RESUMO
The increasing production of goat milk and its derivatives is affected by the occurrence of intramammary infections, which are highly associated with the presence of Staphylococcus species, including some with zoonotic potential. Staphylococci in general can exchange mobile genetic elements, a process that may be facilitated by the isolate's capacity of forming biofilms. In this study we identified, to the species level, Staphylococcus isolated from goat milk samples by MALDI-TOF and confirmed the identification by sequencing housekeeping genes (rrs and tuf). Eight species were identified, more than half being either Staphylococcus epidermidis or Staphylococcus lugdunensis. The isolates were shown by pulsed-field gel electrophoresis to be genetically diverse between the studied herds. Resistance to ampicillin and penicillin was widespread, and 2 Staph. epidermidis isolates contained the methicillin-resistance gene mecA. Most of the isolates that were resistant to at least 1 of the 13 antimicrobials tested harbored plasmids, one of which was demonstrated to be conjugative, being transferred from a Staph. epidermidis to a Staphylococcus aureus strain. Biofilm formation was observed in almost every isolate, which may contribute to their capacity of exchanging antimicrobial resistance genes in addition to acting as a physical barrier to the access of drugs. Our results showed that antimicrobial resistance among goat staphylococci may be emerging in a process facilitated by the exchange of mobile genetic elements between the bacteria and the establishment of biofilms, which calls for careful monitoring and more effective control therapies.
Assuntos
Antibacterianos/farmacologia , Farmacorresistência Bacteriana/genética , Doenças das Cabras/microbiologia , Leite/microbiologia , Infecções Estafilocócicas/veterinária , Staphylococcus/genética , Ampicilina/farmacologia , Animais , Indústria de Laticínios , Feminino , Transferência Genética Horizontal , Cabras , Penicilina G/farmacologia , Infecções Estafilocócicas/microbiologia , Staphylococcus/efeitos dos fármacos , Staphylococcus lugdunensis/efeitos dos fármacos , Staphylococcus lugdunensis/genéticaRESUMO
Staphylococcus lugdunensis is an unusually virulent coagulase-negative species, which causes serious infection similar to S. aureus. We evaluated the expression of virulence factors such as S. lugdunensis synergistic haemolysin (SLUSH), fibrinogen-binding protein (Fbl), biofilm production and biofilm-production-related genes in 23 S. lugdunensis clinical isolates and one type strain that had been previously characterized for their genotypes. In addition, the biofilm composition and the ability of isolates to adhere to and invade human epithelial lung cells were also investigated. The PCR method used detected the presence of slush and intercellular adhesin (ica) virulence genes in all isolates. All isolates produced the Fbl protein and, with the exception of the type strain, all isolates produced the SLUSH haemolysin. Fourteen (60.9â%) isolates produced biofilms. The detachment assay, using sodium metaperiodate or proteolytic enzymes to analyse the biofilm composition, showed protein-mediated biofilms in two representative isolates, one for each colony type (rough and smooth). All strongly biofilm-producing isolates, including three with rough colony morphology, had the same prevalent PFGE pattern. However, among the representative strains tested, only the S. lugdunensis isolate that formed rough colonies was able to adhere to and invade A549 cell monolayers in the same quantities as those observed with S. aureus isolates (Pâ=â1.000). No significant adhesion or invasion was observed for the other isolates in comparison with the S. aureus isolate, independent of biofilm production or clonality. Our results could explain the incredible ability of this pathogen to cause infections that are as aggressive as S. aureus. In addition, the ability of S. lugdunensis to adhere to and invade eukaryotic cells was also noticed for isolates with rough colony morphology, reinforcing the increased virulence in this species.
Assuntos
Aderência Bacteriana/fisiologia , Células Epiteliais/microbiologia , Mucosa Respiratória/citologia , Staphylococcus lugdunensis/citologia , Staphylococcus lugdunensis/genética , Aderência Bacteriana/genética , Proteínas de Bactérias/genética , Proteínas de Bactérias/metabolismo , Biofilmes , Brasil/epidemiologia , Linhagem Celular Tumoral , Regulação Bacteriana da Expressão Gênica/fisiologia , Humanos , Pulmão/citologia , Infecções Estafilocócicas/epidemiologia , Infecções Estafilocócicas/microbiologia , Staphylococcus lugdunensis/fisiologiaRESUMO
Staphylococcus lugdunensis is a rare cause of severe infections and clinical manifestations are similar to those related to S. aureus infection. We describe a hospital-acquired bacteremia due to methicillin-resistant Staphylococcus lugdunensis, misidentified as methicillin-resistant S. aureus. The oxacillin MIC was 16 µg/mL and the mecA gene and SCCmec type V were determined by PCR. Although treatment had been appropriated, the patient died after rapid progressive respiratory failure and another nosocomial sepsis. It is important not only to identify S. lugdunensis in view of its clinical course, but also to determine its susceptibility to oxacillin by detecting the mecA gene or its product.
Assuntos
Bacteriemia/microbiologia , Infecção Hospitalar/microbiologia , Resistência a Meticilina/genética , Infecções Estafilocócicas/microbiologia , Staphylococcus lugdunensis/genética , Idoso , Antibacterianos/farmacologia , Bacteriemia/diagnóstico , Proteínas de Bactérias/genética , Infecção Hospitalar/diagnóstico , Feminino , Humanos , Resistência a Meticilina/efeitos dos fármacos , Staphylococcus aureus Resistente à Meticilina , Oxacilina/farmacologia , Infecções Estafilocócicas/diagnóstico , Staphylococcus lugdunensis/efeitos dos fármacosRESUMO
Staphylococcus lugdunensis is a rare cause of severe infections and clinical manifestations are similar to those related to S. aureus infection. We describe a hospital-acquired bacteremia due to methicillin-resistant Staphylococcus lugdunensis, misidentified as methicillin-resistant S. aureus. The oxacillin MIC was 16 µg/mL and the mecA gene and SCCmec type V were determined by PCR. Although treatment had been appropriated, the patient died after rapid progressive respiratory failure and another nosocomial sepsis. It is important not only to identify S. lugdunensis in view of its clinical course, but also to determine its susceptibility to oxacillin by detecting the mecA gene or its product.