الفهرس 
AcknowledgementOnly 14 pages are availabe for public view
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Abstract
Egypt has witnessed elevated incidence rates of multidrug-resistant Klebsiella
pneumoniae infections in intensive care units (ICUs). The treatment of these
infections is becoming more challenging whilst colistin-carbapenem-resistant
K. pneumoniae is upsurging. Due to the insufficiently available data on the
genomic features of colistin-resistant K. pneumoniae in Egypt, it was
important to fill in the gap and explore the genomic characteristics, as well as
the antimicrobial resistance, the virulence determinants, and the molecular
mechanisms of colistin resistance in such a lethal pathogen. Seventeen
colistin-resistant clinical K. pneumoniae isolates were collected from ICUs in
Alexandria, Egypt in a 6-month period in 2020. Colistin resistance was
phenotypically detected by modified rapid polymyxin Nordmann/Poirel and
broth microdilution techniques. The isolates susceptibility to 20
antimicrobials was determined using Kirby‐Bauer disk diffusion method.
Whole genome sequencing and bioinformatic analysis were employed for
exploring the virulome, resistome, and the genetic basis of colistin resistance
mechanisms. Out of the tested K. pneumoniae isolates, 82.35% were
extensively drug-resistant and 17.65% were multidrug-resistant. Promising
susceptibility levels towards tigecycline (88.24%) and doxycycline (52.94%)
were detected. Population structure analysis revealed seven sequence types
(ST) and K-types: ST383-K30, ST147-K64, ST17-K25, ST111-K63, ST11-
K15, ST14-K2, and ST525-K45. Virulome analysis revealed yersiniabactin,
aerobactin, and salmochelin siderophore systems in ˃50% of the population.
Hypervirulence biomarkers, iucA (52.94%) and rmpA/A2 (5.88%) were
detected. Extended-spectrum β-lactamase- and carbapenemase-producers
accounted for 94.12% of the population, with blaCTX-M-15, blaNDM-5, and blaOXA-
48 reaching 64.71%, 82.35%, and 82.35%, respectively. chromosomal
alterations in mgrB (82.35%) were the most prevailing colistin resistanceassociated
genetic change followed by deleterious mutations in ArnT
(23.53%, L54H and G164S), PmrA (11.76%, G53V and D86E),