Characterising the role of enolase in a stable Small Colony Variant of Staphylococcus aureus isolated from a diabetic foot infection patient with osteomyelitis.

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dc.contributor.authorLee, J.
dc.contributor.authorCarda-Diéguez, M.
dc.contributor.authorVreugde, S.
dc.contributor.authorCooksley, C.
dc.contributor.authorMashayamombe, M.
dc.contributor.authorDawson, J.
dc.contributor.authorFitridge, R.
dc.contributor.authorMira, A.
dc.contributor.authorZilm, P.S.
dc.contributor.authorKidd, S.P.
dc.date.issued2024
dc.description.abstractThe switch to alternate cell types by Staphylococcus aureus creates sub-populations even within an active population, that are highly resilient, tolerant to antibiotics and lack clinical symptoms of infection. These cells present a challenge for clinical treatment where even after initial intervention has seemingly cleared the infection, these alternate cell types persist within tissue to revert and cause disease. Small colony variants (SCV) are a cell type which facilitate persistent infection but clinically isolated SCVs are often unstable in laboratory conditions. We have isolated a pair of S. aureus isolates from an individual patient with osteomyelitis presenting with heterogenous phenotypes; a stable SCV (sSCV) and a SCV that reverts upon laboratory culturing to the usual, active and non-SCV cell type. Thus we are able use this pair to investigate and compare the genetic mechanisms that underlie the clinical variatons of SCV phenotype. The switch to the sSCV phenotype was associated with frameshift mutations in the enolase eno and the histidine kinase arlS. The phenoptye of the sSCV was an impeded growth dependent on amino acid catabolism and modulated biofilm. These mutations present potentially a new molecular mechanism which confer persistence within osteomyelitis.
dc.description.statementofresponsibilityJames Lee, Miguel Carda-Dieguez, Sarah Vreugde, Clare Cooksley, Matipaishe Mashayamombe, Joseph Dawson, Robert Fitridge, Alex Mira, Peter S. Zilm, Stephen P. Kidd.
dc.identifier.citationMicrobial Pathogenesis, 2024; 196:106918-106918
dc.identifier.doi10.1016/j.micpath.2024.106918
dc.identifier.issn0882-4010
dc.identifier.issn0882-4010
dc.identifier.orcidLee, J. [0000-0002-3606-9013]
dc.identifier.orcidVreugde, S. [0000-0003-4719-9785]
dc.identifier.orcidDawson, J. [0000-0001-9229-9545]
dc.identifier.orcidFitridge, R. [0000-0001-6258-5997]
dc.identifier.orcidZilm, P.S. [0000-0001-7554-9717]
dc.identifier.orcidKidd, S.P. [0000-0002-2118-1651]
dc.identifier.urihttps://hdl.handle.net/2440/144796
dc.language.isoen
dc.publisherElsevier
dc.rights© 2024 Published by Elsevier Ltd.
dc.source.urihttps://doi.org/10.1016/j.micpath.2024.106918
dc.subjectdiabetic foot infection
dc.subjectintracellular
dc.subjectosteomyelitis
dc.subjectsmall colony variants
dc.subjectStaphylococcus aureus
dc.subject.meshHumans
dc.subject.meshBiofilms
dc.subject.meshStaphylococcus aureus
dc.subject.meshStaphylococcal Infections
dc.subject.meshOsteomyelitis
dc.subject.meshDiabetic Foot
dc.subject.meshPhosphopyruvate Hydratase
dc.subject.meshBacterial Proteins
dc.subject.meshPhenotype
dc.subject.meshFrameshift Mutation
dc.titleCharacterising the role of enolase in a stable Small Colony Variant of Staphylococcus aureus isolated from a diabetic foot infection patient with osteomyelitis.
dc.typeJournal article
pubs.publication-statusPublished online

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