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Abstract
BackgroundThe increasing resistance of Acinetobacter baumannii to antibiotics has recently been regarded as a notable therapeutic difficulty. Evaluating resistance rates of some A. baumannii isolates to tetracyclines had an impact on understanding the antibiotic resistance dissemination. By comparing genetic characteristics and relatedness of A. baumannii isolates, we are able to determine the transition dynamics of outbreak isolates.MethodsA total of 72 non-duplicate isolates of A. baumannii were recovered in 2011 and 2015 and minimum inhibitory concentration (MIC) range distribution of the isolates to tetracyclines was performed by broth micro dilution (BMD) assay, and to determine the lineage relatedness of the outbreak isolates repetitive extragenic palindromic element based on polymerase chain reaction (rep-PCR) and international clonal (ICs) investigations were performed.ResultsResistance rates to tetracycline, doxycycline and minocycline in 2011 were 73, 2 and 0%, while these rates in 2015 increased up to 90, 84 and 52%, respectively. The tetB existed in 100% of all the isolates of both years. tetA was not found in any of the isolates. According to the rep-PCR assays, up to 83% of all isolates clustered distinctly and only 6% of isolates had a common root. The percentage rates of IC1 decreased from 42% in 2011 to 22% in 2015, while those of IC2 increased from 28 to 36%, from 2011 to 2015.ConclusionsOur data showed that resistance to the first and second generations of tetracyclines is on the rise and the clonal transition dynamics of isolates are in progress in our hospital.
Highlights
The increasing resistance of Acinetobacter baumannii to antibiotics has recently been regarded as a notable therapeutic difficulty
Resistance to the first and second generations of tetracyclines in A. baumannii isolates mainly resulted from the acquired major facilitator superfamily (MFS) efflux pumps, including tetA, tetB, tetG, tetH, tetL, and tet39, resistance nodulation division family (RND) efflux pumps nominated as adeABC, adeIJK, adeFGH, adeM, adeDE [4], and ribosomal protections and enzymatic inactivation [5]. tetA is responsible for the resistance to tetracycline and doxycycline whereas tetB has been found in the isolates that were resistant to minocycline [6]
Thirty-six isolates were collected in 2011, and the other 36 isolates were obtained in 2015. These isolates were identified by API20NE as Acinetobacter baumannii-calcoaceticus complex, and for confirming as A. baumannii, all of the isolates were investigated by OXA51-like β-lactamase and gyrB multiplex PCR amplification according to previous studies [12]
Summary
The increasing resistance of Acinetobacter baumannii to antibiotics has recently been regarded as a notable therapeutic difficulty. Tigecycline, a glycylcycline, has recently approved by US Food and Drug Administration (FDA) antibacterial agent. This minocycline structural analogue is indicated intravenously for the treatment of complicated infections [3]. Resistance to the first and second generations of tetracyclines in A. baumannii isolates mainly resulted from the acquired major facilitator superfamily (MFS) efflux pumps, including tetA, tetB, tetG, tetH, tetL, and tet, resistance nodulation division family (RND) efflux pumps nominated as adeABC, adeIJK, adeFGH, adeM, adeDE [4], and ribosomal protections and enzymatic inactivation [5]. The main resistance mechanisms of tetracyclines are ade efflux systems while coexistence with tetA and tetB determinants resulted in increasing MIC values [7]
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