Abstract
A large outbreak of New Delhi metallo-beta-lactamase (NDM)-1-producing Klebsiella pneumoniae sequence type (ST) 147 occurred in Tuscany, Italy in 2018–2019. In 2020, ST147 NDM-9-producing K. pneumoniae were detected at the University Hospital of Pisa, Tuscany, in two critically ill patients; one developed bacteraemia. Genomic and phylogenetic analyses suggest relatedness of 2018–2019 and 2020 strains, with a change from NDM-1 to NDM-9 in the latter and evolution by colistin, tigecycline and fosfomycin resistance acquisition.
Highlights
A large outbreak of New Delhi metallo-beta-lactamase (NDM)-1-producing Klebsiella pneumoniae sequence type (ST) 147 occurred in Tuscany, Italy in 2018–2019
Protein basic local alignment search tool (BLASTP) analysis was performed on deduced coding sequences (CDSs) obtained by translation of Kp-P1 and Kp-P2 genomes in comparison with CDSs deduced from seven genomes, with different susceptibility to colistin, fosfomycin and tigecycline antibiotics (Table 1), which included those of the three Kp-11Pi, Kp-12Pi and Kp-16Pi strains
A total of 1,645 cases with NDM-carbapenem-resistant Enterobacteriaceae (CRE)-positive microbiological samples were identified in the period from 1 November 2018 to 31 October 2019 in Tuscany [1]
Summary
The study was conducted according to the principles stated in the Declaration of Helsinki. Protein basic local alignment search tool (BLASTP) analysis was performed on deduced coding sequences (CDSs) obtained by translation of Kp-P1 and Kp-P2 genomes (https://rast.nmpdr.org/seedviewer.cgi) in comparison with CDSs deduced from seven genomes, with different susceptibility to colistin, fosfomycin and tigecycline antibiotics (Table 1), which included those of the three Kp-11Pi, Kp-12Pi and Kp-16Pi strains. A mutation (A7→T) in the mgrB gene created a premature stop codon and the complete depletion of the MgrB protein (GenBank accession number: QDC86160.1), the regulator of phoP gene expression, in colistin-resistant Kp-P1, Kp-P2 and Kp-16Pi strains, respectively (Tables 1,2) [8]. Fosfomycin resistance in Kp-P1 and Kp-P2 was due to a mutation in the glpT gene creating a premature stop codon at position 134 (wild type glycerol-3-phosphate transporter (GlpT) is 448 amino acids; GenBank accession number: KLY15715) causing the depletion of the GlpT (Table 2). No mutations were found in MurA, UhpT, FosA, CyaA, Crp, PtsI, UhpB and UhpC proteins related to fosfomycin importation and metabolism [11,12,13]
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