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Flashcards in medical microbio: pathogenesis Deck (42):
1

infection

growth of microbes that are not normally present in the host (regardless of whether or not the host is harmed)

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disease

damage or injury that impairs regular host functions

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pathogen

a microbe that is able to cause disease

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opportunistic pathogen

a microbe that causes disease only in the absence of normal host resistance:
ex. streptococcus pneumoniae- causes pneumonia in immunocompromised patients
ex. e.coli-causes urinary tract infections when bacteria from feces are moved into the urethra

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pathogenicity

the ability to cause disease

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virulence

the severity of the disease that is caused
*often given as an LD50 value
*number of cells of a pathogen (or dose of a toxin) that will cause death in 50% of infected animals
ex. streptococcus pneumoniae - LD50 ~50 cells
ex. salmonella enterica- LD~5000 cells

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pathogenesis

the precess by which a disease develops
*steps that lead to an infection and tissue damage

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virulence factors

genetically encoded traits that contribute to a pathogen's ability to cause disease

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adherence

the ability of a pathogen to stick to a surface and begin colonization

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non-covalent adherence factors

ex. capsules and slime layers
-streptococcus mutans uses slime layer to stick to teeth and form a biofilm
-streptococcus pneumoniae uses capsule to stick to cells in the lungs
-also protects the cell from phagocytes

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other adherence factors

-adhesins- specific surface molecules that allow selective adherence to particular cell types

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examples of adhesins

-strains of enterotoxigenic E.coli produce fimbriae and can adhere specifically to cells in teh small intestine
-Neisseria gonorrhoeae produces fimbriae that allow it to attach to mucosal epithelial cells
*retract to bring bacteria close to the membrane
-opa proteins then specially attach to certain receptors on the host cell

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some pathogens can colonize and grow on the surface of tissues others need to _______

invade tissue

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invasiveness

-the ability of a pathogen to enter into host cells or spread through tissues

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virulence factors that promote invasiveness

-siderophores
-exoenxymes
-invasins

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siderophores

iron binding molecules
-host proteins transferrin and lactoferrin- sequester iron, making it unavailable for microoganisms
*limits the growth of invaders
-siderophores rip iron out of tissues to be used by bacteria

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exoenzymes

-excreted by bacteria to degrade host tissues
*hyaluronidase
*collagenase
*proteases, nucleases and lipases
*fribrinolysin
*coagulase

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hyaluronidase

hydrolyzes hyaluronic acid (cement that holds animal cells together)

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collagenase

degrades collagen (structural component of connective tissue)
allows pathogen to spread through tissues

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proteases, nucleases and lipases

degrade host macromolecules

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fibrinolysin

dissolves fibrin clots
*ex. streptococcus pyogenes makes streptokinase

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coagulase

induces fibrin clots
ex. staphlococcus aureus produces coagulase to protect it from phagocytes
*keeps staph infections localized

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invasins

proteins that allow bacteria to invade and enter directly into host cells

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listeria monocytogenes

*invasins
-non lactic acid, non pore forming psychrotolerant (grows best at lowe temp) member of the firmicutes
-produces invasins that promote phagocytosis by macrophages
*hijacks the cytoskeleton to escape the phagolysosome
*spreads from cell to cell- avoiding humoral immune response

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some pathogens remain localized at the site of infection while others _____

spread

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bacteremia

bacteria in the blood
can be carried to different organs and tissues

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septicemia

bacteria multiplying in the blood (blood borne systemic infection)
-can lead to sepsis

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sepsis

widespread systemic inflammation

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septic shock

can be caused by gram negative bacteria (gram negative sepsis)
-also by gram positives : staphylococci and enterococci

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exotoxins

proteins released by growing bacteria
*inhibit host cell function (or kill host cells)
*usually heat labile
*can be extremely toxic

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bacillus anthracis

-exotoxins
-several virulence factors: capsule, exoenzymes and the anthrax toxin
*interferes with the immune response and kills macrophages

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there are three categories of exotoxins

cytoxins
AB toxins
superantigens

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cytotoxins

disrupt cytoplasmic membrane integrity
cell lysis and death
-hemolysins
-lecithinase or phospholipase
-leukocidins

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hemolysins

lyse many cells (not just red blood cells)
ex. streptococcus pyogenes
-produces streptolysin sterols in the cell membrane

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lecithinase or phospholipase

dissolves membrane lipids
-ex. clostridium perfringens
-alpha-toxin (gas gangrene)

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leukocidins

destroy white blood cells
ex. staphylcoccus aureus - staphylococcal alpha-toxin
toxin subunits insert into the membrane and oligomerize to form a heptamer
a membrane spanning pore
cell contents leak out and the cell dies

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AB toxins

two subunits : active subunit and binding subunit
ex.diphtheria toxin (corynebacterium diphtheriae)
subunit B- specifically binds to a protein on animal cells
subunit A- then moves across the membrane
*interferes with protein synthesis
-gene for diphtheria toxin is not encoded on the chromosome, but instead on a virus

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other AB toxins

tetanus, botulism and cholera toxins

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superantigens

-activate T cells to elicit an extreme immune response
-bind to MHC molecules and TCRs outside the antigen bind sites
-bridge the gap and mimics proper antigen presentation
-huge number of T cells can be activated
-T cells produce cytokines
-extreme immune response
-extreme fever, systemic inflammation, shock, death
ex.staphylococcus aureus's toxic shock syndrome toxin

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endotoxins

lipopolysaccharide from the gram negative outer membrane
-toxic part is lipid A -only released when the cells die
-generally considered less toxic than exotoxins (need a lot to cause symptoms)

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salmonellosis

food borne illness
endotoxin
-salmonella colonizes the intestine-multiply to a huge number of bacteria
*as those bacteria die, they release endotoxin
*fever, diarrhea, generalized inflammation

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gram negative species

endotoxins
-gram negative bacteria multiply in the blood
-killed by immune system, releasing endotoxin
-massive inflammation leads to septic shock an death