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Anti-Microbial Resistance by Medical

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Ann Emerg Med 2009, E-pub ahead of print. 103 Miller LG, Spellberg B: Treatment of communityassociated methicillin-resistant Staphylococcus aureus skin and soft tissue infections with drainage but no antibiotic therapy. Pediatr Infect Dis J 2004;23:795; author reply 6. 104 Yeh J: The role of antibiotics in community-acquired MRSA cutaneous abscesses. Infect Med 2006;23: 166–167. 105 Rybak M, Lomaestro B, Rotschafer JC, et al: Therapeutic monitoring of vancomycin in adult patients: a consensus review of the American Society of Health-System Pharmacists, the Infectious Diseases Society of America, and the Society of Infectious Diseases Pharmacists.

It is possible that suboptimal dosing of quinolones in the presence of strains with elevated quinolone minimal inhibitory concentrations (yet remaining in the ‘susceptible’ range) may account for these differences. Conclusions ESBL-producing organisms are a premier example of the growing threat of resistance in Gram-negative bacilli. In many parts of the world, rates of infection with ESBLs are growing. Yet, at the same time, therapy for ESBL-producing organisms is being compromised by other emerging resistance mechanisms in Gram-negative bacteria.

The mechanism was a chromosomally encoded β-lactamase, termed SHV. The third-generation cephalosporins were introduced into clinical practice in the early 1980s. Shortly after their release, β-lactamases were discovered which could hydrolyze and inactivate these antibiotics. The genes encoding these β-lactamases Table 1. β-lactamases which inactivate third-generation cephalosporins β-lactamase ESBLs KPC AmpC MBLs Ability to hydrolyze cephamycins cefepime carbapenems – + ++ ++ + + – ++ – ++ – + were identical to TEM or SHV except for point mutations which led to an altered amino acid sequence.

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