Antibiotic resistance: Superbugs can be killed by modifying existing drugs, scientists discover
By www.independent.co.uk
One type of antibiotic is found to kill bacteria by ripping it open by brute force, a previously unknown method that could help make a whole new generation of drugs.
In the evolutionary arms-race between deadly bacteria and the antibiotics used by doctors to kill them, the bugs have very definitely been gaining the upper hand in recent years.
But, amid growing reports of bacteria resistant to even the ‘last resort’ antibiotics, comes the news that scientists have found a new way that some existing drugs can still be effective.
Normally antibiotics must bind to a bacteria cell in order to kill it, like putting a key in a locked door.
But the researchers found that one drug exerted such a strong physical force on the bacteria that it “tore the door off its hinges”.
The hunt is now on for other antibiotics with similar properties to create a “new generation” of drugs capable of defeating even the most resistant superbugs.
Last year, growing concern about antibiotic resistance prompted then Prime Minister David Cameron to warn of "catastrophic consequences" if the problem was not dealt with across the world. The UK was instrumental in organising a meeting at the United Nations to discuss the issue.
One of the researchers, Dr Joseph Ndieyira, of University College London, said: “Antibiotics work in different ways, but they all need to bind to bacterial cells in order to kill them.
“Antibiotics have ‘keys’ that fit ‘locks’ on bacterial cell surfaces, allowing them to latch on.
“When a bacterium becomes resistant to a drug, it effectively changes the locks so the key won’t fit any more.
“Incredibly, we found that certain antibiotics can still ‘force’ the lock, allowing them to bind to and kill resistant bacteria because they are able to push hard enough.
“In fact, some of them were so strong they tore the door off its hinges, killing the bacteria instantly.”
The study tested a powerful antibiotic called vancomycin, used as a last-resort treatment for infections like MRSA, and another called oritavancin, used to treat skin infections.
“We found that oritavancin pressed into resistant bacteria with a force 11,000 times stronger than vancomycin,” says Dr Ndieyira.
“Even though it has the same ‘key’ as vancomycin, oritavancin was still highly effective at killing resistant bacteria.
“Until now it wasn’t clear how oritavancin killed bacteria, but our study suggests that the forces it generates can actually tear holes in the bacteria and rip them apart.”
This way of killing bacteria has not been seen before.
“Oritavancin molecules are good at sticking together to form clusters, which fundamentally changes how they kill bacteria,” Dr Ndieyira said.
“When two clusters dig into a bacterial surface they push apart from each other, tearing the surface and killing the bacteria.
“Remarkably, we found that conditions at the bacterial surface actually encourage clustering which makes antibiotics even more effective.”
The researchers have now developed a mathematical model that could be used to screen for new antibiotics that have the same “brute force” approach.
“Our findings will help us not only to design new antibiotics but also to modify existing ones to overcome resistance,” Dr Ndieyira said.
“Oritavancin is just a modified version of vancomycin, and now we know how these modifications work we can do similar things with other antibiotics.
“This will help us to create a new generation of antibiotics to tackle multi-drug resistant bacterial infections, now recognized as one of the greatest global threats in modern healthcare.”
The growth of antibiotic resistance has been driven partly by over-prescription of the drugs for conditions like the common cold, which is a virus, not a bacterium, and is therefore unaffected.
Antibiotics have also been used in agriculture to boost the growth of livestock.
Source: http://www.independent.co.uk/news/science/superbugs-kill-cured-existing-drugs-antibiotic-resistance-new-way-scientists-ucl-a7561686.html
Saturday, May 30, 2026
Esomeprazole (Nexium) - Acid Reflux - Patient guide
Esomeprazole, commonly known by brand Nexium, is proton pump inhibitor used for gastroesophageal reflux disease, erosive esophagitis healing, and acid suppression in selected ulcer-risk situations. It reduces gastric acid production by blocking proton pumps in parietal cells. For many patients with persistent heartburn, nocturnal reflux, or esophageal irritation, esomeprazole can improve symptom control and mucosal healing when used consistently and timed appropriately. Typical use involves once-daily dosing before meals, with duration tailored to indication. Some conditions require short treatment courses, while others need longer maintenance with periodic reassessment. Despite strong efficacy, prolonged acid suppression should be reviewed regularly to avoid unnecessary exposure. Potential long-term concerns include nutrient malabsorption patterns, altered infection risk, and rebound symptoms after abrupt discontinuation in some patients. These factors explain why nexium-esomeprazole for acid and ulcer management should be paired with clear indication review and step-down planning when feasible. Persistent alarm symptoms such as dysphagia, gastrointestinal bleeding signs, unintended weight loss, or severe chest pain require prompt evaluation. Lifestyle supports remain important: meal timing, trigger-food awareness, weight strategy, head-of-bed elevation, and smoking reduction can reduce breakthrough symptoms and medication dependence. Patients should track symptom frequency, nighttime awakenings, rescue-antacid use, and food triggers. Function-based data helps determine whether current regimen remains necessary. For broader comparison of reflux-treatment pathways and long-term acid-control planning, patients can review acid reflux treatment resources before follow-up visits. Clinical review should confirm whether symptoms are acid-driven or overlap with motility, functional, or cardiac causes that need different management. Patients benefit from written dosing instructions, especially regarding pre-meal timing and missed-dose handling. If long-term therapy is needed, periodic dose-minimization trials can reduce exposure while preserving symptom control. Structured follow-up improves safer maintenance. Good communication supports adherence, better step-down success, and fewer rebound symptom episodes. Consistent reassessment keeps therapy effective and appropriately targeted over time.
Subscribe to:
Post Comments (Atom)
No comments:
Post a Comment
Note: Only a member of this blog may post a comment.