title: A comparison of virulence patterns and in vivo fitness between hospital- and community-acquired methicillin-resistant Staphylococcus aureus related to the USA400 clone.
abstract: Methicillin-resistant Staphylococcus aureus (MRSA) isolates genetically related to the CA-MRSA clone MW2/USA400 (ST1-SCCmecIV lineage) from the United States have emerged in hospitals in Rio de Janeiro and are associated with nosocomial bloodstream infections. To understand the virulence mechanisms involved in the adaptability of ST1 isolates as a hospital pathogen in Rio de Janeiro, we compared the virulence traits and fitness properties of the Brazilian isolates with those displayed by the CA-MRSA isolates from the United States. Similar to the USA400 from the United States, all the Brazilian isolates tested carried the genes encoding SEH and LukDE. In contrast, none of the Brazilian isolates carried the lukSF PVL, sea, sec, and sek genes. Competition experiments in mice demonstrated a significant increase in the fitness for the CA-MRSA isolates MW2 and USA400-0051 from the United States compared to other isolates. In the foreign body animal model, 83 % more North-American bacterial cells were recovered compared to the Brazilian ST1 isolates. Differences in gene expression of important virulence factors were detected. Transcription of rnaIII and psmα3 was increased about two-fold in the isolates from the United States, and sasG about two-fold in the Brazilian isolates. Thus, it is possible that the virulence attenuation observed among the Brazilian hospital isolates, associated with the acquisition of multiple resistant determinants, are consequences of microevolutionary events that contributed to the necessary fitness adjustment of this lineage, allowing a typically community-acquired MRSA (MW2/USA400) to emerge as a successful hospital pathogen (Brazilian ST1-SCCmecIV).
authors.affiliation: Departamento de Microbiologia Médica, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
authors.forename: M A
authors.initials: MA
authors.lastname: Guimarães
authors.forename: M S
authors.initials: MS
authors.lastname: Ramundo
authors.forename: M A
authors.initials: MA
authors.lastname: Américo
authors.forename: M C
authors.initials: MC
authors.lastname: de Mattos
authors.forename: R R
authors.initials: RR
authors.lastname: Souza
authors.forename: E S
authors.initials: ES
authors.lastname: Ramos-Júnior
authors.forename: L R
authors.initials: LR
authors.lastname: Coelho
authors.forename: A
authors.initials: A
authors.lastname: Morrot
authors.forename: P A
authors.initials: PA
authors.lastname: Melo
authors.forename: S E L
authors.initials: SE
authors.lastname: Fracalanzza
authors.forename: F A
authors.initials: FA
authors.lastname: Ferreira
authors.forename: A M S
authors.initials: AM
authors.lastname: Figueiredo
mesh_terms: D000818:Animals; D005075:Biological Evolution; D001938:Brazil; D017714:Community-Acquired Infections / Q000382:microbiology*; D003428:Cross Infection / Q000382:microbiology*; D004195:Disease Models, Animal; D005260:Female; D020869:Gene Expression Profiling; D005798:Genes, Bacterial; D005838:Genotype; D006801:Humans; D055624:Methicillin-Resistant Staphylococcus aureus / Q000235:genetics* / Q000254:growth & development / Q000302:isolation & purification / Q000502:physiology*; D051379:Mice; D013203:Staphylococcal Infections / Q000382:microbiology*; D014481:United States; D014774:Virulence; D037521:Virulence Factors / Q000235:genetics*
chemical_list: D037521:Virulence Factors