- Email: [email protected]
Spread of the community-acquired methicillin-resistant Staphylococcus aureus USA300 clone among family members in Japan
J Infect Chemother (2010) 16:372–374 DOI 10.1007/s10156-010-0087-z
NOTE
Spread of the community-acquired methicillin-resistant Staphylococcus aureus USA300 clone among family members in Japan Shizuka Yabe • Tomomi Takano • Wataru Higuchi Shigenao Mimura • Yoshihiro Kurosawa • Tatsuo Yamamoto
•
Received: 31 March 2010 / Accepted: 12 June 2010 / Published online: 14 July 2010 Ó Japanese Society of Chemotherapy and The Japanese Association for Infectious Diseases 2010
Abstract The USA300 clone is a highly-virulent community-acquired methicillin-resistant Staphylococcus aureus, which has been predominant in the United States. In a previous study, we isolated the USA300 clone from an 11-month-old Japanese girl, who lived in Saitama (Japan), and suffered from cellulitis and sepsis, and subsequently osteomyelitis, in 2008. In this study, we searched for the source of such USA300 infection in three related families (the patient’s grandfather and grandmother, having a USA300-infected daughter [F2D], and a mother [F3M] who was a sister of F2D’s mother). In January, 2008, F3M and her family members visited Hawaii and were treated in a hospital for gastroenteritis (with diarrhea) with an intravenous drip for F3M. After their return to Japan in January, F3M suffered from unusually frequent (more than 10 times) skin soft-tissue infections (SSTIs) until successful chemotherapy in July in Saitama. In the same summer season, SSTI was observed in 7 of 11 family members (63.6%). This dense spread of SSTI was followed by cellulitis and sepsis (USA300-isolated case) in October and subsequent osteomyelitis in December in F2D. After successful chemotherapy for the patient (F2D), no new SSTI cases were observed among the family members, and no USA300 colonization was observed when examined in December, 2009. The data suggest the first spread of the USA300 clone in Japan with related families at the core
S. Yabe T. Takano W. Higuchi T. Yamamoto (&) Division of Bacteriology, Department of Infectious Disease Control and International Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan e-mail: [email protected] S. Mimura Y. Kurosawa Ageo Central General Hospital, Saitama, Japan
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and that such USA300 spread in the community is likely to have occurred in the summer season in Japan. Keywords Community-acquired methicillin-resistant S. aureus (CA-MRSA) USA300 clone Family Transmission
Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is a new class of MRSA, which can persist in the community, in contrast with previous MRSA (called hospital-acquired MRSA, HA-MRSA) mainly spreading in hospitals [1–3]. CA-MRSA spreads among otherwise healthy children or adolescents, for example athletes, through skin-to-skin contact, and is primarily associated with skin soft tissue infection (SSTI), including pyrogenic skin infection [1–3]. It is also associated with severe systemic infections, for example sepsis, necrotizing pneumonia, necrotizing fasciitis, and osteomyelitis [1, 3–5]. CA-MRSA often produces Panton–Valentine leukocidin (PVL) [1–3, 6]. Although CA-MRSA is genetically heterogenous, the USA300 clone is currently the most prominent clone in the United States; for instance, the USA300 clone accounts for the vast majority (97%) of MRSA infections among patients in emergency departments [7]. The USA300 clone is highly transmissible and highly virulent, becoming multiple drug-resistant, and behaving like HA-MRSA [8]. Moreover, it is growing as a global clone [9]. The USA300 clone belongs to multilocus sequence type (ST) 8, exhibits spa1 (or t008) and SCCmecIVa, is positive for PVL, and carries the arginine catabolic mobile element (ACME) [10]. In Japan, the USA300 clone (with genotype ST8/ spa985[t711]/SCCmecIVa; strain NN36) was isolated from a 3-month-old Indian girl who was born in a hospital in South Alameda (CA, USA) and stayed there for 1 month,
J Infect Chemother (2010) 16:372–374
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transiently stayed in Tokyo, and suffered from temporal and cervical subcutaneous abscesses in 2007 [11]. The parents had no history of SSTI and no MRSA colonization, indicating that the USA300 strain originated, most probably, in a hospital in California. The second USA300 infection case occurred in 2008. In this case, the USA300 clone (with genotype ST8/spa363 [t024]/SCCmecIVa; strain NN47) was isolated from the blood of an 11-month-old Japanese girl who lived in Saitama, suffered from cellulitis of the lower thigh and sepsis, and subsequently suffered from osteomyelitis [12]. Because the patient and her family members had never been abroad and did not have contact with foreigners, and moreover, there were no reported Japanese USA300 infection cases in Japan at that time, in this study we searched for the source of infection in her family members. All protocols of this study were approved by the ethics review board of Niigata University School of Medicine, Niigata, Japan, and before sampling from children consent was obtained from their parents. Diagnosis of SSTIs in family members, who had not consulted with a doctor in hospital, were done by interview at their homes, by showing photographs of SSTIs including abscesses. Screening of MRSA colonization in the members of related families was performed in December, 2009. For this, the
nares, cheeks, axilla, and inguinal area were examined for MRSA by using swabs. S. aureus was examined for the mecA gene, PVL gene, and ACME by PCR for confirmation of the USA300 clone, as described previously [12]. Susceptibility testing of MRSA strain NN47 was carried out using the agar dilution method with Mueller–Hinton agar, according to previous procedures [13]. The family pedigree of the patient is shown in Fig. 1; the patient (from whom the USA300 clone [strain NN47] was isolated, as described above) was a daughter in family 2 (F2D). The three related families included 11 members (0–52 years old) and all family members lived in Saitama. The mother (M) in family 3 (F3M), together with her three family members (father [F3F] and two daughters [F3D1] and [F3D2]), had visited Hawaii in January, 2008. F3M and F3D1 developed gastroenteritis (with diarrhea) there and were treated in a hospital with peripheral drip intravenous infusion for F3M. They returned to Japan (Saitama) in January, 2008. After their return, F3M suffered from unusually frequent (more than 10 times) recurrent and multifocal SSTIs (including flaring and swelling, and abscesses) of the upper thigh and gluteal regions until July. F3M was diagnosed with impetigo (or insect bites just like spider bites reported in the United States [14]) at a hospital on July 1. Cefdinir (CFDN, a third-generation cephem) at
Family 1
Mother 52 years
Father 52 years
Aug. -Sep., 2008: SSTI of thigh Family 2
Family 3
F3M Mother 26 years Aug. -Sep., 2008: SSTI of thigh
Father 40 years Aug. -Sep., 2008: SSTI of thigh
Mother 23 years Feb. -Jul., 2008: Frequent (recurrent) SSTIs of thigh and gluteal regions
Father 22 years Jul., 2008: SSTI of thigh
F2D Daughter 2 years (11 months in 2008)
Son 5 years
Aug. -Sep., 2008: SSTI of thigh Oct., 2008: Cellulitis of thigh (MRSA*) Dec., 2008: Osteomyelitis of tibial region
Fig. 1 Family pedigree and SSTI of the family members. Closed symbols represent family members who suffered from SSTI, including flaring and swelling (cellulitis), and abscesses in the thigh and gluteal regions. The series of SSTI started when the mother (M) in family 3 (F3M), who had visited Hawaii (in January, 2008), was treated there for gastroenteritis, with an intravenous drip, and suffered from frequent SSTI (February through July) after her return to Japan in January. A daughter (D) in family 2 (F2D) was admitted to a hospital
Daughter 1 4 years
Daughter 2 2 years
Daughter 3 0 years
Jul., 2008: SSTI of thigh
for treatment of cellulitis and sepsis in October; MRSA (USA300), marked with an asterisk in the figure, was isolated from the blood. F2D was also admitted to a hospital for treatment of osteomyelitis in December. All family members were negative for MRSA colonization when examined in December, 2009. The age of the family members is as of December, 2009 (that in 2008 is shown in parentheses)
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100 mg was orally administered three times a day for 7 days. During this time (July 3), it was confirmed that the flaring and swelling were relieved in hospital. However, other family members also suffered from SSTI shortly after F3M. Episodes of SSTIs (July through September) are summarized in Fig. 1. SSTIs included flaring, swelling, and abscesses of the upper thigh. In the series of SSTIs, which started with F3M and spread among the family members, 7 out of 11 members (63.6%) developed SSTI. F2D was also included in this series of SSTIs and suffered from flaring and swelling of the upper thigh in August and September. No family members had experienced frequent SSTIs or a large abscess before 2008. On October 21, F2D (11 months at that time) was admitted to another hospital with fever, and flaring and swelling of the left lower thigh. She was diagnosed with cellulitis and sepsis; USA300 (strain NN47) was isolated from the blood [12]. After successful treatment with cefazolin (CEZ) and vancomycin (VCM), she was discharged on November 7; however, on December 17, she was again admitted to a hospital with recurrent lower thigh swelling. Osteomyelitis involving the entire left tibial region was observed and she was successfully treated with teicoplanin (TEIC) and linezolid (LZD) [12]. She was discharged on January 28, 2009. The MIC values (lg/ml) of CEZ, CFDN, VCM, TEIC, and LZD for USA300 strain NN47 were 2, 2, 1, 0.5, and 2, respectively. In other family members (except F2D), no new cases of SSTI were observed after September, 2008. Members of the three families (shown in Fig. 1) were screened for MRSA colonization in December, 2009; however, no MRSA was isolated from the nares, cheeks, axilla, and inguinal area in any individual. Therefore, USA300 strain NN47 (isolated from a Japanese infant, F2D) could have originated in the United States (most probably in a hospital in Hawaii), and F3M (who was treated in Hawaii with an intravenous drip) could be the source of infection among the family members (including F2D). This study provides supporting evidence of the first spread of the USA300 clone in the community (among family members) in Japan with the hypothesis that such USA300 spread in the community is likely to have occurred in the summer season in Japan, like bullous impetigo. The families in this study had infants and frequently got together on New Year’s Day or other holidays; therefore, it is highly possible that the USA300 clone had been transmitted among family members through close body contact (such as hugs and kisses to infants). It is not known whether the USA300 clone had also spread to people unrelated to these families. Finally, it should be noted that MRSA was actually isolated only from F2D and not from other family members; therefore, USA300 spread
123
J Infect Chemother (2010) 16:372–374
is a possibility based on the SSTI information of family members and is not proved directly by MRSA isolation and characterization. Surveillance of the USA300 clone is needed in Japan.
References 1. Zetola N, Francis JS, Nuermberger EL, Bishai WR. Communityacquired methicillin-resistant Staphylococcus aureus: an emerging threat. Lancet Infect Dis. 2005;5:275–86. 2. Vandenesch F, Naimi T, Enright MC, Lina G, Nimmo GR, Heffernan H, et al. Community-acquired methicillin-resistant Staphylococcus aureus carrying Panton–Valentine leukocidin genes: worldwide emergence. Emerg Infect Dis. 2003;9:978–84. 3. Yamamoto T, Nishiyama A, Takano T, Yabe S, Higuchi W, Razvina O, et al. Community-acquired methicillin-resistant Staphylococcus aureus: community transmission, pathogenesis, and drug resistance. J Infect Chemother 2010. doi:10.1007/ s10156-010-0045-9. 4. Hayani KC, Mathew R, Oyedele T, Hulten KG. Neonatal necrotizing fasciitis due to community-acquired methicillin resistant Staphylococcus aureus. Pediatr Infect Dis J. 2008;27:480–1. 5. Centers for Disease Control and Prevention. Four pediatric deaths from community-acquired methicillin-resistant Staphylococcus aureus—Minnesota and North Dakota, 1997–1999. MMWR Morb Mortal Wkly Rep. 1999;48:707–10. 6. Labandeira-Rey M, Couzon F, Boisset S, Brown EL, Bes M, Benito Y, et al. Staphylococcus aureus Panton–Valentine leukocidin causes necrotizing pneumonia. Science. 2007;315:1130–3. 7. Moran GJ, Krishnadasan A, Gorwitz RJ, Fosheim GE, McDougal LK, Carey RB, et al. Methicillin-resistant S. aureus infections among patients in the emergency department. N Engl J Med. 2006;355:666–74. 8. Tenover FC, McDougal LK, Goering RV, Killgore G, Projan SJ, Patel JB, et al. Characterization of a strain of community-associated methicillin-resistant Staphylococcus aureus widely disseminated in the United States. J Clin Microbiol. 2006;44:108–18. 9. Tenover FC, Goering RV. Methicillin-resistant Staphylococcus aureus strain USA300: origin and epidemiology. J Antimicrob Chemother. 2009;64:441–6. 10. Diep BA, Gill SR, Chang RF, Phan TH, Chen JH, Davidson MG, et al. Complete genome sequence of USA300, an epidemic clone of community-acquired methicillin-resistant Staphylococcus aureus. Lancet. 2006;367:731–9. 11. Shibuya Y, Hara M, Higuchi W, Takano T, Iwao Y, Yamamoto T. Emergence of the community-acquired methicillin-resistant Staphylococcus aureus USA300 clone in Japan. J Infect Chemother. 2008;14:439–41. 12. Higuchi W, Mimura S, Kurosawa Y, Takano T, Iwao Y, Yabe S, et al. Emergence of the community-acquired methicillin-resistant Staphylococcus aureus USA300 clone in a Japanese child, demonstrating multiple divergent strains in Japan. J Infect Chemother 2010. doi:10.1007/s10156-010-0051-y. 13. Clinical and Laboratory Standards Institute. Performance standard for antimicrobial susceptibility testing; 18th informational supplement, vol. 28, no. 1, M100-S18. Wayne, PA: Clinical and Laboratory Standards Institute; 2008. 14. Dominguez TJ. It’s not a spider bite, it’s community-acquired methicillin-resistant Staphylococcus aureus. J Am Board Fam Pract. 2004;17:220–6.
NOTE
Spread of the community-acquired methicillin-resistant Staphylococcus aureus USA300 clone among family members in Japan Shizuka Yabe • Tomomi Takano • Wataru Higuchi Shigenao Mimura • Yoshihiro Kurosawa • Tatsuo Yamamoto
•
Received: 31 March 2010 / Accepted: 12 June 2010 / Published online: 14 July 2010 Ó Japanese Society of Chemotherapy and The Japanese Association for Infectious Diseases 2010
Abstract The USA300 clone is a highly-virulent community-acquired methicillin-resistant Staphylococcus aureus, which has been predominant in the United States. In a previous study, we isolated the USA300 clone from an 11-month-old Japanese girl, who lived in Saitama (Japan), and suffered from cellulitis and sepsis, and subsequently osteomyelitis, in 2008. In this study, we searched for the source of such USA300 infection in three related families (the patient’s grandfather and grandmother, having a USA300-infected daughter [F2D], and a mother [F3M] who was a sister of F2D’s mother). In January, 2008, F3M and her family members visited Hawaii and were treated in a hospital for gastroenteritis (with diarrhea) with an intravenous drip for F3M. After their return to Japan in January, F3M suffered from unusually frequent (more than 10 times) skin soft-tissue infections (SSTIs) until successful chemotherapy in July in Saitama. In the same summer season, SSTI was observed in 7 of 11 family members (63.6%). This dense spread of SSTI was followed by cellulitis and sepsis (USA300-isolated case) in October and subsequent osteomyelitis in December in F2D. After successful chemotherapy for the patient (F2D), no new SSTI cases were observed among the family members, and no USA300 colonization was observed when examined in December, 2009. The data suggest the first spread of the USA300 clone in Japan with related families at the core
S. Yabe T. Takano W. Higuchi T. Yamamoto (&) Division of Bacteriology, Department of Infectious Disease Control and International Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan e-mail: [email protected] S. Mimura Y. Kurosawa Ageo Central General Hospital, Saitama, Japan
123
and that such USA300 spread in the community is likely to have occurred in the summer season in Japan. Keywords Community-acquired methicillin-resistant S. aureus (CA-MRSA) USA300 clone Family Transmission
Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is a new class of MRSA, which can persist in the community, in contrast with previous MRSA (called hospital-acquired MRSA, HA-MRSA) mainly spreading in hospitals [1–3]. CA-MRSA spreads among otherwise healthy children or adolescents, for example athletes, through skin-to-skin contact, and is primarily associated with skin soft tissue infection (SSTI), including pyrogenic skin infection [1–3]. It is also associated with severe systemic infections, for example sepsis, necrotizing pneumonia, necrotizing fasciitis, and osteomyelitis [1, 3–5]. CA-MRSA often produces Panton–Valentine leukocidin (PVL) [1–3, 6]. Although CA-MRSA is genetically heterogenous, the USA300 clone is currently the most prominent clone in the United States; for instance, the USA300 clone accounts for the vast majority (97%) of MRSA infections among patients in emergency departments [7]. The USA300 clone is highly transmissible and highly virulent, becoming multiple drug-resistant, and behaving like HA-MRSA [8]. Moreover, it is growing as a global clone [9]. The USA300 clone belongs to multilocus sequence type (ST) 8, exhibits spa1 (or t008) and SCCmecIVa, is positive for PVL, and carries the arginine catabolic mobile element (ACME) [10]. In Japan, the USA300 clone (with genotype ST8/ spa985[t711]/SCCmecIVa; strain NN36) was isolated from a 3-month-old Indian girl who was born in a hospital in South Alameda (CA, USA) and stayed there for 1 month,
J Infect Chemother (2010) 16:372–374
373
transiently stayed in Tokyo, and suffered from temporal and cervical subcutaneous abscesses in 2007 [11]. The parents had no history of SSTI and no MRSA colonization, indicating that the USA300 strain originated, most probably, in a hospital in California. The second USA300 infection case occurred in 2008. In this case, the USA300 clone (with genotype ST8/spa363 [t024]/SCCmecIVa; strain NN47) was isolated from the blood of an 11-month-old Japanese girl who lived in Saitama, suffered from cellulitis of the lower thigh and sepsis, and subsequently suffered from osteomyelitis [12]. Because the patient and her family members had never been abroad and did not have contact with foreigners, and moreover, there were no reported Japanese USA300 infection cases in Japan at that time, in this study we searched for the source of infection in her family members. All protocols of this study were approved by the ethics review board of Niigata University School of Medicine, Niigata, Japan, and before sampling from children consent was obtained from their parents. Diagnosis of SSTIs in family members, who had not consulted with a doctor in hospital, were done by interview at their homes, by showing photographs of SSTIs including abscesses. Screening of MRSA colonization in the members of related families was performed in December, 2009. For this, the
nares, cheeks, axilla, and inguinal area were examined for MRSA by using swabs. S. aureus was examined for the mecA gene, PVL gene, and ACME by PCR for confirmation of the USA300 clone, as described previously [12]. Susceptibility testing of MRSA strain NN47 was carried out using the agar dilution method with Mueller–Hinton agar, according to previous procedures [13]. The family pedigree of the patient is shown in Fig. 1; the patient (from whom the USA300 clone [strain NN47] was isolated, as described above) was a daughter in family 2 (F2D). The three related families included 11 members (0–52 years old) and all family members lived in Saitama. The mother (M) in family 3 (F3M), together with her three family members (father [F3F] and two daughters [F3D1] and [F3D2]), had visited Hawaii in January, 2008. F3M and F3D1 developed gastroenteritis (with diarrhea) there and were treated in a hospital with peripheral drip intravenous infusion for F3M. They returned to Japan (Saitama) in January, 2008. After their return, F3M suffered from unusually frequent (more than 10 times) recurrent and multifocal SSTIs (including flaring and swelling, and abscesses) of the upper thigh and gluteal regions until July. F3M was diagnosed with impetigo (or insect bites just like spider bites reported in the United States [14]) at a hospital on July 1. Cefdinir (CFDN, a third-generation cephem) at
Family 1
Mother 52 years
Father 52 years
Aug. -Sep., 2008: SSTI of thigh Family 2
Family 3
F3M Mother 26 years Aug. -Sep., 2008: SSTI of thigh
Father 40 years Aug. -Sep., 2008: SSTI of thigh
Mother 23 years Feb. -Jul., 2008: Frequent (recurrent) SSTIs of thigh and gluteal regions
Father 22 years Jul., 2008: SSTI of thigh
F2D Daughter 2 years (11 months in 2008)
Son 5 years
Aug. -Sep., 2008: SSTI of thigh Oct., 2008: Cellulitis of thigh (MRSA*) Dec., 2008: Osteomyelitis of tibial region
Fig. 1 Family pedigree and SSTI of the family members. Closed symbols represent family members who suffered from SSTI, including flaring and swelling (cellulitis), and abscesses in the thigh and gluteal regions. The series of SSTI started when the mother (M) in family 3 (F3M), who had visited Hawaii (in January, 2008), was treated there for gastroenteritis, with an intravenous drip, and suffered from frequent SSTI (February through July) after her return to Japan in January. A daughter (D) in family 2 (F2D) was admitted to a hospital
Daughter 1 4 years
Daughter 2 2 years
Daughter 3 0 years
Jul., 2008: SSTI of thigh
for treatment of cellulitis and sepsis in October; MRSA (USA300), marked with an asterisk in the figure, was isolated from the blood. F2D was also admitted to a hospital for treatment of osteomyelitis in December. All family members were negative for MRSA colonization when examined in December, 2009. The age of the family members is as of December, 2009 (that in 2008 is shown in parentheses)
123
374
100 mg was orally administered three times a day for 7 days. During this time (July 3), it was confirmed that the flaring and swelling were relieved in hospital. However, other family members also suffered from SSTI shortly after F3M. Episodes of SSTIs (July through September) are summarized in Fig. 1. SSTIs included flaring, swelling, and abscesses of the upper thigh. In the series of SSTIs, which started with F3M and spread among the family members, 7 out of 11 members (63.6%) developed SSTI. F2D was also included in this series of SSTIs and suffered from flaring and swelling of the upper thigh in August and September. No family members had experienced frequent SSTIs or a large abscess before 2008. On October 21, F2D (11 months at that time) was admitted to another hospital with fever, and flaring and swelling of the left lower thigh. She was diagnosed with cellulitis and sepsis; USA300 (strain NN47) was isolated from the blood [12]. After successful treatment with cefazolin (CEZ) and vancomycin (VCM), she was discharged on November 7; however, on December 17, she was again admitted to a hospital with recurrent lower thigh swelling. Osteomyelitis involving the entire left tibial region was observed and she was successfully treated with teicoplanin (TEIC) and linezolid (LZD) [12]. She was discharged on January 28, 2009. The MIC values (lg/ml) of CEZ, CFDN, VCM, TEIC, and LZD for USA300 strain NN47 were 2, 2, 1, 0.5, and 2, respectively. In other family members (except F2D), no new cases of SSTI were observed after September, 2008. Members of the three families (shown in Fig. 1) were screened for MRSA colonization in December, 2009; however, no MRSA was isolated from the nares, cheeks, axilla, and inguinal area in any individual. Therefore, USA300 strain NN47 (isolated from a Japanese infant, F2D) could have originated in the United States (most probably in a hospital in Hawaii), and F3M (who was treated in Hawaii with an intravenous drip) could be the source of infection among the family members (including F2D). This study provides supporting evidence of the first spread of the USA300 clone in the community (among family members) in Japan with the hypothesis that such USA300 spread in the community is likely to have occurred in the summer season in Japan, like bullous impetigo. The families in this study had infants and frequently got together on New Year’s Day or other holidays; therefore, it is highly possible that the USA300 clone had been transmitted among family members through close body contact (such as hugs and kisses to infants). It is not known whether the USA300 clone had also spread to people unrelated to these families. Finally, it should be noted that MRSA was actually isolated only from F2D and not from other family members; therefore, USA300 spread
123
J Infect Chemother (2010) 16:372–374
is a possibility based on the SSTI information of family members and is not proved directly by MRSA isolation and characterization. Surveillance of the USA300 clone is needed in Japan.
References 1. Zetola N, Francis JS, Nuermberger EL, Bishai WR. Communityacquired methicillin-resistant Staphylococcus aureus: an emerging threat. Lancet Infect Dis. 2005;5:275–86. 2. Vandenesch F, Naimi T, Enright MC, Lina G, Nimmo GR, Heffernan H, et al. Community-acquired methicillin-resistant Staphylococcus aureus carrying Panton–Valentine leukocidin genes: worldwide emergence. Emerg Infect Dis. 2003;9:978–84. 3. Yamamoto T, Nishiyama A, Takano T, Yabe S, Higuchi W, Razvina O, et al. Community-acquired methicillin-resistant Staphylococcus aureus: community transmission, pathogenesis, and drug resistance. J Infect Chemother 2010. doi:10.1007/ s10156-010-0045-9. 4. Hayani KC, Mathew R, Oyedele T, Hulten KG. Neonatal necrotizing fasciitis due to community-acquired methicillin resistant Staphylococcus aureus. Pediatr Infect Dis J. 2008;27:480–1. 5. Centers for Disease Control and Prevention. Four pediatric deaths from community-acquired methicillin-resistant Staphylococcus aureus—Minnesota and North Dakota, 1997–1999. MMWR Morb Mortal Wkly Rep. 1999;48:707–10. 6. Labandeira-Rey M, Couzon F, Boisset S, Brown EL, Bes M, Benito Y, et al. Staphylococcus aureus Panton–Valentine leukocidin causes necrotizing pneumonia. Science. 2007;315:1130–3. 7. Moran GJ, Krishnadasan A, Gorwitz RJ, Fosheim GE, McDougal LK, Carey RB, et al. Methicillin-resistant S. aureus infections among patients in the emergency department. N Engl J Med. 2006;355:666–74. 8. Tenover FC, McDougal LK, Goering RV, Killgore G, Projan SJ, Patel JB, et al. Characterization of a strain of community-associated methicillin-resistant Staphylococcus aureus widely disseminated in the United States. J Clin Microbiol. 2006;44:108–18. 9. Tenover FC, Goering RV. Methicillin-resistant Staphylococcus aureus strain USA300: origin and epidemiology. J Antimicrob Chemother. 2009;64:441–6. 10. Diep BA, Gill SR, Chang RF, Phan TH, Chen JH, Davidson MG, et al. Complete genome sequence of USA300, an epidemic clone of community-acquired methicillin-resistant Staphylococcus aureus. Lancet. 2006;367:731–9. 11. Shibuya Y, Hara M, Higuchi W, Takano T, Iwao Y, Yamamoto T. Emergence of the community-acquired methicillin-resistant Staphylococcus aureus USA300 clone in Japan. J Infect Chemother. 2008;14:439–41. 12. Higuchi W, Mimura S, Kurosawa Y, Takano T, Iwao Y, Yabe S, et al. Emergence of the community-acquired methicillin-resistant Staphylococcus aureus USA300 clone in a Japanese child, demonstrating multiple divergent strains in Japan. J Infect Chemother 2010. doi:10.1007/s10156-010-0051-y. 13. Clinical and Laboratory Standards Institute. Performance standard for antimicrobial susceptibility testing; 18th informational supplement, vol. 28, no. 1, M100-S18. Wayne, PA: Clinical and Laboratory Standards Institute; 2008. 14. Dominguez TJ. It’s not a spider bite, it’s community-acquired methicillin-resistant Staphylococcus aureus. J Am Board Fam Pract. 2004;17:220–6.