1887

Abstract

Carbapenem resistance in members of the is increasing. To evaluate the effects of tigecycline and polymyxin B against carbapenem-non-susceptible pathogens, 89 representative clinical carbapenem-non-susceptible isolates were recovered from seven hospitals from four cities in China during 2006–2009: 30 , 35 , seven , six , five , four and two isolates. Twenty-eight isolates were indistinguishable. The 35 isolates belonged to 12 clonal strains. Among the 89 isolates, 82 produced KPC-2, seven produced IMP (three produced KPC-2 simultaneously), three did not produce any carbapenemases and nine were deficient in porins. Polymyxin B was much more active than tigecycline against carbapenem-non-susceptible . The MIC and MIC of imipenem, meropenem, ertapenem, polymyxin B and tigecycline were 8 and 32 µg ml, 8 and 32 µg ml, 16 and 128 µg ml, 0.5 and 16 µg ml, and 4 and 16 µg ml, respectively. Rates of susceptibility to imipenem, meropenem, ertapenem and polymyxin B were 30.0 %, 27.5 %, 2.5 % and 89.2 % by CLSI criteria. The rate of susceptibility to tigecycline was 40 % and 17.5 % by Food and Drug Administration (MIC ≤2 µg ml) and European Committee on Antimicrobial Susceptibility Testing (MIC ≤1 µg ml) criteria, respectively. KPC-2- or IMP-producing transconjugants exhibited reduced susceptibility to carbapenems but were susceptible to polymyxin B and tigecycline with an MIC range of 0.5–2 µg ml, 0.25–2 µg ml, 0.5–4 µg ml, 0.5 µg ml and 0.5–1 µg ml. In conclusion, carbapenem resistance in is mainly due to production of KPC-2, and polymyxin B is active for the carbapenem-resistant .

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2011-12-01
2019-09-21
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vol. , part 12, pp. 1813–1819

MICs of carbapenems, polymyxin B and tigecycline, β-lactamase production, and porin expression of carbapenem-non-susceptible , transconjugants and plasmid eliminated strains. [PDF](49 KB)



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