CFDA and propidium iodide fluorescence were detected by flow cytometry. Proliferation was calculated by relating the mean fluorescence intensity to cells grown in IL-2 alone (100 % proliferation) and cells cultured in the presence of the mitosis inhibitor Colcemide (50 ng/mL, Biochrom) (0 % proliferation). This study was supported by grant HA 4318/37hyphen;3
from Deutsche Forschungsgemeinschaft (DFG). Conflict of interest: The authors declare no financial or commercial conflict of interest. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made Cabozantinib cost available as submitted by the authors. “
“The prevalence of OXA-type carbapenemase genes, ISAba1 insertion sequence, carbapenem resistance, biofilm forming ability and genetic heterogeneity in clinical isolates of Acinetobacter spp. from hospitals in Mangalore, South India was studied. Based on the presence of the blaOXA-51-like gene, the 62 isolates of Acinetobacter spp. were identified as 48 A. baumannii and 14 other Acinetobacter spp. The prevalence of blaOXA-23-like, blaOXA-24-like and blaOXA-58-like
genes in A. baumannii was 47.9%, 22.9% and 4.2%, while in other Acinetobacter spp. it was 28.5%, 64.3% and 35.7% respectively. Several A. baumannii isolates (16/48) harbored the insertion sequence ISAba1 in the upstream region of the blaOXA-23-like Sirolimus mw gene. Resistance to meropenem was seen in 39.6% and 14.2% of A. baumannii and other Acinetobacter spp. isolates, respectively. The ability to form biofilm was observed to be higher among A. baumannii in comparison to other Acinetobacter spp. The present study shows that blaOXA-23-like
DOK2 genes are more common in A. baumannii,whereas blaOXA-24-like genes are common to other Acinetobacter spp. The study revealed genetic heterogeneity among the isolates, indicating multiple sources in the hospitals. Acinetobacter spp., particularly, Acinetobacter baumannii have emerged as an important nosocomial pathogen worldwide (1), multiple drug resistance posing a serious problem in the clinical management of infections caused by them. Surveys by the British Society for Antimicrobial Chemotherapy in 2005 showed that >30% of bacteremia isolates were resistant to gentamicin and other drugs, resistance to imipenem being low (2). Carbapenem resistance mechanisms are mediated by beta-lactamases which are classified by two general schemes: the Ambler molecular scheme and the Bush-Jacoby-Medieros scheme (3, 4). In the Ambler molecular scheme, beta-lactamases are classified into four major types, A – D, based on protein homology. This excludes the phenotypic basis that is commonly used in any laboratory. Classes A, C and D are serine-beta-lactamases while class B includes metallo-beta-lactamases.