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Flashcards in Antibiotics II Deck (42)
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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

2
Q

Aminoglycosides are administered via _____

A

IV (parenteral)

3
Q

What are the two toxicities seen with aminoglycosides?

A

Ototoxicity

Nephrotoxicity

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

5
Q

Aminoglycosides cover _____ rods more than _____

A

G(-) > G(+)

6
Q

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

A

A beta-lactam antibiotic

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

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

9
Q

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

A

Amikacin

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.

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)

12
Q

T/F Linezolid has limited distribution in tissues?

A

FALSE

Linezolid is distributed widely in all tissues!

13
Q

Linezolid covers only what kind of organisms?

A

G+ Aerobes

No activity against anaerobes

14
Q

Linezolid binds _____ of bacteria, preventing assembly of _____.

A

Binds 50S, preventing assembly of ribosomes

15
Q

How do bacteria become resistant against Linezolid?

A

Ribosomal alteration to prevent binding

16
Q

T/F Tetracyclines only work against G+ organisms

A

FALSE

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

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?

A

Tigecycline

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?

A

Minocycline

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
Q

What is the most common method of bacterial resistance to chloramphenicol? What are the other methods?

A

Acetylation is most common (via chloramphenicol acetyl transferase, prevents binding to 50S)

Other methods: Efflux, ribosomal mutation

26
Q

Macrolides bind to _____, preventing _____

A

Macrolides bind to 50S, preventing MOVEMENT OF THE POLYPEPTIDE AT THE A SITE TO THE P SITE

27
Q

What are the methods of bacterial resistance to macrolides (4)?

A

1) Efflux
2) Methylation
3) Esterases (hydrolyze lactone ring of macrolides)
4) Ribosomal mutation

28
Q

Macrolides are _____ spectrum antibiotics that are effective against _____, _____, and some _____.

A

Macrolides are NARROW spectrum antibiotics that are effective against RESPIRATORY G+ ORGANISMS, ATYPICAL MYCOBACTERIA, & SOME INTRACELLULAR BUGS

29
Q

Which intracellular pathogens does erythromycin cover (4)?

A

1) Heliobacter/Campylobacter
2) Mycoplasma
3) Chlamydia
4) Legionella

30
Q

Clarithromycin covers the same organisms as erythromycin plus _____ and has better efficiency against _____ & ______

A

Clarithromycin covers the same organisms as erythromycin plus ATYPICAL MYCOBACTERIA has better efficiency against STAPH AND STREP than erythromycin

31
Q

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 _____

A

Less effective against G+ organisms

H. influenza

Good against atypical mycobacteria

32
Q

Which drug is used to treat macrolide resistant organisms causing CAP? Why is its use limited?

A

Telithromycin (ketolide)

Limited use due to its hepatotoxicity

33
Q

Which macrolide can be used as a single dose STD prescription (chlamydia)?

A

Azithromycin

34
Q

Which antibiotic works in a similar fashion to macrolides and turns off exotoxin production by staph and strep?

A

Clindamycin

35
Q

Clindamycin (lincosamide) is a _____ spectrum antibiotic that works against _____ and is excellent against _____

A

Clindamycin is a NARROW spectrum antibiotic that works against G+ and is excellent against ANAEROBES

36
Q

What is the main method of bacterial resistance to clindamycin?

A

Alteration of ribosome (via constitutive/inducible methylase

37
Q

Streptogramin binds _____ like macrolides.

A

50S

38
Q

Streptogramin is a _____ spectrum antibiotic that covers _____ bacteria. It is not effective against _____.

A

Narrow spectrum

Covers G+ bacteria

Not effective against E. faecalis

39
Q

Cross resistance to Macrolides, Lincosamides, and Streptogramins (MLS) is mediated by the _____ gene

A

erm gene

40
Q

When the erm gene (responsible for MLS cross resistance) is turned on, what happens to the bacterial ribosome?

A

It becomes methylated, preventing the binding of MLS to the 50S subunit

41
Q

T/F There are two kinds of erm methylases

A

TRUE
Constitutive (cMLS)
Inducible (iMLS)

42
Q

How is the ability of a bacterial strain to induce methylation assessed in the lab?

A

D-Test