 Hey everybody, Dr. O. Obviously, antibiotics is a huge topic, it's one of the main reasons you take a microbiology class if you're working in the health sciences. So we've got a lot of ground to cover here, but in this video I just want to cover the mechanisms or modes of action of the most common antibiotics. So real quick refresher for you when you learned about the structure and function of bacteria. Remember that two key differences that we exploit are that bacteria have cell walls, heptidoglycan cell walls, and our cells don't need cell walls, and bacteria have a different shaped ribosome than us. So most of our ribosomes are the ADS eukaryotic ribosomes, not counting the ones that are in our mitochondria, while bacteria have 70S ribosomes. So you're going to see that two of the key players here are going to be the antibiotics that disrupt cell wall production, and the antibiotics that inhibit the 70S ribosome of bacteria. So all right, let's just go through the list here. You see on the left hand the cell wall inhibitors, so obviously these are great selectively toxic antibiotics, because if we can disrupt the production of the peptidoglycan cell wall, then we can damage bacteria, and that shouldn't hurt us, because again, we don't have the peptidoglycan cell walls like they do. So these are generally going to be more narrow spectrum antibiotics though, at least the natural ones, because gram positive bacteria care a lot more about their cell walls than gram negative bacteria do. So just remember that your cell wall inhibitors are usually much more effective against the gram positives, but that's okay, because we need them to fight off our staffs, and like you see Vancomycin on this list is one of our last lines of defense against MRSA, these types of things. So the cell wall inhibitors are generally going to impact the gram positive bacteria more. Now we do now have extended spectrum and broad spectrum cell wall inhibitors as well. So we'll cover the individual antibiotics in different videos. All right, we'll just go in order here. So the plasma membrane inhibitors, these are going to be pretty rare, because plasma membranes are the same as you, yours. We have phospholipid bilayer plasma membranes just like bacteria do. So most of these are going to have to either be used topical like polymixin B or they're going to come with side effects like colostin, but colostin is a super, super important antibiotic. We'll do a separate video just on that one, because that is truly our last line of defense against some of the scariest organisms on the planet right now. All right, so your plasma membrane inhibitors. Next group, the ribosome inhibitors, I would say that generally speaking, unless you get to a real high dose, these are more likely to be bacteriostatic than your cell wall inhibitors, because the cell wall inhibitors, as these cells are dividing, their cells are going to get weaker and weaker and then they will rupture or disappear. So that will kill the microbes, the bacteria. The ribosome inhibitors, the protein synthesis inhibitors, they're generally just slowing down or stopping the production of protein. So it might not kill an individual micro, but it'll certainly slow down or stop their growth. Those are the ribosome inhibitors, long list of them there that we'll cover. Metabolic pathway inhibitors, so we do have a couple of metabolic pathways that are kind of interesting. So you see here that some of these, like the sulfa drugs, they inhibit the production of folic acid and that's pretty cool, because we obviously need folate or folic acid and so do microbes, but they have to make it and we actually get it from our diet. So it's another example of a selectively toxic type of antibiotics. We can stop the production of folic acid, but because we don't make it, it shouldn't hurt us at all. At the bottom of that list here, you see the mycolic acid inhibitors. So mycolic acid is that waxy material that's in the cell wall of the mycobacterium, like the causative agents of tuberculosis and leprosy. You're also going to find them in the no-cardia, which aren't as big of a deal. But again, we don't have mycolic acid cell walls. We don't have cell walls. So it's a great thing to inhibit that should hurt the microbes without killing us, their host. Then the last group, you see the DNA and RNA synthesis inhibitors. So these generally do come with quite a few side effects. There's not a lot of drugs in this group for the same reason we've mentioned several times now. We have to make DNA and RNA. So if we can find a way to selectively block the production of microbial DNA and RNA synthesis without hurting how our human cells make it, then that's an awesome thing. So all right. So those are the mechanisms of action of all the antibiotics we'll cover. So we'll do separate videos on each mechanism of action, and then I will also highlight a few individual antibiotics just because of their wickedly importance. So this is just an intro. So stay tuned. All right. I hope this helps. Like all the other videos that I make for you, and therefore you. Have a wonderful day. Be blessed.