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Substitutions of Ser83Leu in GyrA and Ser80Leu in ParC Associated with Quinolone Resistance in Acinetobacter pittii.
Microb Drug Resist. 2015 Jun; 21(3):345-51.MD

Abstract

To investigate the prevalence and the mechanism of quinolone-resistant Acinetobacter pittii, 634 Acinetobacter calcoaceticus-Acinetobacter baumannii complex isolates were collected throughout Zhejiang Province. Identification of isolates was conducted by matrix-assisted laser desorption ionization/time of flight mass spectrometry (MALDI-TOF MS), blaOXA-51-like gene, and partial RNA polymerase β-subunit (rpoB) amplification. Twenty-seven isolates of A. pittii were identified. Among the 634 isolates, A. baumannii, A. pittii, Acinetobacter nosocomialis, and A. calcoaceticus counted for 87.22%, 4.26%, 8.20%, and 0.32%, respectively. Antimicrobial susceptibility of nalidixic acid, ofloxacin, enoxacin, ciprofloxacin, lomefloxacin, levofloxacin, sparfloxacin, moxifloxacin, and gatifloxacin for 27 A. pittii were determined by the agar dilution method. Detection of quinolone-resistant determining regions of gyrA, gyrB, parC, and parE was performed for the A. pittii isolates. In addition, plasmid-mediated quinolone resistance (PMQR) determinants (qnrA, qnrB, qnrS, qnrC, qnrD, aac(6')-Ib-cr, qepA, oqxA, and oqxB) were investigated. All the 27 isolates demonstrated a higher minimum inhibitory concentration (MIC) to old quinolones than the new fluoroquinolones. No mutation in gyrA, gyrB, parC, or parE was detected in 20 ciprofloxacin-susceptible isolates. Seven ciprofloxacin-resistant A. pittii were identified with a Ser83Leu mutation in GyrA. Among them, six isolates with simultaneous Ser83Leu amino acid substitution in GyrA and Ser80Leu in ParC displayed higher MIC values against ciprofloxacin. Additionally, three were identified with a Met370Ile substitution in ParE, and two were detected with a Tyr317His mutation in ParE, which were reported for the first time. No PMQR determinants were identified in the 27 A. pittii isolates. In conclusion, mutations in chromosome play a major role in quinolone resistance in A. pittii, while resistance mechanisms mediated by plasmid have not been found. Ser83Leu substitution in GyrA and Ser80Leu substitution in ParC are associated with quinolone resistance in A. pittii. Whether Met370Ile and Tyr317His substitutions in ParE play a minor role requires further investigation.

Authors+Show Affiliations

1Department of Laboratory Medicine, Second Affiliated Hospital of Zhejiang University, Hang Zhou, China.2Beijing Hospital, Beijing, China.1Department of Laboratory Medicine, Second Affiliated Hospital of Zhejiang University, Hang Zhou, China.1Department of Laboratory Medicine, Second Affiliated Hospital of Zhejiang University, Hang Zhou, China.1Department of Laboratory Medicine, Second Affiliated Hospital of Zhejiang University, Hang Zhou, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25514581

Citation

Gu, Dan-xia, et al. "Substitutions of Ser83Leu in GyrA and Ser80Leu in ParC Associated With Quinolone Resistance in Acinetobacter Pittii." Microbial Drug Resistance (Larchmont, N.Y.), vol. 21, no. 3, 2015, pp. 345-51.
Gu DX, Hu YJ, Zhou HW, et al. Substitutions of Ser83Leu in GyrA and Ser80Leu in ParC Associated with Quinolone Resistance in Acinetobacter pittii. Microb Drug Resist. 2015;21(3):345-51.
Gu, D. X., Hu, Y. J., Zhou, H. W., Zhang, R., & Chen, G. X. (2015). Substitutions of Ser83Leu in GyrA and Ser80Leu in ParC Associated with Quinolone Resistance in Acinetobacter pittii. Microbial Drug Resistance (Larchmont, N.Y.), 21(3), 345-51. https://doi.org/10.1089/mdr.2014.0057
Gu DX, et al. Substitutions of Ser83Leu in GyrA and Ser80Leu in ParC Associated With Quinolone Resistance in Acinetobacter Pittii. Microb Drug Resist. 2015;21(3):345-51. PubMed PMID: 25514581.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Substitutions of Ser83Leu in GyrA and Ser80Leu in ParC Associated with Quinolone Resistance in Acinetobacter pittii. AU - Gu,Dan-xia, AU - Hu,Yun-jian, AU - Zhou,Hong-wei, AU - Zhang,Rong, AU - Chen,Gong-xiang, Y1 - 2014/12/16/ PY - 2014/12/17/entrez PY - 2014/12/17/pubmed PY - 2016/2/18/medline SP - 345 EP - 51 JF - Microbial drug resistance (Larchmont, N.Y.) JO - Microb Drug Resist VL - 21 IS - 3 N2 - To investigate the prevalence and the mechanism of quinolone-resistant Acinetobacter pittii, 634 Acinetobacter calcoaceticus-Acinetobacter baumannii complex isolates were collected throughout Zhejiang Province. Identification of isolates was conducted by matrix-assisted laser desorption ionization/time of flight mass spectrometry (MALDI-TOF MS), blaOXA-51-like gene, and partial RNA polymerase β-subunit (rpoB) amplification. Twenty-seven isolates of A. pittii were identified. Among the 634 isolates, A. baumannii, A. pittii, Acinetobacter nosocomialis, and A. calcoaceticus counted for 87.22%, 4.26%, 8.20%, and 0.32%, respectively. Antimicrobial susceptibility of nalidixic acid, ofloxacin, enoxacin, ciprofloxacin, lomefloxacin, levofloxacin, sparfloxacin, moxifloxacin, and gatifloxacin for 27 A. pittii were determined by the agar dilution method. Detection of quinolone-resistant determining regions of gyrA, gyrB, parC, and parE was performed for the A. pittii isolates. In addition, plasmid-mediated quinolone resistance (PMQR) determinants (qnrA, qnrB, qnrS, qnrC, qnrD, aac(6')-Ib-cr, qepA, oqxA, and oqxB) were investigated. All the 27 isolates demonstrated a higher minimum inhibitory concentration (MIC) to old quinolones than the new fluoroquinolones. No mutation in gyrA, gyrB, parC, or parE was detected in 20 ciprofloxacin-susceptible isolates. Seven ciprofloxacin-resistant A. pittii were identified with a Ser83Leu mutation in GyrA. Among them, six isolates with simultaneous Ser83Leu amino acid substitution in GyrA and Ser80Leu in ParC displayed higher MIC values against ciprofloxacin. Additionally, three were identified with a Met370Ile substitution in ParE, and two were detected with a Tyr317His mutation in ParE, which were reported for the first time. No PMQR determinants were identified in the 27 A. pittii isolates. In conclusion, mutations in chromosome play a major role in quinolone resistance in A. pittii, while resistance mechanisms mediated by plasmid have not been found. Ser83Leu substitution in GyrA and Ser80Leu substitution in ParC are associated with quinolone resistance in A. pittii. Whether Met370Ile and Tyr317His substitutions in ParE play a minor role requires further investigation. SN - 1931-8448 UR - https://www.unboundmedicine.com/medline/citation/25514581/Substitutions_of_Ser83Leu_in_GyrA_and_Ser80Leu_in_ParC_Associated_with_Quinolone_Resistance_in_Acinetobacter_pittii_ L2 - https://www.liebertpub.com/doi/10.1089/mdr.2014.0057?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -