Genomic Analysis of Antibiotic-Resistant Staphylococcus epidermidis Isolates From Clinical Sources in the Kwazulu-Natal Province, South Africa.

Jonathan Asante,Daniel G Amoako,Linda A Bester,Sabiha Y Essack,Bakoena A Hetsa,Akebe L K Abia

doi:10.3389/fmicb.2021.656306

Abstract

Staphylococcus epidermidis has become an important nosocomial pathogen. Multidrug resistance makes S. epidermidis infections difficult to treat. The study aims to describe the genomic characteristics of methicillin-resistant S. epidermidis (MRSE) isolated from clinical sources, to comprehend the genetic basis of antibiotic resistance, virulence, and potential pathogenicity. Sixteen MRSE underwent whole-genome sequencing, and bioinformatics analyses were carried out to ascertain their resistome, virulome, mobilome, clonality, and phylogenomic relationships. In all, 75% of isolates displayed multidrug resistance and were associated with the carriage of multiple resistance genes including mecA, blaZ, tet(K), erm(A), erm(B), erm(C), dfrG, aac(6′)-aph(2′′), and cat(pC221) conferring resistance to β-lactams, tetracyclines, macrolide–lincosamide–streptogramin B, aminoglycosides, and phenicols, which were located on both plasmids and chromosomes. Their virulence profiles were evidenced by the presence of genes involved in adherence/biofilm formation (icaA, icaB, icaC, atl, ebh, and ebp), immune evasion (adsA, capC, and manA), and antiphagocytosis (rmlC, cdsA, and A). The community-acquired SCCmec type IV was the most common SCCmec type. The CoNS belonged to seven multilocus sequence types (MLSTs) and carried a diversity of mobile genetic elements such as phages, insertion sequences, and plasmids. The bacterial anti-phage defense systems clustered regularly interspaced short palindromic repeats/CRISPR-associated (CRISPR-Cas) immunity phage system and restriction-modification system (R-M system) and the arginine catabolic mobile element (ACME) involved in immune evasion and transport of virulence genes were also found. The insertion sequence, IS256, linked with virulence, was found in 56.3% of isolates. Generally, the isolates clustered according to STs, with some similarity but also considerable variability within isolates. Whole-genome sequencing and bioinformatics analysis provide insights into the likely pathogenicity and antibiotic resistance of S. epidermidis, necessitating surveillance of this emerging pathogen.

Highlights

Staphylococcus epidermidis are coagulase-negative staphylococci (CoNS) that are commensals of the skin microbiome
The pathogenicity of S. epidermidis is further enhanced by virulence genes associated with adherence/biofilm formation, phenol-soluble modulins, and various mobile genetic elements (MGEs) such as plasmids, insertion sequences (ISs), transposons, pathogenicity islands, and phages that are involved in the acquisition and transmission of resistance and virulence characteristics (Bouchami et al, 2016; Rolo et al, 2017)
Other factors that have been associated with pathogenicity in S. epidermidis include the metabolic state of the bacterial cell, genomic rearrangements in pathogenic isolates facilitated by IS256, and the conjugative transfer of antibiotic resistance (Cabrera-Contreras et al, 2019)

Summary

Introduction

Staphylococcus epidermidis are coagulase-negative staphylococci (CoNS) that are commensals of the skin microbiome. Among the CoNS, S. epidermidis and Staphylococcus haemolyticus, together referred to as the S. epidermidis group, are the most prevalent in clinical settings (Azih and Enabulele, 2013) and can behave as pathogens by colonizing medical devices, infecting surgical wounds, and causing bacteremia (Cabrera-Contreras et al, 2019). MecA gene, which mediates methicillin resistance, is highly conserved in S. epidermidis, transferred to other staphylococcal species by horizontal transmission (Méric et al, 2015), and borne on the staphylococcal cassette chromosome, SCCmec, which is shared between S. epidermidis and Staphylococcus aureus (Méric et al, 2015). Other factors that have been associated with pathogenicity in S. epidermidis include the metabolic state of the bacterial cell, genomic rearrangements in pathogenic isolates facilitated by IS256, and the conjugative transfer of antibiotic resistance (Cabrera-Contreras et al, 2019)

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Results

Conclusion