Introduction to Bacteria

by Vincent Racaniello, PhD

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    00:01 Hello and welcome to Bacteria. We are going to dive a little bit deeper into how bacteria cause disease and after you've watched this video, you will understand the extent, origin and functions of the human microbiome. You will appreciate the ways that bacteria enter and spread in their hosts. You will be familiar with the different types of bacterial toxins and their activities and you will know the mechanisms of action of members of the different classes of antimicrobials and how resistance emerges.

    00:37 Before we talk about bacteria that cause disease, it's very important to first discuss the human microbiome, all of the microbes that live in and on us. We are home to trillions of microbes, trillions, and that's what we call the microbiome and it is a composition of all the microbes that are everywhere in us and on top of us. A human body is only 25% human cells. Now look, you can see me, you think you're looking at just human cells.

    01:13 75% of what you see here are bacteria, very, very little human cells, bacteria, fungi and archaea. It’s amazing. Wherever the human body is exposed to the outside world, there's a microbial community, the mouth, the lungs, the G.I. tract, the urogenital tract, the skin and probably other places we haven't even found it yet. This microbiome is just beginning to be unraveled in terms of what it does for us. It certainly helps us to extract energy and nutrients from the food we eat, but it also appears to inhibit the growth of pathogens, not only in us, but on our skin. The microbes on our skin produce antimicrobial compounds that protect us, it is remarkable. There is probably much more that the microbiome does, for example, recently it's been shown in animals that the microbiome helps their immune system to develop, it is really, really remarkable. In the coming years we will be able to sort all of this out, but it's quite clear from the very early days of our existence when we were first born, our microbiome forms and it has a huge impact on our health.

    02:39 Microbes contribute an extra 2 million genes to the 20,000 or so genes that our human genome encodes. 99% of our genes are bacterial, isn't it remarkable? Our microbiome weighs two and a half pounds, that is weight you will never be able to get rid of, you can try and lose some of your body fat, but that two and a half pounds of microbiome needs to stay with you, otherwise you are going to be very unhealthy, and don't forget the viruses, all those bacteria and fungi and archaea in us, they also are accompanied by their viruses, in fact viruses outnumber bacteria by about 5 to 1 in us and it's quite clear that they have major roles in regulating the microbiome.

    03:26 The volume of the microbiome is about 3 pints. The next time you drink 3 pints of beers, I want you to remember you’ve just drunk the volume of your microbiome. It’s my way of getting you to remember what I'm telling you here. Now where do you get this microbiome? There are many ways. While you are developing in utero, you are bathed in amniotic fluid provided by your mother, and of course it's going into your mouth and on your skin, and it's got bacteria and viruses in it, so that’s your first encounter. You are acquiring your microbiome in utero. Then as you are born, you acquire more of your microbiome. During birth, if you so happen to have been born by passage through the birth canal, you will start to acquire the bacteria that are present along that canal, not just in your mouth but on your skin. People who are born by cesarean section, they don't go through the birth canal, of course, they come out through an opening in the skin, produced by surgical manipulation, they have a very different skin microbiome from children who were born vaginally. So it's probably better to be born through the normal routes, you acquire probably a more beneficial microbiome, but of course in some cases it's not possible for health reasons. You also acquire a good amount of your microbiome from your mother. Your mother is one of the first to hug and kiss you, and she continues to do so, hopefully, for the rest of your life, and your father also contributes, and any caregivers who may come into your home, they are all contributing to your microbiome. Breast milk is a very important contributor to your gut microbiome, again breast-feeding is not done by everyone, but it has been shown in many studies to be better indicators of subsequent health. You also acquire microbiome from the soil that you may touch. You should let your kids play in the soil, it is probably good for them to help acquire their microbione from the water that you wash yourself in and drink, from the foods that you eat, and any people or pets or plants that you encounter early on in your life. The early years are formative years and then you acquire a relatively stable microbiome that is very similar to that of your family, and only when your health changes, or if you move or change your diet, do you change your microbiome. And the consequences of the microbiome for human health are going to be learned in the next 10 years and we’re really going to find out fabulous ways that we can improve our health by manipulating it.

    06:11 Okay, onto infection basics. Let's talk about some principles by which bacteria can enter the host. We can divide bacterial infections into two broad groups depending on how they're acquired. Some are acquired exogenously, from some external source, like bacteria in the environment or bacteria in the food, the water, the air, the objects we touch, insect bites, or any animals, dog bites for example. And so those are exogenously acquired from elsewhere, and that contrasts with endogenously acquired infections, where our microbiome suddenly turns on us and this could be because we've altered the microbiome by treatments with antibiotics, and Clostridial infections of the intestine are a great example of that, where we alter the composition of this family of microbes and then suddenly clostridia overgrow and cause us problems. Sometimes injuries introduce skin bacteria into us, and this is commonly occurring with Staphylococci, normal inhabitants of the skin, when an injury introduces them below the skin, this can cause a problem. So we get bacteria that cause infections and illness from external sources and from within ourselves.

    07:35 Let's talk a bit about how bacteria gain entry to the host, the exogenous sources of infection.

    07:42 Here is a human body, which provides a very large spectrum of places for bacteria to enter, a very common place is a mucous membrane. We have mucous membranes all throughout our body, our eyes, our mouth and nose, the entire alimentary tract, which is essentially a very long tube starting from our mouth going through our intestines and out the anus, that is all lined with mucous membranes because it has to absorb food and excrete waste, and because it's a mucous membrane, it is vulnerable, it is not sealed against entry. Things like breathing, eating, having sex, all can introduce pathogens into us. Cholera, whooping cough and gonorrhea are example of bacterial infections that are acquired across mucosal membranes. Now we are happened to be covered by a wonderful protective organ called the skin. Skin is the biggest organ in your body, it weights the most, and it has the most square area and it is a great barrier. The outer layer of your skin is dead, so viruses cannot multiply in them, they have to get inside by penetration, but there are ways that the skin can be breached, allowing bacteria to invade the underlying cells and tissues. How can this happen? Insect bites of course, they routinely deliver things below the skin, any kind of scratch or injury, which we are all prone to having, will also breach that wonderful protective barrier. Once you're in a mucosal membrane, there are ways to get across that, which are even easier than in the skin, you typically don't need an injury. Here is a cross-section of the intestinal mucosal barrier and on the left side is the lumen of the gut, the space in the interior, and the first line of defense is an epithelial cell barrier and below that are the submucosal tissues and that also contains capillaries and lymph capillaries, so if a pathogen can get across the epithelial cell sheet, it has access to the circulatory system, which can bring it anywhere, and of course below that are the muscle cells that help to contract the intestine during digestion. If we take a closer look at this intestinal lining, we can see that there are different kind of cells that make up that epithelial sheet, there are enterocytes, which are involved in taking up nutrients, and then interspersed among them are the so-called M cells, in which immune cells come from below lymphocytes and macrophages, and sample the contents of the gut to make sure there isn’t anything nasty there. Both the enterocyte and the M cell can be points where pathogens can cross into the underlying tissues. Once a bacteria has adhered to the epithelium, which many do, as we will talk about later, they can move laterally, reproduce and move across to contiguous tissues, or as I said they can penetrate the epithelial sheet and disseminate to distant sites. Our immune defenses play a big role in limiting such incursions, but they don't always win and bacteria do enter the rest of our body. Once a bacteria or many bacteria are in us, they typically multiply in order to cause disease, and this graph shows a time course of some typical infections: the x-axis shows you time and the y-axis shows you various parameters including the production of bacteria in red, and immune responses.

    11:28 So there is a period initially after the bacteria enter us called the incubation period, this is an extremely important concept. This is a period which is variable among the different infections during which the bacteria are multiplying, but we don't yet have overt disease. During that period, immune responses may be mounting, but again, you may have fever as a consequence of that, chills, aches, and so forth, but you won't have the actual symptoms of the disease, that is the incubation period. Then, as the bacteria multiply, they may either elaborate toxins or they may invade and cause tissue damage, you have a period of disease and if you follow the redline and go above the blue segment of this graph, that says no disease, above the blue is where we have bacterial disease and this can be a consequence of both the immune response and direct effects of bacterial toxins, which we will talk about in a moment, on us. There is a very important part of this graph which shows no disease.

    12:35 Some bacterial infections, where the bacteria are replicating, will not result in disease.

    12:41 These are called asymptomatic infections and many people have these, it's a consequence of them being able to control the replication of the bacteria, and others may have simply more resistance to disease formation. And the outcome, of course, of a bacterial infection can be recovery and cure, and subsequent immunity, it can be, unfortunately, in many cases death or in some cases immunity is not lifelong and we obtain recurrent illnesses with the same pathogens.

    13:12 Let’s talk a bit about bacterial toxins. These are molecules produced by various bacteria that alter the normal metabolism of host cells, and they are often responsible for the major symptoms of bacterial infection. And there are many different kinds of toxins that are produced, which we will talk about briefly. Interestingly, this is in direct contrast to viral infections, in which very few viral toxins have been identified; they cause disease in very different ways from bacteria. Now we recognize different classes of bacterial toxins, some are called exotoxins, because they are secreted by the bacterium into the extracellular environment. These exotoxins shown on this picture have a typical AB structure, they have subunits, separate subunits consisting of an A component and a B component. Typically the way they work, is they are secreted by the bacterium and they bind a receptor, shown here in R, on the surface of the eukaryotic cell, on the surface of our cells. They are then taken up into the cell by the endocytic pathway, and typically the A component, which is the active component, is released from the receptor binding component, makes its way into the cytoplasm where then has its effect on cells. There is another class of toxins called the type III cytotoxins, they are shown on the right of the diagram, where we see an outline of a rod shaped bacterium and what looks like a syringe, injecting molecules into the host cell. Those are type III cytotoxins, they are directly injected into the host cell by a structure on the bacterium called a secretory injection system and these have evolved just to inject toxins into the cell. These secretory systems act by introducing molecules into cells to alter their behavior. Other toxins are produced by bacteria, that act at the surface of host cells, some of them bind to pattern recognition receptors and induce the production of cytokines, which have lethal effects, there are also pore forming toxins which make holes in cell membranes and make them die. And finally there are toxins called superantigens that bind to T cell receptors and major histocompatibility receptors, and induce the synthesis of many, many toxic cytokines. And finally there are proteins called exoenzymes produced by bacteria that modulate targets in the extracellular matrix.

    16:00 Let’s look at toxins in a bit more detail. I mentioned that they typically have an AB structure. The diphtheria toxin consists of one molecule of the A and one molecule of the B, again the B is the receptor binding component, the A is the effector portion that actually has an effect on the host cell. Diphtheria toxin, the A portion blocks cell protein synthesis, the A portion ADP ribosylates, an elongation factor for translation eEF-2, it stops host cell protein synthesis and kills the cell. Cholera toxin is composed of a single A subunit and 5 B subunits. This toxin elevates intracellular cyclic adenosine monophosphate in the epithelium of the small intestine and that causes movement of fluid into the lumen and a classic diarrhea associated with cholera. And finally the Anthrax toxin, the highly lethal anthrax toxin is composed of two A and a B subunits, and again the B subunit binds the cell receptor.

    17:08 Two toxins that are well known, botulinum toxin, produced by C. botulinum and tetanus toxin produced, by C. tetani clostridium, are neurotoxins. These toxins elaborated by their bacteria at different sites make their way through the circulatory system and the lymph system, to the brain, where they cause their effects. Tetanus toxin for example, causes muscles to contract uncontrollably, and they cause what we call spastic paralysis.

    17:39 On the other hand, botulinum toxin blocks muscle contractions, so the muscles get flaccid, this is called flaccid paralysis, so two very different effects on the central nervous system.

    17:54 The type III cytotoxins we mentioned briefly before, they're shown on the right-hand part of this screen, they are injected by the bacterium into the host cell by a type III secretion apparatus. Bacteria have a number of different kinds of secretion apparati which are used to inject effector molecules into the host cell to get them to do what they want, and these have their own ways of altering the biochemistry of the cell to cause pathology.

    18:23 Type III cytotoxins are found in a wide range of bacteria, for example Salmonella, Shigella, Pseudomonas, Cholera and the Plague bacilli, all produce type III toxins of various sorts and we will mention a few of these and how they work in a few moments.

    18:46 Another toxin and a very important one, produced by Gram negative bacteria is endotoxin.

    18:56 Now, if you don’t remember what a gram negative bacteria is, go back to the introductory bacteria lecture and take a look. Endotoxin is sort of like the calling card of gram negative bacteria, it announces to the host, 'I'm here and you better watch out'. Endotoxin is nothing more than lipopolysaccharide, that outer layer on the outer membrane of a gram negative bacteria.

    19:24 So that outer layer is a lipid bilayer, but the outer layer is unusual, it's not the standard kind of lipid, it's made of lipopolysaccharide and that is what is endotoxin. Now despite the name endotoxin, this toxin is not internalized into the host cell, it remains extracellularly, it just happens to be the name that has stuck over the years. Let’s look in closer at that outer membrane, that lipopolysaccharide; here it is in some detail. Remember the very bottom, there are lipid chains that form the outer leaflet of that membrane and that component is called lipid A, that's the active component of endotoxin, that is what has the biological effect, and then there are other portions including the O portion that we talked about, which extends above, completing lipopolysaccharide. Lipopolysaccharide is recognized by pattern recognition receptors located on the surface of the eukaryotic cell. We all have such receptors in order for us to recognize what is foreign, and when foreign molecules are recognized, the result is a production of cytokines, which mobilize the immune response, but may also have detrimental properties. So on the left of this slide are three pattern recognition receptors, one of which recognizes LPS, that portion of the outer membrane of bacteria that we've just been talking about. Another one, FLA, recognizes flagellum, the protein that makes up the flagella of bacteria that helps them to move. So here's a close-up look at the pattern recognition receptor and it again recognizes endotoxin as being present, initiates cytokine synthesis and depending on how much endotoxin is present, low or high, it has different effects on the cell. So you can imagine that early in infection, it has one kind of effect, where the endotoxin is low, and then if the infection proceeds unchecked, you will have higher concentration of endotoxin, you will have a very different effect.

    21:39 These receptors for endotoxin and other bacterial products are called innate receptors, they also sense viral infections as well. So at low concentrations of endotoxin, there are a variety of effects, many of which reflect the attempts at the immune system of eliminating the bacterial infection, so let's take a look at some of these. You can see the four different targets here and the ultimate activities and effects of endotoxin. At low concentrations, endotoxin targets Kupffer cells, macrophages of various sorts, it causes release of cytokines, when it binds to its receptor cytokines are produced, and some of the cytokines cause fever. So endotoxin is well known to be pyrogenic, fever inducing, the mechanism is by being recognized by that innate receptor and producing a cytokine that induces fever. Cytokines, endotoxin also activates macrophages, it makes them more phagocytic, it makes them secrete hydrolases and have just more enhanced killing, the idea being of course, “there is endotoxin here, we sensed it, there must be a gram negative, we are going to kill it, so we are going to get activated”. At low concentrations, endotoxin also activates neutrophils, this has an effect of dilating blood vessels, and allowing immune cells to come in and clear any infections that may be present. Endotoxin also activates B lymphocytes, B lymphocytes of course produce antibodies and these may be useful for clearing the infection. Finally at low concentrations, endotoxin also activates the complement system, whose goal is manyfold, essentially trying to get rid of the bacterial infection, complement can help take up bacteria into macrophages by opsonization, it can increase capillary permeability and it can also poke holes into bacteria, all of this is part of the inflammatory response to infection. Now in contrast, at very high levels of endotoxin, it often can result in shock, fluid loss for example caused by too many cytokines and disseminated intravascular clotting or coagulation.

    24:01 There are other membrane damaging toxins as well, lipases for example, enzymes that digest lipids, an example is the lecithinase from Clostridial species. This enzyme can lyse cells and eliminate defenses and provides nutrients for bacteria. These are bacterial toxins lysing eukaryotic cells to avoid defenses and the lyse cells produce nutrients for the bacteria. Hemolysins can lyse red and white blood cells, and then there are toxins that form pores in the cell membrane, they insert into the membrane and they allow water to flow in and the cell bursts, again a way for bacteria to avoid some of those immune cells that are trying to get rid of the bacteria. We also have what are called heterogeneous pore-forming toxins, these are produced by a variety of bacteria, one well-known one is Streptolysin O, produced by the Streptococci. This pore-forming toxin binds cholesterol and damages liposomes in cells of the host, causes the cells to lyse, part of the reason why tissues are damaged. Another set of toxins that are produced and if you're thinking, “boy, bacteria make a lot of toxins”, you are right, this is their modus operandus.

    25:17 These are called extracellular matrix toxins. The extracellular matrix is the area between cells. Here on this picture, we are showing two cells and the area between them and below them, this is filled with all kinds of substances that provide protection and hold the cell together, this is the extracellular matrix. Bacteria produce enzymes called hyaluronidase.

    25:40 Hyaluronic acid is a component of the extracellular matrix, as you can see here, and this breaks it down. It breaks down connective tissue allowing bacteria to spread better. Streptokinase is an enzyme produced by streptococci, it activates plasminogen, converts it to plasmin, which then attacks blood clots and gets them to dissolve. Bacteria don't like blood clots because it inhibits them from moving about, it may restrict them, so this enzyme takes care of that; and finally collagenases and elastases also digest the extracellular matrix allowing free flow movement of the bacteria.

    26:19 I’d like to end up this discussion by talking about antimicrobial compounds that are used to treat bacterial infections and think we have a bacterial infection in us, we need to treat them with drugs that will kill the bacteria, but will not harm us. In other words, the antibiotics or antimicrobial compounds, have to be selective, they have to target things in the bacteria that are not present in ourselves. Fortunately, this is relatively easy to do, because bacteria are very different from eukaryotic cells. I’ll give you an example of such selectivity. There is a class of antibiotics called the β-lactam antibiotics, and these include the penicillins, the cephalosporins, and the carbapenems. They are called β-lactam antibiotics because they have a chemical ring in them called the β-lactam ring. These antibiotics target the synthesis of murein. Now do you remember from an earlier lecture what murein is? In gram positive bacteria this forms a thick layer on the outside of the bacterium, just above the cell membrane, and it's composed of sugar molecules joined together and cross-linked by amino acids of short length. On the right of this slide is a diagram of the synthesis of murein. Murein is exclusive to bacteria, it does not occur in eukaryotic cells, and on this slide are four different antibiotics, fosfomycin, cycloserine, vancomycin, and penicillin, which block different steps on the synthesis of murein. So these antibiotics work beautifully, because murein is only in bacteria and not in our cells, so they have very, very little toxicity, and you can see we have developed over the years, antibiotics that target different steps in the synthesis of murein, including penicillin, that last step which is assembling the cross-linking amino acids between the sugar chains.

    28:35 Unfortunately, as we develop new antimicrobial compounds, resistance to them rapidly emerges.

    28:45 And today we have resistance to almost every antimicrobial compound that we have developed, and the situation is becoming dire because we have fewer and fewer options with which to treat bacterial infections. Antimicrobial resistance occurs in nature and it’s ancient.

    29:06 Bacteria make antibiotics to compete with each other in nature and many of those we have harnessed to use as antimicrobial treatments of infections of people. We know that these genes that confer resistance have been around for thousands and thousands of years, we can find them in very old sites on earth, and there is plenty of evidence that they existed way before human developed any antimicrobial compound, so we are really taking advantage of something that exists in nature. There are a number of mechanisms by which these antimicrobial genes or I should say antimicrobial resistance genes work. For example, they may direct the synthesis of an enzyme that breaks down the drug, a simple way of doing resistance, they may chemically modify the drug, so it interferes with its function, they could inhibit the uptake of the drug into cells and tissues, so it can no longer access its target, or they could stimulate the export of a drug from the bacterial cell, so it's no longer bactericidal, or they may modify the target site of the drugs. So there are many different mechanisms of antimicrobial resistance, and again these are all encoded on genes that code for proteins that have these various activities.

    30:29 Let's take an example to illustrate that, and we will use an example, the antibiotic, vancomycin. Its target is cell wall modification. So vancomycin acts by blocking the assembly of the murein cell wall. Now at the top of this slide is the normal incorporation of the precursors of murein, so the blue and the green ovals, those are sugar molecules that are going to be part of the growing peptidoglycan chain and these smaller ovals below them.

    31:06 Those are amino acids that will eventually cross-link the murein to make it very strong.

    31:11 So the way this works is that subunits are added to the growing chain, in the second row of this diagram, you can see the growing polypeptide chain. Vancomycin binds to the precursors by binding to the amino acid. Vancomycin is shown here in purple with the V, or maybe that's brown, and it's binding the amino acids and blocking the incorporation into the new chain, therefore this inhibits murein synthesis and kills the bacteria.

    31:39 Resistance to vancomycin, one mechanism of resistance is simply that the bacterium changes the D-ala-D-ala to D-ala-D-lac, and lactose can be incorporated into this chain, it evades vancomycin resistance, and the antibiotic no longer works. That's one example of the way resistance works. Going back to our β-lactam antibiotics, which I mentioned before, and the arrow points to the β-lactam ring, that's common to all members of this class, that's why we call them β-lactams. We have so far identified over 300 β-lactamases. These are enzymes that cut that β-lactam ring, and these β-lactamases encode resistance to the β-lactam antibiotics. So you can see the extent of the problem, β-lactamases are everywhere.

    32:44 Further complicating antibiotic resistance, is that the genes encoding resistance factors, for example that encode β-lactamases, are often able to move from bacterium to bacterium.

    33:01 One way to do that is via plasmids and in fact many of these antibiotic resistance genes are encoded on plasmids. This diagram, which we saw previously in one of our other lectures, shows how plasmids can move from one bacterial cell to another. In the upper left is a bacterial cell with a chromosome in green and a smaller plasmid in red. Let's say this plasmid encodes a β-lactamase, which confers resistance to beta-lactams to that bacterium, well in the second set of bacteria, the two bacteria are now exchanging DNA through a pilus that's joining the two cells, and the plasmid is moving from one cell to another. The result is that that second cell now acquires antibiotic resistance. So you know a problem here is that we often feed our animals that we eat for food lots of antibiotics so they grow up quickly. The effect is that we select for antimicrobial resistance in the animals and then when we eat these foods, we acquire antibiotic resistance genes in us, which are of no consequence initially, but then when we go to have surgery and we need antibiotic therapy, it doesn't work, because we have the resistance already in us. So these antibiotic resistance genes can move around bacteria extensively, this is why they're a problem, not just by plasmid mobility, but by also movement by transduction, the exchange of pieces of DNA by viruses or simply by naked DNA. So gene transfer among bacteria, we call this horizontal gene transfer, is widespread and is a big problem for antimicrobial resistance.

    34:43 Let's end up with a chart showing you some common mechanisms of resistance to antimicrobial agents, for example the penicillins and the cephalosporins are hydrolyzed by β-lactamases which we mentioned, these resistance genes are in fact carried on plasmids. Methicillin resistance is a change in the penicillin binding protein, not in a β-lactamase, but in a separate protein, this happens not to be carried on a plasmid. Tetracycline resistance encodes a pump that pushes the drug out of the bacterial cell; this is a plasmid born resistance factor.

    35:20 So if you look at all these various mechanisms of resistance modification of the drug, synthesis of alternate substrates, and so forth, acetylation, change in binding sites, look how many are encoded on plasmids and that simply means that they are easy to go from bacterium to bacterium, and we have a hard time treating bacterial infections when these resistance genes are so mobile.

    35:47 So after hearing this today, I hope that you understand the extent, origin, and functions of our wonderful microbiome. I hope you appreciate the ways that bacteria enter and spread in their hosts. You should be familiar with the different types of bacterial toxins and their activities, and you should know the mechanisms of action of members of the different classes of antimicrobials, how resistance emerges and how it spreads.

    36:17 Thanks for listening and come back again to hear more about bacterial diseases.

    About the Lecture

    The lecture Introduction to Bacteria by Vincent Racaniello, PhD is from the course Bacteria. It contains the following chapters:

    • Human Microbiome
    • Infection Basics
    • Spread
    • Bacterial Toxins
    • Endotoxin
    • Membrane-damaging Toxins
    • Antimicrobial Compounds
    • Antimicrobial Resistance
    • Introduction Bacteria: Learning Outcomes

    Included Quiz Questions

    1. Bacterial cells
    2. Fungal cells
    3. Epithelial cells
    4. Protozoal cells
    5. Archaeal cells
    1. Aids in extraction of nutrients from food consumed
    2. Enhances cell to cell signalling
    3. Aids in oxidative phosphorylation
    4. Enhances anaerobic digestion
    5. Produces toxins that prevent human cell overgrowth
    1. C-section
    2. Amniotic fluid
    3. Water and soil
    4. Early physical contact
    5. Breast milk
    1. Physical contact
    2. Water
    3. Soil
    4. Food
    5. Plants and animals
    1. It is a part of the normal skin microbiome
    2. It is a common exogenous pathogen
    3. It alters the microbiome, making us more susceptible to infection
    4. It is introduced via insect bites
    5. The microbiome cannot protect against it
    1. Mucus membranes
    2. Insect bites
    3. Open wounds
    4. Skin breakdown
    5. Tissue penetration
    1. Epithelial cell barrier
    2. Mesothelial cell barrier
    3. White blood cells
    4. Submucosal tissues
    5. Enterocytes
    1. Allow for sampling of contents of the gut by lymphocytes and macrophages
    2. Provide a protective barrier in the gut lumen
    3. Are responsible for taking up nutrients
    4. Prevent dissemination of pathogens to distant tissues
    5. Decreases surface area of the Peyer's patches
    1. Incubation period
    2. Asymptomatic infection
    3. Recovery period
    4. Infectious period
    5. Recurrent illness
    1. Bacterial toxins and immune response
    2. Immune response and mechanical tissue damage
    3. Bacterial toxins and mechanical tissue damage
    4. Mechanical tissue damage and pharmacological damage
    5. Pharmacological damage and immune response
    1. Asymptomatic infection
    2. Recurrent disease
    3. Incubation period
    4. Infectious period
    5. Active disease
    1. Contain a secretory injection system
    2. Secreted by bacterium
    3. Most have an AB structure
    4. Often bind receptors on human cells
    5. Break up in cell cytoplasm where they mediate cell damage
    1. Inject toxins directly into human cells
    2. Inactivate host cell receptors, allowing toxin to enter cell directly
    3. Bind directly to host cell receptors to enter cytoplasm
    4. Contain 3 subunits: A, B and C
    5. Directly kill the host cell
    1. Cytokines from host immune cells
    2. PAMPs
    3. Secretory injection system
    4. Exotoxins from bacteria
    5. Pore forming toxins
    1. ADP ribosylation of eEF-2
    2. Increase cAMP via adenylate cyclase activity
    3. Increase ADP which increases cAMP
    4. ADP ribosylation of adenylate cyclase
    5. Inactivation of eEF-2 via an increase in cAMP
    1. Botulinum and tetanus
    2. Anthrax and tetanus
    3. Anthrax and cholera
    4. Cholera and dipheria
    5. Botulinum and anthrax
    1. Anthrax
    2. Salmonella
    3. Shigella
    4. Pseudomonas
    5. Cholera
    1. Lipopolysaccharide
    2. Pore forming proteins
    3. eEF-2
    4. Cytokines
    5. PAMPs
    1. Lipid A
    2. O protein
    3. M protein
    4. AB subunit
    5. MHC
    1. IL-1
    2. Kinins
    3. Complement
    4. LPS
    5. Neutrophils
    1. Provides nutrients for bacteria
    2. Creates pores in host cells
    3. Lyses red blood cells
    4. Decrease susceptibility to opsonization
    5. Increase cytokine release
    1. Activation of plasminogen
    2. Lyses RBCs
    3. Damages lysosomes
    4. Breaks down connective tissue
    5. Breaks down membrane lipids
    1. Prevents release of bacterial toxins
    2. Is bacteriocidal
    3. Prevents formation of bacterial cell wall
    4. Is specific to prokaryotic cells
    5. Does not effect the cell wall of human cells
    1. Genetic mutation resulting in a lack of vancomycin binding site
    2. Increased D-ala-D-ala synthesis
    3. Decreased peptidoglycan wall synthesis
    4. Decreased bacterial utilization of lactose
    5. Increased synthesis of beta-lactam ring
    1. Cephalosporins
    2. Tetracyclins
    3. Vancomycin
    4. Flouroquinolones
    5. Linezolid
    1. Efflux pump
    2. Acetylation
    3. Enzymatic modification
    4. Change in peptidoglycan binding site
    5. Beta-lactamases

    Author of lecture Introduction to Bacteria

     Vincent Racaniello, PhD

    Vincent Racaniello, PhD

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    like everything about the teaching. wish you were my medical school lecturer
    By Lucy N. on 27. March 2017 for Introduction to Bacteria

    like everything about the teaching. wish you were my medical school lecturer

    Hello great informative lecture
    By sandeep N. on 20. January 2017 for Introduction to Bacteria

    Hello great informative lecture, however when will the course be complete? It is missing some important topics.

    Good yield
    By Bjarni J. on 30. December 2016 for Introduction to Bacteria

    Learned a lot that I didn't know before. Great lecture. Minimum 10 words.