Open AccessIntravenous inoculation of Staphylococcus aureus in pigs induces severe sepsis as indicated by increased hypercoagulability and hepatic dysfunction
Author(s) -
Leifsson Páll S.,
Iburg Tine,
Jensen Henrik E.,
Agerholm Jørgen S.,
KjelgaardHansen Mads,
Wiinberg Bo,
Heegaard Peter M.H.,
Astrup Lærke B.,
Olsson Anna E.,
Skov Mette G.,
Aalbæk Bent,
Nielsen Ole L.
Publication year - 2010
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2010.02042.x
Subject(s) - neutrophilia , sepsis , staphylococcus aureus , bacteriology , medicine , hematology , staphylococcal infections , immunology , gastroenterology , biology , bacteria , genetics
Nine pigs were inoculated intravenously once or twice with 10 8 Staphylococcus aureus per kilogram body weight and sacrificed 12, 24 and 48 h after inoculation. Three sham‐infected pigs served as controls. Blood samples were taken for bacteriology, haematology and clinical chemistry. A necropsy was carried out and tissue samples were collected for bacteriology and histology. The onset of clinical disease was seen at 7–8 h after inoculation. The blood bacterial counts remained low throughout the study. All infected pigs developed sepsis characterized by fever, neutrophilia, increased levels of C‐reactive protein (CRP) and IL‐6, and decreased levels of serum iron. The CRP and IL‐6 levels peaked at 36 h, whereas IL‐1β and tumour necrosis factor‐α showed no obvious changes. Thromboelastography showed increasing hypercoagulability from 12 h and onwards, whereas the platelet numbers declined slightly throughout the experiment. The levels of serum aspartate aminotransferase and bilirubin were elevated at 24 and 36 h. In conclusion, sepsis and severe sepsis were induced as evidenced by dysfunction of the blood clotting system and the liver.