Differences in Colistin-resistant Acinetobacter baumannii Clinical Isolates Between Patients With and Without Prior Colistin Treatment.
10.3343/alm.2018.38.6.545
- Author:
Yu Jin PARK
1
;
Duck Jin HONG
;
Eun Jeong YOON
;
Dokyun KIM
;
Min Hyuk CHOI
;
Jun Sung HONG
;
Hyukmin LEE
;
Dongeun YONG
;
Seok Hoon JEONG
Author Information
1. Department of Laboratory Medicine, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Colistin;
Population heterogeneity;
Acinetobacter baumannii;
Resistance;
Lipid A analysis;
Pathogenesis
- MeSH:
Acinetobacter baumannii*;
Acinetobacter*;
Bacteria;
Colistin*;
Drug Resistance;
Humans;
In Vitro Techniques;
Lipid A;
Masks;
Methods;
Molecular Typing;
Mortality;
Population Characteristics
- From:Annals of Laboratory Medicine
2018;38(6):545-554
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: The increasing morbidity and mortality rates associated with Acinetobacter baumannii are due to the emergence of drug resistance and the limited treatment options. We compared characteristics of colistin-resistant Acinetobacter baumannii (CR-AB) clinical isolates recovered from patients with and without prior colistin treatment. We assessed whether prior colistin treatment affects the resistance mechanism of CR-AB isolates, mortality rates, and clinical characteristics. Additionally, a proper method for identifying CR-AB was determined. METHODS: We collected 36 non-duplicate CR-AB clinical isolates resistant to colistin. Antimicrobial susceptibility testing, Sanger sequencing analysis, molecular typing, lipid A structure analysis, and in vitro synergy testing were performed. Eleven colistin-susceptible AB isolates were used as controls. RESULTS: Despite no differences in clinical characteristics between patients with and without prior colistin treatment, resistance-causing genetic mutations were more frequent in isolates from colistin-treated patients. Distinct mutations were overlooked via the Sanger sequencing method, perhaps because of a masking effect by the colistin-susceptible AB subpopulation of CR-AB isolates lacking genetic mutations. However, modified lipid A analysis revealed colistin resistance peaks, despite the population heterogeneity, and peak levels were significantly different between the groups. CONCLUSIONS: Although prior colistin use did not induce clinical or susceptibility differences, we demonstrated that identification of CR-AB by sequencing is insufficient. We propose that population heterogeneity has a masking effect, especially in colistin non-treated patients; therefore, accurate testing methods reflecting physiological alterations of the bacteria, such as phosphoethanolamine-modified lipid A identification by matrix-assisted laser desorption ionization-time of flight, should be employed.
