micro exam #2 Flashcards
endosymbiotic theory
our mitochondria were once free living bacteria
who invented endosymbiotic theory
Lynn margulis 1967
what question did a cell biologist ask himself
how did life go from single cell to multicellular organisms?
what things are organelles?
Golgi apparatus, mitochondira, endoplasmic reticulum, ribosomes
organelle
sub cellular (smaller than a cell) structure that important for life but by them selves organelles are not alive
ribosomes
help with protein synthesis
DNA mRNA ribosomes
enzymes are a type of protein
endocytosis
process where cell “capture” other cell as a food source
aerobic respiration
process of producing cellular energy involving oxygen
first step of endosymbiosis
early cell engulfed aerobic bacteria
second step of endosymbiosis
they lost ability to live by themselves became mitochondria, chloroplast
where does bacteria produce their energy
cell membrane
prokaryotes
single celled organisms lacking membrane bound organelles
chloroplast and mitchchonira both contain their own
dna and ribosomes
circular dna
bacteria and mito
endosymbiosis
cell offers bacteria protection, moist environment (no drying out), food is brought to them
evidence for endosymbiosis
Mitch and bacteria-what in common?
evidence for endosymbiosis 1
Mitch have DNA
evidence for endosymbiosis 2
DNA genes, proteins, enzymes. Mitch has all enzymes needed for ATP
evidence for endosymbiosis 3
mitch have circular DNA like bacteria
evidence for endosymbiosis 4
mitch reproduce like bacteria
evidence for endosymbiosis 5
mitoribosomes, unique ribosomes in mitch
evidence for endosymbiosis 6
atp production and mitoribosomes in inner membrane
evidence for endosymbiosis 7
same size
macromolecule
molecule containing large # of atoms
ex of macromolecule
protein carbohydrate lipid nucleic acid
mitochondria
double membrane bound organelle
does bacteria have mitochondria
no
where is biochemical process of reparation and energy occur
mitochondria
role of mitochondria
produce energy currency of the cell through reparation and regulate cellular metabolism like Krebs cycle
can eukaryotes be both single and multicellular
yes
eukaryotes
membrane bound organelles, nucleus
all bacteria are “ “ and generally have a “ “
prokaryotic, single chromosome
biochemical testing
identify species or genus
GPR biochemical test
MSA, BAP, starch
GNR biochemical test
EMB carbohydrate test, MacConkey test
biochemical tests commonly use the
color system or gram staining
can disaccharide get though bacterium
no
carbohydrates used for
cell wall DNA formation
ex of monosaccharides
glucose fructose galactose
ex of disaccharide
sucrose lactose maltose
what happens of macromolecule is too big to simply cross into bacterium
bacterium must produce exoenzyme to break down macromolecule
endoenzymes
intercellular enzyme that functions within the cell in which it was produce (function within the cell)
lipase
enzymes that catalyzes breakdown of fatty acids
protease
enzymes breaksdown proteins (peptides
ph indicator can detect
fecal contamination
ph indicator
added to solution so acidity basicity can be seen visually
ph changes when
waste given off by bacteria metabolizing medium
periplasmic space
in negative: 2, periplasmic space, peptidoglycan, periplasmic space
in postive: 1 peptidoglycan, periplasmic space, plasma membrane
cell membrane
sorrounding cytoplasm, flexible,
what forms the cell membrane
phsopolidids and proteins
five functions of cell membrane
protects, receptor, cell mobility, regulates transport in and out , receives chemical messengers from other cells
what is ribosomes made of
rna and protiens
what are the two types of sugar molecules in cell wall that are the glycan
NAG and NAM
What acts as a cross bridge to connect NAG AND NAM
Amino acids (enhancing cell wall ridgety)
is penicillins fast or slow
slow
what does penicillin inhibit
synthesizing enyme that some bacteria make
penicillin effect on bacterial cell walls
aren’t enough amino acids connecting bridges and peptidoglycan layer becomes unstable
how does synthesizing enzyme work
allows new bacteria (binary fission) to enlarge by adding amino addicts to peptidoglycan layer, cell wall gets bigger
cocci diplocci
step. pneumonia
cocci chains
step pyogenes
cocci clusters
s. aures
bacilli chain
bacillus anthraces
vibrios
vibrio cholerae
what is the major component of the outer layer of gram negative bacteria
lipopolysaccharide
where is the LPS located
outer layer of the membrane and is exposed to cell surface
LPS also known as
lipoglycans and endotoxins
exotoxin
made internally then released
example of exotoxin
clostridium neurotoxin
what structure is released when bacteria die
endotoxin
lipid a exotoxin or endotoxin
endotoxin
what is in LPS layer
lipopolysaccharide, polysaccharide, lipid a
people die from E. coli when
lipid A is just floating around
what does lipid a do
- initiate blood clotting(kidneys, capillaries) 2. blood clots turn into broken capillaries 3. kidney failure
what does lipid a affect
fever inflammation diarrhea shock blood coagulation
why is it a loose loose situation to give patient antibiotics when there cells shut down
bacteria will die and lipid a will be released
two places E. coli infection
fecal (irrigation) raw beef
does lipid a grow on agar
no
why does lipid a septic shock happen
due to rapid drop of blood pressure due to overwhelming infection (leaky plasma
septic
total organ infection, too leaky leads to infection
3 ways bacteria die
macrophages, antibiotics, naturally
how to treat septic shock
artificial spleen
artificial spleen
device similar to dialysis that rids body of toxins and infection
how does artificial spleen work
blood enters biospleen device through nano beads that have receptor cites that bind to pathogens. the magnet on device pulls beads out of blood, clean blood gets put back in patient
if pathogen comes out negative
then lipid a is causing septic
importance of receptor sites
convey signals that bind to molecules and initiate response
capsules
helps with drying out, slows macrophage digestion or antibiotics, stick to things
a bacteria with capsule
strep pyogenes
biofilm
EPS
the making of biofilm depends on what
critical mass of microbes in one area
hardened biofilm
tarter
textured biofilm
cholera
necessary number to have enough bacteria in one place
quorum
cell to cell communication
quorum release happens with “ “ too
toxin release
colonization resistance
barrier to newcomers
John snow
cholera epidemic, epidemiology, public health, theory of biogenesis, spatial analysis
snows first observation and explanation
snow work with patients and no sick= cholera not respiratory MC
snows second observation and explanation
cholera patients not near other cholera patients = cholera no contact MC
snows third observation and explanation
cholera skip neighborhoods = respiratory
contagion theory
disease are contagious rather than spontaneous generation theory
what did snow do in 1850
add cholera to list of infectious disease
epidemiology
branch of medicine that deals with incidence , distrubution and control
how can disease be transmitted
oral fecal sexually contact airborne
causative agent of cholera
vibrio cholerae
what shape in cholera
comma shaped
what bacteria is high salt tolerant low ph and acid tolerant
cholera
where does cholera hang out
fecally polluted fresh water and salt water
in fish water does cholera have comma shape or rod shaped
rod
where is cholera comma shaped
our gut
protein production is controlled by
quorum sensing
what does comma shape do for the bacteria
more pathogenic
why is cholera comma shape
CrVA protein inhibits growth on one side
cholera toxin in controlled by
quorum sensing
cholera toxin attaches to what and why
sodium and chloride channels and keep from closing.
when cholera toxin attach to channels what does this cause
water flood in the intestine
is small pox airborne
no
small pox transmission
through conact, person to person or saliva droplets in infected persons mouth
antigenic
degree in which you make antibodies low or high output of antibody production
antigen
foreign substance or toxin that induces immune respond
what does antigen activate
lymphocytes
lymphocytes
infection fighting white blood cells
where are mast cells found
connective tissue
what do mast cells release during inflammation or allergic reactions
histamine
macrophages that leak out of capillaries also release
plasma
vasodilation
dilation of blood vessels which decrease blood pressure
what are released from macrophages and signal for more macrophages to relieve or clean up infected site
cytokines
can syphilis be congenital
yes cross placenta
if syphilis isn’t treated where can it spread
bone marrow cartilage and brain
syphilis
STD by direct contact during vaginal or anal sex
causing agent of syphilis
treponema pallidum
STDS
syphilis gonorrhoea, chlamydia
can you make antibodies if you have STD
no
pelivic inflammatory disease
uterus, Fallopian tubes, ovaries can cause infertility if not treated
what is chronic lyme disease due to
persister cells
persister cells
remain dormant until antibiotics are halted(conditions are met) not targeted by antibiotics
what tick
black legged deer tick
why is Lyme disease an example of arthropod-borne infection
because bacterium is transferred through bite of a tick
reservoir host carries bacteria but not harmed
east- white footed mouse
west- black footed moue
step 1 of transmutation of Lyme disease to humans
mouse- reservoir house
step 2 of transmutation of Lyme disease to humans
ticks feed off mouse develop nymphs
step 3 of transmutation of Lyme disease to humans
nymphs attach to mammals
step 4 of transmutation of Lyme disease to humans
nymphs develop into adult ticks then drop off Ito grass
step 5 of transmutation of Lyme disease to humans
ticks picked up my human + bacteria is transferred
zoonosis
infection we get from animal/ found in animal (not insect)
ex of zoonosis
Lyme disease rabies plague
vector
carries how we get infected
ex of vector
tick transferring bacteria from mouse to us
enteric
related to or occurring in the intestines
CSF glucose bacterial meningitis
glucose levels lower
why is glucose levels lower in bacterial meningitis
bacteria uses glucose for itself
CSF protein bacterial meningitis
increase
why is protein levels higher in bacterial meningitis
because cell destruction bu bacteria
CSF glucose viral meningitis
stays same
CSF protein viral meningitis
increase
does viral meningitis grow on broth or agar
no because no preproduction
when do soil microbes form into endospores
when conditions are not met from high salt or sugar
do endospores reproduce or metabolize when dormat
no
endospores can be made only by some
gram postive bacteria
bacillus anthracis
GPR soil toxin made by bacteria damage cells produce anthrax spores
bacillus subtilis
GPR soil and gi tract of humans
strep pyogenes
produce a protease known as SPYcep
group A strep
strep throat
strep mutans
GPR not very pathogenic, biofilm, oral cavity, tooth decay, break down enamel
strep pneumoniae
GPR has capsule
staph aures
GPR postive for catalase
treponema pallidum
GNR, through blood stream
E. coli 0157:H7
GNR shiga toxin, fecal contamination
vibrio cholerae
GNR WATERY diaherra= dehydration
borrelia mayonii
GNR can cause Lyme disease
borrelia burgdorferi
GNR Lyme disease
mycobacterium tuberculosis
wavy coat around cell way
mycobacterium bovis
TB in cattle spread to humans through airway
proteus mirabilis
GNR part of our intestinal microbiome, can cause uti
pseudonmonas aeruginosa
burn patients iv plastic tubbing cf patients
clostridium perfringes
GPR # cause of gangrene dead tissue rotting flesh bacteria emit foul smelling gas
clostridium botulinnum
produces neurotoxins in bodies that inhibit the release of acetylcholine,
clostridium difficile
GPR INTESTINAL
CLOSTRIDIUM TETANI
GPR soil rod shaped neurotoxin releases too much each ORGANIMS MUST PLACE IT IN BLOOD STREAM
NEISSERIA MENINGITIDIS
GNR meningitis
neisseria gonorrhoeae
PID gonnorrhoeae
