Culture Collections

Multidrug resistant Staphylococcus epidermidis lineages added to the NCTC


S Epi

Staphylococcus epidermidis - This image is licensed under the Creative Commons Attribution-Share Alike 4.0 International licence.


Staphylococcus epidermidis exhibits both commensal and pathogenic lifestyles. It is both present on healthy human skin and the cause of significant number of infections worldwide. In 2018 J. Y. H. Lee et al. described three multidrug resistant lineages of S. epidermidis, which are now available from NCTC.

S. epidermidis was once considered to be a benign commensal organism that predominantly colonises the human head and nares1, but is now recognised to be an aetiological agent of opportunistic soft tissue infection, medical device associated infection, mastitis, and bacteraemia. It is infrequently associated with a range of pathologies and reported to be an underlying contributor to other significant morbidity and mortality2,3,4.

While S. epidermidis is perhaps the most virulent coagulase negative Staphylococcus (CoNS) species, it has been described as an “accidental” pathogen5, where the aspects of the biology of the species that sustain its ecology as a commensal organism (such the ability to form biofilm and a robust osmotolerance) provide benefit to the species when it is involved in infection. Its frequent colonisation of human skin may have important implications for the species’ behaviour as a reservoir for antimicrobial resistance genes.

In October 2018, Lee JYH et al. published a review6 describing three previously unidentified multi-drug resistant lineages of S. epidermidis, identifiable by a rifampicin resistant phenotype, which have spread globally. A representative of each lineage has been deposited into Public Health England’s National Collection of Type Cultures as NCTC 14218, NCTC 14219 and NCTC 14220, the details of which are below: 


  NCTC 14218 NCTC 14219 NCTC 14220
Sequence Type  23  2  2
Genome assembly (ENA/GenBank) ERS1019876 GCA_900086615.1 SAMN09093631
    MIC (mg/L)  
Gentamicin 32  64  256
Oxacillin >16  >16  >16
Penicillin  8  >8  >8
Teicoplanin  4  8  4
Vancomycin  2  2  2
Clindamycin  >8  >8 > 8
Erythromycin  >16  >16 >16
Linezolid  2  1  2
Ciprofloxacin  >8  >8  >8
Quinupristin/Dalfopristin  1  0.5  0.5
Daptomycin  0.5  0.5  0.5
Fusidic acid  16  16  16
Rifampicin  >2  >2  >2






















































Table 1 – MIC values coloured green are reported as sensitive, whereas those in orange are reported as resistant.

Regarding the genomic structure and content of the S. epidermidis population that causes infection, J. Y. H. Lee et al. reported that 74% of nosocomial isolates belong to clonal complex 2, of which sequence type (ST) 2 is the founder, and that the ica operon (a key S. epidermidis virulence factor, a set of genes encoding the production of polysaccharide intercellular adhesin) are conserved across these types of isolates. ST2 and ST23 strains are also generally enriched for genes relating to antibiotic resistance and biofilm formation.

NCTC 14219, which also appears in the literature under identifier BPH0662, has been further characterised prior and since. It is the source of the first complete genome sequence of a multi-drug resistant ST2 S. epidermidis7 and has also been the subject of extensive characterisation with regard to its restriction modification systems8.

These three strains are valuable additions to the NCTC, and alongside NCTC 13360 S. epidermidis (equivalent to ATCC 12228, a non-biofilm-forming strain), NCTC 13924 S. epidermidis (a linezolid resistant strain) and 8 other strains of S. epidermidis held by the NCTC, will help contextualise and elucidate S. epidermidis pathology, population structure, evolution and biology.

NCTC is grateful to Jean Y H Lee, Benjamin Howden and their colleagues for characterising and depositing their strains (NCTC14218-14220).


1. Fleer A, Verhoef J. New aspects of staphylococcal infections: emergence of coagulase-negative staphylococci as pathogens. Antonie Van Leeuwenhoek. 1984;50(5-6):729–744. doi:10.1007/bf02386237

2. Sharon Kleinschmidt, Flavia Huygens, Joan Faoagali, Irani U Rathnayake, Louise M Hafner. Staphylococcus Epidermidis as a Cause of Bacteremia. Future Microbiol, 10 (11), 1859-79 2015. doi:10.2217/fmb.15.98

3. Dong Y, Speer CP, Glaser K. Beyond sepsis: Staphylococcus epidermidis is an underestimated but significant contributor to neonatal morbidity. Virulence. 2018;9(1):621–633. doi:10.1080/21505594.2017.1419117

4. A. L. Byrd, Y. Belkaid, J. A. Segre. The Human Skin Microbiome. Nat. Rev. Microbiol., 16(3), 143-155 Mar 2018. DOI:

5. Otto M. Staphylococcus epidermidis--the 'accidental' pathogen. Nat Rev Microbiol. 2009;7(8):555–567. doi:10.1038/nrmicro2182

6. Lee JYH, Monk IR, Gonçalves da Silva A, et al. Global spread of three multidrug-resistant lineages of Staphylococcus epidermidis. Nat Microbiol. 2018;3(10):1175–1185. doi:10.1038/s41564-018-0230-7

7. Lee JYH, Monk IR, Pidot SJ, et al. Functional analysis of the first complete genome sequence of a multidrug resistant sequence type 2 Staphylococcus epidermidis. Microb Genom. 2016;2(9):e000077. doi:10.1099/mgen.0.000077

8. Lee JYH, Carter GP, Pidot SJ, et al. Mining the Methylome Reveals Extensive Diversity in Staphylococcus epidermidis Restriction Modification. mBio. 2019;10(6):e02451-19. doi:10.1128/mBio.02451-19


Copy prepared by Jake D. Turnbull. Follow Jake on Twitter @HotchPotchJake

January 2020.

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