Insights on evolution of virulence and resistance from the complete genome analysis of an early methicillin-resistant Staphylococcus aureus strain and a biofilm-producing methicillin-resistant Staphylococcus epidermidis strain.

@article{citeulike:2465188, abstract = {Staphylococcus aureus is an opportunistic pathogen and the major causative agent of numerous hospital- and community-acquired infections. Staphylococcus epidermidis has emerged as a causative agent of infections often associated with implanted medical devices. We have sequenced the approximately 2.8-Mb genome of S. aureus COL, an early methicillin-resistant isolate, and the approximately 2.6-Mb genome of S. epidermidis RP62a, a methicillin-resistant biofilm isolate. Comparative analysis of these and other staphylococcal genomes was used to explore the evolution of virulence and resistance between these two species. The S. aureus and S. epidermidis genomes are syntenic throughout their lengths and share a core set of 1,681 open reading frames. Genome islands in nonsyntenic regions are the primary source of variations in pathogenicity and resistance. Gene transfer between staphylococci and low-GC-content gram-positive bacteria appears to have shaped their virulence and resistance profiles. Integrated plasmids in S. epidermidis carry genes encoding resistance to cadmium and species-specific LPXTG surface proteins. A novel genome island encodes multiple phenol-soluble modulins, a potential S. epidermidis virulence factor. S. epidermidis contains the cap operon, encoding the polyglutamate capsule, a major virulence factor in Bacillus anthracis. Additional phenotypic differences are likely the result of single nucleotide polymorphisms, which are most numerous in cell envelope proteins. Overall differences in pathogenicity can be attributed to genome islands in S. aureus which encode enterotoxins, exotoxins, leukocidins, and leukotoxins not found in S. epidermidis.}, address = {Microbial Genomics, The Institute for Genomic Research, 9712 Medical Center Dr., Rockville, MD 20850, USA. srgill@tigr.org}, author = {Gill, S. R. and Fouts, D. E. and Archer, G. L. and Mongodin, E. F. and Deboy, R. T. and Ravel, J. and Paulsen, I. T. and Kolonay, J. F. and Brinkac, L. and Beanan, M. and Dodson, R. J. and Daugherty, S. C. and Madupu, R. and Angiuoli, S. V. and Durkin, A. S. and Haft, D. H. and Vamathevan, J. and Khouri, H. and Utterback, T. and Lee, C. and Dimitrov, G. and Jiang, L. and Qin, H. and Weidman, J. and Tran, K. and Kang, K. and Hance, I. R. and Nelson, K. E. and Fraser, C. M. }, citeulike-article-id = {2465188}, doi = {10.1128/JB.187.7.2426-2438.2005}, issn = {0021-9193}, journal = {J Bacteriol}, keywords = {staph}, month = {April}, number = {7}, pages = {2426--2438}, posted-at = {2008-03-04 15:54:00}, priority = {2}, title = {Insights on evolution of virulence and resistance from the complete genome analysis of an early methicillin-resistant Staphylococcus aureus strain and a biofilm-producing methicillin-resistant Staphylococcus epidermidis strain.}, url = {http://dx.doi.org/10.1128/JB.187.7.2426-2438.2005}, volume = {187}, year = {2005} }

TY - JOUR ID - citeulike:2465188 L3 - citeulike-article-id:2465188 TI - Insights on evolution of virulence and resistance from the complete genome analysis of an early methicillin-resistant Staphylococcus aureus strain and a biofilm-producing methicillin-resistant Staphylococcus epidermidis strain. JF - J Bacteriol VL - 187 IS - 7 SP - 2426 EP - 2438 AD - Microbial Genomics, The Institute for Genomic Research, 9712 Medical Center Dr., Rockville, MD 20850, USA. srgill@tigr.org SN - 0021-9193 N2 - Staphylococcus aureus is an opportunistic pathogen and the major causative agent of numerous hospital- and community-acquired infections. Staphylococcus epidermidis has emerged as a causative agent of infections often associated with implanted medical devices. We have sequenced the approximately 2.8-Mb genome of S. aureus COL, an early methicillin-resistant isolate, and the approximately 2.6-Mb genome of S. epidermidis RP62a, a methicillin-resistant biofilm isolate. Comparative analysis of these and other staphylococcal genomes was used to explore the evolution of virulence and resistance between these two species. The S. aureus and S. epidermidis genomes are syntenic throughout their lengths and share a core set of 1,681 open reading frames. Genome islands in nonsyntenic regions are the primary source of variations in pathogenicity and resistance. Gene transfer between staphylococci and low-GC-content gram-positive bacteria appears to have shaped their virulence and resistance profiles. Integrated plasmids in S. epidermidis carry genes encoding resistance to cadmium and species-specific LPXTG surface proteins. A novel genome island encodes multiple phenol-soluble modulins, a potential S. epidermidis virulence factor. S. epidermidis contains the cap operon, encoding the polyglutamate capsule, a major virulence factor in Bacillus anthracis. Additional phenotypic differences are likely the result of single nucleotide polymorphisms, which are most numerous in cell envelope proteins. Overall differences in pathogenicity can be attributed to genome islands in S. aureus which encode enterotoxins, exotoxins, leukocidins, and leukotoxins not found in S. epidermidis. KW - staph AU - Gill, SR AU - Fouts, DE AU - Archer, GL AU - Mongodin, EF AU - Deboy, RT AU - Ravel, J AU - Paulsen, IT AU - Kolonay, JF AU - Brinkac, L AU - Beanan, M AU - Dodson, RJ AU - Daugherty, SC AU - Madupu, R AU - Angiuoli, SV AU - Durkin, AS AU - Haft, DH AU - Vamathevan, J AU - Khouri, H AU - Utterback, T AU - Lee, C AU - Dimitrov, G AU - Jiang, L AU - Qin, H AU - Weidman, J AU - Tran, K AU - Kang, K AU - Hance, IR AU - Nelson, KE AU - Fraser, CM PY - 2005/04// UR - http://dx.doi.org/10.1128/JB.187.7.2426-2438.2005 ER -