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HMS Immunology and Microbiology > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

“spectrum” of an antibiotic

A

The species against which an antibiotic is typically effective. Spectrum can be associated with characteristics of the bacteria

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2
Q

Bacteriostatic antibiotics

A

prevent bacteria from growing, but do not kill them. If a bacteriostatic antibiotic is removed from the bacteria, the bacteria will resume growth

Bacteriostatic antibiotics depend on the host immune response to do some of the work of eliminating the infection

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3
Q

In order for an antibiotic to be effective, it must. . .

A
  1. Reach the target
  2. Be able to bind to the target and inhibit its activity
  3. Resist inactivation
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4
Q

Indifference in antibiotic combinations

A

No additive effects

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5
Q

Antagonism in antibiotic combinations

A

Antibiotics interfere with one another’s activity

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6
Q

Synergy in antibiotic combinations

A

Antibiotics produce summative or cooperative effects

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7
Q

Mechanisms of antibiotic synergy

A
  • One antibiotic allows second antibiotic to reach greater concentration at site of activity
  • One antibiotic enhances binding of a second antibiotic to the target
  • One antibiotic blocks destruction of a second antibiotic
  • Two antibiotics partially inhibit separate steps in a synthetic pathway
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8
Q

Combinations of ___ and ___ antibiotics are often antagonistic

A

Combinations of bactericidal and bacteriostatic antibiotics are often antagonistic

Bactericidal antibiotic often require bacteria to be metabolically active, and so killing is blocked by the bacteriostatic antibiotic

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9
Q

Types of antibiotic interaction plotted as Log Viable Bacteria vs Time

A
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10
Q

minimum inhibitory concentration

A

Minimum concentration of antibiotic which prohibits visible growth

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11
Q

minimum bactericidal concentration

A

concentration of antibiotic which kills 99.9% of the bacteria. MBCs are rarely measured for clinical use as they are labor intensive and difficult to measure

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12
Q

Disk diffusion testing

A

Performed by plating bacteria on solid agar, and then placing discs with (separate) antibiotics on the plate. The zone of inhibition of growth around each disk is measured and used to determine whether that isolate of bacteria is susceptible to each antibiotic.

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13
Q

Results of antibiotic susceptibility tests

A

“susceptible” or “resistant”

“intermediate” is reported when therapeutic success cannot be approximated with confidence

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14
Q

Diffusion Disk Diameter vs Minimum Inhibitory Concentration

A

zone size is inversely correlated to the MIC.

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15
Q

The effect of inflammation on penicillin concentration in the CNS

A

In the absence of inflammation, a small amount of penicillin diffuses across the blood-brain-barrier, into the CSF. It is quickly pumped back out of the CSF by the choroid plexus. But if the choroid plexus is inflamed, penicillin is pumped out of the CSF more slowly, allowing it to reach a higher concentration in the CNS than is achieved in the absence of inflammation.

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16
Q

Choroid plexus

A

A network of blood vessels that produces the cerebrospinal fluid, which surrounds the brain and meninges

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17
Q

Antimetabolites

A

inhibit enzymes in the folate pathway. Tetrahydrofolate is needed for synthesis of nucleotides, which are needed for DNA (and RNA) synthesis

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18
Q

Inhibitors of DNA-stability

A

affect enzymes that regulate the 3-D structure of DNA

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19
Q

Inhibitors of RNA synthesis

A

affect the enzymes that make RNA

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20
Q

Inhibitors of protein synthesis

A

bind to the ribosome and affect protein synthesis

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21
Q

Tetrahydrofolate

A

A form of folic acid that is used to donate carbon in biosynthetic pathways. Tetrahydrofolate is needed to make thymidine (used in DNA), purines (used in DNA and RNA) and some amino acids

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22
Q

Tetrahydrofolate biosynthesis pathway

A
23
Q

Sulfonamides and trimethoprim

A

Synergistic in their inhibition of bacterial cell growth because they each inhibit a separate step in a single synthetic pathway.

These are usually used in combination. The combination has a broad spectrum of effect against bacteria. Alone or in combination, these are bacteriostatic antibiotics

24
Q

Adverse effects of sulfonamides and trimethoprim

A

Sulfonamides: hypersensitivity (rash) is common

Trimethoprim: in people with low folate (due to lack of dietary intake), inhibition of human DHFR leads to suppression of formation of red blood cells, white blood cells and platelets by the bone marrow. This is an uncommon adverse effect.

25
Q

topoisomerases and gyrases

A

regulate supercoiling and to decatenate DNA

26
Q

Quinolones

A

Non-competitive inhibitors of gyrases and topoisomerases.

They prevent the enzymes from repairing the break in the DNA. This leads to death (bactericidal) of the bacterium, however the mechanism by which cell death occurs is not well understood

27
Q

Nalidixic acid

A

Antibiotic. Inhibitor of DNA stability.

Nalidixic acid is rapidly excreted in the urine, and so is only used for treatment of urinary tract infections.

28
Q

Fluoroquinolone

A

Antibiotic. Inhibitor of DNA stability.

Fluoroquinolones have a fluorine atom (arrow), which increases the blood levels, tissue penetration and half-life of the quinolones. Fluoroquinolones can be used to treat a variety of infections.

29
Q

Adverse Effects of Fluoroquinolones

A
  • Cartilage erosion occurs in juvenile animals, however growing experience with children has reduced this concern.
  • Tendinitis with rupture occurs rarely in adults.
  • May predispose to cardiac arrhythmias; avoid use with some antiarrhythmic drugs.
30
Q

Rifamycins

A

Work by binding within a channel in the β-subunit of the RNA polymerase, blocking the movement of the nascent RNA through the channel . These antibiotics are bactericidal.

31
Q

Aminoglycosides

A

Antibiotics. Inhibitors of protein syntesis.

Bind the 30S subunit of the bacterial ribosome. They cause the ribosome to incorporate incorrect amino acids into the nascent protein. Aminoglycosides are bactericidal.

32
Q

Adverse Effects of Rifamycins

A
  • Rifamycins are orange and get into many secreted fluids. As a result, they turn urine, tears, saliva orange.
  • Rarely lead to hepatic failure in patients with another source of injury (e.g. another drug)
  • Induce expression of hepatic metabolic enzymes, leading to increased metabolism of many drugs
33
Q

Tetracyclines

A

Antibiotics. Protein synthesis inhibitors.

Bind the 30S subunit of the ribosome and block the A-site.

34
Q

Adverse effects of tetracyclines

A

Adverse effects of tetracyclines are caused by the high affinity of these antibiotics for calcium:

  • Tetracycline must be taken on an empty stomach, or it will bind to calcium in food and be passed in stool without being adsorbed into the blood. Unfortunately, tetracycline causes GI upset.
  • These antibiotics also damage and discolor growing tooth enamel and so they are not given during pregnancy or to children <8 years old.
35
Q

Adverse effects of Aminoglycosides

A
  • These antibiotics accumulate to high levels in the fluid of the inner ear. At high concentrations, they damage hair cells of the ear (ototoxicity), leading to irreversible hearing loss and vertigo.
  • Aminoglycosides also accumulate to high concentrations within the proximal tubule cells of the kidneys. This leads to acute renal failure that is usually reversible by ending use of the aminoglycoside.
  • An uncommon adverse effect of aminoglycosides is neuromuscular blockade, leading to flaccid paralysis. This can affect the respiratory muscles, preventing respiration.
36
Q

Adverse effects of Clindamycin

A

Clostridioides difficile overgrowth and infection.

Other antibiotics cause C. difficile infection, but clindamycin is most strongly associated with this adverse effect

37
Q

Lincosamides

A

Antibiotic. Inhitibots of protein synthesis that bind the 50S ribosomal subunit of bacteria. The major lincosamide of clinical use is Clindamycin.

Prevents peptide bond formation and binds to the P-site.

38
Q

Macrolides

A

Antibiotics. Inhibitors of protein synthesis via the 50S bacterial ribosome. Include erythromycin and azithromycin.

Bind in the exit tunnel of the 50S ribosomal subunit, blocking elongation of the nascent polypeptide.

39
Q

Adverse effects of Macrolides

A

Macrolides are generally well tolerated.

  • Erythromcyin commonly causes GI upset.
  • Macrolides rarely cause acute cholestatic hepatitis (inflammation of the liver).
40
Q

Major classes of antibiotics that inhibit peptidoglycan synthesis

A

β-lactams (like penicillin and ampicillin) and glycopeptides (like vancomycin)

41
Q

Transglycosylase

A

Enzyme that cross-links peptidoglycans in bacterial cell walls.

Glycopeptides bind to the terminal two D-alanine molecules and block transglycosylation

42
Q

Adverse Effects of Vancomycin

A
  • The common adverse effect of vancomycin is hypersensitivity. Vancomycin interacts with the cell membrane of mast cells, leading to degranulation and histamine release.
  • The manifestations include erythema and pruritus of the head, neck, and trunk. This is called “red man’s” syndrome, named for the erythema.
  • Less common adverse effects of vancomycin are neutropenia and nephrotoxicity.
43
Q

Transpeptidase

A

Catalyzes the cross-linking of the amino acid side chains of the peptidoglycan polymer, the final step in peptidoglycan wall biosynthesis (downstream of transglycosylase).

Irreversibly inhibited by β−lactam antibiotics, which covalently bind to its catalytic serine residue.

44
Q

Suicide substrate

A

Covalent inhibitors that are destroyed or “spent” in the process of knocking down enzyme activity.

Ex: β-lactam antibiotics

45
Q

β-lactam Structures

A
46
Q

Resistance to ____ is common.

A

“Natural” penicillins

The ones actually produced by wild mold. Include Penicillin V and G.

47
Q

Penicillinase-resistant penicillins

A

They are specifically effective against staphylococci that produce a β-lactamase which cleaves natural penicillins (about 90% of S. aureus have this enzyme). They resist destruction by these enzymes because of the addition of a bulky R-group.

48
Q

Adverse effects of penicillin

A

Penicillin allergy!!!

This is common, occurring in 2-8% of people. The manifestations, which can be severe, include pruritus, flushing, wheezing, hypotension and shock. Penicillin allergy is mediated by IgE that binds to penicillin at sites other than the β-lactam ring.

49
Q

Cephalosporins

A

Cephalosporins are divided into five “generations” based on their spectrums of activity (not their structure).

50
Q

Adverse Effects of Cephalosporins

A
  • The most important adverse effect of cephalosporins is allergy. This is less common than allergy to penicillins.
  • Allergy to penicillin increases the risk of allergy to cephalosporins about four-fold. But not everyone who is allergic to penicillins is allergic to cephalosporins.
51
Q

Carbapenems

A

Type of beta-lactam antibiotic.

Carbapenems have very broad spectrums of activity, meaning that resistance to these antibiotics is uncommon

They are resistant to nearly all b-lactamases. Also, they cross into the periplasmic space of Gram-negative bacteria using a different porin than most antibiotics.

If a bacterium is resistant to a lot of non-carbapenem antibiotics because it has lost expression of porin(s), it can still be susceptible to carbapenems.

52
Q

Most protein synthesis inhibitors are _____.

A

Most protein synthesis inhibitors are bacteriostatic!

With the notable exception of aminoglycosides

53
Q

How does inflammation in the nervous system increase the level of penicillin in the cerebrospinal fluid?

A

By reducing exit of penicillin from the CSF

Inflammation reduces the ability of the choroid plexus to pump penicillin out of the CSF and into the blood.

54
Q

Don’t give bacteriostatic antibiotics to patients with ____!!!

A

Don’t give bacteriostatic antibiotics to patients with meningitis!!!

HMS Immunology and Microbiology (27 decks)

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