How did we get to such a drastic point with antibiotics?

Professor Milton Wainwright an expert in the history of antibiotic resistance at the University of Sheffield spoke to us about how the power of antibiotics has become so diminished since its first use in clinical medicine.

Video 1. Professor Wainwright’s interview discussing antibiotic resistance development and factors increasing the development of resistant bacterial strains.

Further to Prof. Wainwright’s explanation of increasing antibiotic resistance, the figure below (fig. 1) shows the incredible rapid rate that bacteria develop antibiotic resistance to all antibiotics developed. This highlights the importance of using what remaining antibiotics we have very wisely.

Fig. 1 Timeline showing the year each antibiotic drug was introduced onto the market with observed antibiotic resistance from specific bacterial strain for that drug on opposite side of timeline. From “Targeting virulence: a new paradigm for antimicrobial therapy” (541-8) by A.E. Clatworth et al. (2007) Nature Chemical Biology.

As Prof. Wainwright explained, one of the factors contributing to this rapid development of antibiotic resistance is their overuse. So why then, in the face of this crisis, do we continue to overuse antibiotics?

Economics studies people’s behaviours under the constraint of scarce resources something which we all face. For our project, patients and doctors face the scarcity of antibiotics in terms of its effectiveness over the time. However, taking antibiotics in some cases does offer benefits, therefore decisions must be made about how much antibiotics should be consumed in total.

To offer a conceptual explanation to this phenomenon we turned to an Economics lecturer at the University of Sheffield, Dr. Jolian McHardy.

From the beginning we were really enthusiastic about our project, as we believed a device addressing the global problem of antibiotic resistance could revolutionise healthcare on an international level.

Where we fit in

We also choose to look at a biomarker, Lipocalin 2, that is produced by the body in response to bacterial infection rather than a biomarker from bacteria. This meant that our device would be able to detect all bacterial infections instead of being specific for a particular bacterial infection. A factor we hoped would give our device greater applicability and therefore impact.

Bibliography:

Clatworth, A.E., Pierson, E. and Hung, D.T., (2007). Targeting virulence: a new paradigm for antimicrobial therapy. Boston: Nature Chemical Biology, 3(9), pp. 541-548.