Since humans started making antibiotics for ourselves from 1940s, bacteria have evolved to counteract our efforts. They are now winning. There are strains of old patterns that withstand with everything we can throw at them. Meanwhile, our arsenal has dried up. Before 1962, scientists developed classes of antibiotics more than 20. Since then, they have made two.
Antibiotics have not only rescued patients; they have played a vital role in achieving major advances in medicine. They have successfully prevented or treated infections diseases those can happen in patients who are receiving chemotherapy as a major treatments; who have chronic diseases such as diabetes, terminal renal disease, or rheumatoid arthritis; or who have had several surgeries such as organ transplantation, joint replacements, or cardiac surgery etc. Antibiotics have also helped to extend expected life spans by changing the outcome of bacterial infections.
Antimicrobial resistance seems when microorganisms (like bacteria, fungi, viruses, and parasites) change when they are exposed to antimicrobial drugs (like antibiotics, antifungals, antivirals, antimalarials, and anthelmintics). Microorganisms those are antimicrobial resistance are sometimes called to as “superbugs or resistant”.
The rapid occurrence of bacteria is seeming worldwide, endangering the efficacy of antibiotics, which have transformed medicine. Many decades after the first patients were treated with antibiotics; but bacterial infections have again get a threat. The antibiotic resistance crisis has been occurred to the overuse and misuse of these medications, as well as a lack of new drug development by the pharmaceutical companies due to reduced economic incentives and challenging regulatory requirement.
And then there’s teixobactin, a still-experimental drug that may make a new era of antibiotic history. A team of scientists led by Kim Lewis from Northeastern University have specified a new agent named teixobactin, which destroyers some bacteria by preventing them from building their outer cellular coats. They used it to successfully treat antibiotic-resistant infections in mice and more importantly, when they tried to deliberately evolve strains of bacteria that resist the drug, they failed.
Teixobactin was highly effective in protecting from such common bacterial as Clostridium difficile, Mycobacterium tuberculosis and Staphylococcus aureus. An estimated 99% of the bacteria that might create antibiotic agents live in earth but refuse to grow in lab. As a result, a world of antibiotic possibilities has been beyond the reach of researchers. So Lewis and his team invented an isolation chip, or iChip, device that “essentially tricks them.
The researchers took bacterial cells and diluted them in media. They made a growing rack that stored huge panels of treated bacterial culture and immersed individual in soil from which the bacteria had originally been collected. Recognizing the familiar surroundings, the bacteria not seems to notice the foreign presence of media and replicated as if they had never been removed from their primordial soup.
Among these new microbes, the team found one species that kills identified bacteria efficiently. It belongs to an entirely new genus and is part of a group that’s not known for making antibiotics. They called it Eleftheria terrae. It yielded a compound—teixobactin—that could kill significant identities like the bacteria causing anthrax and tuberculosis, and Clostridium difficile (which causes severe diarrhoea). The team exposed some of these microbes to minor levels of teixobactin for some weeks, to see if resistant strains would evolve.
Teixobactin works by withholding two molecules—Lipid II, which bacteria required to develop the cell walls around their body, and Lipid III, which stops their existing walls from breaking down. When teixobactin is around, bacterial walls come crumbling down, and don’t get rebuilt. The drug also binds to parts of both Lipid II and III those are remaining across different species. It’s likely that these parts can’t be altered without disastrous events, making it harder for bacteria to skip teixobactin. This might explain why it’s so hard to evolve resistance to the drug. This won’t work on every bacterium. Many of them, like E.coli, Helicobacter and Salmonella, have another membrane around their cell walls which can be deflected by teixobactin.
The development of resistance is inevitable and need to focus on introducing antibiotics faster than pathogens can acquire resistance. About 25,000 people a year in Europe alone already die from infections that are resistant to antibiotics and the World Health Organization has described the rise of antibiotic-resistance as one of the most significant global risks facing modern medicine.
Teixobactin gives us an example of how we can develop an alternative strategy on developing compounds where resistance is not going to rapidly develop.
Priyanka Florina Karmokar is a graduate pharmacist. She has completed her gradation under department of pharmacy of University of Asia Pacific. She has interest on public health and recent health issues. She can be reached at email@example.com
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