Answers are grounded in this paper and cite their sources.
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 bla OXA-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 .
No takes yet. Share an insight, caveat, or question.
Nurtop et al. (2019) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: