April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
An Investigation Into The Prevalence Of spla, pvl And mecA And Their Role In Virulence In Staphylococcus Aureus-associated Keratitis
Author Affiliations & Notes
  • Rose M. Gilbert
    Ophthalmology and Medical Microbiology,
    The Royal Liverpool University Hospital, Liverpool, United Kingdom
  • Henri Sueke
    Ophthalmology and Medical Microbiology,
    The Royal Liverpool University Hospital, Liverpool, United Kingdom
  • Stephen B. Kaye
    Ophthalmology and Medical Microbiology,
    The Royal Liverpool University Hospital, Liverpool, United Kingdom
  • Timothy Neal
    Medical Microbiology,
    The Royal Liverpool University Hospital, Liverpool, United Kingdom
  • Malcolm J. Horsburgh
    Institute of Integrative Biology, University of Liverpool, Liverpool, United Kingdom
  • Andrew Libberton
    Institute of Integrative Biology, University of Liverpool, Liverpool, United Kingdom
  • Footnotes
    Commercial Relationships  Rose M. Gilbert, None; Henri Sueke, None; Stephen B. Kaye, None; Timothy Neal, None; Malcolm J. Horsburgh, None; Andrew Libberton, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 5840. doi:
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      Rose M. Gilbert, Henri Sueke, Stephen B. Kaye, Timothy Neal, Malcolm J. Horsburgh, Andrew Libberton; An Investigation Into The Prevalence Of spla, pvl And mecA And Their Role In Virulence In Staphylococcus Aureus-associated Keratitis. Invest. Ophthalmol. Vis. Sci. 2011;52(14):5840.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Staphylococcus aureus keratitis isolates from community patients in the UK were surveyed for the following genes which may influence bacterial virulence: the splA gene, encoding a serine protease-like protein; the pvl gene, encoding the Panton Valentine leukocidin; and the mecA gene, encoding SCCmec-borne methicillin resistance. The prevalence of splA, pvl and mecA and their effect on clinical outcome in bacterial keratitis were assessed.

Methods: : Bacterial isolates from all cases of ulcerative keratitis from 2003 to 2005 in six UK centres (Birmingham, Bristol, Liverpool, London, Manchester and Newcastle) were collected. S. aureus positive samples were identified in the National Institute of Health Research (NIHR) Biomedical Research Centre, using standard microbiological techniques. Isolates from patients with keratitis and 30 healthy control subjects (nasal isolates collected in 2008) were analysed for the presence of splA, pvl and mecA using primers from conserved internal sequences of the genes. Clinical outcome data was collected from the patients with keratitis and a clinical index of ulcer healing time to ulcer size was calculated.

Results: : 40/96 (40%) S. aureus isolates from patients with ulcerative bacterial keratitis and 3/15 (20%) from healthy control subjects were splA positive. 5/91 (5.5%) isolates were positive for pvl and 8/91 (9%) for methicillin resistance. The pvl positive strains were all from different hospitals. Mean (SD) ulcer size, treatment time, healing time and healing time to ulcer size for the S. aureus isolates were 5.89mm2 (9.34), 21.31days (14.58) 14.57days (12.51) and 5.34days/mm2 (5.06), respectively.

Conclusions: : S. aureus is a frequent cause of bacterial keratitis and has been isolated in up to 31% of cases in the UK. We have found thus far that there is enrichment of splA in S. aureus keratitis isolates relative to S. aureus nasal isolates from healthy controls. This increased prevalence may relate to known SplA cleavage of a peptide sequence found in the ocular surface epithelial mucin 16 (MUC16). The frequency of pvl and mecA in keratitis isolates was similar to that for other S. aureus disease isolates.

Keywords: keratitis • microbial pathogenesis: experimental studies • bacterial disease 
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