Those bacteria that have ways to protect themselves from antibiotics, what are their mechanisms and how do they work?
In: Biology
Lots of ways, the basic concept behind all of them is that all bacteria have some random amount of mutations each generation. Some small portion of them get lucky and have random mutations that prevent the antibiotic from working without harming the bacteria. Those bacteria then survive and all their descendants have the resistant mutation.
As a specific example, penicillin works by breaking down bacterial cell walls. It finds cell walls by binding to proteins that we call penicillin binding proteins. They have jobs unrelated to penicillin, we just call them that because we discovered them in the context of antibiotic function. Some bacteria have mutations in their genes for penicillin binding proteins that make it so penicillin can’t bind anymore but the normal functions are maintained. These bacteria are now immune to penicillin.
Basically, every new bacteria is a super low odds dice roll for antibiotic resistance, they just multiply at unbelievably high rates so the super low odds actually start to come into play. Bacteria can divide every 4-20 minutes, so with optimal conditions a single bacteria can have twenty generations pass and a million living descendants after just 80 minutes. That’s about 400 years of human evolution ever hour. There have been approximately 12,000 generations of humans who have ever lived, bacteria can do that in a couple of months.
I can’t explain the precise mechanism (there are many), but I can explain how they occur.
The dna of any organism undergoes changes, due to errors in copying or damage from various sources. Sometimes, those changes result in a new trait (different coloured hair for example). This is called mutation and it’s entirely random.
If you have a colony of bacteria, and one of them mutates in such a way that antibiotics are no longer very good at killing it, that bacterium will be more likely to reproduce, while the rest of them will likely be killed off. The mutation will pass to the offspring, and since all the competing bacteria have been killed, you’re left with the resistant strain only.
Multiple mechanisms can occur. They all result from random dna mutations. If that random mutation has an affect on the bacteria that it is now resistant to a specific antibiotic then it will divide and divide, while the other cells are killed, thereby the bacteria with the mutation becomes the only bacteria remaining
The mechanisms for resistance can be looked at as:
1. Breakdown the antibiotic : usually an enzyme evolves that will breakdown the antibiotic and do it faster than the antibiotic kills the bacteria. This is one of the reasons some bacteria can be partially resistant as you need large doses of antibiotics to kill the bacteria.
2. Alter the target of the antibiotic: some antibiotics use its interaction with certain molecules in the bacteria to be effective. For example some antibiotics will bind to specific parts of ribosomes to prevent protein synthesis. If that area changes in some way that stops the binding of the antibiotic but still allows protein production, the antibiotic is no longer effective
3. Limiting uptake of the drug: although some drugs will just diffuse into cells without help, many need the drug to be actively taken into them. It is usually something that’s normal purpose is to move some other necessity into the cell. If that mechanism is interrupted and no longer available, the antibiotic can’t get into the cell to do the killing
4. Kick the antibiotic out: the reverse of the above. Although the antibiotic can get into the cell, a mechanism develops that actively removes it from the cell. Therefore there is not enough antibiotic in the cell to cause enough damage to cause bacteria death before the cell can repair itself.
I talked to a researcher a few weeks ago, who’s running clinical trials.
They’re doing clinical human trials now on bacteria (I think it’s salmonella) where they’ve grown genetically modified “good” salmonella that cannot reproduce seeks out “bad” harmful salmonella and destroys it, because it recognizes it as its own “kind”. So, you get a shot or oral dosage of the good modified, it kills the bad, and then your body just treats it like any other cellular waste. They’re planning to do this for lots of other bacteria, and then also viruses.
Also, it’s a million times more cost effective of a treatment as the cells are easy to reproduce in a lab vs. antibiotics or antivirals, and supposedly much safer.
It’ll depend on the antibiotic, but should be a mix of “keep it out” (having a cell wall that blocks the chemicals) or producing a chemical that weakens/breaks down the antibiotic.
Imagine lactose was a deadly, deadly poison. Lactose intolerant people would die because they don’t produce the enzymes that digest lactose.
An antibiotic is like a ne’er-do-well with a copy of a key which, when put in the right lock turns off the cell (or makes it explode). Cells are full of important pieces that can act like this, all needing different keys. Sometimes the cell calls a locksmith and changes the lock–the key no longer fits into it. Sometimes the cell rewires itself so that lock doesn’t do anything anymore and it uses a different mechanism to turn itself on. In some cases the cell may even install something where the lock will spit out the key. As long as it can change *something* about the lock or the mechanisms attached to it it can acquire resistance.
Many others have given good explanations, and I’m not sure I could add much of value. But if you like a visualization answer to your question, [this video](https://youtu.be/plVk4NVIUh8?si=zdRuPBzrX6Zlba4y) from Harvard is really compelling.
Latest Answers