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

• Published in: Infection and immunity 2018-11, Vol.86 (11)
• Main Authors: Richards, Amy C, O'Shea, Marie, Beard, Philippa M, Goncheva, Mariya I, Tuffs, Stephen W, Fitzgerald, J Ross, Lengeling, Andreas
• Format: Article
• Language: English
• Subjects: Abscess - microbiology; Abscess - pathology; Animals; Bacterial Load; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Cellular Microbiology: Pathogen-Host Cell Molecular Interactions; Disease Models, Animal; Gene Deletion; Histocytochemistry; Membrane Proteins - genetics; Membrane Proteins - metabolism; Mice; Skin - microbiology; Skin - pathology; Staphylococcal Skin Infections - microbiology; Staphylococcal Skin Infections - pathology; Staphylococcus - genetics; Staphylococcus - growth & development; Staphylococcus - pathogenicity; Virulence Factors - genetics; Virulence Factors - metabolism
• ISSN: 0019-9567; 1098-5522
• DOI: 10.1128/iai.00631-18

is the leading cause of pyoderma in dogs and is often associated with recurrent skin infections that require prolonged antibiotic therapy. High levels of antibiotic use have led to multidrug resistance, including the emergence of epidemic methicillin-resistant clones. Our understanding of the pathogenesis of skin infection is very limited, and the identification of the key host-pathogen interactions underpinning infection could lead to the design of novel therapeutic or vaccine-based approaches for controlling disease. Here, we employ a novel murine cutaneous-infection model of and investigate the role of the two cell wall-associated proteins (SpsD and SpsL) in skin disease pathogenesis. Experimental infection with wild-type strain ED99 or a gene-deletion derivative deficient in expression of SpsD led to a focal accumulation of neutrophils and necrotic debris in the dermis and deeper tissues of the skin characteristic of a classical cutaneous abscess. In contrast, mice infected with mutants deficient in SpsL or both SpsD and SpsL developed larger cutaneous lesions with distinct histopathological features of regionally extensive cellulitis rather than focal abscessation. Furthermore, comparison of the bacterial loads in induced cutaneous lesions revealed a significantly increased burden of bacteria in the mice infected with SpsL-deficient mutants. These findings reveal a key role for SpsL in murine skin abscess formation and highlight a novel function for a bacterial surface protein in determining the clinical outcome and pathology of infection caused by a major canine pathogen.