Chapter 25 Microbial Pathogenesis – Flashcards
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| Pathogenicity |
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| the ability of a symbiont to cause disease -symbiosis is the state in which two organisms coexist -Because pathogens harm the host they are parasitic symbionts |
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| Pathogen |
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| a pathogen is a microbial agent of disease -it may be used synoymously with parasite -Ectoparasite: lives on the surface of the host Endoparasite: lives inside the host's body *Infection does not always cause disease |
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| Primary pathogens vs. Opportunistic pathogens |
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| Primary pathogen cause disease in healthy hosts Opportunistic pathogens cause disease only in immunocompromised patients |
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| Virulence |
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| is the measure of the degree or severity of disease -a highly virulent pathogen is more likely to cause death A pathogen can be highly infectious but not highly virulent, ex. common cold -Depends on the invasiveness of the pathogen, or ability to proliferate in the host -depends on the toxigenicity or the ability to produce toxins which injure the host tissure |
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| Infectiouis dose vs. Lethal dose |
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| scientist can measure virulence by seing how much of an organism is required to kill 50% of the experimental hosts, thus finding the LD50 or its lethal dose If the pathogen is not virulent, or simply colonizes but does not kill the host we can measure the infectious dose needed to colonize 50% of the hosts. |
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| Infection cycle |
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| The infection cycle is the route the pathogen takes from one organism to another. Horizontal transmission is when the pathogen goes from one member of a species to another, either through: Formites- inanimate objects, such as a used tissure Vectors- animals that carry the pathogen from host to host, such as mosquitoes or ticks Vertical Transmission is from a parent to child Acciental Transmission is when a host who is not part of the normal infectious cycle unintentionally encounters that cycle |
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| A Reservoir |
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| is an animal, bird, or insect that normally harbors the pathogen |
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| Portal of entry |
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| the way that a pathogen infects the host that is best suited to their mechanism of pathogenesis Examples: -Mouth: food-borne pathogens -Respiratory tract: airborne pathogens |
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| Immunopathogenesis |
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| when the immune system's response to an infection damages host cells or tissues |
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| Virulence Factors |
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| are factors that allow or enhance the disease producing capability or pathogenicity of the pathogen. They are encoded by virulence genes, and include toxins, attachment proteins, capsules, and other devices used to avoid the host's immune system They are encoded by virulence genes that can be found in pathogenicity islands in the chromosome, on plasmids, or even on phage genomes. |
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| Pathogenicity Islands |
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| These are clusters of genes that can be found in the chromosome that encode for virulence factors. -many are originally inherited through horizontal transmission -have a GC content different from the rest of the genome -often flanked by phage or plasmid genes that can move the island from one organism to another |
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| Resistance: Nonspecific surface defenses |
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| Structural defenses- epithelium -skin, mucous membranes Mechanical defenses -movement of material through intestines -mucociliary system, mucous production and ciliary movement in nasal cavity -Movement of fluids- eyes are bathed in tears Biochemical defenses -lysozymes in tears and saliva -fatty acids on the skin -bile in the intestines |
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| Resistance: Nonspecific Interior defenses |
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| Inflammation -stimulates phagocytosis; bacteria engulfed and killed by phagocytes -stimulates complement cascades; bacteria lysed by a membrane attack complex |
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| Resistance: Specific Interior Defenses |
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| -activation of B and T cells -production of antibodies and activation of cytotoxic T cells that can kill bacteria-infected cells |
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| Pathogens and disease |
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| Overall ability of a pathogen to cause disease = V/R, where V= Virulence and R= resistance or = I x T/R, where I= invasiveness and T is toxigenicity Toxins ability to cause disease= T/R Certain pathogens can be toxic without actually infecting the host, the host can simply ingest it, example: botulism |
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| Entry |
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| -break in epithelial layer -specific adherence to an epithelial layer -species specificity limits the species of host that can be infected -tissue specificity limits the tissue which can be infected -tissure specificity limits the tissue which can be infected -specificity is mediated by macromolecules on both the surface of the host and pathogen |
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| Pathogen specificity |
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| Fimbriae and pilli proteinaceous structures Capsule-polysaccharides, proteins or glycoproteins Capsules- can also protect pathogens from phagocytosis |
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| Adhesin |
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| the general term for any microbial factor that promotes attachment |
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| Pili (fimbriae) |
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| Many bacteria typically attach to host cells by hair-like appendages called pili (fimbriae): Type I: adhere to mannose residues -produce static attachment to host cell -grow from outer membrane; new subunits are added at the base -adding free mannose will inhibit attachment; mannose sensitive Type IV- involved in "twitching motility" -continually assemble and disassemble -grow from inner membrane |
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| Non-pilus adhesions |
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| Streptococcus pyogenes: M protein which binds to fibronectin and complement factor H Bacteria can also attach to surfaces in bulk forming a biofilm. -play important roles in chronic infections Bordetella pertussis: Pertactin which binds to integrni |
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| Colonization |
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| Once the pathogen is binded to the target cell or tissue, there are a number of factors that determine if it can colonize Colonization requires that the pathogen can grow Factors effecting colonization include pH, redox potential, temperature, and supply of nutrients |
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| Invasion |
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| once it begins colonizing, the pathogen can remain localize and act by liberating toxins or penetrate the epithelium or mucus membrane and grow in the submcuosa or spread to other tissues Some pathogens release toxins while attached to the mucosa others are actively invasive |
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| Collagenase-proteolytic enzyme |
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| this enzyme is capable of degrading the collagen network supporting host tissues |
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| Hyaluronidase |
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| breaks down hyaluronic acid which is the basis of connective tissue |
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| Streptokinase |
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| breaks down coagulated plasma and allows spread of pathogen |
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| Coagulase |
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| allows fibrin clot to form around pathogen and protects pathogen from phagocytes in a localized infection |
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| Avoiding death inside the host cell |
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| Cell ingests pathogens in phagosome -some pathogens use hemolysin to break out ex. Shigella dysenteriae, Listeria monocytogenes Phagosome fuses with acidic lysosome -some pathogens secrete proteins to prevent the fusion ex. Salmonella, Chlamydia, Mycobacterium, Legionella -some pathogens mature in acidic envirinment ex. Coxiella burnetii = Q fever |
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| How do Pathogens avoid death outside of host cell? |
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| Complements, antibodies bind pathogen -some pathogens secrete thick capsule ex. streptococcus pneumoniae, Neisseria meningitidis -Some pathogens make proteins to bind antibodies ex S. aurues cell wall Protein A - Binds Fc fragment -antibodies attach upside down -prevents opsonization Other pathogens can cause apoptosis of phagocytes Others can alter surface antigen periodically |
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| How do bacteria recognize host environment? |
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| -two component signal transduction -detect magnesium concentration, pH -both low in host cell vacuole Quorum Sensing -detects exotoxins made by other ells -Delays toxin synthesis until many bacteria present -may be a possible pathway for preventing pathogen growth? |
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| Induction of disease state |
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| Happens in two ways: 1. thru sheer numbers pathogens block heart or lung function, the large inflammatory response to a huge number of bacteria can also harm the host 2. Many pathogens produce toxins which can harm host tissues |
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| Host Response |
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| the hsot responds to infection or mechancial injury via the innate immune system (inflammatory response) -Macrophages attack pathogens and signal for other responses; blood vessels dilate and become moe ermeable allowing neutrophils to extravasate -Phagolysosomes kill bacteria in several ways |
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| Phagolysosomes |
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| Lower pH by anaerobic fermentation to produce lactic acid Produce hydrolytic enzymes that can degrade bacteria like lipases, proteases, and nucleases Produce reactive O2 and N2 species that can damage bacteria, like singlet oxygen, hydrogen peroxide, hypochlorous acid, and nitrate Function: Bacteria binds to the surface of the phagocytic cell -invagination of the membrane traps the organism inside the cell -a lysosome binds to the phagosome inside the cell and deposits an enzyme that generates reactive O or N species that kill the bacteria |
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| Antigen presentation |
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| Degraded pathogen macromolecules are displayed on cell surfaces of neutrophils and macrophages to intiate the produciton of antibodies |
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| Pathogens Respond |
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| Many pathogens produce leukocydins which lyse phagocytes S. aurues produce carotenoids which can inactivate singlet oxygen Some pathogens escape from the phagosome into the cytoplasm |
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| Further host responses |
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| Lysis of phagocytes releases histamines which increase inflammatory response They also relesae endogenous pyrogen which induces fever Slight increases in temperature accelerate phagocytic responses and antibody response the higher temperature can also slow pathogen growth |
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| Adaptive Immunity |
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| Lymphocytes produce antibodies to bacterial cell componenets and also to toxins. Antitoxins directly inactivate toxins while antibodies stimulate phagocytosis of pathogens that escaped phagocytosis of the innate response |
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| Endotoxins |
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| the LPS layer of Gram negative bacteria is toxic when released from the cell via lysis -heat stable -not extremely immuniogenic or toxigenic -all endotoxins work by same mechanism |
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| Exotoxins |
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| are toxic proteins released form a pathogen as it grows; usually secreted -is a protein -can be from gram pos or gram neg -highly toxic and immunogenic -heat labile, usually destroyed by boiling -acts by binding to taret cell of host and disrupting specific cellular function -Toxins can be coded by chromosome, plasmid, or temperature phage; meaning non virulent strains can become virulent by phage infection, plasmid transfer, or even transposition even of transposon -can act at targets removed from focus of infection Lipid A is relesaed as bacteria die -causes massive release of cytokine from host cells -can trigger fever, shock, and death |
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| Type I Exotoxin: Superantigens |
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| Activate the immune response by binding to a large percentage of T cells and class II MHC molecules on antigen presenting cells T cells are stimulated to grow and divide, machrophages, and phagocytes are activated and mass inflammatory response occurs which causes a disease state. Found in S. aureus food poisoning and toxic shock syndrome Found in S. pyogenes induced scarlet fever |
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| Cytolytic toxins |
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| Phospholipases breakdown cell membranes -pore forming toxins form a pore in the host cell membranes causing lysis "cell membrane distrupter" |
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| Alpha toxin |
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| produced by s. aureus -forms a transmembrane, seven-member pore in target cell membranes also a "cell membrane disrupter" |
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| AB toxins |
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| Consist of two differen subunits -toxic activity is in subunit A -subunit B binds to host cell receptors -many AB toxins have 5 B subunits and a single A subunit The A subunit enters the host cel and alters the host metabolism Some toxic activities of subunit A: ADP-ribosyltransferase -Diphtheria toxin -Cholera toxin |
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| ADP-Ribosylating Toxins |
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| Diphtheria toxin -made by Corynebacterium diphtheriae -ribolysates elongation factor 2 -blocks ribosome function; cell dies -forms pseudomembrane over trachea Cholera toxin - made by Vibrio cholerae -Ribosylates to overactivate adenylate cyclase -cAMP activates ion transport; water follows -Uncontrollable diarrhea |
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| Anthrax toxin |
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| Made by Bacillus anthracis Has two active toxins: Edema factor raises cAMP levels -causes fluid secretion, tissue swelling Lethal factor cleaves protein kinases -blocks immune system from attacking |
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| Protein Type II secretion |
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| similiar to type IV pilus, just modified to secrete proteins -can extend and retract -proteins to be secreted first make their way to the periplams -are then folded before secretion |
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| Protein type III secretion |
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| use a molecular syringe to inject proteins from the bacterial cytoplasm directly to the host cell -similar to flagellum -genes on pathogenicity island -found in salmonella, Yersinia, and shigella |
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| Protein Type IV secretion |
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| Similar to conjugation pilus -modified to secrete proteins only or proteins plus DNA -can secrete proteins from cytoplasm or periplasm -found in Agrobacterium tumefaciens and Bordetella pertussis |
