title: A non-traumatic Staphylococcus aureus osteomyelitis model in pigs.
abstract: BACKGROUND
  The propensity for bacterial localization within bones of juvenile pigs is similar to the situation in humans, where haematogenously based osteomyelitis most commonly occurs in infants and children. In both pigs and humans, Staphylococcus aureus is a dominant cause of pyaemic lesions including osteomyelitis. The aim of the present study was to evaluate the pig as a model for the development of osteomyelitis following haematogenous spread of S. aureus.
  
  
  METHODS
  Twelve animals were challenged intravenously once or twice with 1x10(8) bacteria/kg body weight and euthanased consecutively from 6 h to 48 h after challenge. Following euthanasia, tissues were sampled from the lungs and bones for histology and immunohistochemical staining of vessels, different inflammatiory cells, apoptosis cells, and S. aureus.
  
  
  RESULTS
  Disseminated microabscesses developed within the lungs by 6 h but had disappeared at 48 h. Within the metaphyseal area of bones, microabscesses developed after 12 h and progressed until 48 h after challenge. Within bones, lesions were localized in separate foci from where the infection progressed towards the growth plate, which was in some cases bypassed due to bacterial spread through transphyseal vascular channels. Often, bone lesions resulted in trabecular osteosis, in which apoptotic cells were sometimes present.
  
  
  CONCLUSIONS
  The model revealed a pattern of development and presence of lesions similar to the frequently occurring osteomyelitic lesions, especially in pre-pubertal children following haematogenous spread of S. aureus. Therefore, this model can be reliably applied in studies of this disease with respect to pathophysiology, pathomorphology, impact of strain virulence, and therapy.
authors.affiliation: Department of Veterinary Disease Biology, Faculty of Life Sciences, University of Copenhagen, Ridebanevej 3, DK-1870, Frederiksberg C, Denmark. elvang@life.ku.dk
authors.forename: Henrik Elvang
authors.initials: HE
authors.lastname: Jensen
authors.forename: Ole Lerberg
authors.initials: OL
authors.lastname: Nielsen
authors.forename: Jørgen Steen
authors.initials: JS
authors.lastname: Agerholm
authors.forename: Tine
authors.initials: T
authors.lastname: Iburg
authors.forename: Louise Kruse
authors.initials: LK
authors.lastname: Johansen
authors.forename: Eleonora
authors.initials: E
authors.lastname: Johannesson
authors.forename: Maiken
authors.initials: M
authors.lastname: Møller
authors.forename: Line
authors.initials: L
authors.lastname: Jahn
authors.forename: Liselotte
authors.initials: L
authors.lastname: Munk
authors.forename: Bent
authors.initials: B
authors.lastname: Aalbaek
authors.forename: Pall Skuli
authors.initials: PS
authors.lastname: Leifsson
mesh_terms: D000818:Animals; D017209:Apoptosis; D004195:Disease Models, Animal; D005260:Female; D007150:Immunohistochemistry; D007275:Injections, Intravenous; D008168:Lung / Q000382:microbiology / Q000473:pathology; D008171:Lung Diseases / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology; D010019:Osteomyelitis / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D011884:Radius / Q000382:microbiology / Q000473:pathology; D013203:Staphylococcal Infections / Q000473:pathology / Q000503:physiopathology*; D013211:Staphylococcus aureus / Q000472:pathogenicity; D034421:Sus scrofa; D014774:Virulence