AUTHOR=Chen Lida , Tan Pinghai , Zeng Jianming , Yu Xuegao , Cai Yimei , Liao Kang , Guo Penghao , Chen Yili , Wu Zongwen , Qu Pinghua , Cai Renxin , Chen Cha , Huang Bin 

TITLE=Impact of an Intervention to Control Imipenem-Resistant Acinetobacter baumannii and Its Resistance Mechanisms: An 8-Year Survey

JOURNAL=Frontiers in Microbiology

VOLUME=11

YEAR=2021

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2020.610109

DOI=10.3389/fmicb.2020.610109

ISSN=1664-302X

ABSTRACT=<sec><title>Background</title><p>This study aimed to examine the impact of an intervention carried out in 2011 to combat multi-drug resistance and outbreaks of imipenem-resistant <italic>Acinetobacter baumannii</italic> (IRAB), and to explore its resistance mechanism.</p></sec><sec><title>Methods</title><p>A total of 2572 isolates of <italic>A. baumannii</italic>, including 1673 IRAB isolates, were collected between 2007 and 2014. An intervention was implemented to control <italic>A. baumannii</italic> resistance and outbreaks. Antimicrobial susceptibility was tested by calculating minimal inhibitory concentrations (MICs), and outbreaks were typed using pulsed-field gel electrophoresis (PFGE). Resistance mechanisms were explored by polymerase chain reaction (PCR) and whole genome sequencing (WGS).</p></sec><sec><title>Results</title><p>Following the intervention in 2011, the resistance rates of <italic>A. baumannii</italic> to almost all tested antibiotics decreased, from 85.3 to 72.6% for imipenem, 100 to 80.8% for ceftriaxone, and 45.0 to 6.9% for tigecycline. The intervention resulted in a decrease in the number (seven to five), duration (8–3 months), and departments (five to three) affected by outbreaks; no outbreaks occurred in 2011. After the intervention, only <italic>bla</italic><sub>AMPC</sub> (76.47 to 100%) and <italic>bla</italic><sub>TEM–</sub><sub>1</sub> (75.74 to 96.92%) increased (<italic>P</italic> &lt; 0.0001); whereas <italic>bla</italic><sub>GES–</sub><sub>1</sub> (32.35 to 3.07%), <italic>bla</italic><sub>PER–</sub><sub>1</sub> (21.32 to 1.54%), <italic>bla</italic><sub>OXA–</sub><sub>58</sub> (60.29 to 1.54%), <italic>carO</italic> (37.50 to 7.69%), and <italic>adeB</italic> (9.56 to 3.08%) decreased (<italic>P</italic> &lt; 0.0001). Interestingly, the frequency of class B β-lactamase genes decreased from 91.18% (<italic>bla</italic><sub>SPM–</sub><sub>1</sub>) and 61.03% (<italic>bla</italic><sub>IMP–</sub><sub>1</sub>) to 0%, while that of class D <italic>bla</italic><sub>OXA–</sub><sub>23</sub> increased to 96.92% (<italic>P</italic> &lt; 0.0001). WGS showed that the major PFGE types causing outbreaks each year (type 01, 11, 18, 23, 26, and 31) carried the same resistance genes (<italic>bla</italic><sub>KPC–</sub><sub>1</sub>, <italic>bla</italic><sub>ADC–</sub><sub>25</sub>, <italic>bla</italic><sub>OXA–</sub><sub>66</sub>, and <italic>adeABC</italic>), AdeR-S mutations (G186V and A136V), and a partially blocked porin channel CarO. Meanwhile, plasmids harboring <italic>bla</italic><sub>OXA–</sub><sub>23</sub> were found after the intervention.</p></sec><sec><title>Conclusion</title><p>The intervention was highly effective in reducing multi-drug resistance of <italic>A. baumannii</italic> and IRAB outbreaks in the long term. The resistance mechanisms of IRAB may involve genes encoding β-lactamases, efflux pump overexpression, outer membrane porin blockade, and plasmids; in particular, clonal spread of <italic>bla</italic><sub>OXA–</sub><sub>23</sub> was the major cause of outbreaks. Similar interventions may also help reduce bacterial resistance rates and outbreaks in other hospitals.</p></sec>