Laboratory for Bacterial Evolution and Pathogenesis (LBEP)

S. pseudintermedius surface protein L (SpsL) is required for abscess formation in skin infection

New article shows that the SpsL protein of the bacteria influences the type of infection produced in the skin of a mouse model

We have just published a new article entitled "Staphylococcus pseudintermedius Surface Protein L (SpsL) Is Required for Abscess Formation in a Murine Cutaneous Infection Model" in the journal Infection & Immunity. This work was led by Amy Richards, in collaboration with other research groups in the Roslin Institute. Well done!

The bacteria Staphylococcus pseudintermedius is the primary cause of bacterial skin infections in dogs including eczema-related infections. Dogs prone to eczema often have recurrent S. pseudintermedius infections that become increasingly difficult to treat. This is particularly concerning because we know very little about the tools the bacteria uses to produce a skin infection. To address this, we investigated the role of two proteins produced by S. pseudintermedius in a model of skin infection. No function was identified for one of the proteins but the second protein, called SpsL, influenced the type of infection produced. In the presence of SpsL protein, the bacteria produce a skin abscess –a community of bacteria surrounded by host immune defence cells. In the absence of SpsL protein, the bacteria produce cellulitis– a dispersed infection that affects a larger area of the skin. These differences show that the SpsL protein of the bacteria influences the type of infection produced in the skin. More research is needed but this knowledge could aid the design of new treatment options.

You can find the paper here for more information.

Full citation:

Richards AC, O'Shea M, Beard PM, Goncheva MI, Tuffs SW, Fitzgerald JR, Lengeling A. Staphylococcus pseudintermedius Surface Protein L (SpsL) Is Required for Abscess Formation in a Murine Cutaneous Infection Model. Infect Immun. 2018 Sep 4. doi: 10.1128/IAI.00631-18.