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MSU MMG 301 - Module 31

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Module 31Be able to describe the steps involved in pathogenesis, leading from exposure to tissuedamageexposure to pathogen → adherence to skin/mucosa → invasion through epithelium → infection (growth of virulence factors) → toxicity (local and systemic) and invasiveness (futher growth at regional and distant sites) → tissue damage and disease manifestationDefine an opportunistic pathogenCan cause disease because the normal resistance mechanism of host are weakened.Define virulence and provide examples of virulence factors - Virulence- measure of pathogenicity- Factors- molecules produced by pathogen that make them more easily pathogenic to hoseUnderstand the meaning of ID50 and LD50 and how virulence is measuredMeasured with LD50Know what adherence factors are and how they aid virulenceMolecules on pathogens surface that aid in attachment to host, adherence proteins found on fimbrae and piliDescribe examples of enzyme virulence factors and the mechanism by which they contribute to virulenceVirulence factors increase virulence by aiding adherence (capsules, slime layers, pili, fimbrae), colonization/growth, and invasionHyaluronidase: breaks down hyaluronic acid polymer that glues host cells together.Collagenase: breaks down collagen in connective tissueStreptokinase: destroys fibrin of blood clots - blood starts clotting around bacteria to localize it, but streptokinase will break this up and stop localizationCoagulase: Found on the exterior of pathogenic Staphylococcus aureus cells - creates a fibrin later around the cell that prevents immune system from detecting the bacteria - self recognitionmolecule, will be recognized as host tissue and that everything is okayContrast bacteremia and septicemiaInvasion can result in bacteria in the blood.Bacteremia is when bacteria are in the circulating blood. Pathogens can easily e transported to other tissues and organs. In some cases, a systemic inflammatory response occurs because of bacteria in the blood or lymph system (leading to life-threatening sepsis)Be able to define virulence, virulence factors, and virulence genes- Virulence: measure of pathogenicity- Virulence Factors: a pathogen-produced substance (usually a protein, enzyme, adherence factor, or toxin) that promotes the establishment of an infection disease.- Virulence Genes: a gene whose presence or activity in an organism's genome is responsible for the pathogenicity of an infective agentUnderstand how to quantify virulence Quantified using the ID50 and LF50 test it can measure virulence by exposing populations of test animals to increasing doses of a bacterial pathogen; graph shows virulence, as measured bya LD50 value. Highly virulent microbes have low LD50 - few cells are needed for efficient killing of the mouse hostCompare the differences between endotoxin and exotoxin- Exotoxin: are proteins that are excreted by bacteria and are toxic to host cells, toxicity can come from bacteria growing at an infection site, colonizing a site without invasion, and direct ingestion of pre-formed toxin through contaminated food; cytotoxins, AB toxins, superantigens; a protein that is released extracellularly by a microorganism as it grows and that produces immediate cell damage.- Endotoxins: lipopolysaccharides of Gram-negative bacteria that are. released into surrounding tissue after lysis of the cell; the lipopolysaccharide portion of the cell envelope of certain gram-negative Bacteria, which is a toxin when solubilizedDefine enterotoxinExotoxins that affect the small intestineUnderstand the function of each of cytolytic toxins, AB toxins, and superantigens- Cytotoxins: cause damage to host cell membranes; can cause host cell lysis and death; often called hemolysis - ability to lyse red blood cells, some are phospholipase (cleave phosphohead ground form the lipid tail, destabilizing them and damaging the membrane, lysis of host cell- AB toxins: consist of two subunits; B subunit binds to surface of specific host cells and A subunit enters host well where it acts as an enzyme to produce host cell damage- Superantigens: proteins that cause a hyper-stimulated immune response resulting in excessive inflammation and tissue damageKnow the pathogens and mechanisms of action of diphtheria, tetanus, botulism, and cholera toxins- Diptheria: extremely cytoxic - only one toxin molecule kills one host cell; produced by Corynebacterium diphtheria, a bacterial pathogen of the upper respiratory tract. An AB toxin - B component binds to host cell receptors while A component is an enzyme that enters cell and blocks tRNA from entering the ribosome by catalyzing modification of elongation factor (chemical modification of the EF2 subunit so that tRNA can no longer bring and cannot build cell- Tetanus: AB toxin, blocks neurotransmitter release from nerve cells that signal muscles, and produced by a species of the spore-forming anaerobe Clostridium (normally found in soils); Clostridium retain, bacterium colonizes and grows in deep anoxic wound, exotoxin spreads throughout the body - toxin binds to inhibitory interneurons, preventing their function and as a result, muscles are constantly stimulated to interact - results in spastic paralysis (muscle cannot relax - persistent spasms and exaggerated tendon reflexes because of damage to the central nervous system); vaccination using a chemically inactivated purified toxin can prevent tetanus for years.- Botulism: AB toxin, blocks neurotransmitter release from nerve cells that signal muscles, and produced by a species of the spore-forming anaerobe Clostridium (normally found in soils); produced by Clostridium botulinum, 7 types, but Type A has medical uses; Botulism usually results from improper food preservation where bacterium grows and produces toxin, this toxin spreads throughout the body, eventually affecting many muscles and resulting in flaccid paralysis (weakness or paralysis and reduced muscle tone without other obvious cause), binds to neural cells and blocks the release ofinhibiting contraction, so they cannot contract- Cholera: caused by Vibrio cholerae; bacterium colonizes small intestinal wall and produces cholera toxin; An AB toxin that binds to intestinal epithelial cells, the A subunit enters host cell and acts as an enzyme to stimulate formation of cyclic AMP; Increased cyclic AMP alters regulation of ion movement across the epithelium - results in increasedion concentration within the small intestine and osmosis results in large

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