Systemic dissemination and cutaneous damage in a mouse model of staphylococcal skin infections. Microb Pathog 2009 Jul;47(1):16-23
Date
04/29/2009Pubmed ID
19397991Pubmed Central ID
PMC2831771DOI
10.1016/j.micpath.2009.04.007Scopus ID
2-s2.0-67349152679 (requires institutional sign-in at Scopus site) 24 CitationsAbstract
Serious staphylococcal infections frequently begin in the skin. The present study used a mouse model of such infections to evaluate the ability of Staphylococcus aureus to disseminate from the skin and to determine if cutaneous damage from the infections was required for dissemination. The mice were inoculated with S. aureus onto flank skin prepared by a tape-stripping method that caused minimal disruption of the epidermal keratinocyte layers. After these inoculations the staphylococci were found to disseminate to the spleen and kidneys of almost all animals within 6h. Induction of leucopenia did not affect this process. Cutaneous damage was prominent in these experimental infections and included loss of the epidermis, neutrophil infiltration into the epidermis, and complete necrosis of the dermis. The latter also occurred in cyclophosphamide-treated animals, indicating that the organisms themselves and not the host inflammatory responses were responsible. Dermal necrosis did not develop until 48h after inoculation, a time by which dissemination had already occurred. Therefore, in this mouse model system S. aureus is capable of penetrating the epidermal keratinocyte layers and disseminating rapidly after inoculation; the experimental infections do produce significant dermal damage, but the latter develops after dissemination has already taken place.
Author List
Hahn BL, Onunkwo CC, Watts CJ, Sohnle PGMESH terms used to index this publication - Major topics in bold
AnimalsBacteremia
Colony Count, Microbial
Female
Kidney
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Spleen
Staphylococcal Skin Infections
Staphylococcus aureus
Time Factors