Co-existence of virulence factors and antibiotic resistance in new Klebsiella pneumoniae clones emerging in south of Italy

Abstract

BackgroundEndemic presence of Klebsiella pneumoniae resistant to carbapenem in Italy has been due principally to the clonal expansion of CC258 isolates; however, recent studies suggest an ongoing epidemiological change in this geographical area.Methods50 K. pneumoniae strains, 25 carbapenem-resistant (CR-Kp) and 25 susceptible (CS-Kp), collected from march 2014 to march 2016 at the Laboratory of Bacteriology of the Paolo Giaccone Polyclinic University hospital of Palermo, Italy, were characterized for antibiotic susceptibility and fully sequenced by next generation sequencing (NGS) for the in silico analysis of resistome, virulome, multi-locus sequence typing (MLST) and core single nucleotide polymorphism (SNP) genotypesResultsMLST in silico analysis of CR-Kp showed that 52% of isolates belonged to CC258, followed by ST395 (12%), ST307 (12%), ST392 (8%), ST348 (8%), ST405 (4%) and ST101 (4%). In the CS-Kp group, the most represented isolate was ST405 (20%), followed by ST392 and ST15 (12%), ST395, ST307 and ST1727 (8%). The in silico β-lactamase analysis of the CR-Kp group showed that the most detected gene was blaSHV (100%), followed by blaTEM (92%), blaKPC (88%), blaOXA (88%) and blaCTX-M (32%). The virulome analysis detected mrk operon in all studied isolates, and wzi-2 was found in three CR-Kp isolates (12%). Furthermore, the distribution of virulence genes encoding for the yersiniabactin system, its receptor fyuA and the aerobactin system did not show significant distribution differences between CR-Kp and CS-Kp, whereas the Klebsiella ferrous iron uptake system (kfuA, kfuB and kfuC genes), the two-component system kvgAS and the microcin E495 were significantly (p < 0.05) prevalent in the CS-Kp group compared to the CR-Kp group.Core SNP genotyping, correlating with the MLST data, allowed greater strain tracking and discrimination than MLST analysis.ConclusionsOur data support the idea that an epidemiological change is ongoing in the Palermo area (Sicily, Italy). In addition, our analysis revealed the co-existence of antibiotic resistance and virulence factors in CR-Kp isolates; this characteristic should be considered for future genomic surveillance studies.

Successful High-Dosage Monotherapy of Tigecycline in a Multidrug-Resistant Klebsiella pneumoniae Pneumonia–Septicemia Model in Rats

“…Due to the complex relationship between antibiotic resistance and virulence factors, it is important to report the genotypic data of bacterial strains used in microbiological studies [13,14]. Polymerase chain reaction (PCR) assays were used to verify the presence of the following resistance genes: cefotaxime (CTX)-M β-lactamase groups 1, 2, 8, 9, 25 [15]; temoniera (TEM) β-lactamase [16]; sulfhydryl reagent variable (SHV) β-lactamase [17]; oxacillinase (OXA) 1-like β-lactamase groups 1, 48 [18,19]; KPC [20]; and New Delhi metallo-β-lactamase 1 (NDM) [21].…”

<p>Hybrid Genome Assembly and Annotation of a Pandrug-Resistant <em>Klebsiella pneumoniae</em> Strain Using Nanopore and Illumina Sequencing</p>

“…7 Interestingly, recent studies have shown that multidrugresistant K. pneumoniae clones have a mobile pool of antimicrobial resistance and virulence genes capable of causing life-threatening infections in healthy individuals. 8,9 Thus, there is a pressing need for detailed molecular studies that provide comprehensive insights into the evolutionary processes of this species and help in monitoring and controlling drug-resistant infections.…”

Emerging high-risk ST101 and ST307 carbapenem-resistant Klebsiella pneumoniae clones from bloodstream infections in Southern Italy

“…Recent epidemiological reports showed that ST101 and ST307 are emerging in several countries; therefore, these STs are considered candidates for becoming the prevalent high-risk CR-KP in the near future [10,16,17,[19][20][21][22][23][24][25]. Genetic features of these clones may contribute to their adaptation to hospital environments and to the human host, both of which result promote further spread of antibiotic resistance [26,27].…”