Peter Panizzi

Peter Panizzi

Auburn University, USA

Title: Contribution of host thrombosis and fibrinolytic cascades to the pathogenesis of gram-positive infections


Peter Panizzi, Ph.D., is an Assistant Professor at Auburn University. He received his doctorate from Vanderbilt University in 2004 and completed at post-doctoral fellowship at the Center for Systems Biology at the Massachusetts General Hospital from 2007-2010. He has co-authored >32 high- impact articles and was awarded a NIH pathway to Independence Grant (K99R00) from NHLBI before coming to Auburn. His research focus is to better understand how certain bacteria are able to cause human disease and in turn use this knowledge against the microbe to detect specific sites of infections and identify casual pathogen.


Exploiting or usurping host pathways are critical elements to proper establishment of infections in vivo by many human pathogens. Gram-positive Staphylococcus aureus (S. aureus) and Streptococcus pyogenes are among the deadliest pathogens to humans and clinical interest into mechanisms that govern their infectivity has increased, partly due to their increased antibiotic resistance. Exemplified here, coagulase-positive S. aureus is one of these emerging Superbugs that hijacks the clotting cascade to effectively limit phagocytic immune cell infiltration. In vivo bacterial colonization occurs at sites of endothelial damage and complex fibrin-networks quickly develop. S. aureusforms thisprotective barrier throughexpression of a redundant virulence factors, namely staphylocoagulase and von Willebrand factor binding protein (vWbp) that bind the zymogen prothrombin, thereby forming a prothrombin-activator complex that cleaves fibrinogen to fibrin. Recently, we took advantage of this unique mechanism of prothrombin recruitment to detect S. aureus in vivo in a mouse model of endocarditis via noninvasive fluorescence and PET-CT methods by systemic injection of specifically designed prothrombin analogs. Use of strains of S. aureus deficient in one or both bacterial prothrombin activators, provided the first in vivo validation to the importance of these factors in the establishment of endocarditis. Much unlike S. aureus, Streptococcus pyogenes harnesses host fibrinolytic pathways to mediate potential dissemination of the pathogen in vivo. The mechanisms employed by these pathogens will be discussed to highlight this interplay between the misregulation of host systems and pathogens during infection

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