Hepatitis C virus core antigen for screening organ donors and recipients.

Organ donors and recipients are routinely screened for hepatitis C virus (HCV) infection, typically via anti-HCV detection. We analyze the utility of an alternative HCV core antigen (HCV-Ag) quantification system, the ARCHITECT HCV Ag Assay, in this setting. We simultaneously tested 315 samples from potential organ donors and recipients using two chemiluminescent microparticle immunoassays: ARCHITECT Anti-HCV and HCV Ag (Abbott, Germany). HCV-Ag was detected in 81 of the serum samples (25.71%) and anti-HCV in 87 (27.62%). Seventy-five of the HCV-Ag-positive samples were positive for anti-HCV (92.59%). Overall concordance between the two assays was 94.29%. Of the six HCV-Ag-positive/anti-HCV-negative patients, five had HCV-Ag values <32 fmol/L, and the sixth had a concentration of 477.50 fmol/L (viral load, 137,000 IU/mL). The HCV AG Assay detects HCV infections missed by the Anti-HCV Assay. Both markers should be used to screen for HCV infection in potential organ donors and recipients.

Antimicrobial resistance, virulence factors and genetic lineages of hospital-onset methicillin-resistant Staphylococcus aureus isolates detected in a hospital in Zaragoza.

INTRODUCTION: MRSA population dynamics is undergoing significant changes, and for this reason it is important to know which clones are circulating in our nosocomial environment. MATERIALS AND METHODS: A total of 118 MRSA isolates were collected from clinical samples from patients with previous hospital or healthcare contact (named as hospital-onset MRSA (HO-MRSA)) during a one year period. Susceptibility testing was performed by disk diffusion and microdilution. The presence of resistance genes and virulence factors were tested by PCR. All isolates were typed by SCCmec, spa and agr typing. PFGE and MLST were applied to a selection of them. RESULTS: Eighty-three HO-MRSA isolates (70.3%) were resistant to any antibiotic included in the macrolide-lincosamide-streptogramin B group. Among these isolates, the M phenotype was the most frequent (73.5%). One hundred and seven of HO-MRSA isolates (90.7%) showed aminoglycoside resistance. The combination aac(6')-Ie-aph(2″)-Ia+ant(4')-Ia genes was the most frequent (22.4%). Tetracycline resistance rates in HO-MRSA isolates were low (3.4%), although a high level of mupirocin resistance was observed (25.4%). Most of the HO-MRSA isolates (approximately 90%) showed SCCmec type IVc and agr type II. Fifteen unrelated pulsotypes were identified. CC5 was the most prevalent (88.1%), followed by CC8 (5.9%), CC22 (2.5%), CC398 (2.5%) and CC1 (0.8%). CONCLUSION: CC5/ST125/t067 lineage was the most frequent. This lineage was related to aminoglycoside resistance, and to a lesser extent, with macrolide resistance. The presence of international clones as EMRSA-15 (CC22/ST22), European clones as CC5/ST228, community clones related to CC1 or CC8 and livestock associated clones, as CC398, were observed in a low percentage.

Molecular epidemiology, resistance profiles and clinical features in clinical plasmid-mediated AmpC-producing Enterobacteriaceae.

During the 30 months of surveillance period, 85 pAmpC-producing isolates were detected (prevalence 0.56% overall): blaCMY-2 gene in 70 E. coli, 2 K. pneumoniae and 6 P. mirabilis isolates; and the blaDHA-1 gene in 4 E. coli and 3 K. pneumoniae. In 8.23% of them, other ß-lactamases (predominantly OXA-1) were identified. All pAmpC-producing isolates were susceptible to carbapenems, whereas high resistance to nalidixic acid, ciprofloxacin and trimethoprim-sulfamethoxazole was observed among pAmpC-producing isolates (80%, 60%, and 44.7%, respectively). In hospital patients, predisposing factors such as prior antibiotic use, previous hospitalization, presence of an indwelling device, invasive urinary tract procedures and mechanical ventilation were observed. In the community setting, urinary tract infection was the most common type of infection related to pAmpC-producing isolates. A wide heterogeneity of clones was found among our E. coli isolates by PFGE, suggesting that this mechanism of resistance is not due to the dissemination of a clonal strain. Surveillance of these resistance mechanisms in the community is thus needed. Awareness of pAmpC dynamic is required to prevent introduction into hospitals and to control the spread of this emerging resistance within the community.

Molecular mechanisms of quinolone resistance in clinical isolates of Aeromonas caviae and Aeromonas veronii bv. sobria.

Mutations in quinolone targets were studied together with quinolone efflux pump activation and plasmid-mediated quinolone resistance determinants in nalidixic-acid-resistant isolates of Aeromonas caviae and Aeromonas veronii. Among 135 clinical Aeromonas spp. isolated from stools of patients with gastrointestinal symptoms, 40 nalidixic acid-resistant strains belonging to A. caviae and A. veronii were selected and their susceptibility to different quinolones (ciprofloxacin, norfloxacin, ofloxacin) further evaluated. Susceptibility to nalidixic acid and ciprofloxacin in the presence/absence of Phe- Arg-ß-naphthylamide was also determined. The 16 nalidixic-acid-resistant strains identified as A. caviae were more resistant than the 24 A. veronii bv. sobria strains to ciprofloxacin, norfloxacin, and ofloxacin. All strains showed a mutation (single or double) at position 83 of the QRDR sequence of gyrA, with Ser-83 → Ile as the most frequent substitution. By contrast, no mutations were found at position 87 of gyrA. Double substitutions (GyrA-ParC) were detected in 50% of A. veronii bv. sobria isolates and in 43.75% of A. caviae strains. Both species showed decreases in the MICs of ciprofloxacin. A qnrS gene was found in an A. caviae strain. Thus, in the two species of nalidixic-acid-resistant Aeromonas isolates examined, resistance mediated by efflux pumps contributed only slightly to ciprofloxacin resistance. While two isolates were positive for the aac(6')-Ib gene, no -cr variants were detected.