3) 1 (8.3) 4 (33.3) 1 (8.3) 5 (41.7)
21 (8.2) 236 (91.8)
0 167 (100) ST239 (3/16) ST241 (10/16) ST1374 (4/16)
0 18 (100) ST239 (1/3) ST241 (2/3)
1 (3.9) 25 (96.2) ST59 (1/3) ST966 (1/3) ST967 (1/3)
18 (94.7) 1 (5.3) ST59 (3/3)
0 4 (100) ST239 (1/1)
0 11 (100) ST5 (2/2)
2 (16.7)b 10 (83.3)
Minor types (n = 12)
a
MLST was determined in 25 randomly selected strains of PFGE types A to F. ST241 and ST1374 are single-locus variant (SLV) and double-locus variant, respectively, of ST239. ST966 and ST967 are both SLVs of ST59. The number of isolates with the ST followed by the numbers of isolates tested is given in parentheses. b Two PVL-positive isolates were respectively carrying SCCmecIV and SCCmec VT.
the instruction provided in the MLST Web site (http://www. mlst.net). The genes encoding Panton–Valentine leukocidin (PVL) were detected using a single polymerase chain reaction method (Lina et al., 1999). Temporal trends in the proportions of community-onset isolates, of isolates expressing particular SCCmec types and antibiograms, were tested by the Mantel–Haenszel χ2 method using SAS 9.1 for
Windows (SAS Institute Inc., Cary, NC). Statistical significance was defined as P b 0.05. The distributions of PFGE patterns, SCCmec types, and MLST are displayed in Table 1. Combining the 3 genotyping methods classified a majority of the 257 MRSA blood isolates into 3 clonal types: ST239-PFGE(A/B/E)-SCCmecIII (182 isolates, 70.8%), ST5-PFGE(F)-SCCmecII (12 isolates, 4.7%), and ST59-PFGE(C/D)-SCCmec IV/VT (48
Table 2 The origin and clonal type-specific characteristics of MRSA blood isolates in a teaching hospital in Taiwan Characteristics Origin, no. (%) HA
CO
Clonal type, no. (%) ST5
Total isolates 197 60 12 Days from admission to specimen collection ≤2 days 0 60 2 (17) N2 days 197 0 10 (83) Mean 39 ± 47 0.5 ± 0.7 21 ± 18 Median 23 0 14.5 (range) (3–303) (0–2) (1–55) PVL genes Presence 16 (8) 5 (8) 0 Resistance to Fusidic acid (0) (0) (0) Erythromycin (96) (97) (100) Clindamycin (88) (88) (100) Minocycline (56) (47) (0) SXT (77) (72) (0) Gentamicin (88) (85) (100) Multidrugc (90) (82) (100)
Fig. 1. The transition of ST239, ST59, and ST5 clonal types among MRSA blood isolates during the period 1995 to 2006 (A) and the resistance profile of ST59 clonal type during 1998 to 2006 (B).
Pa
ST239
ST59
182
48
41 (23) 141 (77) 31 ± 45 18 (0–303)
14 (29) 34 (71) 28 ± 47 11 (0–251)
.337
0
20 (42)
b.001
(0) (97) (87) (69) (96) (98) (99)
(0) (94) (85) (8.3) (15) (48) (46)
.369b .722 b.001 b.001 b.001 b.001
.658
CO = community onset; SXT = trimethoprim–sulfamethoxazole. a P value derived from comparison of isolates of ST239 and ST59 clonal type. b Fisher's exact test. c Multiresistance to at least 3 of the 6 non–β-lactam antibiotics listed above.
C.-J. Chen et al. / Diagnostic Microbiology and Infectious Disease 65 (2009) 199–201
isolates, 18.7%). PVL genes were exclusively present in isolates of ST59 lineage, including 3 (9.7%) of 31 isolates carrying SCCmec IV, 17 (100%) of 17 isolates carrying SCCmec VT, and 1 isolate of PFGE type D carrying nontypeable SCCmec. Among the 257 isolates, 60 (23.3%) were community onset. The rate remained stable throughout the study period (P value for trend = 0.1407). The isolates of ST239 clonal type prevailed over the entire 12-year period, with a rate declining from more than 90% in the first 3 years to 47.6% in the last years of study (P value for trend = 0.0015, Fig. 1A). This trend was accompanied by increasing incidences of isolates of ST5 and ST59 clonal types with borderline significances (P value for trend = 0.0532 and 0.0665, respectively). Similar to the strains of ST239 clonal type, more than 70% of the strains of ST59 clonal type were isolated from the blood specimen obtained beyond 2 days of admission (Table 2). The mean durations from admission to specimen collection were not significantly different in the 2 clonal types. Isolates of ST59 clonal type expressed high incidences of resistance to non–β-lactam antibiotics and multiple drugs, although at lower rates than did ST239 clonal type (Table 2). The resistance profile of ST59 did not change significantly since its emergence in 1998 in this hospital (P value for trend = 0.2699 for isolate with multiresistance, Fig. 1B). Results from this study indicate that the overwhelming majority (95.3%) of MRSA isolates causing BSIs during the period 1995 to 2006 in this hospital can be clustered into minor variants of 3 clonal types, ST239, ST5, and ST59. The dominance of the ST239 lineage, however, remained until 2006 and began to wane in this hospital after emergence of 2 new MRSA lineages, ST5 and ST59, respectively. ST59 with SCCmec IV/VT emerged as the BSI pathogen in 1998 and accounted for 17% of HA-MRSA blood isolates from 1995 to 2006 (Table 2). More than 70% of them were obtained from patients who had been hospitalized more than 48 h. The data indicate that the CA-MRSA ST59 clone originated in the community, entered the hospital, and accounted for a substantial proportion of nosocomial BSIs in this university hospital. CA-MRSA with ST59 background emerged in Taiwan in the late 1990s (Chen and Huang, 2005). The identification and increasing incidence of ST59 strains as a nosocomial BSI pathogen since 1998 suggest that this clone adapts quickly to the hospital environment without major evolution. The multiresistant characteristic may have provided an advantage for the CA-MRSA strains to easily enter and rapidly proliferate in health care facilities. It is quite possible that ST59 will become the major clone responsible for nosocomial infections in Taiwan soon. It appeared that the emergence of CA-MRSA isolates as an important cause of nosocomial infections has
201
occurred more widely than previously expected. The introduction of the dominant CA-MRSA clone, USA300, into health care setting in the United States, resulting in serious infections, has been well documented (Davis et al., 2006; Gonzalez et al., 2006; Maree et al., 2007). Our investigation provided evidence of the ability of another CA-MRSA clone, ST59, to cause serious nosocomial infections in a tertiary care hospital. The implication of the rise of CA-MRSA strains responsible for nosocomial infections remained unclear. In a cohort study of 100 consecutive patients with nosocomial MRSA infections, Davis et al. (2006) reported similar microbiologic and clinical cure rates between patients with SCCmec II/III strains and those with SCCmec IV strains infections. Further study is warranted to investigate the impact of CA-MRSA in hospital-acquired infections. References Chen CJ, Huang YC (2005) Community-acquired methicillin-resistant Staphylococcus aureus in Taiwan. J Microbiol Immunol Infect 38: 376–382. Chen CJ, Huang YC, Chiu CH, Su LH, Lin TY (2005) Clinical features and genotyping analysis of community-acquired methicillin-resistant Staphylococcus aureus infections in Taiwanese children. Pediatr Infect Dis J 24:40–45. Chen FJ, Lauderdale TL, Huang IW, Lo HJ, Lai JF, Wang HY, Shiau YR, Chen PC, Ito T, Hiramitsu K (2005) Methicillin-resistant Staphylococcus aureus in Taiwan. Emerg Infect Dis 11:1760–1763. Davis SL, Rybak MJ, Amjad M, Kaatz GW, McKinnon PS (2006) Characteristics of patients with healthcare-associated infection due to SCCmec type IV methicillin-resistant Staphylococcus aureus. Infect Control Hosp Epidemiol 27:1025–1031. Gonzalez BE, Rueda AM, Shelburne 3rd SA, Musher DM, Hamill RJ, Hulten KG (2006) Community-associated strains of methicillin-resistant Staphylococcus aureus as the cause of healthcare-associated infection. Infect Control Hosp Epidemiol 27:1051–1056. Huang YC, Ho CF, Chen CJ, Su LH, Lin TY (2008) Comparative molecular analysis of community-associated and healthcare-associated methicillinresistant Staphylococcus aureus isolates from children in northern Taiwan. Clin Microbiol Infect 14:1167–1172. Huang YC, Su LH, Wu TL, Liu CE, Young TG, Chen PY, Hseuh PR, Lin TY (2004) Molecular epidemiology of clinical isolates of methicillinresistant Staphylococcus aureus in Taiwan. J Clin Microbiol 42: 307–310. Lina G, Piemont Y, Godail-Gamot F, Bes M, Peter MO, Gauduchon V, Vandenesch F, Etienne J (1999) Involvement of Panton–Valentine leukocidin-producing Staphylococcus aureus in primary skin infections and pneumonia. Clin Infect Dis 29:1128–1132. Lo WT, Lin WJ, Tseng MH, Wang SR, Chu ML, Wang CC (2006) Community-acquired methicillin-resistant Staphylococcus aureus in children, Taiwan. Emerg Infect Dis 12:1267–1270. Maree CL, Daum RS, Boyle-Vavra S, Matayoshi K, Miller LG (2007) Community-associated methicillin-resistant Staphylococcus aureus isolates causing healthcare-associated infections. Emerg Infect Dis 13: 236–242. Wang CC, Lo WT, Chu ML, Siu LK (2004) Epidemiological typing of community-acquired methicillin-resistant Staphylococcus aureus isolates from children in Taiwan. Clin Infect Dis 39:481–487.
Diagnostic Microbiology and Infectious Disease 65 (2009) 199 – 201 www.elsevier.com/locate/diagmicrobio
Change in the molecular epidemiology of methicillin-resistant Staphylococcus aureus bloodstream infections in Taiwan☆ Chih-Jung Chena,c , Po-Ren Hsuehe , Lin-Hui Sub,d , Cheng-Hsun Chiua,d , Tzou-Yien Lina,d , Yhu-Chering Huanga,d,⁎ a
Divisions of Pediatric Infectious Diseases, Department of Pediatrics, Chang Gung Children's Hospital, 333, Taoyuan, Taiwan b Department of Clinical Pathology, Chang Gung Memorial Hospital, Taoyuan, Taiwan c Graduate Institute of Clinical Medical Science, College of Medicine, Chang Gung University, 333, Taoyuan, Taiwan d Pediatric Research Center, Chang Gung Memorial Hospital, Taoyuan, 333, Taiwan e Department of Laboratory Medicine, National Taiwan University Hospital, 100, Taipei, Taiwan Received 1 February 2009; accepted 29 May 2009
Abstract A multiresistant community-associated methicillin-resistant Staphylococcus aureus clone (sequence type 59) established itself as a significant cause of nosocomial bloodstream infections soon after emergence in the communities. Multiresistance might be one of the characteristics that could have contributed to its quick adaptation to hospital environments. © 2009 Elsevier Inc. All rights reserved. Keywords: Methicillin-resistant Staphylococcus aureus; Community-associated infections; Bloodstream infections; Taiwan
Methicillin-resistant Staphylococcus aureus (MRSA) that met the epidemiologic definition for community-associated (CA) infection was first documented in Taiwan in 1997 and identified in 9.8% to 36% of all childhood CA S. aureus infections between 1997 and 2001 (Chen et al., 2005a; Wang et al., 2004). The rate rapidly increased to 56% during 2004 and 2005 (Huang et al., 2008). Genotypic analysis demonstrated that a clone (ST59, defined by multilocus sequence typing [MLST]) carrying a SCCmec IV or VT element and expressing multiresistance to non–β-lactams (including erythromycin and clindamycin) was responsible for the major outbreaks of CA-MRSA infections in this island (Lo et al., 2006; Wang et al., 2004). Further, the ST59 clone caused a substantial proportion of health care-associated (HA)-MRSA infections in a children's hospital during 2000 and 2001 (Chen et al., 2005a, 2005b). The finding suggested ☆ The study was supported by a grant from Chang Gung Memorial Hospital (CMRPG450122). ⁎ Corresponding author. Division of Pediatric Infectious diseases, Department of Pediatrics, Chang Gung Memorial Hospital, Taoyuan 333, Taiwan. Tel.: +886-3-3281200; fax: +886-3-3288957. E-mail address: [email protected] (Y.-C. Huang).
0732-8893/$ – see front matter © 2009 Elsevier Inc. All rights reserved. doi:10.1016/j.diagmicrobio.2009.05.020
that the multiresistant CA-MRSA clone might have spread into the hospitals soon after its emergence in the communities. To better understand the change in epidemiology of MRSA infections in the health care facilities and estimate the magnitude of the multiresistant CA-MRSA clone in causing serous nosocomial infections in Taiwan, we conducted a longitudinal study by comparing the antibiograms and molecular features of 257 MRSA blood isolates collected from 1995 to 2006 in the National Taiwan University Hospital, Taipei, Taiwan. The 257 isolates comprised the first 10% of consecutive and nonduplicate MRSA bloodstream infections (BSIs) isolates in each year of the study. Community-onset MRSA was defined as isolates from bloodstreams obtained within 48 h of admission, whereas HA-MRSA was defined as those from bloodstreams obtained beyond that time. Susceptibilities to various antibiotics (Table 2) were determined with disc diffusion methods according to the guidelines set forth by Clinical and Laboratory Standards Institute. The pulsed-field gel electrophoresis (PFGE) of SmaI digests of chromosomal DNAs and SCCmec typing was according to previously described methods (Huang et al., 2004). MLST was performed for representative strains of each major PFGE type according to
200
C.-J. Chen et al. / Diagnostic Microbiology and Infectious Disease 65 (2009) 199–201
Table 1 Distributions of SCCmec elements, presence of PVL genes, and MLST among 257 MRSA blood isolates according to PFGE types No. of subtypes
SCCmec types II III IV VT Nontypeable PVL genes Present Absent MLST type(s)a
Overall no. (%)
PFGE patterns, no. (%) A (n = 167)
B (n = 18)
C (n = 26)
D (n = 19)
E (n = 4)
F (n = 11)
90
37
7
16
12
2
4
12 (4.7) 182 (70.8) 31 (12.1) 17 (6.6) 15 (5.8)
0 164 (98.2) 0 0 3 (1.8)
0 13 (72.2) 0 0 5 (27.8)
0 0 26 (100) 0 0
0 0 1 (5.3) 16 (84.2) 2 (10.5)
0 4 (100) 0 0 0
11 (100) 0 0 0 0
1 (8.3) 1 (8.3) 4 (33.3) 1 (8.3) 5 (41.7)
21 (8.2) 236 (91.8)
0 167 (100) ST239 (3/16) ST241 (10/16) ST1374 (4/16)
0 18 (100) ST239 (1/3) ST241 (2/3)
1 (3.9) 25 (96.2) ST59 (1/3) ST966 (1/3) ST967 (1/3)
18 (94.7) 1 (5.3) ST59 (3/3)
0 4 (100) ST239 (1/1)
0 11 (100) ST5 (2/2)
2 (16.7)b 10 (83.3)
Minor types (n = 12)
a
MLST was determined in 25 randomly selected strains of PFGE types A to F. ST241 and ST1374 are single-locus variant (SLV) and double-locus variant, respectively, of ST239. ST966 and ST967 are both SLVs of ST59. The number of isolates with the ST followed by the numbers of isolates tested is given in parentheses. b Two PVL-positive isolates were respectively carrying SCCmecIV and SCCmec VT.
the instruction provided in the MLST Web site (http://www. mlst.net). The genes encoding Panton–Valentine leukocidin (PVL) were detected using a single polymerase chain reaction method (Lina et al., 1999). Temporal trends in the proportions of community-onset isolates, of isolates expressing particular SCCmec types and antibiograms, were tested by the Mantel–Haenszel χ2 method using SAS 9.1 for
Windows (SAS Institute Inc., Cary, NC). Statistical significance was defined as P b 0.05. The distributions of PFGE patterns, SCCmec types, and MLST are displayed in Table 1. Combining the 3 genotyping methods classified a majority of the 257 MRSA blood isolates into 3 clonal types: ST239-PFGE(A/B/E)-SCCmecIII (182 isolates, 70.8%), ST5-PFGE(F)-SCCmecII (12 isolates, 4.7%), and ST59-PFGE(C/D)-SCCmec IV/VT (48
Table 2 The origin and clonal type-specific characteristics of MRSA blood isolates in a teaching hospital in Taiwan Characteristics Origin, no. (%) HA
CO
Clonal type, no. (%) ST5
Total isolates 197 60 12 Days from admission to specimen collection ≤2 days 0 60 2 (17) N2 days 197 0 10 (83) Mean 39 ± 47 0.5 ± 0.7 21 ± 18 Median 23 0 14.5 (range) (3–303) (0–2) (1–55) PVL genes Presence 16 (8) 5 (8) 0 Resistance to Fusidic acid (0) (0) (0) Erythromycin (96) (97) (100) Clindamycin (88) (88) (100) Minocycline (56) (47) (0) SXT (77) (72) (0) Gentamicin (88) (85) (100) Multidrugc (90) (82) (100)
Fig. 1. The transition of ST239, ST59, and ST5 clonal types among MRSA blood isolates during the period 1995 to 2006 (A) and the resistance profile of ST59 clonal type during 1998 to 2006 (B).
Pa
ST239
ST59
182
48
41 (23) 141 (77) 31 ± 45 18 (0–303)
14 (29) 34 (71) 28 ± 47 11 (0–251)
.337
0
20 (42)
b.001
(0) (97) (87) (69) (96) (98) (99)
(0) (94) (85) (8.3) (15) (48) (46)
.369b .722 b.001 b.001 b.001 b.001
.658
CO = community onset; SXT = trimethoprim–sulfamethoxazole. a P value derived from comparison of isolates of ST239 and ST59 clonal type. b Fisher's exact test. c Multiresistance to at least 3 of the 6 non–β-lactam antibiotics listed above.
C.-J. Chen et al. / Diagnostic Microbiology and Infectious Disease 65 (2009) 199–201
isolates, 18.7%). PVL genes were exclusively present in isolates of ST59 lineage, including 3 (9.7%) of 31 isolates carrying SCCmec IV, 17 (100%) of 17 isolates carrying SCCmec VT, and 1 isolate of PFGE type D carrying nontypeable SCCmec. Among the 257 isolates, 60 (23.3%) were community onset. The rate remained stable throughout the study period (P value for trend = 0.1407). The isolates of ST239 clonal type prevailed over the entire 12-year period, with a rate declining from more than 90% in the first 3 years to 47.6% in the last years of study (P value for trend = 0.0015, Fig. 1A). This trend was accompanied by increasing incidences of isolates of ST5 and ST59 clonal types with borderline significances (P value for trend = 0.0532 and 0.0665, respectively). Similar to the strains of ST239 clonal type, more than 70% of the strains of ST59 clonal type were isolated from the blood specimen obtained beyond 2 days of admission (Table 2). The mean durations from admission to specimen collection were not significantly different in the 2 clonal types. Isolates of ST59 clonal type expressed high incidences of resistance to non–β-lactam antibiotics and multiple drugs, although at lower rates than did ST239 clonal type (Table 2). The resistance profile of ST59 did not change significantly since its emergence in 1998 in this hospital (P value for trend = 0.2699 for isolate with multiresistance, Fig. 1B). Results from this study indicate that the overwhelming majority (95.3%) of MRSA isolates causing BSIs during the period 1995 to 2006 in this hospital can be clustered into minor variants of 3 clonal types, ST239, ST5, and ST59. The dominance of the ST239 lineage, however, remained until 2006 and began to wane in this hospital after emergence of 2 new MRSA lineages, ST5 and ST59, respectively. ST59 with SCCmec IV/VT emerged as the BSI pathogen in 1998 and accounted for 17% of HA-MRSA blood isolates from 1995 to 2006 (Table 2). More than 70% of them were obtained from patients who had been hospitalized more than 48 h. The data indicate that the CA-MRSA ST59 clone originated in the community, entered the hospital, and accounted for a substantial proportion of nosocomial BSIs in this university hospital. CA-MRSA with ST59 background emerged in Taiwan in the late 1990s (Chen and Huang, 2005). The identification and increasing incidence of ST59 strains as a nosocomial BSI pathogen since 1998 suggest that this clone adapts quickly to the hospital environment without major evolution. The multiresistant characteristic may have provided an advantage for the CA-MRSA strains to easily enter and rapidly proliferate in health care facilities. It is quite possible that ST59 will become the major clone responsible for nosocomial infections in Taiwan soon. It appeared that the emergence of CA-MRSA isolates as an important cause of nosocomial infections has
201
occurred more widely than previously expected. The introduction of the dominant CA-MRSA clone, USA300, into health care setting in the United States, resulting in serious infections, has been well documented (Davis et al., 2006; Gonzalez et al., 2006; Maree et al., 2007). Our investigation provided evidence of the ability of another CA-MRSA clone, ST59, to cause serious nosocomial infections in a tertiary care hospital. The implication of the rise of CA-MRSA strains responsible for nosocomial infections remained unclear. In a cohort study of 100 consecutive patients with nosocomial MRSA infections, Davis et al. (2006) reported similar microbiologic and clinical cure rates between patients with SCCmec II/III strains and those with SCCmec IV strains infections. Further study is warranted to investigate the impact of CA-MRSA in hospital-acquired infections. References Chen CJ, Huang YC (2005) Community-acquired methicillin-resistant Staphylococcus aureus in Taiwan. J Microbiol Immunol Infect 38: 376–382. Chen CJ, Huang YC, Chiu CH, Su LH, Lin TY (2005) Clinical features and genotyping analysis of community-acquired methicillin-resistant Staphylococcus aureus infections in Taiwanese children. Pediatr Infect Dis J 24:40–45. Chen FJ, Lauderdale TL, Huang IW, Lo HJ, Lai JF, Wang HY, Shiau YR, Chen PC, Ito T, Hiramitsu K (2005) Methicillin-resistant Staphylococcus aureus in Taiwan. Emerg Infect Dis 11:1760–1763. Davis SL, Rybak MJ, Amjad M, Kaatz GW, McKinnon PS (2006) Characteristics of patients with healthcare-associated infection due to SCCmec type IV methicillin-resistant Staphylococcus aureus. Infect Control Hosp Epidemiol 27:1025–1031. Gonzalez BE, Rueda AM, Shelburne 3rd SA, Musher DM, Hamill RJ, Hulten KG (2006) Community-associated strains of methicillin-resistant Staphylococcus aureus as the cause of healthcare-associated infection. Infect Control Hosp Epidemiol 27:1051–1056. Huang YC, Ho CF, Chen CJ, Su LH, Lin TY (2008) Comparative molecular analysis of community-associated and healthcare-associated methicillinresistant Staphylococcus aureus isolates from children in northern Taiwan. Clin Microbiol Infect 14:1167–1172. Huang YC, Su LH, Wu TL, Liu CE, Young TG, Chen PY, Hseuh PR, Lin TY (2004) Molecular epidemiology of clinical isolates of methicillinresistant Staphylococcus aureus in Taiwan. J Clin Microbiol 42: 307–310. Lina G, Piemont Y, Godail-Gamot F, Bes M, Peter MO, Gauduchon V, Vandenesch F, Etienne J (1999) Involvement of Panton–Valentine leukocidin-producing Staphylococcus aureus in primary skin infections and pneumonia. Clin Infect Dis 29:1128–1132. Lo WT, Lin WJ, Tseng MH, Wang SR, Chu ML, Wang CC (2006) Community-acquired methicillin-resistant Staphylococcus aureus in children, Taiwan. Emerg Infect Dis 12:1267–1270. Maree CL, Daum RS, Boyle-Vavra S, Matayoshi K, Miller LG (2007) Community-associated methicillin-resistant Staphylococcus aureus isolates causing healthcare-associated infections. Emerg Infect Dis 13: 236–242. Wang CC, Lo WT, Chu ML, Siu LK (2004) Epidemiological typing of community-acquired methicillin-resistant Staphylococcus aureus isolates from children in Taiwan. Clin Infect Dis 39:481–487.