0:00 Armando Hasuduna in Biology and Medicine videos. Please make sure to subscribe. 0:05 Join the forming group for the latest videos. Please visit Facebook. Armando 0:09 Hasuduna. 0:10 This video on abscess of the skin will continue on from the previous video that 0:18 looked at skin anatomy, physiology and microbiology as an overview. 0:23 So if you haven't watched that, you can watch it if you want. 0:26 So abscess. Abscess of the skin. 0:31 So an abscess, it's a common infection characterized by localized accumulation 0:38 of neutrophils with tissue necrosis. 0:40 And it's mainly caused by the bacteria staphylococcus aureus. 0:46 So before we look at the pathophysiology or pathogenesis, you can say of an abs 0:51 cess of the skin, 0:52 we have to first understand the bacteria staphylococcus aureus, or at least to 0:58 some extent. 1:00 So staphylococcus aureus is a commensal pathogen in our body, on our skin, 1:06 especially. 1:07 Staphylococcus aureus is a cocus, so it's round bacteria. 1:13 The bacteria has circular DNA as well as plasmids, which are also genetic 1:19 material, usually containing some forms of resistant genes. 1:24 Now let's look at some virulent factors of the bacteria, which allows it to 1:31 infiltrate and invade other organisms. 1:36 So the staphylococcus aureus is a gram positive bacteria and so has a cell wall 1:43 with a thick peptidoglycan layer and an inner lipid membrane layer. 1:48 Staphylococcus aureus has a capsule that surrounds it, which allows it to 1:53 resist phagocytosis. 1:55 So when it infiltrates a body or invades a body, our body for example, the phag 2:01 ocytes within our body are unable to eat this bacteria up in some instances. 2:08 Staphylococcus aureus also contains adhesins, which are protein molecules or 2:13 carbohydrates that bind latches onto cells within the body, allowing it to 2:20 invade the cell. 2:22 These adhesins include fibronectin binding protein and collagen binding protein 2:27 . 2:28 Staphylococcus aureus also has a special protein known as protein A on its 2:32 surface. 2:33 Protein A protects the bacteria from antibodies, you can say, because 2:38 antibodies usually bind onto the bacteria so that the bacteria can be destroyed 2:44 . 2:45 But protein A binds onto the antibody from the back so the antibody doesn't 2:50 actually end up binding to the bacteria. 2:54 So here you can see the FC portion, which is the constant region of the 2:59 antibody, binding onto the protein A and the actual variable region on the top 3:05 doesn't latch onto the bacteria. 3:09 Staphylococcus aureus also produces some exotoxins, such as TSST1 and nteriotox 3:19 ins, which I won't talk into. 3:23 Staphylococcus aureus also produces invasins and produces two important invas 3:30 ins. 3:31 The first is known as coagulase. 3:33 Coagulase is an enzyme that converts fibrinogen, which is found in our body, 3:38 into fibrin. 3:40 This will form a fibrin clot. 3:45 So coagulase will essentially form a fibrin type clot. 3:51 And then it has the other invasin known as staphylokinase. 3:56 Now this enzyme activates plasmidogen and converts it to plasmid. 4:01 And this helps in breaking down fibrin clots. 4:05 So just to recap, coagulase will help the bacteria form a fibrin clot. 4:11 Staphylokinase will help the bacteria break a fibrin clot. 4:16 Now this is a really important concept to remember and understand about these 4:21 two enzymes. 4:22 You can imagine that when staphylococcus aureus invades our body, it can form a 4:31 fibrin clot around itself, 4:33 essentially protecting it from the immune cells of the host. 4:38 And then it can hide for some time and then using staphylokinase, it can break 4:42 down this clot and then continue its invasion process. 4:47 So it's a very, very unique sort of mechanism of infiltration. 4:55 So now that we know a little bit about staphylococcus aureus and its enzymes 4:59 and what sort of structures it has that allows it to resist phagocytosis, 5:04 you know, hide and stuff like that, let's look at how it forms an abscess. 5:09 So here we're looking at the section of our skin. 5:12 Here is the hair follicle, the layers of the skin, epidermis and the dermis. 5:18 Now within the layers of the skin, we can find some cells, some immune cells 5:23 that help protect our body from foreign substances and bacteria and pathogens. 5:28 We have dendritic cells on the epidermis. 5:31 We also have macrophages and epidermis and in the dermis, as well as mast cells 5:36 . 5:37 Mast cells contain histamine. 5:40 Here is our blood vessel, which is quite massive, but it's just used to 5:45 illustrate the concept. 5:47 And within the blood vessel, we have red blood cells. 5:50 So on top of our skin, we have staphylococcus aureus, which as I mentioned are 5:55 commensal bacteria because they live there in unison with our body. 5:59 But this commensal bacteria, which is also an opportunistic bacteria, can 6:04 invade the body when the skin is damaged in some way, such as an abrasion, a 6:11 burn or a cut or something like that. 6:13 And this will essentially open up an entry point for the staphylococcus aureus. 6:19 So you can imagine, because of the entry point, the bacteria staphylococcus a 6:22 ureus can enter the body. 6:24 And when it enters the body, these immune cells reciting here will detect it 6:29 and will begin initiating an immune response. 6:31 It will try to destroy the bacteria first. 6:33 At the same time, it will secrete inflammatory cytokines. 6:37 These inflammatory cytokines include TNF-alpha, interleukin-1, as well as hist 6:42 amine from the mast cells. 6:44 These inflammatory cytokines cause a number of things to happen, including vas 6:49 odilation of the blood vessel. 6:52 And cause an increase in vascular permeability, as well as recruiting more 6:59 immune cells to the area. 7:02 So here in the blood vessel, we have vasodilation. 7:06 Within the blood vessel, we have normally neutrophils circulating around the 7:10 body. 7:11 So when there's an increase in vascular permeability here, and there's like a 7:16 chemotactic effect, the neutrophils will enter this tissue area of invasion and 7:22 try to help the other immune cells. 7:25 So here we have now many neutrophils in the area. 7:28 They're coming like an army that will try to destroy the bacteria. 7:34 And now, because there's so many neutrophils in this area, the neutrophils are 7:40 essentially phagocytes that will blow up once it's destroyed, once it's eaten 7:46 something. 7:47 So it's like a kamikaze cell. 7:51 So these neutrophils, you can imagine, are going to try to eat up this bacteria 7:54 , try to destroy it at the same time it will blow up. 7:58 And due to this sort of fight between the bacteria and the neutrophils, this 8:04 will form an abscess. 8:06 Now an abscess is essentially pus. 8:10 Pus containing dead leukocytes, which are the neutrophils, as well as other 8:14 immune cells it can be. 8:16 And there's also dead skin cells, the epithelial cells, and connective tissue. 8:21 There's also bacteria, which is staph clockisaurus. 8:26 Now the abscess is capsulated. 8:30 It doesn't disperse everywhere. 8:33 It's within a border, you can say. 8:36 And this is due to the fact that bacteria produces these enzymes that allow it, 8:41 that protects it, such as the fibrin clot. 8:44 And so you have this bombardment of neutrophils trying to destroy it. 8:49 And this just essentially creates all this pus. 8:54 At the same time, you have the fibroblasts in the connective tissue layer 9:00 trying to repair itself. 9:02 And so this will also help form the capsule, the boundary of the abscess. 9:08 I hope you understood that made sense and you enjoyed this video on abscess 9:12 formation. 9:13 Thank you.
