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MICR 2420 > Immunization and Antibiotics > Flashcards

Immunization and Antibiotics Flashcards

1
Q

what is immunologic specificity?

A

the degree to which an antibody recognizes an antigen

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2
Q

what is variolation?

A

ground up scabs of people infected with small pox and shoot the powder up their nose; 2% chance of death

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3
Q

what virus caused small pox?

A

VARIOLA

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4
Q

what is cross protection?

A

milk maids who got cow pox had immunity to small pox

produce the same major antigens

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5
Q

describe vaccines that kill the whole organism

A

ex. hep A vaccine, SALK VACCINE

pros: easy to produce, many antigens present for a robust response

cons: hard to inactivate

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6
Q

what was the cutter incident?

A

some batches of the SALK polio vaccine contained the live virus, caused 250 cases of polio

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7
Q

what is live, attenuated vaccines?

A

ex. BCG (TB vaccine), SABIN polio vaccine

organisms have been weakened in some way

pros: pathogen presented to the right part of the body, allows for a robust response

cons: difficult to produce, cannot give to immunocompromised, cold chain distribution needed

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8
Q

what are subunit vaccines?

A

ex. streptococcus pneumoniae capsular antigen, viral capsids from HPV, TOXOID VACCINES (tetanus)

selected, purified antigenic components of pathogens

pros: easy to produce, no chance of infection

cons: hard to find protective agent

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9
Q

what are nucleic acid vaccines?

A

Ex. COVID vaccine

contain mRNA that codes for a specific antigen, wrapped in a lipid layer and injected

mRNA has a short life, rapidly dealt with by NK cells

benefits: easy to manufacture, quick to get to market, NO CHANCE OF INFECTION

cons: cold chain distribution, hesitancy

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10
Q

why are booster shots needed?

A

first dose causes synthesis of IgM, then IgG

booster shot results in a rapid response, since memory B cells formed during first response

booster ensures sufficient antibodies with sufficient reactivity

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11
Q

describe antigenic changes

A

some pathogens can change their shape or antibodies

ex. COVID, influenza

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12
Q

describe waning memory

A

memory T-cells and B-cells do not have an indefinite life span

can lose specificity when they replicate

ex. tetanus shot every 10 years

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13
Q

what are the best type of vaccines?

A

LIVE ATTENUATED

activates the immune system properly, to the right part of the body, prevents a mild form of the infection being passed onto others

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14
Q

what is herd immunity?

A

for diseases spread person to person, vaccinating a large part of the population interrupts transmission of the disease

important for immunocompromised individuals

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15
Q

what is vaccine hesitancy?

A

problematic atm due to social media and a lack of fact checking

people believed Jenner’s vaccine would turn them into cows

measles outbreak in New Brunswick

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16
Q

who actually discovered antibiotics first?

A

ernst dechesne discovered antibiotic properties of penicillin moulds

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17
Q

who stabilized penicillin?

A

HOWARD FLOREY and ERNST CHAIN

won nobel prize with femming

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18
Q

who was GERHARD DOMAGK?

A

german physician, daughter got infection from a pinprick

injected her with a dye called PRONTOSIL, cured her

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19
Q

how does PRONTOSIL work?

A

SULFA DRUGS

prontosil is metabolized to sulfanilmide in the body, inhibits the enzyme that makes folic acid, inturrupting bacterial metabolism

20
Q

what was WAKSMAN’S contribution?

A

screened soil bacteria for antimicrobial activity

discovered STREPTOMYCIN

21
Q

what is SELECTIVE TOXICITY?

A

drug is toxic against one part of the pathogen and leaves host alone

ex. targets peptidoglycan, ribosomes

22
Q

how do bacteriostatic drugs work?

A

prevent growth, but DO NOT KILL it
suspends growth and buys time for immune system to kick in and kill it

23
Q

what does antibiotic effectiveness depend on?

A

organism being treated
attainable tissue levels of the drug
route of administration

24
Q

how can we measure inhibitory concentration?

A

serial dilutions of a 96-well plate
E-strips
kirby-bauer disk diffusion

ALL TAKE TIME

25
Q

what will antibiotics target?

A

cell WALL synthesis
cell MEMBRANE integrity
DNA synthesis
RNA synthesis
PROTEIN synthesis
METABOLISM

26
Q

which antibiotics are cell wall inhibitors?

A

penecillins, cephalosporins, vancomycins, bacitracin, monobactams

27
Q

what antibiotics are cell membrane inhibitors?

A

polymyxins, daptomycins, gramicidin

28
Q

what are cell wall antibiotics?

A

sugar molecules N-acetylmuramic acid (NAM) and N-acetylglucosamine (NAG) are made in the cytosol

linked together by TRANSGLYCOLASE enzyme at cell wall

side chains of of adjacent NAM molecukes are cross-linked by a transpeptidase to provide rigidity to the cell wall

different antibiotics will inhibit different steps

29
Q

what are beta-lactam antibiotics?

A

derived from fungi, consist of a beta lactam ring struction, of which R groups can be added

transpeptidase and transglycolase are called PENECILLIN BINDING PROTEINS

the ring prevents the microbe from binding to the cell wall properly

30
Q

describe resistance to beta-lactam antibiotics

A

INHERITANCE of the beta lactamase gene, ex. New Delhi NDM-1, can be overcome by inhibitors, such as clavulanic acid

INHERITANCE of an altered PBP that does not bind to the antibiotic, ex. MRSA

31
Q

what does BACITRACIN do?

A

binds to the bactoprenol lipid carrier and inhibits growth of peptidoglycan chain

only used topically

32
Q

what does CYCLOSERINE do?

A

inhibits enzymes that make a percursor peptide of the NAM side chain

ex. TB

33
Q

what does VANCOMYCIN do?

A

binds to the D-Ala terminal end of the disaccharide and prevents binding of transglycosylases and transpeptidases

34
Q

is resistance always a good thing for the microbe?

A

no, causes slower growth

35
Q

what drugs affect bacterial membrane integrity?

A

gramicidin: cyclic peptide that inserts into the bacterial membrane
polymyxin: binds to inner and outer membranes of Gram NEGATIVE bacteria, disrupts inner membrane
daptomycin: aggregates in gram POSITIVE bacterial membrane to form channels

36
Q

what drugs affect DNA synthesis and integrety?

A

SULFA drugs: interfere with NA and THF synthesis
QUINOLONES: target topoisomerase (toxic to mitochondria)
METRONIDAZOLE: anaerobic bacteria, nicks DNA at random once activated (tooth infections)

37
Q

what drugs affect RNA synthesis?

A

rifampicin and actinomycin D
binds to exit tunnel of bacterial RNA polymerase
halts transcription

38
Q

what are protein synthesis inhibitors?

A

interfere with rRNA
ribosomes of prokaryotes are very different from eukaryotes

39
Q

what is a prokaryotic ribosome made out of?

A

30s and 50s subunit = 70S ribosome

40
Q

what drugs are protein synthesis inhibitors?

A

aminoglycosides: bind to 16s, cause translation misreadings of mRNA
tetracyclines: bind to and distort the ribosomal A site (not given to pregnant women)

41
Q

what proteins target the 50S subunit?

A

macrolides and lincosamide: inhibit translocation of growing chain
chloramphenicol: inhibits peptidyltransferase activity
oxazolidinones: prevent formation on 70S complex
streptogramins: bind to peptidyltansferase cites

42
Q

what is mupirocin?

A

binds to bacterial enzymes that attach amino acids to the end of tRNA molecules, halting protein synthesis
Gram POSITIVE bacteria

43
Q

why is antibiotic resistance becoming a problem

A

exerting SELECTIVE PRESSURE on bacteria

44
Q

how do microbes keep antibiotics outside the cell?

A

destroy bacteria before it can enter cell
decrease membrane permeability
pump antibiotics out using specific transporters

45
Q

how do microbes prevent antibiotics from binding to the target?

A

modify the target so it cannot bind to the antibiotic
add modifying groups

46
Q

how do microbes dislodge an antibiotic bound to its target?

A

ribosome protection or rescue
G+ organisms can make proteins that bind to ribosomes and dislodge or prevent binding of antibiotics that bind near the peptidyltransferase site

47
Q

how can AMR spread?

A

mutation, vertical transmission, horizontal transmission

MICR 2420 (9 decks)

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