Staphylococcus pseudintermedius Surface Protein L (SpsL) Is Required for Abscess Formation in a Murine Model of

Amy C Richards1, Marie O'Shea1, Philippa M Beard1

  • 1The Roslin Institute, Royal (Dick) School of Veterinary Sciences, University of Edinburgh, Edinburgh, United Kingdom.

Infection and Immunity
|September 6, 2018
PubMed

Insights

Staphylococcus pseudintermedius causes canine pyoderma, leading to antibiotic resistance. This study reveals the SpsL protein is crucial for abscess formation in mice, offering new therapeutic targets for canine skin infections.

Area of Science:

  • Veterinary Dermatology
  • Bacterial Pathogenesis
  • Host-Pathogen Interactions

Background:

  • Staphylococcus pseudintermedius is a primary cause of canine pyoderma, frequently leading to recurrent skin infections and extensive antibiotic use.
  • The rise of multidrug-resistant strains, including methicillin-resistant Staphylococcus pseudintermedius, necessitates a deeper understanding of infection mechanisms.
  • Limited knowledge of S. pseudintermedius pathogenesis hinders the development of novel treatments and vaccines.

Purpose of the Study:

  • To investigate the roles of two cell wall-associated proteins, SpsD and SpsL, in the pathogenesis of S. pseudintermedius skin infections.
  • To elucidate the host-pathogen interactions critical for disease development.
  • To identify potential targets for new therapeutic or vaccine strategies.

Main Methods:

  • Development and utilization of a novel murine cutaneous infection model for S. pseudintermedius.
  • Experimental infections using wild-type S. pseudintermedius and gene-deletion mutants lacking SpsD, SpsL, or both.
  • Histopathological analysis of skin lesions to characterize inflammation and tissue damage.
  • Quantification of bacterial loads within infected tissues.

Main Results:

  • Infection with wild-type or SpsD-deficient S. pseudintermedius resulted in focal cutaneous abscesses.
  • Mutants deficient in SpsL, or both SpsD and SpsL, induced larger lesions with features of cellulitis rather than abscesses.
  • A significantly higher bacterial burden was observed in lesions infected with SpsL-deficient mutants compared to wild-type.

Conclusions:

  • The bacterial surface protein SpsL plays a critical role in the formation of skin abscesses caused by S. pseudintermedius in a murine model.
  • SpsL influences the clinical outcome and pathology of S. pseudintermedius skin infections.
  • These findings provide insights into host-pathogen interactions and suggest SpsL as a potential target for controlling canine pyoderma.

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