Antibacterial compounds have been used to help humans overcome otherwise difficult bacteria since 1928, when Alexander Fleming discovered penacillin. Penicillin then came into use in the late 1940s, where it helped my grandfather overcome an ear infection that had afflicted him for over a year. Since then, other new classes of antibiotics have been developed that target other bacterial processes than penicillin, but no new class has come out in the 25 years, until now.
The new compound, teixobactin, seems almost inexplicably impervious to evolution in trials so far. Isolated from bacteria found in a grassy field in Maine, USA, this brand new protein may hold the most promise of any antibacterial currently on the drawing board. It works through a previous unexploited mechanism of action against (so far) all gram positive bacteria and appears to have no negative effects on mouse cells even at the highest dose used (125 µg ml−1), while killing all gram positive bacteria tested even at the lowest dose. This is actually pretty unique, and very exciting.
Some, but not all, anti-bacterial compounds are also “effective” against animal and/or plant cells, like kanamycin which targets the prokaryotic ribosome (which turns genetic information into proteins, to put it really simply) that are also present in the mitochondria (which can be thought of as power plants) in both animal and plant cells. Others are risky for human due to allergies or interactions with other systems (like sulfonamides, which compete with penicillins for being the first class of antibiotics developed).
There are a number of different types and classes of antibiotics, but so far essentially all existing classes had protein targets. Although the new drug (teixobactin) also interferes with cell wall synthesis (the same general target as penicillin), it doesn’t have a protein target. Protein based targets are prone to trigger an evolutionary arms race in which the bacteria evolve to create slightly different proteins which are then no longer targeted by existing antibiotics. Instead, teixobactin appears to targets lipids (fats) involved in bacterial cell wall synthesis instead of proteins. This makes it far more difficult for the bacteria to adapt to.
Add on the fact that it doesn’t harm mice, and it sounds like a miracle drug for otherwise dangerous and multi-resistant bacteria. Of course it would technically be possible for bacteria to develop a protein that could degrade or inhibit teixobactin (similar to ß-latamase against several different types including penicillins), but there has yet to be any evidence of this.
We also have to acknowledge that fact that this study by Ling, Schneider et al developed a new mechanism for refining and finding antibacterial compounds, as well as coaxing wild strains of bacteria to grow in the lab (which the authors claim 99% of wild bacteria normally cannot). This is at least as exciting as the discovery and characterization this new compound.
Teixobactin treatment, even at the lowest levels, led to absolutely no resistant bacteria while also appearing to leave mouse cells safe. Although the use of any full-spectrum antibiotic should be reserved for emergencies, since such compounds also kill normal/symbiotic bacteria in your body (there are some exceptions: not all antibacterials are so unselective, like fidaxomicin), it is exciting to a have a brand new solution for treating a wide range of otherwise multi-resistant bacteria that have become a problem in hospitals around the world and are described by the WHO as a global threat.