A surprising Rutgers Health study reveals why common antibiotics like ciprofloxacin may be making infections harder to treat. Instead of wiping out bacteria, these drugs could be inadvertently training them to survive and evolve resistance faster.

The study focused on ciprofloxacin, a go-to antibiotic for urinary tract infections. Researchers found that while the drug causes an “energy crash” in bacteria by depleting ATP (the cellular energy source), it doesn't always kill them. The studyfocused on ciprofloxacin, a commonly given medication for urinary tract infections. The researchers discovered that the medicine causes a type of "energy crash" in bacteria. Instead of dying, many bacteria respond by increasing their metabolism, allowing them to withstand the attack and change more quickly. 

The lead researcher, Barry Li, stated, "We saw the opposite of what people expected." The germs did not slow down. They accelerated. They used this stress to survive and even develop resistance faster." 

When bacteria are exposed to certain antibiotics, their internal energy levels, particularly ATP (adenosine triphosphate), which powers all cellular processes, plummet dramatically. This abrupt energy scarcity puts them in a state known as bioenergetic stress. Instead of dying off altogether, many bacteria react to the crisis in two unexpected and deadly ways. 

First, some cells become persisters, a type of dormant cell that can withstand antibiotics without dying. These cells essentially "play dead" until the antibiotic threat is removed, then reactivate to continue infection. In laboratory research, stressed bacteria produced ten times as many persister cells as normal bacteria. 

Second, the few survivors begin to mutate quicker. Stress causes them to produce reactive oxygen species (ROS), harmful molecules that damage their DNA. Instead of dying, bacteria use error-prone repair processes that promote genomic changes. This unintended consequence actually and potentially leading to antibiotic resistance. 

Together, these studies demonstrate how bacteria under stress their ability to fight drugs in the future. 

Jason Yang, co-author of the study and an assistant professor at Rutgers, stated, "Bacteria turn our attack into a training camp. If we can turn off the power to that camp, we can keep our antibiotics operating longer." 

This result calls into question long-held beliefs that bacteria survive by slowing down after antibiotic treatment. Instead, rapid metabolic responses may be the true culprits driving growing resistance. 

Even more concerning, preliminary research indicates that other antibiotics, such as gentamicin and ampicillin, may have comparable impacts on bacterial energy systems. If these findings are consistent across different viruses, they could change how we treat infections. 

Antibiotic resistance is already responsible for 1.27 million deaths . The rising crisis jeopardises ordinary surgeries, cancer treatment, and even childbirth, all of which rely significantly on efficient antibiotics. 

The Rutgers team advocates for a new approach to antibiotics, both in laboratories and clinics. They emphasise that novel antibiotics should be evaluated not only for their ability to kill germs but also for potential adverse effects on bacteria's metabolism that may increase resistance. To make therapies more effective over time, they suggest combining antibiotics with chemicals that inhibit bacterial stress responses or reduce toxic substances such as reactive oxygen species. Importantly, they warn against using excessively high doses, which may backfire by encouraging germs to build even stronger defences. These changes, taken together, have the potential to retain antibiotic effectiveness for future generations. 

Li and Yang are currently exploring compounds that energy state will make them more susceptible to treatment. 

This study highlights a terrible irony: the medications used to kill bacteria may be making them smarter and stronger. As Yang put it, if we don't address the metabolic consequences of antibiotics, we risk giving bacteria exactly what they need to destroy us.