Blood coagulation often accompanies bacterial infections and sepsis and is generally accepted as a consequence of immune
responses. Though many bacterial species can directly activate individual coagulation factors, they have not been shown to
directly initiate the coagulation cascade that precedes clot formation. Here we demonstrated, using microfluidics and surface
patterning, that the spatial localization of bacteria substantially affects coagulation of human and mouse blood and plasma.
Bacillus cereus and Bacillus anthracis, the anthrax-causing pathogen, directly initiated coagulation of blood in minutes when
bacterial cells were clustered. Coagulation of human blood by B. anthracis required secreted zinc metalloprotease InhA1, which
activated prothrombin and factor X directly (not via factor XII or tissue factor pathways). We refer to this mechanism as ‘quorum
acting’ to distinguish it from quorum sensing—it does not require a change in gene expression, it can be rapid and it can be
independent of bacterium-to-bacterium communication
