ORIGINAL RESEARCH

Genetic polymorphism of Staphylococcus epidermidis strains in patients of the Neonatal Intensive Care Unit

About authors

1 Department of Microbiology and Clinical Pharmacology,
Kulakov Research Center for Obstetrics, Gynecology and Perinatology, Moscow, Russia

2 Department of Clinical and Molecular Genetics,
Kulakov Research Center for Obstetrics, Gynecology and Perinatology, Moscow, Russia

3 Department of Neonatology and Pediatrics,
Kulakov Research Center for Obstetrics, Gynecology and Perinatology, Moscow, Russia

Correspondence should be addressed: Alexey B. Gordeev
ul. Akademika Oparina, d. 4, Moscow, Russia, 117997; ur.sertorp.agev@weedrog

About paper

Funding: this study was supported by the Grant Agreement No. 14.607.21.0019 of the Ministry of Science and Education of the Russian Federation
dated June 5, 2014 (ID 2014-14-579-0001-065).

Contribution of the authors to this work: Gordeev AB — bioinformatics analysis of nucleotide sequences, analysis of literature, drafting of a manuscript; Lyubasovskaya LA — micribiological studies, analysis of literature, data interpretation, drafting of a manuscript; Rodchenko JV, Dubodelov DV — microbiological studies, drafting of a manuscript; Mukosey IS, Kochetkova TO — whole genome suquencing and genome assembling; Nikitina IV — research planning, data interpretation; Ionov OB, Zubkov VV — research planning, organization of biomaterial sampling; Trofimov DYu — research planning, organization of whole genome sequencing; Priputnevich TV — research planning, organization of microbiological studies, data interpretation, drafting of a manuscript. All authors participated in editing of the manuscript.

Received: 2017-02-02 Accepted: 2017-02-18 Published online: 2017-03-11
|
Table 1. Genome assembly o S. epidermidis strains based on whole-genome sequencing data
Table 2. Antibiotic resistance of S. epidermidis strains
Note. R — resistant strain, S — sensitive strain.
Table 3. Resistance genes in S. epidermidis
Note. Symbols + and – represent the presence and absence of the resistance gene in the strain genome. Gene aacA-aphD  mediates resistance to amikacin, gentamycin, kanamycin, and tobramycin; gene aadD mediates resistance to amikacin, kanamycin, neomycin and tobramycinl; aphA mediates resistance to kanamycin and neomycin; blaZ — to penicillins; mecA — to beta-lactam antibiotics; fusB and fusC to fusidic acid; vanA, vanB, and vanZ  to vancamycin; lnu(A), vga(A), and vga(B) — to licosamides (clindamycin); msr(A) and mph(C) — to macrolide antibiotics (erythromycin); erm(A), erm(B), and erm(C) — to macrolide antibiotics and lincosamides; vat(B) — to streptogramin B; tet(M) and tet(K) — to tetracycline; dfr(G) and dfr(K) — to trimethoprim.
Table 4. Genes associated with virulence in S. epidermidis
Note. Symbols + and – represent the presence and absence of a resistance gene in the strain genome.