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FSU MCB 2004 - Chapter 15: Microbial Mechanisms of Pathogenicity

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Chapter 15: Microbial Mechanisms of PathogenicityPathogenicity: the ability to cause disease by overcoming the defenses of a hostVirulence: the degree of extent of pathogenicityI. How Microorganisms Enter a Hosta. Portals of Entryi. Mucous Membranes1. Many bacteria and viruses gain access to the body by penetrating mucous membranes lining the respiratory tract, gastrointestinal tract, genitourinary tract, and conjunctiva2. Most enter through the gastrointestinal and respiratory tractsii. Skiniii. The Parenteral Route1. When they are deposited directly into the tissues beneath the skin or into mucous membranes when these barriers are penetrated or injuredb. The Preferred Portal of Entryi. Pathogens do not always cause a diseaseii. Occurs most likely when entry into the body is by the preferred portal of entryiii. Ie: Salmonella typhi causes typhoid fever when swallowed, but only produces a slight inflammation is rubbed on the skinc. Numbers of Invading Microbesi. The likelihood of disease increases as the number of pathogens increaseii. ID50: the infectious dose for 50% of a sample populationiii. LD50: lethal dose for 50% of a sample populationd. Adherencei. The most common way pathogens attach themselves to host tissues at their portal of entryii. Adhesins/ligands: the attachment between pathogen and host is accomplished by these surface moleculesiii. Receptors: complementary to the adhesins/ligands1. Majority of adhesins are glycoproteins or lipoproteins2. Majority of receptors are sugars, such as mannoseiv. Biofilms: the ability to come together in masses, cling to surfaces, and take in and share available nutrients- the communities, which constitute masses of microbes and their extracellular products that can attach to living and nonliving surfaces 1. The first microbes to attach are usually bacteria; once they adhere to the surface, they multiply and secrete a glycocalyx that further attaches the bacteria to each other and to the surface2. Biofilms resist disinfectants and antibioticsII. How Bacterial Pathogens Penetrate Host Defensesa. Capsulesi. Capsules increase the virulence of speciesii. Capsules resist the host’s defenses by impairing phagocytosisiii. The chemical nature of the capsule appears to prevent the phagocytic cell from adhering to the bacteriumb. Cell Wall Componentsi. The cell walls of certain bacteria contain chemical substances that contribute to virulenceii. M protein: a heat-resistant and acid-resistant protein found on both the cell surface and fimbriae; the M protein mediates attachment of the bacterium to epithelial cells of the host and helps the bacterium resist phagocytosis by white blood cells—the protein thereby increases the virulence of the microorganismiii. Opa: used by microorganisms along with fimbriae to attach to host cellsiv. Waxy lipid: also increases virulence by resisting digestion by phagocytes and can even multiply inside phagocytesc. Enzymesi. Coagulases: bacterial enzymes that coagulate (clot) the fibrinogen in bloodii. Fibrinogen- a plasma protein produced by the liver, is converted by coagulases into fibrin, the threads that form a blood clot1. the fibrin clot may protect the bacterium from phagocytosis and isolate it from other defenses of the hostiii. Kinsases: bacterial enzymes that break down fibrin and thus digest clots formed by the body to isolate the infectioniv. Fibrinolysis- a well known kinasev. Hyaluronidase: an enzyme secreted by certain bacteria that hydrolyzes hyaluronic acid, a type of polysaccharide that holds together certain cells of the body, particularly cells in connective tissuevi. Collagenase: is produced by several species of Clostridium and facilitates the spread of gas gangrene- breaks down the protein collagen, which forms the connective tissue of muscles and other body organs and tissuesvii. IgA proteases: have the ability to destroy IgA antibodiesd. Antigenic Variationi. Changes in surface antigens that occur in a microbial populatione. Penetration into the Host Cell Cytoskeletoni. Invasins: rearrange nearby actin filaments of the cytoskeletonii. Membrane ruffling: invasins of the microbe cause the appearance of the host cell plasma membrane to resemble the splash of a drop of liquid hitting a sold surface—this is the result of disruption in the cytoskeleton of the host cell; the microbe sinks into the ruffle and is engulfed by the host cellIII. How Bacterial Pathogens Damage Host Cellsa. Using the Host’s Nutrients: Siderophoresi. Siderophores: some pathogens secrete this protein in order to obtain free ironb. Direct Damagei. Once pathogens attach to host cells, they can cause direct damage as the pathogens use the host cell for nutrients and produce waste productsii. Many viruses and some intracellular bacteria and protozoa that grow in host cells are release when the host cell ruptures; following their releasepathogens that rupture cells can spread to other tissues in even greater numbersc. The Production of Toxinsi. Toxins: poisonous substances that are produced by certain microorganismii. They are often the primary factor contributing to the pathogenic properties of these microbesiii. Toxigenicity: the capacity of microorganisms to produce toxinsiv. Toxins transported by the blood or lymph can cause serious ,and sometimes fatal, effectsv. Toxins can also inhibit protein synthesis, destroy blood cells and blood vessels, and disrupt the nervous system by causing spasmsvi. Toxemia: refers to the presence of toxins in the bloodvii. Toxins are of two general types, based on their position relative to the microbial cell: exotoxins and endotoxins1. Exotoxins:a. Are produced inside some bacteria as part of their own growth and metabolism and are secreted by the bacterium into the surrounding medium or released by lysisb. Proteinsc. Small amounts are quite harmful or even lethald. Can be gram-negative or gram-positivee. The genes for most are carried on bacterial plasmids or phagesf. Soluble in body fluids- they can easily diffuse into the blood and are rapidly transported throughout the bodyg. They work by destroying particular parts of the host’s cells or by inhibiting certain metabolic functionsh. Highly specific in their effects on body tissuesi. Disease specificj. The body produces antitoxins that provide immunity to exotoxinsk. Toxoids: altered exotoxins from inactivation from heat or by chemicals such as formaldehyde or iodinei. Naming Exotoxins1. Exotoxins are divided into three


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