During human meningococcal infections, bacteria adhere to the endothelium, accumulate in the form of aggregates and finally fill up blood vessels, causing severe diseases such as septicemia and meningitis. However, the mechanisms governing formation of bacterial aggregates and their impact on infection remained elusive. Here, we show that aggregates of Neisseria meningitidis behave as a viscous liquid similar to honey. This is due to type-IV pili, long adhesive filaments which are constantly extending and retracting at the bacterial surface. By these means, bacteria can find each other and transiently come into contact. Aggregation is therefore based on an intermittent process of attraction between bacteria, and gives rise to a new type of active fluid. Importantly, the unique physical properties of meningococcal aggregates allow them to remain cohesive while rapidly adapting to the complex geometry of the vascular network. As a consequence, this active fluid efficiently colonize blood vessels leading to disease progression. Finally, I will focus on the interaction of bacteria with host cells, and present some open questions related to the forces at play upon type-IV pili mediated adhesion to the host cell plasma membrane and to their consequences on the global mechanical state of the host cell.