Paul J Planet1, Lorena Diaz2, Sergios-Orestis Kolokotronis3, Apurva Narechania4, Jinnethe Reyes2, Galen Xing5, Sandra Rincon2, Hannah Smith5, Diana Panesso6, Chanelle Ryan5, Dylan P Smith2, Manuel Guzman7, Jeannete Zurita8, Robert Sebra9, Gintaras Deikus9, Rathel L Nolan10, Fred C Tenover11, George M Weinstock12, D Ashley Robinson13, Cesar A Arias14. 1. Division of Pediatric Infectious Diseases, Department of Pediatrics, Columbia University, College of Physicians and Surgeons Sackler Institute for Comparative Genomics, American Museum of Natural History. 2. Molecular Genetics and Antimicrobial Resistance Unit, International Center for Microbial Genomics, Universidad El Bosque, Bogotá, Colombia. 3. Sackler Institute for Comparative Genomics, American Museum of Natural History Department of Biological Sciences, Fordham University, Bronx, New York. 4. Sackler Institute for Comparative Genomics, American Museum of Natural History. 5. Division of Pediatric Infectious Diseases, Department of Pediatrics, Columbia University, College of Physicians and Surgeons. 6. Division of Infectious Diseases, Department of Internal Medicine Molecular Genetics and Antimicrobial Resistance Unit, International Center for Microbial Genomics, Universidad El Bosque, Bogotá, Colombia. 7. Centro Médico Caracas, Venezuela. 8. Hospital Vozandes, Pontificia Universidad Catolica, Quito, Ecuador. 9. Genome Center, Mount Sinai Hospital, New York City. 10. Division of Infectious Diseases, Department of Internal Medicine. 11. Cepheid, Sunnyvale, California. 12. The Jackson Laboratory for Genomic Medicine, Farmington, Connecticut. 13. Division of Infectious Diseases, Department of Microbiology, University of Mississippi Medical Center, Jackson. 14. Division of Infectious Diseases, Department of Internal Medicine Department of Microbiology and Molecular Genetics, University of Texas Medical School at Houston Molecular Genetics and Antimicrobial Resistance Unit, International Center for Microbial Genomics, Universidad El Bosque, Bogotá, Colombia.
Abstract
BACKGROUND: The community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) epidemic in the United States is attributed to the spread of the USA300 clone. An epidemic of CA-MRSA closely related to USA300 has occurred in northern South America (USA300 Latin-American variant, USA300-LV). Using phylogenomic analysis, we aimed to understand the relationships between these 2 epidemics. METHODS: We sequenced the genomes of 51 MRSA clinical isolates collected between 1999 and 2012 from the United States, Colombia, Venezuela, and Ecuador. Phylogenetic analysis was used to infer the relationships and times since the divergence of the major clades. RESULTS: Phylogenetic analyses revealed 2 dominant clades that segregated by geographical region, had a putative common ancestor in 1975, and originated in 1989, in North America, and in 1985, in South America. Emergence of these parallel epidemics coincides with the independent acquisition of the arginine catabolic mobile element (ACME) in North American isolates and a novel copper and mercury resistance (COMER) mobile element in South American isolates. CONCLUSIONS: Our results reveal the existence of 2 parallel USA300 epidemics that shared a recent common ancestor. The simultaneous rapid dissemination of these 2 epidemic clades suggests the presence of shared, potentially convergent adaptations that enhance fitness and ability to spread.
BACKGROUND: The community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) epidemic in the United States is attributed to the spread of the USA300 clone. An epidemic of CA-MRSA closely related to USA300 has occurred in northern South America (USA300 Latin-American variant, USA300-LV). Using phylogenomic analysis, we aimed to understand the relationships between these 2 epidemics. METHODS: We sequenced the genomes of 51 MRSA clinical isolates collected between 1999 and 2012 from the United States, Colombia, Venezuela, and Ecuador. Phylogenetic analysis was used to infer the relationships and times since the divergence of the major clades. RESULTS: Phylogenetic analyses revealed 2 dominant clades that segregated by geographical region, had a putative common ancestor in 1975, and originated in 1989, in North America, and in 1985, in South America. Emergence of these parallel epidemics coincides with the independent acquisition of the arginine catabolic mobile element (ACME) in North American isolates and a novel copper and mercury resistance (COMER) mobile element in South American isolates. CONCLUSIONS: Our results reveal the existence of 2 parallel USA300 epidemics that shared a recent common ancestor. The simultaneous rapid dissemination of these 2 epidemic clades suggests the presence of shared, potentially convergent adaptations that enhance fitness and ability to spread.
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