Aggregating resistant Staphylococcus aureus induces hypocoagulability, hyperfibrinolysis, phagocytosis, and neutrophil, monocyte, and lymphocyte binding in canine whole blood

Abstract

Background Staphylococcus aureus is an opportunistic pathogen with the ability to form mobile planktonic aggregates during growth, in vitro. The in vivo pathophysiologic effects of S aureus aggregates on host responses are unknown. Knowledge of these could aid in combating infections. Objective This study aimed to investigate the effect of increasing concentrations of two different aggregating S aureus strains on the hemostatic and inflammatory host responses in canine whole blood. The hypothesis was that aggregating bacteria would induce pronounced hemostatic and inflammatory responses. Methods Citrate‐stabilized whole blood from 10 healthy dogs was incubated with two strains of aggregating S aureus at three different concentrations. Each sample was analyzed using tissue factor‐thromboelastography (TF‐TEG) and the formed clot was investigated with electron microscopy. The plasma activated partial thromboplastin time (aPTT), prothrombin time (PT), fibrinogen, and D‐dimer tests were measured. Bacteria‐leukocyte binding was evaluated with flow cytometry, and neutrophil phagocytosis was assessed using light and transmission electron microscopy. Results The highest concentration of bacteria resulted in a significantly shortened TF‐TEG initiation time, decreased alpha, maximum amplitude, global strength, and increased lysis. In addition, significantly shortened PT, decreased fibrinogen, and increased D‐dimers were demonstrated at the highest concentration of bacteria. Lower concentrations of bacteria showed no differences in TF‐TEG when compared with controls. The findings were similar for both S aureus strains. Increased concentration‐dependent binding of bacteria and leukocytes and neutrophil bacterial phagocytosis was observed. Conclusions Two strains of S aureus induced alterations of clot formation in concentrations where bacterial aggregates were formed. A concentration‐dependent cellular inflammatory response was observed.