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59 Cards in this Set
- Front
- Back
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Normal microbiota (microflora) |
The microorganisms that are usually found associated with healthy body tissue |
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Pathogen |
Microorganism capable of causing harm to a host |
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Primary pathogen |
Causes disease in a proportion of healthy individuals Vibrio cholerae Salmonella Typhi |
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Opportunistic pathogen |
Causes disease if given opportunity (weak, immunocompromised hosts) Pseudomonas aeruginosa |
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Pathogenicity |
The ability of pathogen or parasite to inflict damage on host E.coli 0157:H7 vs E.coli ATTC 9723e |
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Pathogenesis |
Process by which a pathogen causes disease |
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Resistance or susceptibility of host |
May vary (lack of sleep, personal hygiene, malnutrition, underlying medical condition, age, genetics) |
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Host pathogen relationship |
Dynamic
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PAI |
Pathogenicity Island Region of a chromosome containing multiple genes concerned with pathogenicity (coding for various virulence factors) May be transferred via HGT |
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HGT |
Horizontal Gene Transfer Process of avirulent bacterium obtaining genes for virulence factors (transduction, transfromation, conjugation) Avirulent microbe may become virulent and produce disease |
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Transduction Conjugation Transformation |
Via phage Via related bacterial strains Via released DNA from other bacteria |
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Virulence LD50 IC50 |
Measure of pathogenicity (number of pathogen cells or viruses that will elicit pathogenic response in host at specific time) Dose that is lethal for 50% of population Infectious concentration |
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Virulence factors |
Recognizable characteristics that contribute to microorganisms ability to cause harm (toxins, capsule, enzime activity, adhesins) |
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Infection |
Any situation in which microorgansim is established and growing in host |
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Disease |
Damage or injury to host that impairs host function Overt symptoms may require threshold in pathogen numbers to be exceeded |
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Invasiveness |
Ability of microorganism to invade tissues and establish an infection |
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Toxicity |
Ability of microorganism to cause disease by means of a preformed toxin |
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Microbial ecology of human body |
Each region/organ differs chemically and physical from others Selective environment where growth of certain microorganisms is favored |
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GI tract is lined by |
Mucous membrane |
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Bacteria in the ileum and colon |
differ based on acidity of body area |
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Pathogenisis of microorganisms |
1. Exposure 2. Adhere to mucosa or skin (adhesion receptor interaction) 3. Invasion through epithelium (or not) 4. Colonization and growth - produce virulence factors 5. Toxicity (local or systemic) and Invasiveness 6. Tissue damage and disease |
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Adhesins - specific factors that enhance ability of microbe to attach to host cell |
Capsule - slime layer, glycocalyx, exopolymeric substance EPS Fimbriae, pili - ETEC possess CFA (colinization factor antigen - a fimbrial protein) EPEC, EHEC - produce adhesion molecule called intimin |
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Receptor - molecule on surface of host cell to which adhesin may specifically bind |
Often protein - glycoprotein Neisseria gonorrheae binds strongly to urogenital epithelium Bacterial surface protein (Opa) interacts specifically with epithelial cell surface protein (CD66) |
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Colonization |
Usually needed to invoke damage May be restricted by nutrient lack (Fe - sidrophore production) May be localized or pathogen may spread via blood, lymph systems (bacteremia) May cause systemic infection |
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Bacterial mechanisms for obtaining iron |
Sidrophores - grab iron from iron binding protein Bacterial transport proteins - bring iron complex to bacteria Low pH - cause Fe to unbind from IBP Hemolysin - lyses hemoglobin and Fe escapes to bacteria |
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Virulence Factors Common in salmonella |
Edotoxin in LPS O antigen Enterotoxin Siderophores Capsule Flagellum Fimbriae |
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Fibrin clots |
May be formed at site of microbial invasion Wall off invaders |
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Streptokinase |
Clot dissolving substance Streptococcus pyogenes Makes further invasion possible |
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Coagulase |
Fibrin clotting substance Staphylococcus aureus Fibrin deposition on its surface may protect bacterium from attacking host cells Many staph infections are localized such as boils by fibrin matrix |
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Exotoxins |
Proteins released extracellularly as the microorganism grows 1) cytolytic toxin (cytolysin) ii) AB toxin iii) superantigen toxin |
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Cytolysin |
Hemolysin - Affect erythrocytes (RBC) and other host cells (strep pyogenes) Leukocidin - affects WBC Phospholipases, lecithinases, pore forming toxins |
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Staphylococcal alpha-toxin - pore forming cytolysin |
1. S. aureus secretes alpha toxin monomer 2. Monomer binds to membrane receptor 3. Additional monomers bind and oligomerize 4. Conformation change and insertion of hydrophobic segments into membrane forms a pore |
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AB toxin |
Diphtheria toxin B Chain: binds to host cell A Chain: enters host cell cytoplasm, catalyzes toxic reaction |
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Normal protein synthesis |
EF2 brings aa-tRNA to ribosome during protein synthesis |
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Protein synthesis stops |
diptheria toxin inactivates EF2 and disrupts protein synthesis in host cells |
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Entry and action of diphtheria toxin |
B subunit binds to host cell receptor Receptor-mediated endocytosis is induced Endosome acidification confirmationchange in toxin protein --> B subunit forms channel enables entry of A subunit into host cytoplasm A subunit performs action (ADP-ribosylation of EF2) --> protein synthesis ceases |
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Diphtheria |
Infection of upper respiratory tract by Corynebacterium diphtheriae Bacteria grow on throat tissues- form pseudomembrane (hosts inflammatory response) Systemic exotoxin release -tissue damage tox gene carried by lysogenic bacteriophage- lysogenized bacteria cause serious disease |
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DTaP vaccine |
Diphtheria is now rare D component - formalin-treated diphtheria toxin - toxoid Toxoid- nontoxic, immunogenic |
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Other AB toxins |
Botulin - clostridium botulinum Tetanus toxin - clostridium tetani Pertussis toxin - whooping cough, bordetella pertussis Shiga toxin - bacterial dysentery, shigella dysenteriae - Ecoli 0157:H7 |
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Enterotoxin |
Actos on small intestine Cholera toxin (also AB) |
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Enterotoxin system |
1. Normal ion movement Na from lumen to blood, no net Cl movement 2. Colonization and toxin production 3. Activation of epithelial adenyl cyclase by toxin 4. Na movement blocked, net cl movement to lumen 5. Massive water movement to lumen |
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A subunit of cholera |
ADP-ribosylates Gprotein --> G locked in active form -adenylate cyclase continuously active -cAMP levels continuously high -water, ion imbalance |
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Other enterotoxins |
Ecoli and Salmonella similar to cholera Saureus - superantigen Cperfringens - cytolytic |
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Endotoxin |
LPS portion of cell envelope of gram - bacteria Acts as a toxin when solubilized (lipid A is toxic) |
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LPS is made up of LOS and Oantigen |
LOS: -Lipid A: unusual fatty acids, toxic activity, links LPS to outer membrane -Core PS: various sugars with side chains, genus or species specific O antigen: -many repeating units of PS, strain specific, target of immune response, used for serotyping |
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Membrane layers |
LPS Outer membrane Periplasm Cytoplasmic membrane |
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LOS- lipooligosaccharide |
Certain gram negatives have similar activity to LPS Neisseria bordetella |
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Lipoteichoic acid LTA |
gram + may also cause inflammation, possible septic shock |
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Fever Complement activation |
Inhibition of pathogen replication, increase in immune cell activities Lysis by MAC formation, induction of inflammation |
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Inflammation Bcell proliferation |
Transport of immune cells and molecules to site of infection Antibody production |
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IFN expression from T cells Stimulation of clotting cascade |
Activation of macrophages and NK cells Prevention of pathogen spread |
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Presence of LPS, LOS, LTA in low levels |
contributes to these effects ^^^^^^
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...in high doses
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May result in death due to hemorrhagic shock and tissue necrosis
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Capsule |
presence may help pathogen avoid phagocytosis, increases invasiveness |
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Streptococcus pneumoniae |
gram positive, causes pneumonia smooth strains are virulent (capsule) rough strains are avirulent (no capsule) |
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extracellular enzymes - hyaluronidase |
spreading factor catylzes break down of hyaluronic acid (intracellular cement in animal tissue) Streptococci, staphylococci, clostridia |
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extracellular enzymes- collagenase |
catalyzes break down of collagen network supporting tissues clostridia |
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extracellular enzymes - proteases, nucleases, lipases |
depolymerise host proteins, nuleic acids, lipids |
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gas gangrene |
Cperfringens -perfringolysin: pore froming cytolysin -alpha toxin: lecithinase -tissue disrupting enzymes Tissue necrosis, gas production, fermentation activity |
