Clinical Correlates of Panton-Valentine Leukocidin (PVL), PVL Isoforms, and Clonal Complex in the Staphylococcus aureus Population of Northern Australia

Steven Tong, Rachael Gorie, Emma Bishop, Allen Cheng, Deborah Holt, Malcolm McDonald, Philip Giffard, Bart Currie, Craig Boutlis

    Research output: Contribution to journalArticleResearchpeer-review

    Abstract

    Background: Regional differences in the prevalence of Panton-Valentine leukocidin (PVL) and PVL isoform- harboring strains as well as in the local population structure of Staphylococcus aureus may influence the clinical spectrum of S. aureus infections. 

    Methods: Using a prospective collection of S. aureus isolates from northern Australia, we determined differences between infections caused by (1) PVL+ and PVL- isolates, (2) PVL histidine (H) isoform- and PVL arginine (R) isoform-harboring isolates, and (3) different lineages, including the genetically divergent clonal complex (CC) 75 and the PVL+ CC93. 

    Results: PVL+ isolates comprised 54% (128/239) of community-associated methicillin-resistant isolates and 40% (95/239) of methicillin-susceptible S. aureus (MSSA) isolates. There were 113 H isoform- and 110 R isoform- harboring isolates. PVL was associated with truly community-acquired disease, younger age, and presentation with sepsis. We found no differences in infections due to H isoform-harboring isolates, compared with R isoform- harboring isolates. CC93 was the most prevalent lineage. The genetically divergent CC75 caused clinical disease similar to that of other S. aureus clones. 

    Conclusions: PVL+ and PVL- infections are clearly distinct. MSSA contributes a large but underrecognized burden of PVL+ disease. Compared with elsewhere in the world, there is a relative abundance of the clade that contains CC93 and CC121 in both northern Australia and Asia. 
    Original languageEnglish
    Pages (from-to)760-769
    Number of pages10
    JournalJournal of Infectious Diseases
    Volume202
    Issue number5
    DOIs
    Publication statusPublished - 1 Sep 2010

    Fingerprint

    Staphylococcus aureus
    Protein Isoforms
    Population
    Methicillin
    Infection
    Panton-Valentine leukocidin
    Northern Asia
    Methicillin Resistance
    Histidine
    Arginine
    Sepsis
    Clone Cells

    Cite this

    @article{7fb90a291d11481090bf1d07e76e97e5,
    title = "Clinical Correlates of Panton-Valentine Leukocidin (PVL), PVL Isoforms, and Clonal Complex in the Staphylococcus aureus Population of Northern Australia",
    abstract = "Background: Regional differences in the prevalence of Panton-Valentine leukocidin (PVL) and PVL isoform- harboring strains as well as in the local population structure of Staphylococcus aureus may influence the clinical spectrum of S. aureus infections. Methods: Using a prospective collection of S. aureus isolates from northern Australia, we determined differences between infections caused by (1) PVL+ and PVL- isolates, (2) PVL histidine (H) isoform- and PVL arginine (R) isoform-harboring isolates, and (3) different lineages, including the genetically divergent clonal complex (CC) 75 and the PVL+ CC93. Results: PVL+ isolates comprised 54{\%} (128/239) of community-associated methicillin-resistant isolates and 40{\%} (95/239) of methicillin-susceptible S. aureus (MSSA) isolates. There were 113 H isoform- and 110 R isoform- harboring isolates. PVL was associated with truly community-acquired disease, younger age, and presentation with sepsis. We found no differences in infections due to H isoform-harboring isolates, compared with R isoform- harboring isolates. CC93 was the most prevalent lineage. The genetically divergent CC75 caused clinical disease similar to that of other S. aureus clones. Conclusions: PVL+ and PVL- infections are clearly distinct. MSSA contributes a large but underrecognized burden of PVL+ disease. Compared with elsewhere in the world, there is a relative abundance of the clade that contains CC93 and CC121 in both northern Australia and Asia. ",
    keywords = "arginine, histidine, isoprotein, Panton Valentine leukocidin, adult, age, aged, article, Australia, bacterial strain, bacterium isolate, cladistics, clinical feature, communicable disease, correlation analysis, female, genetic variability, human, major clinical study, male, methicillin resistant Staphylococcus aureus, nonhuman, priority journal, sepsis, Staphylococcus aureus, Staphylococcus infection, Adult, Anti-Bacterial Agents, Bacterial Toxins, Community-Acquired Infections, Exotoxins, Female, Humans, Leukocidins, Male, Methicillin, Methicillin-Resistant Staphylococcus aureus, Northern Territory, Prevalence, Protein Isoforms, Staphylococcal Infections",
    author = "Steven Tong and Rachael Gorie and Emma Bishop and Allen Cheng and Deborah Holt and Malcolm McDonald and Philip Giffard and Bart Currie and Craig Boutlis",
    year = "2010",
    month = "9",
    day = "1",
    doi = "10.1086/655396",
    language = "English",
    volume = "202",
    pages = "760--769",
    journal = "Journal of Infectious Diseases",
    issn = "0022-1899",
    publisher = "Oxford University Press",
    number = "5",

    }

    Clinical Correlates of Panton-Valentine Leukocidin (PVL), PVL Isoforms, and Clonal Complex in the Staphylococcus aureus Population of Northern Australia. / Tong, Steven; Gorie, Rachael; Bishop, Emma; Cheng, Allen; Holt, Deborah; McDonald, Malcolm; Giffard, Philip; Currie, Bart; Boutlis, Craig.

    In: Journal of Infectious Diseases, Vol. 202, No. 5, 01.09.2010, p. 760-769.

    Research output: Contribution to journalArticleResearchpeer-review

    TY - JOUR

    T1 - Clinical Correlates of Panton-Valentine Leukocidin (PVL), PVL Isoforms, and Clonal Complex in the Staphylococcus aureus Population of Northern Australia

    AU - Tong, Steven

    AU - Gorie, Rachael

    AU - Bishop, Emma

    AU - Cheng, Allen

    AU - Holt, Deborah

    AU - McDonald, Malcolm

    AU - Giffard, Philip

    AU - Currie, Bart

    AU - Boutlis, Craig

    PY - 2010/9/1

    Y1 - 2010/9/1

    N2 - Background: Regional differences in the prevalence of Panton-Valentine leukocidin (PVL) and PVL isoform- harboring strains as well as in the local population structure of Staphylococcus aureus may influence the clinical spectrum of S. aureus infections. Methods: Using a prospective collection of S. aureus isolates from northern Australia, we determined differences between infections caused by (1) PVL+ and PVL- isolates, (2) PVL histidine (H) isoform- and PVL arginine (R) isoform-harboring isolates, and (3) different lineages, including the genetically divergent clonal complex (CC) 75 and the PVL+ CC93. Results: PVL+ isolates comprised 54% (128/239) of community-associated methicillin-resistant isolates and 40% (95/239) of methicillin-susceptible S. aureus (MSSA) isolates. There were 113 H isoform- and 110 R isoform- harboring isolates. PVL was associated with truly community-acquired disease, younger age, and presentation with sepsis. We found no differences in infections due to H isoform-harboring isolates, compared with R isoform- harboring isolates. CC93 was the most prevalent lineage. The genetically divergent CC75 caused clinical disease similar to that of other S. aureus clones. Conclusions: PVL+ and PVL- infections are clearly distinct. MSSA contributes a large but underrecognized burden of PVL+ disease. Compared with elsewhere in the world, there is a relative abundance of the clade that contains CC93 and CC121 in both northern Australia and Asia. 

    AB - Background: Regional differences in the prevalence of Panton-Valentine leukocidin (PVL) and PVL isoform- harboring strains as well as in the local population structure of Staphylococcus aureus may influence the clinical spectrum of S. aureus infections. Methods: Using a prospective collection of S. aureus isolates from northern Australia, we determined differences between infections caused by (1) PVL+ and PVL- isolates, (2) PVL histidine (H) isoform- and PVL arginine (R) isoform-harboring isolates, and (3) different lineages, including the genetically divergent clonal complex (CC) 75 and the PVL+ CC93. Results: PVL+ isolates comprised 54% (128/239) of community-associated methicillin-resistant isolates and 40% (95/239) of methicillin-susceptible S. aureus (MSSA) isolates. There were 113 H isoform- and 110 R isoform- harboring isolates. PVL was associated with truly community-acquired disease, younger age, and presentation with sepsis. We found no differences in infections due to H isoform-harboring isolates, compared with R isoform- harboring isolates. CC93 was the most prevalent lineage. The genetically divergent CC75 caused clinical disease similar to that of other S. aureus clones. Conclusions: PVL+ and PVL- infections are clearly distinct. MSSA contributes a large but underrecognized burden of PVL+ disease. Compared with elsewhere in the world, there is a relative abundance of the clade that contains CC93 and CC121 in both northern Australia and Asia. 

    KW - arginine

    KW - histidine

    KW - isoprotein

    KW - Panton Valentine leukocidin

    KW - adult

    KW - age

    KW - aged

    KW - article

    KW - Australia

    KW - bacterial strain

    KW - bacterium isolate

    KW - cladistics

    KW - clinical feature

    KW - communicable disease

    KW - correlation analysis

    KW - female

    KW - genetic variability

    KW - human

    KW - major clinical study

    KW - male

    KW - methicillin resistant Staphylococcus aureus

    KW - nonhuman

    KW - priority journal

    KW - sepsis

    KW - Staphylococcus aureus

    KW - Staphylococcus infection

    KW - Adult

    KW - Anti-Bacterial Agents

    KW - Bacterial Toxins

    KW - Community-Acquired Infections

    KW - Exotoxins

    KW - Female

    KW - Humans

    KW - Leukocidins

    KW - Male

    KW - Methicillin

    KW - Methicillin-Resistant Staphylococcus aureus

    KW - Northern Territory

    KW - Prevalence

    KW - Protein Isoforms

    KW - Staphylococcal Infections

    UR - http://www.scopus.com/inward/record.url?scp=77954753232&partnerID=8YFLogxK

    U2 - 10.1086/655396

    DO - 10.1086/655396

    M3 - Article

    VL - 202

    SP - 760

    EP - 769

    JO - Journal of Infectious Diseases

    JF - Journal of Infectious Diseases

    SN - 0022-1899

    IS - 5

    ER -