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Y Microbiology > Antibiotics (Dustin) > Flashcards

Antibiotics (Dustin) Flashcards

1
Q

Define antibiotic

A

a substance produced by a living organism that inhibits other microorganisms’ growth and/or reproduction

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2
Q

Define chemotherapeutic

A

artificially created antimicrobial substance

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3
Q

How are bacteriostatic antiobiotics evaluated?

A

By their MIC: Minimal Inhibitory Concentration

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4
Q

How are bactericidal antibiotics evaluated?

A

By their MBC: minimal bactericidal concentration

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5
Q

What do the beta lactam antibiotics do?

A

Inhibit cell wall synthesis.

They have a beta lactam ring that competitively binds to/inhibits transpeptidase enzyme (aka PBP or penicillin binding protein).

With PBP inhibited, 5-glycine crossbridges cannot form -> cell wall deformation, weakening, and lysis (bactericidal effect)

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6
Q

What mechanism helps gram negative bacteria to be more resistant to beta lactam antibiotics?

A

Their protective outer membrane has porins that have evolved to be selective against beta lactams

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7
Q

What are the 5 subdivisions of beta lactam antibiotics?

A
  1. Penicillins
  2. Cephalosporins
  3. Carbapenems
  4. Monobactams
  5. Beta Lactamase Inhibitors (although theyre a bit different)

beta monkeys carve ceramic pens

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8
Q

What are 2 advantages of cephalosporins over penicillins?

A
  1. More resistance to beta lactamase
  2. New R group makes it easier to modify it in the lab and make new drugs, meaning at this point 5 generations of cephalosporins have been made
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9
Q

Can you name a broad-spectrum antibiotic in the penicillin category?

A

Ampicillin

(penicillin itself is narrow-spectrum)

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10
Q

Why would you give beta lactamase inhibitors in conjunction with (other) beta lactam antibiotics?

A

Bacteria have evolved a defense mechanism against beta lactam antibiotics by producing the enzyme beta lactamase, which breaks these antibiotics

By giving beta lactam inhibitors, that enzyme is unable to destroy the real antibiotic and thus it’s more effective

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11
Q

Can you name two beta lactamase inhibitors?

A

clavulanic acid

sulbactam

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12
Q

Can you name two carbapenem antibiotics?

One monobactam?

(prob wont need to know until the final)

A

2 Carbapenems: meropenem, imipenem

Monobactam: aztreonam

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13
Q

What is the main Glycopeptide antibiotic we need to know?

Bacteriostatic or -cidal?

Which bacteria is it effective against?

A

Vancomysin

Bacteriocidal

Effective against many Gram positives - even used in culture media to prevent Gram positive growth when you want to culture the Gram negs.

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14
Q

What do glycopeptide antibiotics do?

A

Interfere with peptidoglycan synthesis in only gram-positive bacteria

Interacts with the D-ala-D-ala termini of side chains -> blocks formation of bridges between peptidoglycan chains

Also destroy cytoplasmic membrane, prevent RNA synthesis

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15
Q

What do Polypeptide Antibiotics do?

A

i.e. Bacitracin and polymyxins, these antibiotics inhibit cell wall synthesis / interfere with the phospholipid construction (bactericidal effect). They have amphipathic agents that disrupt membrane phospholipids

Commonly used as a topical antibiotic in creams etc.

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16
Q

Can you name the 7 antibiotic classes that inhibit protein synthesis?

(ugh..)

A
  1. Aminoglycosides
  2. Chloramphenicol
  3. Macrolides
  4. Streptogramins
  5. Tetracyclines
  6. Linezolid
  7. Clindamycin

“ample chlorine makes steaks taste like crap”

17
Q

What are 5 antibiotics that inhibit protein synthesis by binding to the 50S ribosomal subunit?

A
  1. Macrolides (like Erythromycin)
  2. Chloramphenicol
  3. Linezolid
  4. Clindamicin
  5. Streptogramins (note this is the only bacteriocidal of these 5, the rest are bacteriostatic)

“50 Chloroform Clinics Makes Life Stressful”

(I don’t know, I spent too long trying to think of a mnemonic and this will have to do)

18
Q

What are two risks for taking macrolides? Toxicity?

A

Can interact with statin drugs to cause myopathy

Can cause QT prolongation (and thus a reentry tachycardia risk)

However, have very little toxicity

19
Q

What type of bacteria are macrolides good for?

A

Effective against intracellular bacteria, anaerobic streptococci, and campylobacter

Covers mycoplasma, chlamydia, legionella, N. gonorrhea, H. influenzae, Legionella spp.

20
Q

On Chloramphenicol, decribe its MOA

toxicity

-static or -cidal?

broad or narrow spectrum?

A

Interferes with attachment of tRNA on the 50S ribosome subunit

Very toxic, rarely used, destroys RBCs, causes “Gray Baby Syndrome”. Can inhibit protein synthesis in the bone marrow and cause aplastic anemia

Bacteriostatic

broad-spectrum

21
Q

Describe the MOA of linezolid

What kind of bacteria does it target?

A

Inhibits formation of 70S complex after binding to 50S unit. May be useful in otherwise ATB-resistant staph, strep, and enterococci bacteria

Narrow-spectrum, targets gram positive bacteria

22
Q

How do Quinupristin and Dalfopristin (the streptogramins) work?

A

Quinupristin binds at the same site as macrolides (50S subunit) and has similar effect

Dalfopristin directly blocks peptide bond formation by inhibiting peptidyl transferase

They have a strong, bactericidal effect. Specifically against gram-positive cocci, often used against resistant ones like MRSA, VRSA, VRE

23
Q

What 2 antibiotics inhibit protein synthesis by bindind to the 30S ribosomal subunit?

A

Aminoglycosides

Tetracyclines

24
Q

What type of bacteria are resistant to aminoglycosides?

A

Anaerobic bacteria, because O2 is used to transport this antibiotic into cells

It is mostly given for gram negative rod infections, but works on some gram positives as well.

25
Q

What are some notable side effects of Tetracycline?

Bacteriostatic or -cidal?

A

Deposits in teeth and bone - never give to children or pregnant women. Makes the person photosensitive. Renal and hepatic toxicity.

Bacteriostatic (other 30S-acting ATB - Aminoglycosides - are bacteriocidal)

26
Q

What are the antibiotics acting as antimetabolites?

A

Sulfonamides

Sulfamethoxazole (bacteriostatic) commonly taken with Trimethoprim (bactericidal) - has synergistic effect

27
Q

How does sulphamethoxazole work?

A

Sulphamethoxazole compete with aminobenzoic acid, preventing synthesis of folic acid

(Mammals don’t synthesize folic acid, so short-term not really a problem for us to take these ATBs like it is for the bacteria)

28
Q

Whats the mechanism of Trimethoprim?

Which bacteria is the Sulphomethoxazole + Trimethoprom combination good at killing?

A

Inhibits dihydrofolate reductase, thus interfering with folic acid metabolism and inhibiting synthesis of thymidine.

Good activity against Gram + and - bacteria, incl MRSA

Covers Stenotrophomonas maltophilia, Nocardia, and enteric gram-negative rods.

Exceptions: Pseudomonas aeruginosa, Group A strep, enterococcus, Gram neg anaerobes

29
Q

How do Quinolones work?

Bacteriostatic or -cidal?

Broad or narrow spectrum?

A

Inhibit bacterial DNA Gyrase (topoisomerase II or IV)

DNA becomes overwound, cannot replicate or synthesize proteins

Bacteriocidal

Broad spectrum

30
Q

How does Metronidazole work?

Bacteriostatic or -cidal?

Which bacteria is it good for?

A

Forms radicals that react with bacterial nucleic acids, causing cell death (bacteriocidal)

Works on obligate anaerobic and microaerophilic bacteria (also protozoa)

31
Q

How does Rifampin work?

Bacteriostatic or -cidal?

Which bacteria is it good for?

A

Inhibits RNA polymerase

Bactericidal

Commonly used prophylatctically: prevention of N. meningiditis and H. influenzae. Good against gram positive cocci, Brucella, Mycobacterium. Part of the RIPE antibiotics used for the long-term treatment of tuberculosis.

32
Q

Which penicillin is injected? Which is taken orally?

A

Injected: Penicillin G (not acid stable, cannot survive the stomach)

Orally: Penicillin V

33
Q

Which bacteria is penicillin still effective for?

A

Many gram positives, but also Neisseria spp and the spirochetes.

It is the best treatment for Treponema pallidum (syphilis)

34
Q

What is a bacteria called if its cell wall becomes deformed by an antibiotic (like beta lactams that alter cell wall synthesis), but the bacteria is still alive?

A

Spheroplast

35
Q

What are 4 mechanisms of antibiotic resistance?

(not talking about plasmids and how they are acquired)

A
  1. Porin deficiency / Alteration - Gram negs can prevent ATB entry by reducing the number of porins
  2. Efflux pumps - multidrug resistant protein expression
  3. Enzymatic Inactivation - e.g. beta lactamase
  4. Modification of Antibiotic Targets - e.g. altering PBP so that beta lactams cannot bind to it, as is the case in MRSA

Y Microbiology (9 decks)

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