TY - JOUR
T1 - Promoters of Colistin Resistance in Acinetobacter baumannii Infections
AU - Nurtop, Elif
AU - Baylndlr Bilman, Fulya
AU - Menekse, Sirin
AU - Kurt Azap, Ozlem
AU - Gönen, Mehmet
AU - Ergonul, Onder
AU - Can, Fusun
N1 - Publisher Copyright:
© Copyright 2019, Mary Ann Liebert, Inc., publishers 2019.
PY - 2019/9
Y1 - 2019/9
N2 - Objectives: We aimed to describe the mechanisms of colistin resistance in Acinetobacter baumannii. Materials and Methods: Twenty-nine patients diagnosed with colistin-resistant A. baumannii infection were included to the study. The mutations in pmrCAB, lpxA, lpxC, and lpxD genes, expression of pmrCAB, carbapenemases, and mcr-1 positivity were studied. Results: Twenty-seven (93%) of the patients received IV colistin therapy during their stay, and the case fatality rate was 45%. All mutations in pmrC and pmrB were found to be accompanied with a mutation in lpxD. The most common mutations were I42V and L150F in pmrC (65%), E117K in lpxD (65%), and A138T in pmrB (58.6%). The colistin minimum inhibitory concentrations (MICs) of the isolates having any of these four mutations were higher than the isolates with no mutations (p < 0.001). The two most common mutations in pmrC (I42V and L150F) were found to be associated with higher expressions of pmrA and pmrC and higher colistin MIC values (p = 0.010 and 0.031). All isolates were blaOXA-23 positive. Conclusion: Coexistence of the lpxD mutation along with mutations in pmrCAB indicates synergistic function of these genes in development of colistin resistance in A. baumannii.
AB - Objectives: We aimed to describe the mechanisms of colistin resistance in Acinetobacter baumannii. Materials and Methods: Twenty-nine patients diagnosed with colistin-resistant A. baumannii infection were included to the study. The mutations in pmrCAB, lpxA, lpxC, and lpxD genes, expression of pmrCAB, carbapenemases, and mcr-1 positivity were studied. Results: Twenty-seven (93%) of the patients received IV colistin therapy during their stay, and the case fatality rate was 45%. All mutations in pmrC and pmrB were found to be accompanied with a mutation in lpxD. The most common mutations were I42V and L150F in pmrC (65%), E117K in lpxD (65%), and A138T in pmrB (58.6%). The colistin minimum inhibitory concentrations (MICs) of the isolates having any of these four mutations were higher than the isolates with no mutations (p < 0.001). The two most common mutations in pmrC (I42V and L150F) were found to be associated with higher expressions of pmrA and pmrC and higher colistin MIC values (p = 0.010 and 0.031). All isolates were blaOXA-23 positive. Conclusion: Coexistence of the lpxD mutation along with mutations in pmrCAB indicates synergistic function of these genes in development of colistin resistance in A. baumannii.
KW - A. baumannii
KW - colistin
KW - resistance
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U2 - 10.1089/mdr.2018.0396
DO - 10.1089/mdr.2018.0396
M3 - Article
C2 - 30964377
AN - SCOPUS:85070070894
SN - 1076-6294
VL - 25
SP - 997
EP - 1002
JO - Microbial Drug Resistance
JF - Microbial Drug Resistance
IS - 7
ER -