We got a colistin resistance Klebsiella pneumoniae which induced in vitro by serial passages in media containing increasing colistin concentrations.
1、By Re-sequencing, we found that there was no gene mutation(including gene insertion, gene deletion and point mutation) in the known drug resistance genes(phoP/Q,mgrB,pmrA/B,crrB).
2、Through RNA-seq, we found that mgrB gene expression was down-regulated and PhoQ / P gene expression was up-regulated。
3、We detected the LPS of drug-resistant bacteria by MS and found that the LPS of drug-resistant bacteria was modified by L-Ara4N rather than modified by pEtN. This result is consistent with the result of RNA-seq.
4、This Cositin resistance can be stably inherited, that is, when we remove cositin, this strain still has Cosition resistance(MIC=16-32).
5、How can I explain this phenomenon？Or what methods do I need to find the cause of stable genetic resistance？
6、In fact, this phenomenon has been reported in some papers（DOI：10.2807/1560-7917；DOI：10.1016/j.ijantimicag.2014.07.020；DOI：10.1128/JCM.01017-15；DOI：10.3389/fmicb.2017.02262；DOI：10.1128/CMR.00064-16）, but most of them are in clinical strains, and no further research has been done。
Detection of colistin resistance currently relies on MIC determinations using broth microdilution (BMD), a slow process that, despite being the gold standard for polymyxin susceptibility testing, has been subject to reliability and standardization problems
Hersh Maan
1、The first paragraph you mentioned is right.
2、When I remove colistin,the resistant stain still grows in CAMHB and this Cositin resistance can be stably inherited.
3、The RNAseq performed on the samples from this resistant strain , when grown in remove of colisitn.
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