title: Virulence genes and genotypic associations in nasal carriage, community-associated methicillin-susceptible and methicillin-resistant USA400 Staphylococcus aureus isolates.
abstract: It is not well understood why strains of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA), a major cause of skin and soft tissue infections, became successful so quickly, overtaking the place of methicillin-sensitive S. aureus (MSSA) in many communities. To evaluate the genetic basis of differences in their virulence traits, 293 S. aureus isolates consisting of three cohorts, genotypically defined clinical CA-MRSA (n = 77), clinical MSSA (n = 103), and nasal carriage MSSA (n = 113), collected over a 19-year period in two Midwestern states in the United States, were (i) extensively genotyped and (ii) screened for 40 known virulence genes which included those for enterotoxins, leukocidins, hemolysins, and surface proteins and several newly identified putative toxin genes from the USA400 lineage of CA-MRSA. Genotypically, nasal carriage and clinical MSSA isolates were much more diverse than was the CA-MRSA group, which was found to be of USA400 lineage only. Virulence gene profiles of the three groups showed that CA-MRSA strains harbored significantly higher percentages (≥95%; P value, <0.05) of the sea, sec, sec4, seg2, seh, sek, sel, sel2, ear, ssl1, lpl10, lukSF-PV, lukD, lukE, and clfA genes than did the carriage and the clinical MSSA group (range, 0% to 58%). Genes of the enterotoxin gene cluster, seg, sei, sem, sen, and seo, were present in the clinical and carriage isolates but not in the CA-MRSA group. These results suggest that the presence of additional virulence factors in USA400 CA-MRSA strains compared to the nasal carriage and clinical MSSA strains probably contributed to their enhanced virulence.
authors.affiliation: Molecular Microbiology Laboratory, Marshfield Clinic Research Foundation, Marshfield, WI 54449, USA. shukla.sanjay@mcrf.mfldclin.edu
authors.forename: Sanjay K
authors.initials: SK
authors.lastname: Shukla
authors.forename: Mary E
authors.initials: ME
authors.lastname: Karow
authors.forename: Jennifer M
authors.initials: JM
authors.lastname: Brady
authors.forename: Mary E
authors.initials: ME
authors.lastname: Stemper
authors.forename: Jennifer
authors.initials: J
authors.lastname: Kislow
authors.forename: Natalie
authors.initials: N
authors.lastname: Moore
authors.forename: Katherine
authors.initials: K
authors.lastname: Wroblewski
authors.forename: Po-Huang
authors.initials: PH
authors.lastname: Chyou
authors.forename: David M
authors.initials: DM
authors.lastname: Warshauer
authors.forename: Kurt D
authors.initials: KD
authors.lastname: Reed
authors.forename: Ruth
authors.initials: R
authors.lastname: Lynfield
authors.forename: William R
authors.initials: WR
authors.lastname: Schwan
mesh_terms: D002353:Carrier State / Q000382:microbiology*; D017714:Community-Acquired Infections / Q000382:microbiology*; D004269:DNA, Bacterial / Q000235:genetics; D005838:Genotype; D006801:Humans; D016106:Methicillin Resistance; D009297:Nasal Mucosa / Q000382:microbiology; D016133:Polymerase Chain Reaction; D013203:Staphylococcal Infections / Q000382:microbiology*; D013211:Staphylococcus aureus / Q000235:genetics* / Q000302:isolation & purification; D014481:United States; D037521:Virulence Factors / Q000235:genetics*
chemical_list: D004269:DNA, Bacterial; D037521:Virulence Factors