Abstract

Acinetobacter baumannii is an opportunistic pathogen and is one of the primary etiological agents of healthcare-associated infections (HAIs). A. baumannii infections are difficult to treat due to the intrinsic and acquired antibiotic resistance of strains of this bacterium, which frequently limits therapeutic options. In this study, five A. baumannii strains (810CP, 433H, 434H, 483H, and A-2), all of which were isolated from a child with leukemia M2, were characterized through antibiotic susceptibility profiling, the detection of genes encoding carbapenem hydrolyzing oxacillinases, pulsed-field gel electrophoresis (PFGE), multilocus sequence typing (MLST), adherence and invasion assays toward the A549 cell line, and the whole-genome sequence (WGS). The five strains showed Multidrug resistant (MDR) profiles and amplification of the blaOXA-23 gene, belonging to ST758 and grouped into two PFGE clusters. WGS of 810CP revealed the presence of a circular chromosome and two small plasmids, pAba810CPa and pAba810CPb. Both plasmids carried genes encoding the Sp1TA system, although resistance genes were not identified. A gene-by-gene comparison analysis was performed among the A. baumannii strains isolated in this study and others A. baumannii ST758 strains (HIMFG and INCan), showing that 86% of genes were present in all analyzed strains. Interestingly, the 433H, 434H, and 483H strains varied by 8–10 single-nucleotide variants (SNVs), while the A2 and 810CP strains varied by 46 SNVs. Subsequently, an analysis using BacWGSTdb showed that all of our strains had the same resistance genes and were ST758. However, some variations were observed in relation to virulence genes, mainly in the 810CP strain. The genes involved in the synthesis of hepta-acylated lipooligosaccharides, the pgaABCD locus encoding poly-β-1-6-N-acetylglucosamine, the ompA gene, Csu pili, bap, the two-component system bfms/bfmR, a member of the phospholipase D family, and two iron-uptake systems were identified in our A. baumannii strains genome. The five A. baumannii strains isolated from the child were genetically different and showed important characteristics that promote survival in a hospital environment. The elucidation of their genomic sequences provides important information for understanding their epidemiology, antibiotic resistance, and putative virulence factors.

Highlights

  • Acinetobacter baumannii is an emerging opportunistic pathogen involved in healthcare-associated infections (HAIs) with elevated morbidity and mortality, in immunocompromised patients

  • The pediatric patient was previously healthy, presented at Hospital Infantil de México Federico Gómez (HIMFG) in December 2014 for pancytopenia and a mediastinal tumor, and by means of bone marrow aspirate, the patient was diagnosed with acute myeloid leukemia subtype M2

  • Two weeks after receiving the first cycle of chemotherapy, the patient was admitted to the emergency ward for a 24-h evaluation, which was characterized by a fever of 38◦C, vomiting, colicky abdominal pain, and decreased stools

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Summary

Introduction

Acinetobacter baumannii is an emerging opportunistic pathogen involved in healthcare-associated infections (HAIs) with elevated morbidity and mortality, in immunocompromised patients. Treatment for A. baumannii infections is complex due to the increasing antibiotic resistance of this pathogen, which involves several intrinsic and acquired resistance mechanisms, such as the production of β-lactamase inhibitors and low-permeability outer membrane and efflux pumps (Peleg et al, 2008). The study of the molecular epidemiology of bacterial pathogens is an essential tool for establishing control measures for hospital infections, such as the elimination or prevention of the further spread of A. baumannii strains inside a hospital. Diverse molecular typing methods have been used for epidemiological characterization of HAIs pathogens, including A. baumannii strains. Several studies have showed typified A. baumannii strains using two MLST methods: the Oxford and Pasteur schemes (Bartual et al, 2005; Diancourt et al, 2010)

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