micro poop 3. Flashcards

1
Q

What are the newest antibiotics targeting?

A

plasma membrane - bacteria have a step in plasma membrane making that we don’t

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2
Q

Why is there so much antibiotic resistance?

A

use on farm animals before they’re even exposed

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3
Q

natural (intrinsic) resistance

A

chromosomally mediated and is predictable

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4
Q

mutational resistance

A

random mutation - secondary resistance occurring after therapy with the antimicrobial has begun

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5
Q

transferable resistance

A

plasmid-mediated through conjugation (mating), transaction (bacteriophge transmission), transformation (uptake of DNA from environment)

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6
Q

What are the two transposable genetic elements?

A

transposons and insertion sequences —> “jumping genes”

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7
Q

What is the essential element to the transposition process?

A

that both elements are flanked on either end by short identical sequences of DNA in reverse order (inverted repeats)

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8
Q

What is required for transposons and insertion sequences to work?

A

existence on a replicon (chromosome, bacteriophage, plasmid) because they are incapable of autonomous self-replication

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9
Q

insertion sequences

A

mobile genetic elements that are known to encode only functions involved in insertion events (ability to turn on/off because they don’t want to waste energy on things they don’t need)

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10
Q

What does Staphylococci have to give it resistance?

A

insertion sequence

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11
Q

transposon

A

central sequence containing the phenotypic marker gene and transposase genes (have other gene material outside of what an insertional sequence has)

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12
Q

integron

A

DNA elements with the ability to capture genes by site-specific recombination - provides a convenient insertion site for antibiotic-resistance genes from foreign DNA sources

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13
Q

What is the difference between an integral and a transposon?

A

transposon is mobile, integrons (nonmotile) can be within transposon

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14
Q

gene cassettes

A

discrete genetic elements that may exist as free, circular, non-replicating DNA molecules when moving from one genetic site to another - include a gene and an integrase-specific recombinationn site

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15
Q

How can cassettes be added/deleted/moved?

A

due to the attC site

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16
Q

What are the 7 mechanisms of antibiotic resistance?

A

enzymatic inactivation, decreased permeability, efflux (kick antibiotic out), alteration of target site, protection of target site, overproduction of target, bypass of inhibited process

17
Q

How do organisms resist b-lactam antibiotics?

A

with beta-lactamases (bacterial enzyme) that inactivate beta-lactam antibiotics by hydrolysis of the beta-lactamase bond

18
Q

How does beta lactamase work?

A

require a serine or zinc atom moiety at the active site to hydrolyze the beta-lactam ring

19
Q

How are beta lactams being modified to avoid resistance?

A

created beta-lactamase inhibitors and inhibitor combinations (bind irreversibly to beta-lactamases)

20
Q

What is special about the extended spectrum cephalosporins and carbapenams?

A

they are resistant to beta-lactamases

21
Q

What drug is most effective against ESBL-producing enterobacteriaceae?

A

carbapenems (any drug that ends in penem)

22
Q

What common organisms primarily have extended-spectrum beta-lactamases?

A

klebsiella, e coli, proteus

23
Q

What are AmpC Beta-lactamases?

A

differ from ESBLs because they are resistant to available beta-lactamase inhibitors and can hydrolyze the cephamycins - usually produced at low levels by organisms - resistance when produced at high levels (only carbapenems and 4th generation cephalosporins still effective)

24
Q

What are super bugs?

A

carbapenem-hydrolyzing enzymes - most diverse group of all beta-lactamases - resistant to inhibition by beta-lactam inhibitors (plasmid encoded)

25
Q

NDM-1 producing enterobacteriaceae

A

no antibiotics that touch it - carbapenase

26
Q

How does staphylococci resist beta-lactams?

A

production of beta-lactamases and production of modified transpeptidase targets that are impervious to antibiotic activity (such as MRSA)

27
Q

What type of microorganism is now resistant to penicillin? What has been our response?

A

pneumococci and enterococcus - we no longer use antibiotics for simple things like ear infection unless it is a repeated one

28
Q

IS431

A

integron that can trap and cluster resistant genes for other antibiotics (found on the MecA gene plasmid - how MRSA is resistant)

29
Q

How is S. Aureus methicillin resistant?

A

expression of the mecA gene which encodes PBP2a - protein with low affinity for beta lactam antibiotics

30
Q

PBPs

A

transpepdidases in the cytoplasmic membrane - catalyze the synthesis of the peptidoglycan that forms the cell wall - alterations to this can lead to beta-lactam antibiotic resistance (such as PBP2A on the mega gene)

31
Q

How does vancomycin work?

A

blocks cell wall synthesis by binding to the C-terminal D-Ala-D-Ala residue

32
Q

How are strains becoming resistant to vancomycin?

A

adaptive multifactorial response to sublethal vancomycin exposure - thicker cell walls trap vancomycin, blocking action

33
Q

How does acquired resistance to ahminoglycosides happen?

A

combination of decreased drug uptake, efflux pump activity, enzymatic modification of the drug

34
Q

How does resistance to tetracycline happen?

A

efflux pump and ribosomal protection (sometimes both)

35
Q

How does resistance to macrolides happen?

A

alteration of target site (ribosome) and efflux

36
Q

How does resistance to sulfonamides happen?

A

mutational (alteration of metabolic pathway or target site)

37
Q

How does resistance to trimethoprim happen?

A

changes in cell permeability and altered metabolic pathway

38
Q

How does resistance to fluoroquinolone happen?

A

alteration of target enzymes (esp DNA gyros and topoisomerase)