FSII Flashcards
Essentially, to bring something big in, secrete enzymes to break it up OUTSIDE then bring the components back in. In gram positive, they go directly out of cyto mem, in gram -, they must traverse outer membrane too
Excretion of hydrolytic exoenzymes and pathogenic proteins
sterilize broth in air guy + prove spontaneous generation wrong
pasteur
bacteriocin that works agaisnt diverse bacteria inclusing strep mutans and e faecalis
nisin
classify bacteria as pathogenic
koch’s postulate in 1876
PAI
genes that can insert into host DNA. often in tRNA genes and can be transfered to new bac, thus conferring virulence to benign strains
- commensal don’t have PAI but can get it from horizontal gene transfer
- move using transformation
suprres transcription of gene by binding to operator
repressor
homolactic fermentation
excess sugar. this is essentially EMP pathway that turns pyruvate into 2 lactic acid
cefazolin and ceftriaxone
If can’t take meds and allergic:
cooperativity
substrate is an activator. curve is not hyperbolic but sigmoidal (s shape)
selects for gram-positive bacteria agar growth
Sodium azide
periodontitis what to give
(gingivitis is transient) give amox (bactericidal), or azithromycin (bacteriostatic). COMBO: metronidazole + amox
If allergic then just metronidazole
how do cells resist b lactams and glycopeptides, tetracyclins
hydrolysis, efflux and altered target using genes. make b lactamases. resistance genes are AmpC, blaZ
- can be avoided by b lactamase inhibitors like augmentin
- - failure to make peptidoglycans like in mycoplasma
glycopeptides are altered target
tetracyclines avoided by efflux, ribosomal protection proteins, and altered target.
- tet gene protects the ribosome
isofunctional enzyme
branches of both path can inhibit their branches
how do acidic bacteria survive in those pH
increase surface negative charge that stabilize them, pump out H+ ions actively, high isoelectric point to maintain proton motive force
- most bacteria are neutrophils
selection of antibiotics
1) site of infection (bone vs blood)
2) age of patient (dose)
3) place of infection (hospital is more likely to be antibiotic resistant than community)
4) host factors like immunocomp
sulphonamide
have S group. Prontosil, sulphanilamide, “sulf”. Prevent growth but cause allergic reaction
PABA analogs that are nonfunctional so can’t make folic acid so no growth
static. prevent nucleic acid synth
can bind to DNA primers. cut and put into plasmid and clone OR transfer to other organisms and do hybridization test OR blot on membrane and probe for target and do agarose gell for size testing
internal probe
icosahedral symmetry
20 triangular faces and spherical crystal
heterotrophic co2 fixation in some bacteria
- reverse krebs cycle!
adsorption to host, inject dna into host, phage replicates, maturation, new release and new infection
lytic cycle
- virulent phages
peptidoglycan cell wall gram +
b1-4 linkage connected by transglycolase
- pentaglycine cross link done by transpeptidase
- alanine, glutamine, lysine, alanine then clave the 5th AA and link the 3rd and 4th AA via pentaglycine
trp operon
repressible so no repressor makes tryp and pressor is bound when 2 tryptophan, the corepressor is bound
F factor
low copy number plasmid with only 1-2 copies made
proteinase production
can they digest egg or gelatin
quorum sensing
- regulate gene expression in response to cell population density
- secrete autoinducer to check concentration then at low density, molecules diffuse away but in high density, trigger changes in other cells
when inhibitor binds to allosteric site of ENZYME SUBSTRATE COMPLEX
noncompetitive inhibition. significantly lower curve
EMP pathway for glycolysis
phosphorylation, isomerzation, phosphorylation, then split into 2 molec and reduce NADH
c6 to c3 oxidation
hepatitis
infectious is type a
serum or blood type is B (DNA virus)
C is cured
unfolded protein transport across membrane
Sec pathway
- sec b binds to sec A and YEG
peptidoglycan cell wall gram -
b1-4 linkage connected by transglycolase
- no pentaglycine cross link
- alanine, glutamine, MESODAP, alanine then cleave the 5th and do direct amide bond
quinolines
Inhibits DNA gyros and topoisomerase for repair too
bactericidal
starting point of conjugative transfer
oriT
for fungi. Must make daily, corrosive, reduces activity of organic matter, skin and eye irritant
Hypochlorite
gene transfer and antibiotic resistance
Genes carried on plasmids can become part of chromosome and inherited. Transposons are rearrangeable order of genes in bac, leading to resistance to antibiotics
- can do transformation, conjugation, transfuction
biofilm composition and behaviour depend on
cooperation and antagonism and can create environments for each other, nutritional cooperatuion, mutualism, oxygen detox and gene regulation
combine which two drugs to stop biofilm in mouth
nisin and entV
axial filaments
wrap around cell but like flagella
- internal is spirochete
- outer is spirillum
take sample, if it binds to antibody that means there was a history of host response before. Diff from nucleic acid reception since it doesn’t show active infection. Help in research since bac are identified by genus, species then serotype!
serology or antibody test
PTS
phosphotransferase system
glucose across membrane
- PEP to pyruvate then pass the P on to EI then HPr then to E2A then E2B that phosphorylases glucose using 2C glucose
there is a different 2C for different sugars. more of those = more ability to bring c sources in
brings mono or disac in
characteristics of antibiotics
activity type (cidal vs static), chem structure, spectrum (some bac or lots)
capsid
- protect nucleic acid from environmental enzymes
- can have helical, icosahedral or complex crystal symmetry
resolving power of 0.2 micro m. (1/3 width of prokarya cell)
Specimens that fluoresce or with antibodies labelled with fluorochromes (emit fluorophore when stimulated AND when it binds to the right bac)
Light microscope
facultative anaerobic growth in aerobic conditions
directly fixes PEP with oxaloacetate (connect EMP to krebs)
resistance to antibiotics, forming new species and evade host defense via transmission of virulence
consequences of horizontal gene transfer
cumulative feedback
both branches can inhibit first reaction seuallty
bactericidal, cheap, but degrades stuff, reduces activity of organic matter, evaporates, not good for eco
Alcohol
bacteriocin that works agaisnt s mitis and gram + bac
mutacins
s mitis is commensal so not good for oral cavity to disrupt
binds forming a antibody sandwich. Substrate is added and the reaction changes color
antigen is added first, then add anti-antibody
indirect eliza
bacitracin, vancomycin (a glycopeptide), aminoglycosides, polymixins
topical agents
bacteriocin that works agaisnt candida albicans
EntV
amoxicillin
If can take meds not allergic
s mutans quorum sensing *** luxS
LuxS pathway: only species to really have this to communicate to other species using AI2 molecule. establish pathogenesis
- nonspecific autoinducer
herpes virus and adhesion
- dna virus with latent infection and many types
- all species can get it
- first infects then sits in trigem and sacral
- envelope has 12 glycoproteins.
gD is adhesion then stimulates gL and gH membrane fusion that turn on gB to bind host proteoglycans
operon anatomy
regulatory gene then promoter then operator in reg region then structural genes. regulatory gene is NOT included in operon
acid fast bacteria
glycolipids, fa, was on outside
Arabitogalactan (heteropolysac) that connects outer layer to peptido cell call via phosphodiester bond
lipoarabinomanan displayes species specific heterogenuity
Very resistant to disinfectant and dry conditions
Mycobacterium avid-intracellulare complex infects humans
Ulceration
Impermeable cell walls
cell wall
- thin peptido but have waxy mycolic acid on the outside which is hydrophobic (can’t remove the dye)
- stain: using carbolfuchsin with phenol
flagella, capsule, exotoxin, outer membrane, endotoxin bacterial antigen
- serological determinants!
Principle component analysis
each dot is a sample. Color is where its from. Proximity is how similar their microbiomes are (gut of two diff people will be closer than bac of gut to own bac of hair)
bacteriophage
transduction movement
- inject DNA in cytoplasm
- classified by morphology and nucleic acid composition
capsid protein coat with capsomeres (self assemble) what are pentamer (12 vertices) and hexamer (20 faces)
- tail is contractile or non contractile sheat that is hollow
baseplate is spiked with 6 tail fibers that recognize and penetrate host cell wall
- can degrade EPS using depolymerases and active against planktonic and sessile bac. therapy alternative to antibiotics
s mutans quorum sensing *** comCDE
antimicrobial peptides, toxins and adherence
papova/papilloma
- non enveloped DNA virus, persistent
- cause warts
- capsid protein is l1
- mucosal/genital disease with 40 types but mostly 16+ 18 are bad
- cause cervical cancer and head and neck, oropharyngeal
- vax is for 16 + 18 and uses l1 protein
macronutrients needed in smaller amounts that do enzymatic catalysis
K, na, fe, mg, ca, cl
plasmid
- circular, cloned DNA that has many copies, small # of genes but uslaly antibiotic resistance
- can conjugate BUT if can’t replicate if incompatible OR can’t partition either
- can recombine two plasmids innto 1 and transfer antibiotic resistance
sensitization of population, changes in normal microbiota, masking of infection without eradication, drug toxicity, drug resistance
dangers of indiscriminate antibac use
transposons
need transposase enzyme that binds to inverted repeating sequence, catalyze movement and insert it into new genome place
- some require specific sequence to insert and some don’t
- when inserted, it cuts and refils the gaps with direct repeats!
chloramphenicol
binds 50s then stops new AA binding to peptide chain by stopping peptide transferase
letting hfr cell do the thing but measuring it in time
this is gene mapping
- by disrupting at different times, can map the genome
gram -
outer membrane
thin peptido
lipopolysaccarides
counterstain pink
- involved in periodontitis
cell wall
- highly resistant to antibiotics due to outer membrane slow diffusion
- LPS contains lipid A (glycolipid that is endotoxin) with o antigen that is highly variable among species
- lipoprotein links outer membrane to peptido and is very abundant
- periplasmic space has binding proteins (specific) and hydrolytic enzymes, detox enzymes that inactivate antibiotics, and membrane derived oligosacc (MDO)
LPS structure
- O antigen: repeating sugar units specific to bacterial serotype
- core: outer has hexoses, inner has 1-4 kdos and up to 15 residues, phosphate - charge
- core connected to lipid via acid labile linkage (hydrophilic so can detach easy!)
- Lipid A: hydrophobic, with phosphate group and glucosamine disac attached via b1-6 linkage. two acyl chains where the second is esterified
cephalexin, azithromycin or clarithromycin
If allergic to penicillin and can take meds:
maltose operon
positive control
maltose inducer bind activator to transcribe
positive control
positive control is when promoter binds and inducer binds to make thing
** induces polymerase to BIND and repressess the repressor
- positive is also inhibitor binds the promoter so NO transcription
h202 to oxidize NADH
peroxidase
PHB
inclusion bodies to store stuff in bacteria
tetracycline
inhibit the synthesis of bacterial proteins of 30S subunit by stopping aa-tRNA
More side effects now so use derivatives
static
pentose phosphate pathway PPP
makes a precursor for nucleic acid called ribulose 5 phosphate (c5)
- then does all the rest nadh stuff
first person to see bacteria
leeuwenhoek in 1675
Bac replication
replisome is the machinery
forks and bubbles
helicase unwinds
primase lays down RNA primers for lagging strand
leading strand is cts synth
- many replications on same area at once!
bacteriophage therapeutic delivery
limited penetration and degraded by enironment
overcome BY:
- nanoparticle power that improve binding when + charge cargo
- liposomes penetration
film and fiber do constant release of phage and coat them
- hydrogel
heterolactic fermentation
makes ethanol and lactic acid essentially PPP pathway
dark image on light background. Can see living stuff without stain
phase contrast
flagella
movement
- long and thick
- bacterial locomotion
- chemotaxis
- ANTIGEN
take almost 40 different gene products to make. First the basal body is assembled then inserted into cell envelope, then hook is added then filament is assembled by addition of flagellating subunits to its growing tip-
- move using proton motive force
- 2 protein links per mem (so 4 for outer)
is origin of vegetative replication. start of sequence replicated in a recipient cell
oriV
enzyme linked immunoassay. Suitable for liquid phase (not biofilms or tissues)
ELISA
cephalotrichous
head of hair on either side! amphi is only one flagella on either side
carbohydrate breakdown test
if bac produces acidic products. good for anaerobic bacteria
s mutans quorum sensing *** comRS
comRA: swich on competance genes for transformation
glycopeptide
LAST RESORT since very low resistance to it. very sick but bad side effects. inhibit cell wall biosynth by competitive binding to substrate at d-ala terminus
bactericidal
lps with all the structures is what form
smooth, S form
can see motility of bac. See more than light microscope
- see smaller than 0.2 micro m
dark field microscope
pilli moveemnt
twitching using type IV
-gliding using slime and sliding by growth (fake)
nuclear envelope
Dna surrounded by cytoplasmic protein, peptidoglycan cell wall, outer membrane (in gram -)
staph aureus quorum sensing (NOT AS IMP) gram +
- Quorum sensing increases virulence, toxins and adhesion via AIP
pseudomonas aeruginosa gram -
3 mechanisms, AHL and PQS that control virulence and biofilms
prophylactic vs therapeuric antibiotics
prophylactic is for risk of infection like endocarditis so give 1 hr pre op and may continue 2-3 days post op
- b lactams and quinolines
therapeutic is already have infection. clindamycin works here because it treats infection not just preventative
- metronidazole is good for anaerobic
- tetracyclins and macrolides
*infetion types are odontogenic, periodontitis and sinusitis
like azithromycin (FOR PENICILIN ALLERGY) bind to 50S and interfere with initiation complex
macrolides, lancosamides
- static
eukarya cell comparison
ester linked membrane, unbranched, polyunsaturated with sterols and 80s ribosome
- many replicating units with different rep origins so slow
cultivation (alive), molecular techniques (ded)
how to ID bac
virus features
- DNA/RNA capsid.
- lipid envelope.
- glycoprotein spikes
- capsomere
- subunit replication is where pieces are made separately then assembled
- act as antigens
- get into cell by binding to glycoproteins. antibodies try to stop it here
- fiber and knob extensions get virus into cell
sucrose and caries
- sucrose makes lactic acid and acetic acid and make EPS that is sticky needed for biofilm
- coadhesion coaggregation acidic and aciduric to demineralize teeth
- higher number of bac in bioflim in sucrose BUT higher planktonic bac in gluc and fruc since good substrate source!
- BUT it can also do one form of sucrose, not the other 5! another bacteria that can ferment 4/5 types maybe disrupt the biofilm!
endodontic lesions
enterococci
e faecalis
favor growth of some stuff with use of inhibitory agent
Selective
ex. macConkey agar contains bile
bacteria cell comparison
murein in cell wall, ester linked unbranced saturated or monounsaturated lipids, 70s
- defined rep region and proceeds bidirectionally and ONE unit (fast)
carbohydrate utilization by strep mutans
CCR is carbohydrate catabolite repression where you don’t rbeakdown nonpreffered substrate when good source is present
- gram +
E2B does glycolysis and makes substance that binds CCPA then bind CRE that increase or decrease metabolism of strep mutans
bacteriophage assembly
assembly: host cell makes proteins, scaffold bind to portal, this is procapsid. matura capsid has ejected scaffold proteins and DNA is inside. proteins prevent leakage and then tail and baseplate are added = mature
first person to think of microscopic organisms
hooke’s micrographia in 1665
more than 10% ox is harmful
found close to surface of beaker
microaerophile
less bad, localized and mass is fluctuant and tender, peripheral red, pus, anaerobic bac and moderate severity
Abscess
how do gram - transport proteins across membranes
complex
- two step is sec or tat is type 2 or 5
- types 1,3,4,6 can transport across a host cell membrane
- require atp
actinomyces bacterophages
distrupt strep cocc actinomyces interactions that are commensal and needed for homseostasis
archaea cell comparison
ether linked, branched, saturated with 70s ribosomes
conjugation and HFR
high frequency recombination
- transport chromosome genes efficiently
- form bridge, nick the DNA, send it out and can be deleted by the other cell OR it is taken up and now both cells are HFR
sometimes, it gets combined with F+ plasmid but it takes some with it and LOOSES F+ function
- can evage host cell, aquire resistance, form new species
plasmid and transposon movement
conjugation
when low glucose in cell
CAP/ catabolite activator protein/ CRP
- always expressed to report glucose levels to lac operons and other genes
- glucose low, less ATP so add P to E2A then make camp (hunger signal)
- CAP binds to region before lac promoter to help rna pol to bind (CAP/CAMP complex) promotes transcription
- can also promote this using inducer lactose to inactivate repressor lacI and make lac operon
- high glucose then lacI is bound
negative control
protease inhibitors
-treat HIV/AIDS and hep C that binds viral specific proteases involved in precursor so no maturation of virus
what messes with biofilm formation
- disturbance of the bacterial cell wall
helical symmetry
RNA virus. stacked repeating proteins like helix and sometimes folded back when enveloped
first person to think boil = sterile
spallanzani
direct vs indirect contact
direct is with pathogen, indirect is due to some kind of puncture (usually viral stuff)
strep mutans and capsule/glycocalyx
- use glycosyl transferase and fructosyl transferase to make sugars from sucrose, then it makes a glue and secrete acidic products
- do this using a saliva coated hydroxyapatite disk
70s ribosome structure breakdown
50s and 30s (with the 16srRNA)
nongenetic drug resistance
non replicating bac are NOT susceptible to antibiotics so not in spores! if they multiply they are
- sometimes, replication makes them loose the target for drug (organisms that loose a certain cell wall protein so penicillin won’t work). phenotypic resistance
- L form switching where orgs that don’t have that cell wall thing then it can’t get it!
- bacteria may also be at sites where antimicrobials are excluded or inactive!
see viruses with diameters of 0.01 - 0.2 micro m
TEM
what sugars allow strep mutans to form biofilms vs just grow
sucrose allows EPS formation so make plaque. with glucose and sucrose, still won’t form biofilm!!
housekeeping function operon that is always on
constitutive
complex symmetry
pox virus
- kidney bean shape with outer envelope
injection of DNA into host, integrates into chromosome, then hangs out until signal to infect
temperature, lysogenic cycle
70s ribosome structure breakdown
50s and 30s (with the 16srRNA)
bacterial genome
- haploid DNA
- supercoiled DNA done by topoisomerase and gyrase that present unwinding
- single chromosome, usually circular (lil linear) but aggrebacterium has 1 linear and 1 circular
- smaller size genome for obligate intracellar but some can be large
- operons that have single promoter reg retion
- PAIs
gram positive quorum sensing***
use autoinducing peptide AIP
- binds to kinase in hgih concentration that phospho a transcription factor. two component system
shape of bacteria guy
cohn
primary colonizer
streptococci
gram neg quorum sensing ***
produce n acyl homoserine lactone AHL as signal. bind DIRECTLY to trasncription factor to regulate expression
- BUT some can use two component system too
bergey
manual of systematic bateriology in 1923. publication classifies all known bacteria that have been cultured
lac operon
inducible where repressor binds and nothing happens then inducer lactose binds and make enzyme
organism that makes ATP by aerobic respiration if ox is present, but can ferment without ox
facultative anaerobe
rifampin
dna dependent rna pol inhibitor
spores
invagination then forespore gorms, it is coated and then lysis of sporangium, resistance to pH, temp, boiling water and disinfectants
running
lophotrichous
bacteria in our body function
Bac secrete mucus and also little bit of antimicrobial peptide to stop weird bacc. colonization. Help in digestion in mouth and intestines. Maintain pH and peroxide to kill other bac. Fortify immune system in the skin
enveloped virus
lipid has glycoproteins and sensitive to detergent
tumbling
petrichous
facultative anaerobic growth in anaerobic conditions
PEP fixed to oxalo but there is reductive branch and oxidative branch
- oppositely orientated half circles
local vs generalized infection
- local is when short incubation time, specific body part, like cold/flu with many strains but limited antigen made
- no viremia (virus in blood) and short incubation time
- short term immunity
generalized is long incubation time, goes into blood, limited strains of virus but lots of foreign antigen made which means good immune memory!
superoxide anion to h202
superoxide dismutase
look for certain stuff in bacterial species like a ability to produce acid.
Can ID species because their enzymes create a zone of clearing like in hemolysis
differential growth
e faecalis treat by
engineered bacterophages
in a thick** specimen, can see different layers by adjusting beam focus. Can also make the layers take on different colours (false color images)
confocal scanning laser microscope
genes encoding the F pilus and DNA transfer elements
transfer genes Tra region
trifluridine
- nucleoside for blindness that works because it goes into the eye which doesn’t make any dna!
- selective inhibition is where viral dna synth is ongoing and limited host dna synth on the eye site
non enveloped virus
contain cell attachment proteins. not sensitive to detergent
selection of antibiotics
empirical therapy is broad spec mixture
susceptibility test to see if bacteria is resistant (put it on plate with spots of drug and see which kills it. no spot is resistant)
- do a strip with concentrations of antibiotics to see what is most potent dosage
Environmental sensing
two component signal transduction where it interacts with environment. Sudden change of pH, nutrients, oxygen, etc. regulate transcription to induce or repress
how to bring glycerol into bac
facilitated
h202 to water
catalase
the only bac that doesn’t have anything to convert superoxide radical and h202
obligate anaerobe, uses peroxidase
select for gram - agar growth
Bile salts
morphology, stains, antigen testing or DNA, culture isolation, susceptibility testing (isolate sample, bring to lab, grow it and test it to ID), immune response to infectious agent
phenotypic methods of diagnostic classification
pilli/ fimbriae
pilli
- conjugation
- type IV does attachment and twitching
- short and thin ones do adhesion
- almost always gram -
fimbriae are used as attachment and virulence factor
made of protein called pilin. Have adhesions protein on the tip to attach which can be used to move (think throwing a rope and pulling yourself up called twitching). Can be pathogenic, do sex and ID cells
decreases folate
trimethoprim and sulfonamides
which is critical for bacteria. PABA is essential metabolite and needs ATP dependent condensation to make folic acid to make nucleic acids
most common bacteria in human temps
mesophiles
hydrogen sulfide assay
do bac produce H2S from AA for gram - rods. black colour
superbugs *** 5
resistant to TONS of antibiotics. naturally!
- carbapenem resistant acinetobacter
- candida auris
- clostridioides difficile
- cadbapenem resistant enterobacteriaceae
- drug resistant neisseria gonorrhoeae
- treat by makinng NEW anntibiotics from weird places like soil
environmental influence vs test tube, dormant vs biofilm vs planktonic, inequal distribution of drug in tissues and fluid, rate of tissue-drug contact, interfering substances like pH and stuff
all factors that influence drug pathogen interaction
isolate sample DNA and denature it. Allowing primers to bind to target size which then create lots of DNA copies
PCR
macrolide
inhibit protein synthesis of 50S by stopping elongation
static
global control system
control many operons together using a regulon that work in some stimuli like stress or environment
polymyxins
detergent like cyclic peptides that damage membrane proteins ONLY of bac and fungi
cell wall agent
which bacteria will you find in fridge temp
psychrophiles
non selective media growth
everything grows on it pretty much
- easy to show colony patterns
sequential feedback inhibition
end products of branch can inhibit previous reaction
Lipid A toxicity
host cell recognition and once cell is lysed, causes inflam, fever, diarrhea, tissue necrosis, activate immune
- LPS recudes cell viability by inducing ROS generation
aeration process
during respiration, superoxide anion and h202 are made
LPS without o antigen
rough lps, R form
genetic drug resistance
- chromosomal resistance: spontaneous mutation (mistake) very rare
- extrachromosomal: most common. plasmids that carry resistance via enzymes that destroy drugs or something (ex b lactamases in penicillin) OR change permeability to drug so it doesn’t come in
- altered structural target (receptor changes so stop binding of drug). can also be when drug effects it less than beofre
- destroys drug
- altered metabolic pathway: no PABA required so use another folic acid source (while drug blocks the pathway)
- efflux pump
- no synthesis of peptido or specific peptido
- lack of PBP permeability barrier
how do acid fast secrete proteins
type 7 that forms a channel across the mycomembrane. unknown
odontogenic infxn what to give
penicillin, amoxicillin, clindamycin, azithromycin, CLINDAMYCIN only if allergy to penicillin
increases transcription of a gene by facilitating RNA polymerase binding to the promoter
activator
severe and general pain, large and diffuse access, red, thick, hot and severe pain and Loss of fin, pus, very serious with mixed bac
cellulitis odontogenic infection
ampicillin and cefazolin and ceftriaxone
Can’t take meds not allergic then
quantification of bacteriophage and growth cycle
quantification
- plaque count on agar (GOLD STANDARD) using plaque forming units (ded bacteria circles)
- dilution or measuring time to lyse (bad)
- TEM to count bac in area and multiply
cycle is sigmoidal where its flat, rises up slowly (point where it lyses some bac and stops when its lysed ALL the bac)
inner membrane is sac, but outer is its with ER. Selectively perm due to pores, histones bind via ionic interactions
nucleus
F nucleatum
- plaque formation with p gingivalis
- gram neg
- obligate anaerobe
- ALSO has different 3 amino acid = lanthionin
what stops nag and nam joining
lysozyme. block the b1-4 bond
- works best on gram +!
folded protein transport across membrane
tatB and tatC bind to tatA
the only bac that doesn’t have anything to convert superoxide radical and h202
obligate anaerobe
bacteriocins
protein or peptide tocins made by bacteria to stop other bacteria that are similar
works in planktonic BUT not super specific enough (but it is a bit)
negative control
negative conntrol is inducer binds the REPRESSOR so transcription happens
- INDUCES it to allow transcription by FALLING OFF
- when COREPRESSOR binds repressor, then no transcription
acyclovir
- blocks viral DNA synth by messing up only viral enzyme thymidine kinase
- stops replication so no outbreaks and stopping spread in body BUT it doesn’t cure it nor stop infection
respiration and ETC
start and end with oxaloacetate. two acetyl coas are fixed
make H+ gradient made from transport e from NADH and FADH2 to make atp
- chemiosmosis using H+ gradient to make ATP
- NADH dehydrogenase, then cyto b, cyto ox, atp synthase
- proton gradient and membrane potential are proton motive force
- protons pumped across the inner cyto mem
periodontitis treat by
aggregatibacter
how to serotype bacteria
using OH types. surface antigens
- tge O157:H7 is most important
- vaccine will have many serotypes of capsular polysacc to cover all the bases
lower resolving power than TEM but can see 3D images
SEM
antibiotic problems
- allergic reactions
- superinfection when you kill some bac but not others so ANOTHER different bac/fungi creates a niche
- toxicity, drug intneractions, patient compliance, bac resistance
** bacteria resistance is NATURAL strategy to protect against biome toxins, nothing to do with antibiotics themselves
small molecule that either activates or represses transcription by interacting with a repressor or activator
inducer
bacteriocin that works as probiotic
salivaricins
DNA fragments that integrate copies of themselves into a recipient chromosome
insertion sequences IS and #
gram +
thick peptido
teichoic acids
stain purple
spores in rods
capsule/glycocalyx/ slime
ecm polysaccharides and help in attachment
- hydrophilic with high mw of polysac or polypeptide or both
- WON”T protect against dessication
- 1-6 beta linkage
glycocalyx
- adherence and form biofilms
capsule
- adds to invasiveness of pathogenic bacteria and excludes particles
- made of monosacc linear or branched. 1-6 B linkages
slime layer
- when glycocalyx is loosely associated with the cell and doesn’t exclude stuff
competence and transformation in gram +
must be competent
- bind competence factor from somewhere
- make it to make autolysin which activates DNA binding protein and nuclease to transform!
transformation
- DNA is bound to cell surface, then its nicked and one strand degraded by nuclease
- make new strand and incorporate into genome
adenovirus
- matures in nucleus
- icosahedral. double stranded DNA
- used to deliver covid spike proteineus
normal mouth pH
7.2 to severe caries (5.5)
drug concentration
absorption whether its excretion amount or inactivation of the drug. it fluctuates and the amt that gets to pathogen varies
- distribution: drug concentration is diff in diff tissues
- vairability of concentration. critical to maintain an effective concentration at location for time. large dose is larger time interval
- post antibiotic effect: delayed regrowth of bacteria after exposure to agents. some do and some don’t
bacterial adaptation via regulation
- they don’t make catabolic enzymes unless there is substrate ex lactose and pathways are usually reversible for quick adaptation
- adapt via regulation of stuff using environmental signals!
mostly done at transcriptional level to control flux of metabolies - can either alter the activity of enzyme (fast) or amount of enzyme
- transcriptional stuff is regulated by promoters/reg proteins that bind to DNA. level of expression is determined by ability of promoter to bind
proteinaceous structures
fimbriae, capsule/glycoaclays, flagellum, pilus
drugs for virus
- stop entry, protease and maturation
bacteria and planet
make o2, recycle CHNOPS, fix nitrogen, digest complex carbs
b lactam
Inhibit bacteria cell wall biosynthesis. Binds the transpeptidase enzyme so no peptidoglycan links (penicillin binding proteins PBPs) but must penetrate to work so NO SPORES.
bactericidal
antibody on plate, test antigen is added and they bind, then antibody for antigen
direct eliza
mycoplasma
- No cell wall, no peptido??? Has Sterols, smallest, mostly harmless but pneumonia is known pathogen
In air, it is mycelial form. Anaerobic it does binary fission
Gram negative stain works
2 lenses. 100x resolving power. Use dyes to stain
Bright field
greater than 150 degree wettability
super hydrophobic!
amino acid synthesis is a
amphibolic pathway
COVID
- vaccine based on spike protein
- virus is + mrna but only one target of vaccine
lipid nanoparticle helps deliver mrna vaxx
drift and shift
- drift is change in spike mutations to avoid antibodies. mistakes in transcription and natural.
involves mutation in antibody neutralizing site, protease or NEW glycosylation sites
- shift is major change in hemaglutinin (ex. combining two virus to mutate like H3N2 and H1N3 make H1N2
orthomyoxyviridae
RNA
- flu!
- types B and C are only humans, type A is for both animals and humans
- target the rna dep dna pol to transcribe
- H and N
- matures in cytoplasm
Hep C
nnon a non b
- liver damage
- positive strand RNA
treat using protease inhibitor AND viral polymerase so no chance for mutation
salk vs sabin polio vaxx
2 polio is paralyzing
- salk is muscular and gives lifelong immunity and inactive cirus NO IgA
- sabin is oral and attenuated live virus that gives IgG and IgA
BUT it causes virus because mutation in body!
picornavirus
RNA + strand
- uncoats in vescicle, puts dna in nucleus, then insert in empty capsid and maturation and release
- MATURATION IN CYTOPLASM
- VP1 protein of the polyprotein does capsid, recognizing the receptor and neutralizing antibody
polio
flu antiviral drugs
- neuraminidase inhibitors that must be given early
end in VIR - don’t prevent infection but can lessen duration and shorten sickness
- one is a endonuclease inhibitor that stops replication called boloxavir
HIV
many targets like protease inhibitor, transcription inhibitor- named by type/species/location/# of isolate/year isolated and the HxNx number
can prevent hiv after exposure
maybe mrna vaxx
regulatory mechanisms
at legel of transcription to alter enzyme or amt
- control flux of metabolites
causes of endocarditis in oral cavity
mutans, mitis, gallolyticus, aureus, faecalis
- enterococci
HACEK: haemophilus, aggregatibacter, cardiobacterium, eikenella, kingella
DON”T USE clindamycin to treat since can increase risk of c difficile!
cell wall active agents
b lactams, glycopeptides, bacitracin, polymixin
antiribosomal agents
tetracyclines, amonglycosides, macrolides, lincosamides, chloramphenicol
virus classification
genome, linear vs circular,
morphology,
proteins/glycoproteins,
biologic properties (host, pathogenicity, transmission)
- can be DNA/RNA?circular/segmented/linear/single or double strand
virus quantification
virus isolation is gold standard
plaque assay
herpes vaccine
using envelope glycoproteins either block entry by using antibody to mess with the gD receptor OR aggregate the virus
- block entry or cause aggregation
- blco protease, maturation of virus
- nucleoside analogues, aclycovir and protease inhibitors
acute, persistant, latent infection types of virus
- acute means virus and symptoms line up
- persistent is virus is present and only causes symptoms at the very end of life
- latent is that there are periods of infection that match viral but it increases and decreases
- persistent: latent but less often
Flu H and N
- the hemaglutinin binds sialic acid (A RECEPTOR) on cell surface and has 4 spots of antigenic variation required for penetration and fusion
- mutations in Ha = pathogenicity
- neuraminidase cleaves host cell surface protein to allow virus release
- critical in drift and shift
flu virus naming
- named by type/species/location/# of isolate/year isolated and the HxNx number
rabies incubation time
10 days to 3 mos
herpes cycle
cycle
- virus brings its own machinery to make proteins too. maturation of nucleocapsid is when its coated with envelope and glycoproteins
- uncoated at plasma mem (fuses with cell membrane) then releases dna into nucleus OR can do endocytosis then fucion
- all proteins made in cytoplasm go back to nucleus for assembly. form scaffold and units attach then protease puts dna inside by digesting scaffold and nucleic acid is pulled into capsid
- leave nucleus with primary envelope but then lose it and golgi picks up a membrane and leaving it also picks another mem and secreted out (ony 1 mem then)
- matures in CYTOPLASM
nucleoside analogues
- way to block Herpes and hiv
- take the place of a natural nucleic acid to stop synth and enzymes
aminoglycosides
work against 30S ribozome and stops initiation complex and translocation of thingx
- bacteriocidal
teichoic and lipoteichoic acids
teichoic acids
- ribitol and glycerol (conneccted via phosphodiester bond)
- 30-40 repeating units and are diverse
- linked to PG
lipoteichoic
- 45-50 units that have polyglycerol phosphate
- linked to glycolipids on membrane
teichoic and lipoteichoiic functiosn
*both do - charge, rigidity (esp in rod shape), cell divition by interaction with peptido biosynthesis
- resistant to high temp and salt
- protect against cationic AMP by forming polyanionic SMTH
- adhere to host cells then activate immune response via toll-like receptor
p gingivalis
plaque formation with f nucleatum
- capsule to make it virulent
- gram neg
- obligate anaerobe
- high pH
- nisin works with it
c diff
spores, eubacteria, superbug
s mutans
caries, gram +, acidophilic, lactic acid fermentation, uses carbs cool,
candida albicans
pathogenic yeast (fungi but eukarya_
m smithii
archea in microbiome and human gut
