Antibiotics II Flashcards

(42 cards)

1
Q

What are the seven classes of protein synthesis inhibitors we learned?

A

1) Aminoglycosides (only bactericidal)
2) Oxazolidinones
3) Tetracycline/Glycycycline
4) Chloramphenicol
5) Macrolide/Azalide/Ketolide
6) Lincosamide
7) Streptogramins

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2
Q

Aminoglycosides are administered via _____

A

IV (parenteral)

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3
Q

What are the two toxicities seen with aminoglycosides?

A

Ototoxicity

Nephrotoxicity

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4
Q

T/F Aminoglycosides cover both aerobic and anaerobic organisms

A

FALSE

Aminoglycosides require oxygen to enter bacteria, and therefore do not work against anaerobes

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5
Q

Aminoglycosides cover _____ rods more than _____

A

G(-) > G(+)

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6
Q

Aminoglycosides have limited coverage against G(+) organisms when combined with _____

A

A beta-lactam antibiotic

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7
Q

Describe the three mechanisms of aminoglycoside action

A

1) Binds/fixes 30S-50S complex at start codon, blocking INITIATION of protein synthesis
2) Binds 30S, causing MISREADING & PREMATURE TERMINATION
3) Binds 30S, causes incorporation of incorrect amino acid, resulting in the production of a NONFUNCTIONAL PROTEIN

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8
Q

What are the mechanisms of resistance against aminoglycosides (3)?

A

1) Enzymatic modification of drug (cannot bind 30S)
- via acetylases, adenylases & phosphorylases

2) Impaired uptake
3) Ribosomal mutation

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9
Q

Which aminoglycoside is used when the infection is resistant to other aminoglycosides?

A

Amikacin

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10
Q

Ampicillin + _____ is used to kill Enterococcus (gram + cocci). Why is this combination effective?

A

Ampicillin + Gentamicin kills Enterococcus

Ampicillin makes chinks in peptidoglycan layer that gentamicin can enter to kill the organism.

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11
Q

What synthetic inhibitor of protein synthesis is especially effective against VRE, MSSA, MRSA? It also has moderate effectiveness against TB.

A

Linezolid (Oxazolidinone)

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12
Q

T/F Linezolid has limited distribution in tissues?

A

FALSE

Linezolid is distributed widely in all tissues!

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13
Q

Linezolid covers only what kind of organisms?

A

G+ Aerobes

No activity against anaerobes

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14
Q

Linezolid binds _____ of bacteria, preventing assembly of _____.

A

Binds 50S, preventing assembly of ribosomes

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15
Q

How do bacteria become resistant against Linezolid?

A

Ribosomal alteration to prevent binding

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16
Q

T/F Tetracyclines only work against G+ organisms

A

FALSE

Both G+ and G-, though G+ activity > G- activity

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17
Q

Which tetracycline is used to treat complicated intraabdominal infections and soft tissue infections, has both G+ and G- activity, and is ineffective against P. aeruginosa and Proteus?

18
Q

Tetracyclines are effective against intracellular pathogens. What are some of the intracellular infections covered by these drugs (5)?

A

1) Rickettsial infections
2) Mycoplasma infetions
3) Chlamydia infections
4) Bacillary infections
5) Spirochete infections

19
Q

How is doxycycline used other than as an antibiotic?

A

As an anti-inflammatory drug.

Subinhibitory concentrations are used to treat rosacea

20
Q

T/F There is more bacterial resistance to tigecycline than tetracycline

A

FALSE

There’s lots of resistance out there to tetracycline, less so to tigecycline

21
Q

Which tetracycline is particularly effective against Staphylococcus?

22
Q

Which of the following statements are true regarding chloramphenicol?

1) Broad spectrum
2) Treats anaerobes and intracellular
3) No toxicities
4) Bactericidal
5) Crosses BBB

A

1, 2, and 5 are true

3) Use of chloramphenicol has decreased due to its toxicities.
4) Chloramphenicol is bacteriostatic, not bactericidal

23
Q

What specific infections does chloramphenicol cover (4)?

A

1) Typhoid Fever (S. typhi)
2) Bacterial meningitis (N. meningitiditis)
3) Anaerobic infections
4) Rocky Mountain Spotted Fever (Ricketssial disease)

24
Q

Chloramphenicol binds to _____, preventing _____.

A

Chloramphenicol binds to 50S, preventing ADDITION OF AMINO ACIDS to the growing peptide chain

25
What is the most common method of bacterial resistance to chloramphenicol? What are the other methods?
Acetylation is most common (via chloramphenicol acetyl transferase, prevents binding to 50S) Other methods: Efflux, ribosomal mutation
26
Macrolides bind to _____, preventing _____
Macrolides bind to 50S, preventing MOVEMENT OF THE POLYPEPTIDE AT THE A SITE TO THE P SITE
27
What are the methods of bacterial resistance to macrolides (4)?
1) Efflux 2) Methylation 3) *Esterases* (hydrolyze lactone ring of macrolides) 4) Ribosomal mutation
28
Macrolides are _____ spectrum antibiotics that are effective against _____, _____, and some _____.
Macrolides are NARROW spectrum antibiotics that are effective against RESPIRATORY G+ ORGANISMS, ATYPICAL MYCOBACTERIA, & SOME INTRACELLULAR BUGS
29
Which intracellular pathogens does erythromycin cover (4)?
1) Heliobacter/Campylobacter 2) Mycoplasma 3) Chlamydia 4) Legionella
30
Clarithromycin covers the same organisms as erythromycin plus _____ and has better efficiency against _____ & ______
Clarithromycin covers the same organisms as erythromycin plus ATYPICAL MYCOBACTERIA has better efficiency against STAPH AND STREP than erythromycin
31
Azithromycin is slightly less effective against _____ than erythromycin and clarithromycin, but is more effective than them in treating infections by _____. It is also good for use against _____
Less effective against G+ organisms H. influenza Good against atypical mycobacteria
32
Which drug is used to treat macrolide resistant organisms causing CAP? Why is its use limited?
Telithromycin (ketolide) Limited use due to its hepatotoxicity
33
Which macrolide can be used as a single dose STD prescription (chlamydia)?
Azithromycin
34
Which antibiotic works in a similar fashion to macrolides and turns off exotoxin production by staph and strep?
Clindamycin
35
Clindamycin (lincosamide) is a _____ spectrum antibiotic that works against _____ and is excellent against _____
Clindamycin is a NARROW spectrum antibiotic that works against G+ and is excellent against ANAEROBES
36
What is the main method of bacterial resistance to clindamycin?
Alteration of ribosome (via constitutive/inducible methylase
37
Streptogramin binds _____ like macrolides.
50S
38
Streptogramin is a _____ spectrum antibiotic that covers _____ bacteria. It is not effective against _____.
Narrow spectrum Covers G+ bacteria Not effective against E. faecalis
39
Cross resistance to Macrolides, Lincosamides, and Streptogramins (MLS) is mediated by the _____ gene
erm gene
40
When the erm gene (responsible for MLS cross resistance) is turned on, what happens to the bacterial ribosome?
It becomes methylated, preventing the binding of MLS to the 50S subunit
41
T/F There are two kinds of erm methylases
TRUE Constitutive (cMLS) Inducible (iMLS)
42
How is the ability of a bacterial strain to induce methylation assessed in the lab?
D-Test