Final Flashcards
How does a capsule protect a pathogen?
- Prevents PAMP-PRR interactions
- if it has sialic acid it can bind to serum protein H and degrade opsonin C3b
- some prevent formation of C3 convertase
Capsules with silica acid do what?
bind to serum protein H which leads to degradation of opsonin C3b
How does the host fight a capsule?
produce opsonizing antibodies specifically against the capsule
Streptococcus progenies evades complement how?
M protein binds serum factor H which degrades C3b
How do pathogens get around antimicrobial peptides?
- charge repulsion
- peptidases
- reduced uptake of peptides because of capsule
- efflux pumps
- biofilm
virulence factors enable bacteria to do what?
- attach and colonize
- invade and disseminate
- evade host immune system
- eat and grow
- spread
How can you evade the adaptive immune system?
- antigenic variation
- molecular mimicry
- IgA proteases
- protein A, protein G
- biofilm
How does Neisseria use antigenic variation to escape antibodies?
pili as adhesins and different subsets of pili
How do flu viruses use antigenic variation to escape antibodies?
- mutations and seasonal variations of flu strains
- antigenic drift
- antigenic shift
molecularly mimicry example
streptococcus capsule is made of hyaluronic acid which is commonly found in the body
Which proteins does streptococcus produce?
proteins A and G
What do proteins A and G do?
bind to Fc region of antibodies (instead of epitopes)
How can pathogens avoid cytotoxic T cells?
- kill them
- interfer with MHC
pseudomonas classification
- aerobic
- Gram -
- metabolically diverse
- saprophytes (feed on decaying organisms)
is pseudomonas motile?
yes it has polar flagella
Why do some strains of pseudomonas appear mucoid?
polysaccharide alginate
what does pseudomonas smell like?
grapey
what color is pseudomonas and why?
blue green pigment pyocyanin
p aeruginosa is what type of infection?
opportunistic and often nosocomial
How does p aeruginosa spread?
environment (NOT patient to patient)
How does p aeruginosa attach?
pilus and non-plus adhesins
What type of motility does p aeruginosa have?
- swimming
- swarming
- twitching
What enzymes does p aeruginosa make?
- toxins
- proteases
- DNAases
what type of pili does p aeruginosa use to attach to host cells?
type 4
What type of toxins does p aeruginosa secrete?
type 3
What does staphylococcus aureus look like?
a bunch of golden grapes
Staphylococcus classification
- gram +
- non-motile
- non-spore forming
- facultative anaerobe
staphylococcus aureus is what type of pathogen?
commensal and nosocomial
How does MRSA do?
change penicillin binding protein (PBP)
How do vancomycin do?
inhibits cell wall synthesis by binding to hanging chain of peptidoglycan
How do VRSA do?
modify binding site and replace with low-affinity precursors
what are the staphylococcus aureus adhesins
fibrinogen, fibronectin binding surface proteins Fnbp A and B, ClfA and B, IsdA, and WTA
how does staphylococcus aureus inhibit phagocytosis
- capsule
- proteins A and G which bind to Fc region of IgG antibodies and avoid opsonization
how does staphylococcus aureus inhibit neutrophil migration
- inhibitory protein (CHIPS) binds to and inhibit chemotactic receptors
extracellular adherence protein (Eap) decreases ICAM-1 expression on endothelial cells
How does staphylococci aureus inactivate reactive oxygen species?
- golden carotenoid pigment
- superoxide dismutase (SOD)
how does staphylococcus aureus reduce the activity of antimicrobial peptides?
protease aurolysin causes the AMP to hydrolyze
how doe staphylococcus aureus alter the adaptive immune response?
- super antigens which activate T cells by cross linking TCR with MHC II molecules
- this bypasses the requirement for specific TCR recognition of MHC II-peptide complex
facultative intracellular pathogens
- listeria
- mycobacterium
- salmonella
obligate intracellular pathogens
- coxiella
- chlamydia
the phagolysosome contains what?
- reactive oxygen and nitrogen species
- superoxide anion
- hydroxyl radical
- hypochlorite
- hydrolytic enzymes
- lysozymes
- lactoferrin
- AMPs
- acidic pH
neutrophil extra cellar traps (NETs)
- specific tool that allows neutrophils to capture and effectively destroy a broad range of pathogens while minimizing host damage
- extracellular fibrous structures composed of decondenses intracellular DNA associated with AMPs such as neutrophil elastase (NE), lactoferrin, MPO, calprotectin, cathepsin G, histones, and some other cytoplasmic proteins
How does mycobacterium survive?
arrests the maturation of phagolysosome in an easy endosome-like vesicle
which bacteria lyse the phagosomal membrane and escape into the cytoplasm?
listeria and shigella
which bacteria fuses with ER
legionella
which bacteria directs the maturation of a phagolysosome-like compartment
coxiella
which bacteria activate acid tolerance gene allowing adaptation to the acidic pH?
salmonella
mycobacterium tuberculosis classification
- obligate aerobe
- nonsporulating
- non motile
- rods
- slow growing
how to kill mycobacterium tuberculosis
reistant to acid, alkali, drying, germicides, antibodies, and complement
mycobacterium tuberculosis strategy one to conquer macrophages
- interferons with phagosome functions by inhibiting the phagolysosome biogenesis
- the vacuole does not mature following the normal endocytic pathway and resembles an immature endosome
- blocks phagosomal acidification
- inhibits H+ V-ATPase complex assembly and its subsequent fusion with the phagosomal membrane resulting in the stabilization of the phagosomal pH between 6.2 and 6.5
mycobacterium tuberculosis strategy two for conquering a macrophage
access the cytosol through ESX-1 secretion system
mycobacterium tuberculosis strategy three to conquer a macrophage
cytosolic mycobacterium tuberculosis induces host cell death programs to enhance its dissemination
which bacteria can disrupt the phagosomal membrane and cause the release of bacterial products, including its own DNA, into the macrophage cytosol
mycobacterium tuberculosis
which bacteria blocks the assembly of iNOS with phagosomes and resists damage by NO
mycobacterium tuberculosis
listeria classification
- facultative intracellular anaerobe
- non-spore forming
- Gram + rods
- flagella mediating tumbling motility
what the temperatures can listeria grow at
1-45C
how is a listeria infection initiated
infect the M cells in intestinal Peyer’s patches and then spread intracellularly
how does listeria avoid being killed?
- delays the maturation of the phagosome
- destroys the phagosomal membrane and replicates in the cytosol
key steps in listeria intracellular survival
- internalization
- internals A and B mediate uptake, even by non-phagocytic cells
- phagosomal escape
- listeriolysin O is a pore forming toxin that facilitates bacterial escape from the phagosome
- spread from cell to cell
- ActA polymerizes host actin into tails that propel the bacteria into neighboring cells
legionella classification
- facultative intracellular
- small Gram - rods
does legionella do human to human transmission
no
what bacteria enter the ER lumen and how
legionella by altering phagosome transport to send them to the ER and turns the phagosome ER-like
coxiella burnetii classification
- weak Gram -
- obligate intracellular
- requires acidic pH for replication
coxiella burnetii transmission
normally from farm animals, not usually human to human
LD50 of coxiella burnetii
one (one will kill 50% of the test organisms)
how does coxiella burnetii do?
actively directs the maturation of a phagolysosome-like compartment known as the coxiella containing vacuole or a parasitophorous vacuole
coxiella burnetii is phagocytosed through what mechanism
actin dependent
the coxiella containing vacuole acquired what following internalization
RAB5
what accumulates in the CCV?
cathepsin D
what two staphylococcus aureus toxins are superantigens
- TSST-1 - topic shock syndrome toxin
- SE - staphylococcal enterotoxin
staphylococcus aureus exfoliative toxin (ET)
- exoenzyme (a group of proteases)
staphylococcus aureus staphylokinasze (Sak)
- exoenzyme that dissolves clots and helps bacteria move through tissue and escape abscesses
staphylococcus aureus alpha-toxin
- exotoxin that forms pores in human cell membrane
- defense against neutrophils and other immune cells
- implicated in necrotizing pneumonia caused bu CA-MRSA
staphylococcus aureus leukocidin
kills leukocytes and damages cell membranes
how does staphylococcus aureus regulate toxin expression
- quorum sensing
- Repressor Of Toxins (ROT) - repressor protein that regulates 146 genes (most are toxins)
- RNAIII molecule interacts with rot mRNA to degrade the repressor and produce the toxins
live attenuated vaccine pros
- promotes humoral and cell mediated responses
- often lifelong immunity
live attenuated vaccine cons
- strong reaction
- may mutate back to pathogenic form
- may need to be refrigerated
how to make live attenuated vaccines
culture the strains in different host cells (example monkey) for long periods of time to decrease their virulence
faster way to create live attenuated vaccines
- mutate or delete the virulence gene
killed vaccines pro
- heat or chemical inactivates so no reversion to pathogenic form
- more shelf stable generally
killed vaccine cons
- often requires boosters
- doesn’t replicate in the host
subunit vaccines
only use selected antigens not the whole organism
subunit vaccine uses what derived from pathogen
purified macromolecules
tetanus and diphtheria macromolecules are what
inactivated exotoxins/toxoids
haemophilus macromolecules are what?
capsular polysaccharides
Hep B and HPV macromolecules are what?
surface glycoproteins or recombinant protein Ag
toxoid vaccines (subunit vaccines) creation
- inactivate the exotoxin by chemicals
- body creates toxin neutralizing antibodies
toxoid vaccine pro
doesn’t activate cytotoxic T cells
toxoid vaccine con
requires several boosters (tetanus shot)
how do you increase the efficacy of subunit vaccines
conjugate certain antibodies to carriers (macromolecules)
