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D1 BS1 + II/ FSI + II > FSII > Flashcards

FSII Flashcards

1
Q

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

A

Excretion of hydrolytic exoenzymes and pathogenic proteins

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2
Q

sterilize broth in air guy + prove spontaneous generation wrong

A

pasteur

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3
Q

bacteriocin that works agaisnt diverse bacteria inclusing strep mutans and e faecalis

A

nisin

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4
Q

classify bacteria as pathogenic

A

koch’s postulate in 1876

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5
Q

PAI

A

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

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6
Q

suprres transcription of gene by binding to operator

A

repressor

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7
Q

homolactic fermentation

A

excess sugar. this is essentially EMP pathway that turns pyruvate into 2 lactic acid

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8
Q

cefazolin and ceftriaxone

A

If can’t take meds and allergic:

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9
Q

cooperativity

A

substrate is an activator. curve is not hyperbolic but sigmoidal (s shape)

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10
Q

selects for gram-positive bacteria agar growth

A

Sodium azide

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11
Q

periodontitis what to give

A

(gingivitis is transient) give amox (bactericidal), or azithromycin (bacteriostatic). COMBO: metronidazole + amox
If allergic then just metronidazole

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12
Q

how do cells resist b lactams and glycopeptides, tetracyclins

A

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

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13
Q

isofunctional enzyme

A

branches of both path can inhibit their branches

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14
Q

how do acidic bacteria survive in those pH

A

increase surface negative charge that stabilize them, pump out H+ ions actively, high isoelectric point to maintain proton motive force

  • most bacteria are neutrophils
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15
Q

selection of antibiotics

A

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

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16
Q

sulphonamide

A

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

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17
Q

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

A

internal probe

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18
Q

icosahedral symmetry

A

20 triangular faces and spherical crystal

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19
Q

heterotrophic co2 fixation in some bacteria

A
  • reverse krebs cycle!
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20
Q

adsorption to host, inject dna into host, phage replicates, maturation, new release and new infection

A

lytic cycle
- virulent phages

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21
Q

peptidoglycan cell wall gram +

A

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

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22
Q

trp operon

A

repressible so no repressor makes tryp and pressor is bound when 2 tryptophan, the corepressor is bound

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23
Q

F factor

A

low copy number plasmid with only 1-2 copies made

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24
Q

proteinase production

A

can they digest egg or gelatin

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25
Q

quorum sensing

A
  • 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
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26
Q

when inhibitor binds to allosteric site of ENZYME SUBSTRATE COMPLEX

A

noncompetitive inhibition. significantly lower curve

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27
Q

EMP pathway for glycolysis

A

phosphorylation, isomerzation, phosphorylation, then split into 2 molec and reduce NADH

c6 to c3 oxidation

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28
Q

hepatitis

A

infectious is type a
serum or blood type is B (DNA virus)
C is cured

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29
Q

unfolded protein transport across membrane

A

Sec pathway
- sec b binds to sec A and YEG

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30
Q

peptidoglycan cell wall gram -

A

b1-4 linkage connected by transglycolase
- no pentaglycine cross link
- alanine, glutamine, MESODAP, alanine then cleave the 5th and do direct amide bond

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31
Q

quinolines

A

Inhibits DNA gyros and topoisomerase for repair too

bactericidal

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32
Q

starting point of conjugative transfer

A

oriT

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33
Q

for fungi. Must make daily, corrosive, reduces activity of organic matter, skin and eye irritant

A

Hypochlorite

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34
Q

gene transfer and antibiotic resistance

A

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

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35
Q

biofilm composition and behaviour depend on

A

cooperation and antagonism and can create environments for each other, nutritional cooperatuion, mutualism, oxygen detox and gene regulation

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36
Q

combine which two drugs to stop biofilm in mouth

A

nisin and entV

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37
Q

axial filaments

A

wrap around cell but like flagella
- internal is spirochete
- outer is spirillum

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38
Q

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!

A

serology or antibody test

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39
Q

PTS

A

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

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40
Q

characteristics of antibiotics

A

activity type (cidal vs static), chem structure, spectrum (some bac or lots)

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41
Q

capsid

A
  • protect nucleic acid from environmental enzymes
  • can have helical, icosahedral or complex crystal symmetry
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42
Q

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)

A

Light microscope

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43
Q

facultative anaerobic growth in aerobic conditions

A

directly fixes PEP with oxaloacetate (connect EMP to krebs)

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44
Q

resistance to antibiotics, forming new species and evade host defense via transmission of virulence

A

consequences of horizontal gene transfer

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45
Q

cumulative feedback

A

both branches can inhibit first reaction seuallty

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46
Q

bactericidal, cheap, but degrades stuff, reduces activity of organic matter, evaporates, not good for eco

A

Alcohol

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47
Q

bacteriocin that works agaisnt s mitis and gram + bac

A

mutacins

s mitis is commensal so not good for oral cavity to disrupt

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48
Q

binds forming a antibody sandwich. Substrate is added and the reaction changes color
antigen is added first, then add anti-antibody

A

indirect eliza

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49
Q

bacitracin, vancomycin (a glycopeptide), aminoglycosides, polymixins

A

topical agents

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50
Q

bacteriocin that works agaisnt candida albicans

A

EntV

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51
Q

amoxicillin

A

If can take meds not allergic

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52
Q

s mutans quorum sensing *** luxS

A

LuxS pathway: only species to really have this to communicate to other species using AI2 molecule. establish pathogenesis
- nonspecific autoinducer

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53
Q

herpes virus and adhesion

A
  • 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
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54
Q

operon anatomy

A

regulatory gene then promoter then operator in reg region then structural genes. regulatory gene is NOT included in operon

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55
Q

acid fast bacteria

A

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

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56
Q

flagella, capsule, exotoxin, outer membrane, endotoxin bacterial antigen

A
  • serological determinants!
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57
Q

Principle component analysis

A

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)

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58
Q

bacteriophage

A

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
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59
Q

s mutans quorum sensing *** comCDE

A

antimicrobial peptides, toxins and adherence

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60
Q

papova/papilloma

A
  • 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
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61
Q

macronutrients needed in smaller amounts that do enzymatic catalysis

A

K, na, fe, mg, ca, cl

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62
Q

plasmid

A
  • 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
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63
Q

sensitization of population, changes in normal microbiota, masking of infection without eradication, drug toxicity, drug resistance

A

dangers of indiscriminate antibac use

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64
Q

transposons

A

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!

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65
Q

chloramphenicol

A

binds 50s then stops new AA binding to peptide chain by stopping peptide transferase

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66
Q

letting hfr cell do the thing but measuring it in time

A

this is gene mapping
- by disrupting at different times, can map the genome

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67
Q

gram -

A

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

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68
Q

cephalexin, azithromycin or clarithromycin

A

If allergic to penicillin and can take meds:

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69
Q

maltose operon

A

positive control
maltose inducer bind activator to transcribe

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70
Q

positive control

A

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

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71
Q

h202 to oxidize NADH

A

peroxidase

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72
Q

PHB

A

inclusion bodies to store stuff in bacteria

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73
Q

tetracycline

A

inhibit the synthesis of bacterial proteins of 30S subunit by stopping aa-tRNA
More side effects now so use derivatives

static

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74
Q

pentose phosphate pathway PPP

A

makes a precursor for nucleic acid called ribulose 5 phosphate (c5)
- then does all the rest nadh stuff

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75
Q

first person to see bacteria

A

leeuwenhoek in 1675

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76
Q

Bac replication

A

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!

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77
Q

bacteriophage therapeutic delivery

A

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

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78
Q

heterolactic fermentation

A

makes ethanol and lactic acid essentially PPP pathway

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79
Q

dark image on light background. Can see living stuff without stain

A

phase contrast

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80
Q

flagella

A

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)

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81
Q

is origin of vegetative replication. start of sequence replicated in a recipient cell

A

oriV

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82
Q

enzyme linked immunoassay. Suitable for liquid phase (not biofilms or tissues)

A

ELISA

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83
Q

cephalotrichous

A

head of hair on either side! amphi is only one flagella on either side

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84
Q

carbohydrate breakdown test

A

if bac produces acidic products. good for anaerobic bacteria

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85
Q

s mutans quorum sensing *** comRS

A

comRA: swich on competance genes for transformation

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86
Q

glycopeptide

A

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

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87
Q

lps with all the structures is what form

A

smooth, S form

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88
Q

can see motility of bac. See more than light microscope
- see smaller than 0.2 micro m

A

dark field microscope

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89
Q

pilli moveemnt

A

twitching using type IV
-gliding using slime and sliding by growth (fake)

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90
Q

nuclear envelope

A

Dna surrounded by cytoplasmic protein, peptidoglycan cell wall, outer membrane (in gram -)

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91
Q

staph aureus quorum sensing (NOT AS IMP) gram +

A
  • Quorum sensing increases virulence, toxins and adhesion via AIP
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92
Q

pseudomonas aeruginosa gram -

A

3 mechanisms, AHL and PQS that control virulence and biofilms

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93
Q

prophylactic vs therapeuric antibiotics

A

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

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94
Q

like azithromycin (FOR PENICILIN ALLERGY) bind to 50S and interfere with initiation complex

A

macrolides, lancosamides
- static

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95
Q

eukarya cell comparison

A

ester linked membrane, unbranched, polyunsaturated with sterols and 80s ribosome
- many replicating units with different rep origins so slow

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96
Q

cultivation (alive), molecular techniques (ded)

A

how to ID bac

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97
Q

virus features

A
  • 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
98
Q

sucrose and caries

A
  • 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!
99
Q

endodontic lesions

A

enterococci
e faecalis

100
Q

favor growth of some stuff with use of inhibitory agent

A

Selective

ex. macConkey agar contains bile

101
Q

bacteria cell comparison

A

murein in cell wall, ester linked unbranced saturated or monounsaturated lipids, 70s
- defined rep region and proceeds bidirectionally and ONE unit (fast)

102
Q

carbohydrate utilization by strep mutans

A

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

103
Q

bacteriophage assembly

A

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

104
Q

first person to think of microscopic organisms

A

hooke’s micrographia in 1665

105
Q

more than 10% ox is harmful
found close to surface of beaker

A

microaerophile

106
Q

less bad, localized and mass is fluctuant and tender, peripheral red, pus, anaerobic bac and moderate severity

A

Abscess

107
Q

how do gram - transport proteins across membranes

A

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

108
Q

actinomyces bacterophages

A

distrupt strep cocc actinomyces interactions that are commensal and needed for homseostasis

109
Q

archaea cell comparison

A

ether linked, branched, saturated with 70s ribosomes

110
Q

conjugation and HFR

A

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

111
Q

plasmid and transposon movement

A

conjugation

112
Q

when low glucose in cell

A

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

113
Q

protease inhibitors

A

-treat HIV/AIDS and hep C that binds viral specific proteases involved in precursor so no maturation of virus

114
Q

what messes with biofilm formation

A
  • disturbance of the bacterial cell wall
115
Q

helical symmetry

A

RNA virus. stacked repeating proteins like helix and sometimes folded back when enveloped

116
Q

first person to think boil = sterile

A

spallanzani

117
Q

direct vs indirect contact

A

direct is with pathogen, indirect is due to some kind of puncture (usually viral stuff)

118
Q

strep mutans and capsule/glycocalyx

A
  • 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
119
Q

70s ribosome structure breakdown

A

50s and 30s (with the 16srRNA)

120
Q

nongenetic drug resistance

A

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!

121
Q

see viruses with diameters of 0.01 - 0.2 micro m

A

TEM

122
Q

what sugars allow strep mutans to form biofilms vs just grow

A

sucrose allows EPS formation so make plaque. with glucose and sucrose, still won’t form biofilm!!

123
Q

housekeeping function operon that is always on

A

constitutive

124
Q

complex symmetry

A

pox virus
- kidney bean shape with outer envelope

125
Q

injection of DNA into host, integrates into chromosome, then hangs out until signal to infect

A

temperature, lysogenic cycle

126
Q

70s ribosome structure breakdown

A

50s and 30s (with the 16srRNA)

127
Q

bacterial genome

A
  • 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
128
Q

gram positive quorum sensing***

A

use autoinducing peptide AIP
- binds to kinase in hgih concentration that phospho a transcription factor. two component system

129
Q

shape of bacteria guy

A

cohn

130
Q

primary colonizer

A

streptococci

131
Q

gram neg quorum sensing ***

A

produce n acyl homoserine lactone AHL as signal. bind DIRECTLY to trasncription factor to regulate expression
- BUT some can use two component system too

132
Q

bergey

A

manual of systematic bateriology in 1923. publication classifies all known bacteria that have been cultured

133
Q

lac operon

A

inducible where repressor binds and nothing happens then inducer lactose binds and make enzyme

134
Q

organism that makes ATP by aerobic respiration if ox is present, but can ferment without ox

A

facultative anaerobe

135
Q

rifampin

A

dna dependent rna pol inhibitor

136
Q

spores

A

invagination then forespore gorms, it is coated and then lysis of sporangium, resistance to pH, temp, boiling water and disinfectants

137
Q

running

A

lophotrichous

138
Q

bacteria in our body function

A

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

139
Q

enveloped virus

A

lipid has glycoproteins and sensitive to detergent

140
Q

tumbling

A

petrichous

141
Q

facultative anaerobic growth in anaerobic conditions

A

PEP fixed to oxalo but there is reductive branch and oxidative branch
- oppositely orientated half circles

142
Q

local vs generalized infection

A
  • 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!

143
Q

superoxide anion to h202

A

superoxide dismutase

144
Q

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

A

differential growth

145
Q

e faecalis treat by

A

engineered bacterophages

146
Q

in a thick** specimen, can see different layers by adjusting beam focus. Can also make the layers take on different colours (false color images)

A

confocal scanning laser microscope

147
Q

genes encoding the F pilus and DNA transfer elements

A

transfer genes Tra region

148
Q

trifluridine

A
  • 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
149
Q

non enveloped virus

A

contain cell attachment proteins. not sensitive to detergent

150
Q

selection of antibiotics

A

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

151
Q

Environmental sensing

A

two component signal transduction where it interacts with environment. Sudden change of pH, nutrients, oxygen, etc. regulate transcription to induce or repress

152
Q

how to bring glycerol into bac

A

facilitated

153
Q

h202 to water

A

catalase

154
Q

the only bac that doesn’t have anything to convert superoxide radical and h202

A

obligate anaerobe, uses peroxidase

155
Q

select for gram - agar growth

A

Bile salts

156
Q

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

A

phenotypic methods of diagnostic classification

157
Q

pilli/ fimbriae

A

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

158
Q

decreases folate

A

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

159
Q

most common bacteria in human temps

A

mesophiles

160
Q

hydrogen sulfide assay

A

do bac produce H2S from AA for gram - rods. black colour

161
Q

superbugs *** 5

A

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

162
Q

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

A

all factors that influence drug pathogen interaction

163
Q

isolate sample DNA and denature it. Allowing primers to bind to target size which then create lots of DNA copies

A

PCR

164
Q

macrolide

A

inhibit protein synthesis of 50S by stopping elongation

static

165
Q

global control system

A

control many operons together using a regulon that work in some stimuli like stress or environment

166
Q

polymyxins

A

detergent like cyclic peptides that damage membrane proteins ONLY of bac and fungi

cell wall agent

167
Q

which bacteria will you find in fridge temp

A

psychrophiles

168
Q

non selective media growth

A

everything grows on it pretty much
- easy to show colony patterns

169
Q

sequential feedback inhibition

A

end products of branch can inhibit previous reaction

170
Q

Lipid A toxicity

A

host cell recognition and once cell is lysed, causes inflam, fever, diarrhea, tissue necrosis, activate immune
- LPS recudes cell viability by inducing ROS generation

171
Q

aeration process

A

during respiration, superoxide anion and h202 are made

172
Q

LPS without o antigen

A

rough lps, R form

173
Q

genetic drug resistance

A
  • 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
174
Q

how do acid fast secrete proteins

A

type 7 that forms a channel across the mycomembrane. unknown

175
Q

odontogenic infxn what to give

A

penicillin, amoxicillin, clindamycin, azithromycin, CLINDAMYCIN only if allergy to penicillin

176
Q

increases transcription of a gene by facilitating RNA polymerase binding to the promoter

A

activator

177
Q

severe and general pain, large and diffuse access, red, thick, hot and severe pain and Loss of fin, pus, very serious with mixed bac

A

cellulitis odontogenic infection

178
Q

ampicillin and cefazolin and ceftriaxone

A

Can’t take meds not allergic then

179
Q

quantification of bacteriophage and growth cycle

A

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)

180
Q

inner membrane is sac, but outer is its with ER. Selectively perm due to pores, histones bind via ionic interactions

A

nucleus

181
Q

F nucleatum

A
  • plaque formation with p gingivalis
  • gram neg
  • obligate anaerobe
  • ALSO has different 3 amino acid = lanthionin
182
Q

what stops nag and nam joining

A

lysozyme. block the b1-4 bond
- works best on gram +!

183
Q

folded protein transport across membrane

A

tatB and tatC bind to tatA

184
Q

the only bac that doesn’t have anything to convert superoxide radical and h202

A

obligate anaerobe

185
Q

bacteriocins

A

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)

186
Q

negative control

A

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

187
Q

acyclovir

A
  • 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
188
Q

respiration and ETC

A

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

189
Q

periodontitis treat by

A

aggregatibacter

190
Q

how to serotype bacteria

A

using OH types. surface antigens
- tge O157:H7 is most important
- vaccine will have many serotypes of capsular polysacc to cover all the bases

191
Q

lower resolving power than TEM but can see 3D images

A

SEM

192
Q

antibiotic problems

A
  • 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

193
Q

small molecule that either activates or represses transcription by interacting with a repressor or activator

A

inducer

194
Q

bacteriocin that works as probiotic

A

salivaricins

195
Q

DNA fragments that integrate copies of themselves into a recipient chromosome

A

insertion sequences IS and #

196
Q

gram +

A

thick peptido
teichoic acids
stain purple
spores in rods

197
Q

capsule/glycocalyx/ slime

A

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

198
Q

competence and transformation in gram +

A

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

199
Q

adenovirus

A
  • matures in nucleus
  • icosahedral. double stranded DNA
  • used to deliver covid spike proteineus
200
Q

normal mouth pH

A

7.2 to severe caries (5.5)

201
Q

drug concentration

A

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

202
Q

bacterial adaptation via regulation

A
  • 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
203
Q

proteinaceous structures

A

fimbriae, capsule/glycoaclays, flagellum, pilus

204
Q

drugs for virus

A
  • stop entry, protease and maturation
205
Q

bacteria and planet

A

make o2, recycle CHNOPS, fix nitrogen, digest complex carbs

206
Q

b lactam

A

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

207
Q

antibody on plate, test antigen is added and they bind, then antibody for antigen

A

direct eliza

208
Q

mycoplasma

A
  • 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
209
Q

2 lenses. 100x resolving power. Use dyes to stain

A

Bright field

210
Q

greater than 150 degree wettability

A

super hydrophobic!

211
Q

amino acid synthesis is a

A

amphibolic pathway

212
Q

COVID

A
  • vaccine based on spike protein
  • virus is + mrna but only one target of vaccine
    lipid nanoparticle helps deliver mrna vaxx
213
Q

drift and shift

A
  • 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
214
Q

orthomyoxyviridae

A

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

215
Q

Hep C

A

nnon a non b
- liver damage
- positive strand RNA
treat using protease inhibitor AND viral polymerase so no chance for mutation

216
Q

salk vs sabin polio vaxx

A

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!
217
Q

picornavirus

A

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

218
Q

flu antiviral drugs

A
  • 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
219
Q

HIV

A

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

220
Q

regulatory mechanisms

A

at legel of transcription to alter enzyme or amt
- control flux of metabolites

221
Q

causes of endocarditis in oral cavity

A

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!

222
Q

cell wall active agents

A

b lactams, glycopeptides, bacitracin, polymixin

223
Q

antiribosomal agents

A

tetracyclines, amonglycosides, macrolides, lincosamides, chloramphenicol

224
Q

virus classification

A

genome, linear vs circular,
morphology,
proteins/glycoproteins,
biologic properties (host, pathogenicity, transmission)
- can be DNA/RNA?circular/segmented/linear/single or double strand

225
Q

virus quantification

A

virus isolation is gold standard
plaque assay

226
Q

herpes vaccine

A

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

227
Q

acute, persistant, latent infection types of virus

A
  • 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
228
Q

Flu H and N

A
  • 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
229
Q

flu virus naming

A
  • named by type/species/location/# of isolate/year isolated and the HxNx number
230
Q

rabies incubation time

A

10 days to 3 mos

231
Q

herpes cycle

A

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
232
Q

nucleoside analogues

A
  • way to block Herpes and hiv
  • take the place of a natural nucleic acid to stop synth and enzymes
233
Q

aminoglycosides

A

work against 30S ribozome and stops initiation complex and translocation of thingx
- bacteriocidal

234
Q

teichoic and lipoteichoic acids

A

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

235
Q

teichoic and lipoteichoiic functiosn

A

*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

236
Q

p gingivalis

A

plaque formation with f nucleatum
- capsule to make it virulent
- gram neg
- obligate anaerobe
- high pH
- nisin works with it

237
Q

c diff

A

spores, eubacteria, superbug

238
Q

s mutans

A

caries, gram +, acidophilic, lactic acid fermentation, uses carbs cool,

239
Q

candida albicans

A

pathogenic yeast (fungi but eukarya_

240
Q

m smithii

A

archea in microbiome and human gut

D1 BS1 + II/ FSI + II (12 decks)

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