Corynebacterium striatum is a potentially pathogenic microorganism that causes nosocomial outbreaks. However, little is known about its virulence factors that may contribute to healthcare-associated infections (HAIs). We investigated the biofilm production on abiotic surfaces of multidrug-resistant (MDR) and multidrug-susceptible (MDS) strains of C. striatum of pulsed-field gel electrophoresis types I-MDR, II-MDR, III-MDS and IV-MDS isolated during a nosocomial outbreak in Rio de Janeiro, Brazil. The results showed that C. striatum was able to adhere to hydrophilic and hydrophobic abiotic surfaces. The C. striatum 1987/I-MDR strain, predominantly isolated from patients undergoing endotracheal intubation procedures, showed the greatest ability to adhere to all surfaces. C. striatum bound fibrinogen to its surface, which contributed to biofilm formation. Scanning electron microscopy showed the production of mature biofilms on polyurethane catheters by all pulsotypes. In conclusion, biofilm production may contribute to the establishment of HAIs caused by C. striatum.

Background Corynebacterium striatum is an emerging multidrug-resistant (MDR) pathogen associated with immunocompromised and chronically ill patients, as well as nosocomial outbreaks. In this study, we characterized 23 MDR C. striatum isolated of bloodstream and catheter-related infections from a hospital of Rio de Janeiro. Methods C. striatum isolates were identified by 16S rRNA and rpoB genes sequencing. The dissemination of these isolates was accomplished by pulsed-field gel electrophoresis (PFGE). All isolates were submitted to antimicrobial susceptibility testing by disk diffusion and by minimum inhibitory concentration using E-test strips methods. Antimicrobial resistance genes were detected by polymerase chain reaction. Quantitative tests were performed on four different abiotic surfaces and the ability to produce biofilm on the surface of polyurethane and silicone catheter was also demonstrated by scanning electron microscopy. Results Eleven PFGE profiles were found. The PFGE profile I was the most frequently observed among isolates. Five different MDR profiles were found and all PFGE profile I isolates presented susceptibility only to tetracycline, vancomycin, linezolid and daptomycin. Only the multidrug-susceptible isolate did not show mutations in the quinolone-resistance determinant region (QRDR) of the gyrA gene and was negative in the search of genes encoding antibiotic resistance. The other 22 isolates were positive to resistance genes to aminoglycoside, macrolides/lincosamides and chloramphenicol and showed mutations in the QRDR of the gyrA gene. Scanning electron microscopy illustrated the ability of MDR blood isolate partaker of the epidemic clone (PFGE profile I) to produce mature biofilm on the surface of polyurethane and silicone catheter. Conclusions Genotyping analysis by PFGE revealed the permanence of the MDR PFGE profile I in the nosocomial environment. Other new PFGE profiles emerged as etiologic agents of invasive infections. However, the MDR PFGE profile I was also found predominant among patients with hematogenic infections. The high level of multidrug resistance associated with biofilm formation capacity observed in MDR C. striatum is a case of concern. Electronic supplementary material The online version of this article (10.1186/s12879-019-4294-7) contains supplementary material, which is available to authorized users.

Staphylococcus haemolyticus is the most common organism among clinical isolatesof methicillin-resistant staphylococci. Aim: This study evaluated the ability to produce biofilm with the presence of the antibiotics (1/4 minimum inhibitory concentrations) of S. haemolyticus strains isolated from blood culture. Methods: Clonal distribution was assessed in pulsed-field gel electrophoresis. PCR assays were performed to detect mecA, icaA, aap, atlE, atl, fbp genes. S. haemolyticus strains grown in the presence of the antibiotics were investigated for biofilm formation on glass, polystyrene and catheter surfaces. Results: Biofilm formation was independent of the presence of the icaA and mecA genes, pulsed-field gel electrophoresis type. Vancomycin, oxacillin, moxifloxacin, rifampicin, teicoplanin, tigecycline and linezolid did not inhibit biofilm formation on abiotic surfaces. Conclusion: This study demonstrated that the biofilm formation process is complex and may not be related to ica gene carriage. Furthermore, in this study the biofilm formation was increased in the presence of antimicrobial agents.

Biofilm-related infections are considered a major cause of morbidity and mortality in hospital environments. Biofilms allow microorganisms to exchange genetic material and to become persistent colonizers and/or multiresistant to antibiotics. Corynebacterium pseudodiphtheriticum (CPS), a commensal bacterium that colonizes skin and mucosal sites has become progressively multiresistant and responsible for severe nosocomial infections. However, virulence factors of this emergent pathogen remain unclear. Herein, we report the adhesive properties and biofilm formation on hydrophilic (glass) and hydrophobic (plastic) abiotic surfaces by CPS strains isolated from patients with localized (ATCC10700/Pharyngitis) and systemic (HHC1507/Bacteremia) infections. Adherence to polystyrene attributed to hydrophobic interactions between bacterial cells and this negatively charged surface indicated the involvement of cell surface hydrophobicity in the initial stage of biofilm formation. Attached microorganisms multiplied and formed microcolonies that accumulated as multilayered cell clusters, a step that involved intercellular adhesion and synthesis of extracellular matrix molecules. Further growth led to the formation of dense bacterial aggregates embedded in the exopolymeric matrix surrounded by voids, typical of mature biofilms. Data also showed CPS recognizing human fibrinogen (Fbg) and fibronectin (Fn) and involvement of these sera components in formation of "conditioning films". These findings suggested that biofilm formation may be associated with the expression of different adhesins. CPS may form biofilms in vivo possibly by an adherent biofilm mode of growth in vitro currently demonstrated on hydrophilic and hydrophobic abiotic surfaces. The affinity to Fbg and Fn and the biofilm-forming ability may contribute to the establishment and dissemination of infection caused by CPS.