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108 Cards in this Set
- Front
- Back
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myocarditis is caused by
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cocksackievirus
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what is one of the major side effects of gas gangrene
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toxins produced by clostridia lyse red blood cells
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what causes rocky mountain spotted fever
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rickettsia
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what type of immunity is an example of rocky mountain spotted fever
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infected cells are eradicated by killer lymphocytes, cell mediated immunity
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why does shigella survive being taken up by phagocytosis
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can stop apoptosis
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HIV and HSV have what effect on apoptosis
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can make it go premature
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what effect does epstein barr have on apoptosis
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delay it
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what can happen as a consequence of ascaris infection
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intestinal or gall bladder duct occlusion
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what happens when filariae become lodged in lymphatics
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elephantits
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infection of the meninges can cause what
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hydrocephalus
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two parts of infection
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inflammation, immune response
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what happens to patients suffering from septicemia when the complement system is overactivated
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death
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what is responsible for most of the major symptoms of a bacterial infection
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toxins
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exotoxins and type 3 cytotoxins modulate what targets
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intracellular targets
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endotoxin, membrane damaging toxins, and superantigens act on what
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cell surface
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exoenzymes modulate what
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targets in the extracellular matrix
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three pattern recognition receptors that are located on cell surface
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lipoteichoic acid, endotoxin lipopolysaccharide, and flagella
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where are exotoxins secreted by bacterium
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surrounding medium
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what methods are used to transport exotoxins out of cells
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type 1 secretion and type 2 secretion
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type 1 secretion system
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autotransport system built into the toxin
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type 2 secretion mechanism
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apparatus within the bacterial cell membrane
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what bacteria dont make toxins but cause damage though toxin independent mechanisms
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pneumococci
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how many toxins are responsible for causing cholera
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one
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how many toxins are responsible for causing diptheria
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one
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how many toxins are responsible for causing tetanus
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one
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how many toxins are responsible for causing botulism
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one
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which three bacteria produce more than one toxin
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staphylococci, streptococci, bordetellae
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what are toxin genes usually located on
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plasmids or temperate bacteriophages
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during what two phases can a bacteria produce toxins
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continuously or during stationary phase
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what is usually grown during stationary phase
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antibiotics
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why is toxin only usually released when cell growth is slow
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because that is when cells are starved for nutrients, release toxins to get more
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sporulating bacteria produce spores during what
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spore formation
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which three diseases are caused by sporulating bacteria exotoxins
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botulism, gas gangrene and tetanus
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what genus of bacteria causes the above
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clostridium
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what genus of bacteria causes anthrax
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bacillus
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in what type of environment will you have continuous production of spore endotoxin
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wound gash, heterogenius environment, some bacteria will be growing some will be sporulating
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exotoxins are produced with what two domains
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A and B
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what is the purpose of the B doman
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binding to the cell membrane
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what is the purpose of the A domain
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to be delivered into the actual host cell
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which domain has specificity for each toxin
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A domain
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what specific enzymatic activity is exemplified by diptheria toxin, cholera toxin and endotoxin A of pseudomonas arugenosa
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ADP ribosyltransferases
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page 130
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memorize the table
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what are the two domains of anthrax
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A1, A2, A1 is adenylate cyclase and A2 is the protease
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how are exotoxins activated
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by binding to host cell membranes
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what is the biochemical mechanism of activation
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cleavage of a disulfide bond that holds the A and B domains together
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how are toxins taken into the cell
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receptor mediated endocytosis - A domain is translocated
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what is unique about shiga toxin
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it modifies host cell RNA and inhibits protein translation
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what two exotoxins are neurotoxins
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botulism and tetanus (zinc proteases)
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how does diptheria toxin work
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inhibiting host cell protein synthesis
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what does diptheria A toxin ribosylate to halt GTP hydrolysis
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elongation factor 2 (EF 2)
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how many A domains need to be internalized in order to kill a cell
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1
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what compound inactivated EF2
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ADP ribose
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how does cholera toxin modify normal cell functions
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increases cAMP levels
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what is the target tissue for cholera toxin
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small intestine
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how does cholera toxin structure affect binding
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B subunit binds to intestinal epithelium, A subunit upregulates cAMP via adenylate cyclase
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what is the end result of the sudden increase of cAMP levels
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massive fluid shift into the intestinal lumen
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e coli heat labile exotoxin works how
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ADP ribosylation of G proteins that increase cAMP via adenyl cyclase
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what similar method does pertussis toxin work
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increases cAMP levels in leukocytes
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clostridium is anerobic?
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yes
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how does botulism toxin work
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A subunit binds to nerve ending and inhibits vesicle fusion
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what kind of neurotransmitter does botulism inhibit
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stimulatory
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what kind of neurotransmitter does tetanus inhibit
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inhibitory
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does tetanus actually travel through the nervous system?
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no, only the toxin migrates into the CNS
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how are type 3 cytotoxins delivered to the cell?
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directly into the host cell via contact dependent mechanism
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how is the toxin inserted into the cell for type 3 cytotoxic
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type 3 secretion apparatus to form a pore for entry
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salmonella, shigella, pseudomonas, and cholera bacilli and plague are example of what
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type 3 cytotoxins
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what is the usual target for type 3 cytotoxins
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actin skeleton
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Where do endotoxins work
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at the cell surface
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what is endotoxin classified as with gram negative bacteria
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lipopolysaccharide
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what does endotoxin do at low concentrations
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alarm reactions (fever, complement system, etc)
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what does endotoxin do at high concentrations
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shock/death
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when does endotoxin lead to a toxic effect
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only at high concentrations
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why is an endotoxin infection unique
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will stimulate the innate immune system as an early sign of infection
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what is the term for early stages of infection
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pattern recognition receptors
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what causes early activation of the innate immune system
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pattern recongition receptors
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what does the innate immune system cascade stimulate
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adaptive immune system
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what is the active part of the bacterial lipopolysaccharide
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lipid A
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lipid A function is restored/deactivated in what
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water soluble, but reactivated when complexed with proteins
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what is the primary target for endotoxin
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mononuclear phagocytes ( blood monocytes, macrophages, kupffer cells)
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What cells posses TLR
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nutrophils, platelets, and B lymphocytes
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pyrogenic
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small amount of endotoxin produce fever
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endotoxin serves as a low level what
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a very small amount of enteric bacteria is usually released into the bloodstream, this causes a small stimulation of the immune system
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what two cytokines stimulate the activation of the innate immune system from phagocytes
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IL-1 and TNF - A
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what is the above process called
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acute phase response
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how do gram positive bacteria stimulate the innate immune system
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lipoteichoic acid stimulated IL1 anf TNF
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how does endotoxin activate complement
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alternative pathway
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what is the most likely consequence to the production of endotoxin
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activation of the membrane attack complex
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what part of the alternative pathway causes opsonization
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c3b
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anaphylatoxins
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C3a, C5b - increase capillary permeability and release of lysosomal enzymes from neutrophils
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what is the end result of an endotoxin infection
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inflammation
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biological response modifiers
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endotoxins that are being used for tumor treatment as they recruit large numbers of macrophages to the tumor site
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what stimulates the division of B lymphocytes
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IL 1 from endotoxin
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what is the name for increasing the amount of antibodies in circulation
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immunological adjuvant
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large amounts of endotoxin produce what condition
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sepsis
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what 3 bacteria produce sepsis
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e coli, meningococci, p.aeruginosa
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what two conditions result from sepsis
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DIC and endotoxix shock (hypotension)
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what are they mediators of endotoxin induced hypotension
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IL1 and TNF
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what organ is most effected by DIC
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kidney - cortical necrosis
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meningococcal infection can lead to what
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waterhouse-friedichsen syndrome
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gram what bacteria is characteristic of endotoxin
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negative
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lipases
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insert self into membrane to form pores
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lecthinase
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lipase toxin produced by clostridium of gas gangrene
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hemolysins
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kill white and red blood cells
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pore-forming toxins
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insert directly into host membrane to form pores
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a toxin of staph aureus is what type of pore former
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homogenous pore former - all have the same protein arrangement
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heterogenous pore forming TOXIN
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produces pores of varying numbers of toxin molecules
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best example of the above
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streptolysin O, produced by certain streptocci
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exoenzymes
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break down the ECM via a hyaluronidase
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