Microbial Mechanisms of Pathogenicity-sp10
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Mi c robial M ec hani s m s of Pathog e ni c ity Chapt e r 15
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Microbial Mechanisms of Pathogenicity
Transcript of Microbial Mechanisms of Pathogenicity-sp10
Microbial Mechanisms of Pathogenicity
Chapter 15
Mechanisms of Pathogenicity
Pathogenicity: The ability to cause diseaseV irulence: The extent of pathogenicityPrimary pathogenOpportunistic pathogen
How Microbes Enter a HostPortals of Entry
Mucous membranesSkinParenteral routePrefer red portal of entry
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mucous membran is the most used portal of entry of microbes.
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sometimes micros can enter through intact skin ( not broken skin) through the opening of hair particles. opening of swet glandes
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is when the skin barrier if broken (also burned skin or contaminated skin)
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different micros prefer different ways of entry. some have one way others have multiple ways, but each one has a preferred portal of entry even tho they have multiple ways of entry. ( when they enter through the preferred portal of entry they have a higher chance of infection)
Numbers of Invading Microbes
ID50: Infectious dose for 50% of the test population
L D50: Lethal dose (of a toxin) for 50% of the test population
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ID 50 (infection dose, number of microbes that are required to make 50 out of 100 people ill)
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lethal dose ( not for the pathogen but for the toxin. amount of toxin to kill 50% of the test population.)
Portal of Entry ID50
Skin 10 50 endospores
Inhalation 10,000 20,000 endospores
Ingestion 250,000 1,000,000 endospores
Bacillus anthracis
Adherence
Adhesins/ligands bind to receptors on host cells
Glycocalyx: Streptococcus mutansF imbriae: Escherichia coliM protein: Streptococcus pyogenes
Biofilms
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unless these microbes attache to some surfaces they will get flushed aways by body fluids.
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all there are adhesins
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begins with one pathogen attached to a surface leading to other pathogen attached to the same surface leading to a lot of pathogens in one area
Adherence
Figure 15.1
How Pathogens Penetrate Host Defenses
Capsules and cell wall components contr ibute to pathogenicity.Effects of coagulases, kinases, hyaluronidase, and collagenase.Antigenic var iation.
enter the cell.
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at this point most pathogens will get killed by defense mechanisms tho to there special enzymes
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not penetrate but evade
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4 different ways to avoid
Cell Wall Components
M protein resists phagocytosisStreptococcus pyogenes
Opa protein inhibits T helper cellsNeisseria gonorrhoeae
Mycolic acid (waxy lipid) resists digestionMycobacterium tuberculosis
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avoid phagocytosis
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the presence of mycolic acid
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has opa protein that inhibits t helper cells
Enzymes
Coagulase: Coagulates fibr inogenK inases: Digest fibr in clotsHyaluronidase: Hydrolyzes hyaluronic acidCollagenase: Hydrolyzes collagenIgA proteases: Destroy IgA antibodies
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coaguates fibrinogen leads to formation of blood cloth. if bacteria are within the blood cloth they are invisible to defense mechanisms.
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kinases spread the microbes in ur body by desolving the blood cloth
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hyaluronic acid that closes the gaps between the cells. some microbes can digest the hydrolyzes and sperate the cells
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collagenase will damage collagen which allow the microbes to spread in ur body
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the reason Iga is the only antibody that is being destroyed because iga is everywhere in ur body.
Membrane Ruffling
Figure 15.2
Antigenic Variation
Alter surface proteins
Figure 22.16
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many bacteria and viruses have the ability to change their antigens
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by the time antibodies are ready for A pili the microbes have switched to type B pili so the antibodies are never effective. same is for the flu virus thats why we need vaccines every year
InvasinsSalmonella alters host actin to enter a host cell
Use actin to move from one cell to the next
Listeria
Penetration into the Host Cell Cytoskeleton
Figure 15.2
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sometimes bacteria can penetrate inside ur cells. trying to hide and also use the nutrients inside the cell.
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dont need to know
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these invasins will cause membrane ruffling ( the alteration of the membrane)
Figure 15.4
How Pathogens Damage Host Cells:Exotoxins and Endotoxins
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toxins are the by produces of microbial growth. they are not intentional for avoiding the immume system.
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lipid A serves as Endotoxin Gram negative. it can cause a person to into a shock.
Exotoxin
Source Mostly Gram +Relation to microbe By-products of growing cell
Chemistry ProteinFever? NoNeutralized by antitoxin? YesLD50 Small
Figure 15.4a
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small quantity
Source Gram
Relation to Microbe Outer membrane
Chemistry Lipid A
Fever? Yes
Neutralized by Antitoxin? No
LD50 Relatively large
Endotoxins
Figure 15.4b
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large amount of it
Superantigens
Cause an intense immune response due to release of cytokines from host cells
Symptoms: fever , nausea, vomiting, diar rhea, shock, and death
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dont need to know
Mechanisms of Pathogenicity
Figure 15.9
