Coagulase-negative Staphylococcus (CNS) strains are frequently associated with bacteremia and hospital-acquired infections, particularly in patients with catheters or other plastic devices. They include a great variety of species such as S. epidermidis, S. hominis, S. haemolyticus, S. saprophyticus, S. simulans and S. warneri, which have shown increasing resistance to antibiotic treatment, mainly to penicillin and synthetic b-lactams represented by oxacillin. Many of these oxacillin-resistant microorganisms (OXA-R) also present resistance to other antimicrobes, thus limiting the use of glycopeptides like vancomycin and teicoplanin. Staphylococcus isolations with reduced susceptibility to vancomycin have been described. [1][2][3] OXA-R CNS strains posses the mecA gene, which codes for a modified 78-kDa protein, PBP 2a, which is responsible for the resistance to b-lactams such as dicloxacillin, methicillin, nafcillin and oxacillin. The protein is able to bind to these antibiotics with very low affinity. The presence of the mecA gene in Staphylococcus strains is a synonym for OXA-R and so the NCCLS (National Committee for Clinical Laboratory Standards) recommends that OXA-R CNS strains isolated from patients with serious infections should be tested for the mecA gene or PBP 2a presence. 4,5) Biofilms are microbial communities wrapped in a matrix of exo-polysaccharides produced by the bacteria, which are adhered to an inert surface. This property becomes important in immunocompromised patients, because it produces chronic infections. S. epidermidis is thus far the most well known biofilm producer. 6,7)Little is known about the mechanism of resistance (R) to antimicrobial agents in bacterial biofilm producers but apparently it limits antimicrobial diffusion and induces physiological alterations associated with low bacterial growth and the appearance of atypical phenotypes in these cells. 8-15)The objectives of the present paper were to detect mechanisms of antimicrobial resistance and biofilms production in clinical isolates of CNS strains. MATERIALS AND METHODSCNS Identification 293 CNS strains were isolated from 744 samples from a dialysis center in S. M. de Tucumán, Argentina: 156 (53%) from urine, 107 (37%) from catheters and 30 (10%) from hemocultures. The bacteria isolated were characterized with conventional biochemical methods: catalase, bacitracin susceptibility and coagulase testing. The scheme proposed by Kloos and Schleifer, 1986, was used, which allowed identification of the CNS strains with the following tests: novobiocin resistance; urea hydrolysis; fermentation of: sucrose, xylose, maltose, trehalose, mannitol, cellobiose and raffinose; phosphatase; nitrate reduction and use of arginine. 16,17) Susceptibility to Antimicrobial Agents Antimicrobial sensitivity was carried out with the disc-diffusion technique in solid medium according to the NCCLS. The following antimicrobial agents were assayed: oxacillin (OXA) 1 mg, vancomycin (VAN) 30 mg, teicoplanin (TEI) 30 mg, gentamicin (GEN) 10 mg, ciprofloxacin ...

Carbapenemase-producing Klebsiella pneumoniae (CRKP) are increasingly reported worldwide being necessary the local epidemiological monitoring. Our aim was to characterize the hypermucoviscous CRKP isolates collected in our hospital during a 6 months period. Carriage of the carbapenemase genes ( bla KPC , bla NDM , bla VIM and bla OXA-48 ), extended spectrum β-lactamases ( bla SHV-2 , bla CTX-M ) and the virulence genes ( mag A, k2A, rmp A, wab G, uge , all S, ent B, ycf M, kpn , wca G, fim H, mrk D, iut A, iro N, hly and cnf -1) were determined by multiplex-PCR. Genetic relationship among the isolates was performed by PFGE and MLST. A total of 35 isolates were recovered, being the urinary and respiratory tract the most common infection sites (34.2%). The bla KPC-2 gene was present in all the isolates, coexisting with bla CTX-M-2 (45.7%), bla SHV-2 (28.6%), and bla CTX-M-2 / bla SHV-2 (14.3%). The capsular serotype K2 corresponded with 68.6% of the isolates. Virulence factors frequency were variable [adhesins (97.1%), siderophores (94.3%) and phagocytosis resistance ( wab G 48.5%, uge 80% and ycf M 57.1%)]. A total of 10 STs were identified although 40% of them clustered on ST25-CC65, and 17% to ST17. The incidence of KPC-2-producing K. pneumoniae reported by the hospital was 0.290 per 1000 admissions. In summary we described an epidemic scenario of multidrug resistant hypermucoviscous KPC-2 producing ST25 K. pneumoniae in our institution.

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