Unit 4 Flashcards
what makes bacteria different from eukaryotes? list the two most important things first.
70% protein in membrane no sterols (except mycobacteria) synthesize own folate peptidoglycan (except mycobacteria) no nucleus no organelles plasmids transformation different sized ribosomes (70S vs 80S)
peptidoglycan: describe the structure for me
5 aa, come off of Nam
alternating Nam -- Nag
Dala-Dglut-DAP-Dala gram neg
Dala
Dala-Dglut-Llys-Dala gram pos
Dalawhere does lysozyme target?
between Nam–Nag
where do antibiotics target on the peptidoglycan?
between Dala–Dala cross links
describe the lipopolysaccharide
O: differentiates types
P: anchor/linker
A: endotoxin
describe capsules
allow evasion of immune system, avoid antibiotics
protective layer, antiphagocytic
can be antigenic (e.g.: anthrax is vs. strep which is HA which is naturally occurring in body. why we get multiple strep infections)
glycocalyx
staph epi
biofilms, slime layers
can have large biofilm that has many other things populating it
staphylo
clusters
strepto
chains
diplo
a pair
cocci
spherical
bacilli
rod
what are the two flagella?
polar-1
peritrichus-everywhere
what directions do the flagella rotate?
counterclockwise: run
clockwise: tumble
what happens with chemotaxis and flagellar motions?
run>tumble towards thing you want
run
pilli have what 2 jobs?
attach
conjugation
pills are or aren’t antigenic
they are antigenic
eg: gonhorrea=gram - diplococci. can switch pilli
secretion systems
gram negative
can inject into a cell
electron transport chain, tell me all about it with bacteria
flagella runs on proton motor force
must run electron transfer chain across the cell membrane
flagella are important for DNA, flagella, transfer
ribosomes in bacteria
70S
what is it when you can replicate and synthesize DNA at the same time?
polycystronic
what is the shape most bacterial DNA exists in?
1 large circular double stranded line of DNA
there can be single double strands, multiple rings of double stranded DNA or plasmids
there are often many plasmids in a bacteria
what is necessary to have on a plasmid?
an ORI for replication
an ORI for movement
bacteriophage
virus that attacks bacteria
important for diptheria
how do bacteria divide?
binary fission
what are fastidious bacteria?
need extra stuff, fussy
what are heterophilic bacteria?
organic C users
what are autotrophic bacteria
CO2 as C and Energy
aerobe
cannot ferment
anerobe
ferment only
indifferent
ferments in presence of O2, doesn’t respirate
facultative
respires but can ferment
microphilic
low O2 it grows (5%)
what does O2 do to bacteria? how do they survive with it?
O2 creates ROS. to deal with this the bacteria need to have catalase (takes H2O2 to H2O and O2), or superoxidase disputes (takes ROS/O* to O2)
fermentation
obtain energy from organic or inorganic electron donors and acceptors
no O2 usually
respiration
generate ATP
aerobic O2
anerobic not O2
which are the only 2 bacteria that cause spores?
bacillis and clostridium
salmonella is know to switch what antigen?
H antigen
DNA arrangement
on Flagella
bacteria can switch what to express different things?
DNA
salmonella can change H antigen
gonhorrea can change pilli
spontaneous mutation
small changes
strep–>toxins (exotoxin B–>necrotizing faascitis–>due to spontaneous mutation)
recombination
2 sets of homologous zones recombine
often can happen with plasmids
transposons
mediate own movement
will inactivate genes it inserts into
up regulates things it is next to
insertional transposon
only thing it codes for is transposase
complex transposon
codes for transposase + something else
pathogenicity islands
only certain bacteria have
large portions of chromosome that encode for a virulence factor
transformation
where cell can take up DNA
makes it competent
can force competency by lowering temp and adding CaCl
transduction
gene transfer mediated bacteriophage can be chromosomal or plasmid virus picks up a bit of bacteria dan instead of viral DNA transfers bacterial resistance lytic an lysogenic
lytic state
viral production and lysis
lysogenic
needs repression protein to stop
secretly waits until it is triggered to go
every time bacteria divides, it takes some of the dna with it
herpes (waits and divides until the immune system down, then attacks)
bacteriophage conversion
infected=pathogenic
only phenotypic change=production of toxin (diphtheria, shigella)
temperate version needed!!!!
conjugation
F factor can synthesize sex pills
has an origin of transfer-oriT (plasmid has 1/2 go through tube, other half stays in the bacteria and rebuilt)
can remain a plasmid or integrate into DNA
can have a conjugative transposon
conjugative transposon
a transposon that is transferred during conjugation
can move, leave when conjugation is occuring
how do you show a toxin has a role in pathogenesis?
- show toxin alone has same symptoms of infection by the microbe producing it
- show antitoxin prevents disease
- show virulence correlates with amount of toxin
- show nontoxinogenic mutants are not virulent/reduced virulence. virulence is restored if they can make toxin again
Koch’s Postulates
- show that phenotype/property being investigates is associated with pathogenic species/strain of microbe
- show inactivation of genes that encode virulence factor cause decrease in microbe virulence
- show replacement of gene to wild type restores virulence
list the toxins that inhibit protein synthesis
diptheria toxin and pseudomonas aerugionosa exotoxin A
shiga toxin and E coli toxin and ricin
inactivate elongation factor 2
list the toxins that modify intracellular pathways
heat labile enterotoxins pertussis toxin heat stable enterotoxin anthrax edema factor anthrax lethal factor C. diff toxins
list the toxins that inhibit neurotransmitter release
botulinim
tetanus
diptheria toxin (DT) and pseudomonas aeruginosa exotoxin A (PAE)
inactivate elongation factor 2–EF2 (required for peptide chain elongation)
ADP ribosyltransferases (transfer ADP-ribose from NAD to dipthamide on EF2, which inactivates EF2 in cytoplasm)
bind to different receptors in the cell
DT is heart, kidney, neurons
PAE is liver
shiga toxins and Ecoli toxin and Ricin
specific RNA N-glycosidases that remove adenine residue from 28s RNA of 60S ribosome
inactivates it
stops translation
heat labile enterotoxins
vibrio cholerae and escheria
ADP ribosyltransferases
increase cell membrane adenylate cyclase activity
ADP ribosylate and activate the G regulatory protein (stimulatory).
increased cAMP causes chloride secretion and diarrhea
pertussis toxin
ADP ribosyltransferase
increases adenylate cyclase activity
ADP ribosylates and inactivates the inhibitory G reg. protein of cyclase
increased cAMP causes tissue specific effects
heat stabile enterotoxin 1 of ecoli (ST-1)
activates cell membrane guanylate cyclase
increased CGMP in enterocytes causes diahrrea
anthrax edema factor (EF)
from bacillus anthracis and adenylate cyclase toxin from pertussis
adenylate cyclades that cause increased cAMP and produce dependent effects
requires activation by calmodulin and Ca
binds cell membrane and makes a pore
anthrax lethal factor (LF)
endopeptidase that cleaves MAP kinase proteins
inactivates function in signal transduction
c. diff toxins A and B
glucosyl transferases
alter actin cytoskeleton of cells
transfer glucose from UDP-glucose to Rho family GTP ases
inactivates them
botulinim toxin (7 types)
causes flaccid paralysis of skeletal muscles
inhibits release of acetylcholine at mineral junctions
A, B, E cause disease most often in humans
tetaus toxin (1 type)
cause contraction, spastic paralysis
inhibit release of neurotransmitter from inhibitory interneurons in spinal cord
tetanus toxin and botulinim toxins are dependent on what?
zinc!!!!
zinc dependent endopeptidases
incactivate SNARE proteins required for neuroexocytosis (VAMP), 25 kDa SNAP-25, syntaxin
each toxin cleaves one protein at a site
individual serotypes differ in specificity
botulinim is used therapeutically for what?
for focal dystonias, involuntary movement disorders (strabismus, blepharospasm)
used cosmetically
antitoxic antibodies
bind toxins and prevent toxicity
antitoxin
don’t prevent infection, or reverse toxic effects after it enters the host cell
toxoids
derivatives of toxins, retain immunogenicity
lack toxicity
used as vaccines for long term protection agains toxin mediated disease
passive immunization
administration of antibodies to patient to provide immediate, temporary protection against toxin or agent
duration immunity limited by degradation of antibodies in patient
active immunization
administration of toxoid to patient to get anti-toxic antibodies
- primary series of immunizations, booster doses
- active immunity can persist due to memory cells
immunotoxins/hormonotoxins
hybrid molecules of toxin fragment lacking a receptor binding domain of native toxin
linked by chemical conjugation/as recombinant fusion protein to a ligand or a hormone to receptor binding domain
specific for a receptor that is different from native toxin
intoxicate cells by delivering the toxic fragment of native toxin
many are designed to kill tumor cells that display a tumor specific toxin, but not kill normal cells without that receptor
endotoxin
lipopolysaccharide
A region
PAMP
LPS infection (associated with shock, DIC)
exotoxin
heat labile
secreted out of cell
secretor system, strep pyo–scarlet fever
can be injected
list the gram + cocci
staph aureus staph epidermidis strep pyogenes viridans strep enterococcus faecalis/faecium
list the gram + rods
c. diff
c. Tetani
c. botulinum
c. perfringes
list the gram - cocci
gonhorrea
list the gram - rods
e coli
pseudomonas aeruginosa
list anerobic organisms
bacteroides fragilis
lists intracellular bacteria
clamydia trachomatis
list the bacteria with no cell wall
mycoplasma pneumoniae
