Effect of Flow on Bacterial Endocarditis

Undergraduate #325
Discipline: Technology and Engineering
Subcategory: Biomedical Engineering

Jamie Nunez - University of Washington
Co-Author(s): Wendy Thomas, Olga Yakovenko, and Jasmine Hawkins, University of Washington, Seattle, WA

---

Bacterial endocarditis is an infection on the inner lining of the heart. Even though this disease has been studied for decades, there is still not much known about this complex disease. We hypothesize that flow conditions play a critical role in the initiation and progression of bacterial endocarditis. In the heart, flow is pulsatile, meaning that the flow oscillates between two different flow rates. This could allow bacteria to bind in times of low flow and then stay attached when the flow increases once again; however, this has often been ignored or deemed insignificant. Scientists will often use constant flow rather than pulsatile to study these types of bacteria and their adhesive properties. In order to test our hypothesis, we first started with a parallel flow chamber to ensure that we can get a response time, the time it takes for a particular system to respond to an input, low enough to mimic a heart beating 60 times per second. A low response time is important since rapidly changing flow rates may not give our device enough time to reach the maximum and minimum flow rate desired. To lower the response time, the set up for our system, including tubing, a syringe pump, syringe, and flow chamber, was altered. We then used Particle Imaging Velocimetry to analyze the response time and how it was changed by these alterations. So far, we have achieved a response time of about 0.3 seconds, which allows us to simulate a heart beating 15 times per minute. We then tested how Streptococcus gordonii, a strain of bacteria that is known to cause bacterial endocarditis, bound in constant and pulsatile flow with this set up and found that the two conditions caused almost equal amounts of bacteria to bind. Also, binding was still present for both conditions in the high shear stresses present in the heart, 2-8 Pa. This data shows that, while pulsatile flow does not cause more adhesion than constant flow, it does not cause less binding, either. To further evaluate this data and its physiological relevance, we will continue to lower the response time to better simulate what happens in the heart. Once this is accomplished, we can again study S. gordonii’s adhesive properties and draw further conclusions.

Funder Acknowledgement(s): This research was funded by National Institute of Health (1R01 AI106987-01), NASA Space Grant, LSAMP, the University of Washington GenOM Project (NIH 5R25HG007153-03), a gracious donation from Dr. Anne Dinning and Dr. Michael Wolf, and the Genentech Foundation.

Faculty Advisor: Wendy Thomas, wendyt@uw.edu