Antibacterial susceptibility of a vancomycin-resistant Staphylococcus aureus strain isolated at the Hershey Medical Center

Abstract

Staphylococcus aureus strain HMC3 isolated at the Hershey Medical Center, was resistant to vancomycin (VRSA) through the presence of the vanA resistance gene; it also contained mecA, erm(A), erm(B), tet(K) and aac(6')-aph(2"), conferring resistance to licensed beta-lactams, macrolides, tetracycline and aminoglycosides. HMC3 also had alterations in GyrA and GrlB and was resistant to available quinolones. Experimental drugs with low MICs (<2 mg/L) for VRSA HMC3 included cephalosporins BAL9141 and RWJ-54428; glycopeptides oritavancin and dalbavancin; the lipopeptide daptomycin; the glycolipodepsipeptide ramoplanin; new fluoroquinolones WCK 771 A, WCK 1153, DK-507k and sitafloxacin; and the DNA nanobinder GS02-02. These agents were all bactericidal as were trimethoprim/sulfamethoxazole and teicoplanin (MIC 4 mg/L). Oxazolidinones linezolid and ranbezolid; the injectable streptogramin quinupristin/dalfopristin; DNA nanobinders GS2-10547 and GS02-104; peptide deformylase inhibitors NVP-PDF713 and GS02-12; tetracycline derivative tigecycline; the antifolate iclaprim; mupirocin and fusidic acid were all active in vitro but bacteriostatic.

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Bacterial Etiology of Skin and Wound Infections along with Antibiogram Profiling in Reference to Emerging Antibiotic Resistance in Animals

“…In the developing countries nowadays multiple antibiotic resistance have been observed among important pathogens viz., Escherichia coli; MRSA, VREF; Klebsiella; Vibrio etc (Bozdogan et al, 2003;Byarugaba, 2004;Soulsby, 2005;Zhang et al, 2006). Uncontrolled and widespread application of antibiotics in both human and veterinary medicines is equally responsible for increase in prevalence of antibiotic-resistant bacterial infections, and emergence of new antimicrobial resistant pathogenic strains of various infectious agents.…”

Study Comparing the Effectiveness of Chlorhexidine, Calcium Hydroxide and Linezolid Based Medicaments Against Enterococcus Faecalis

“…LZ acts by preventing the formation of 70S ribosome complex that is responsible for the initiation of protein synthesis, by binding to the 23S subunit of the 50S subunit [25]. However, enterococcal resistance to the drug occurs due to mutation of the ribosomal binding site [26].…”