Surface Actions Enable Antibiotics to Work Against Resistant Bacteria
Certain antibiotics can invade drug-resistant bacteria by using brute force at the surface level.
The emergence of bacteria that are resistant to powerful antibiotics has been an alarming issue in the healthcare field, with the creation of new drugs that can fight these bacteria a priority. According to the Centers for Disease Control and Prevention (CDC), more than 2 million people in the United States contract infections that are resistant to antibiotics. Out of these 2 million, 23,000 die.
Part of the problem can be attributed to antibiotic overuse, wherein healthcare providers prescribe antibiotics for patients even in cases where they are not warranted, such as with the common cold. All bacteria are constantly evolving and will eventually “outwit” the drugs used to kill them; however, antibiotic overuse speeds up this process—hence, the urgent need for new drugs. Yet, in the midst of this flurry of development of new antibiotics has come the discovery that certain antibiotics actually can kill supposedly drug-resistant bacteria. It all depends on the particular molecular changes that happen at the surface level.
As described in a recent research study, a team of scientists at University College London used the cantilever technique to quantify the surface forces that resulted when four different antibiotics—oritavancin, vancomycin, ristomycin, and chloroeremomycin—were tested against both drug-susceptible and drug-resistant bacteria. Although no significant differences among the bacteria were seen when they encountered the drug-susceptible bacteria, their behavior when introduced to the drug-resistant bacteria varied quite a bit. In fact, oritavancin was shown to be 11,000 times stronger against drug-resistant targets than vancomycin, which is often considered the treatment of last resort against drug-resistant bacteria such as methicillin-resistant staphylococcus aureus.
According to Joseph Ndieyira, PhD, a senior scientist at University College London and the study’s lead author, the precise mechanisms by which antibiotics work their magic include surface changes on the bacteria: “Antibiotics work like a key that fits into a lock on the bacterial cell surface, and by opening the lock, the antibiotic is able to kill the bacteria. When bacteria develop resistance, the key is no longer able to open the lock. However, with our new approach, the antibiotic is modified so as to force open the lock using brute force. Oritavancin is a much stronger drug against bacteria than vancomycin because it is able to form clusters that lead to generation of strong forces which tear holes in the surface of bacteria and rip them apart.”
The study team came up with a mathematical model highlighting the way antibiotics behave when encountering the surface area of different bacteria. “This model can be used to design new antibiotics or optimize existing ones so that they are more powerful at killing bacteria using brute force,” Dr. Ndieyira said.
The University College London team is not the only group of researchers developing innovative ways to deal with drug-resistant bacteria. Scientists at the Imperial College of London and Nottingham University Medical School recently released a study highlighting their use of Bdellovibrio bacteriovorus, a naturally occurring predatory bacterium, in the fight against Shigella bacteria, which can cause diarrhea and abdominal cramping.
Laurie Saloman, MS, is a health writer with more than 20 years of experience working for both consumer and physician-focused publications. She is a graduate of Brandeis University and the Medill School of Journalism at Northwestern University. She lives in New Jersey with her family.