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MICR > L19 > Flashcards

L19 Flashcards

1
Q

Antimicrobial agents

A

Agents that kill or inhibit growth of microbes

Physical or chemical - have no or low selectivity

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2
Q

Chemical antimicrobial agents

A
  • chemotherapeutic agents = antimicrobial drugs or antimicrobials, including:
  • antibiotics = microbial products or derivatives e.g. penicillin
  • synthetic antimicrobials e.g. sulphonamides
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3
Q

The modern era began with the work of German physician Paul Ehrlich. What did he do

A
  • Dyes can bind to microbial cells
  • 1910: magic bullet- arsenic based salvarsan to treat SYPHILIS
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4
Q

1927: GERARD DOMAGK discovered what

A
  • Prontosil red, a coal-tar dye for staining
    leather, had antibiotic properties
  • treat streptococcus infections
  • active ingred: sulphanilamide
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5
Q

1928: The first antibiotic, penicillin, discovered by Alexander Fleming

A
  • S. aureus with mould that killed staphylococcus
  • mould: Penicillium notatum, which produced penicillin G – diffused into agar – lysed bacteria
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6
Q

Florey & Heatley

A
  • improved penicillin
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7
Q

1944: next was streptomycin

A

TB drug

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8
Q

Broad spectrum

A
  • inhibits/kills a broad range of microbes
  • Tetracycline inhibits Gram-ve, Gram+ve, Chlamydia, Rickettsia
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9
Q

Narrow spectrum

A
  • inhibits/kills narrow range of microbes
  • specificity due to the differences in their cell envelope structures
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10
Q

Static agents

A
  • growth is inhibited but no killing occurs
  • upon removal of the agent the microbe will recover and resume growth
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11
Q

Chloramphenicol static or cidal

A

bacteriostatic

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12
Q

Cidal agents

A
  • cidal agents result in irreversible microbe death, some cause cell lysis
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13
Q

Penicillins static or cidal

A

bactericidal

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14
Q

Antimicrobial drugs must be selectively toxic bc?

A
  • kill or inhibit microbial pathogen
  • damage host as little as possible
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15
Q

§ toxic dose:

A

dose at which drug becomes too toxic for the host

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16
Q

therapeutic dose:

A

dose needed to treat the infection

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17
Q

Therapeutic Index

A

Therapeutic dose

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18
Q

The ____ the therapeutic index, the better the chemotherapeutic agent

A

larger

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19
Q

targets of antibiotic action

A
  1. Inhibitors of protein synthesis
  2. Inhibitors of cell wall synthesis
  3. Metabolic antagonists/antimetabolites
  4. Inhibitors of DNA/RNA synthesis
  5. Cell membrane disruption
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20
Q
  1. Inhibitors of protein synthesis
A
  • Selective toxicity is fairly good, they target bacterial ribosomes, not eukaryotic ribosomes
  • aminoglycosides
  • tetracyclines
  • macrolides
  • chloramphenicol
21
Q

aminoglycosides

A
  • cidal
  • bind to 30S subunit of ribosome, cause misreading of genetic code
  • streptomycin
  • Broad
  • mainly aerobic Gm –ve’s
22
Q

tetracyclines

A
  • static
  • bind to 30S subunit of the ribosome
  • tetracycline, doxycycline
  • Broad - bacteria
23
Q

macrolides

A
  • static
  • bind to 23S rRNA of 50S subunit
  • erythromycin
  • broad (good for anaerobes)
24
Q

chloramphenicol

A
  • static
  • bind to 23S rRNA of 50S subunit
  • chloramphenicol
  • broad (most bacteria)
25
Q

Broad Inhibitors of protein synthesis

A

Tetracyclines, macrolides, chloramphenicol

26
Q
  1. Inhibitors of cell wall synthesis
A
  • Selective toxicity excellent, they target bacterial cell wall which is not present in eukaryotic cells
  • penicillins - cidal - inhibit transpeptidations enzymes - penicillin G narrow - ampicillin braod
27
Q

penicillins
(β-lactams)

A
  • cidal
  • inhibit transpeptidation enzymes (=penicillinbinding proteins or PBPs) involved in cross-linking peptidoglycan cell wall
  • penicillin G, methicillin –> narrow (Gm+ve only)
  • ampicillin, piperacillin–> broad (Gm+ve, & some Gm-ve)
28
Q

Penicillins contain β-lactam ring, what does it do?

A
  • resembles the terminal Dalanyl-D-alanine of the peptides
  • Thus penicillins block cross-link formation
  • Growing cell wall becomes less able to resist osmotic pressure - penicillins lyse growing cells
29
Q

Semisynthetic penicillins

A
  • to overcome limitations with natural
  • New side chains added to β-lactam ring
  • Advantages: broader spectrum of activity, acid stability so can be taken orally, resistance to some penicillinases
30
Q

Natural penicillins produced by
Penicillium fungus (penicillin G,
penicillin V, active against Gram
positives, have limitations

A
  • Pen G destroyed by stomach acid, so must be given by injection
  • Penicillin-resistance via penicillinases soon developed
31
Q

penicillin G, penicillin V B/N

A

narrow (Gm+ve only), G is acid-sensitive, penicillinase-sensitive

32
Q

[B/N] ampicillin

A

broad, (Gm+ve and Gm – ve), acid-stable

33
Q

[B/N]

A

narrow (Gm-ve including Ps. aeruginosa)

34
Q

[B/N] methicillin

A

narrow, anti-Staphylococcus (MRSA)

35
Q

[B/N] piperacillin

A

extended spectrum (many Gm+ & Gm-ve, resistant to many but not all penicillinases)

36
Q

cephalosporins (β-lactams) characteristics

A
  • Cidal
  • MoA: contain βlactam ring
  • cefalexin, cephalothin,cefoxitin
  • broad (Gm+ve, some Gmve), useful if penicillin allergy
37
Q

vancomycin characeristics

A
  • Cidal
  • MoA: inhibits transpeptidation, binds to D-ala-Dala so differs from penicillins (its not accessible)
  • vancomycin
  • narrow (Gm+ve), drug of last resort in some cases e.g. MRSA, enterococci. *ototoxic, nephrotoxic
38
Q
  1. Metabolic antagonists/antimetabolites
A
  • Humans don’t synthesise folic acid
  • sulfonamides (e.g. SMX) inhibit folic acid synthesis
  • trimethoprim blocks later step in folate cycle
  • high synergism: less of each drug needed in combination than when alone
  • THF needed to form DNA bases (A, G, T) and methionine in bacteria
39
Q

high synergism:

A

less of each drug needed in combination than when alone

40
Q
  1. Inhibition of nucleic acid synthesis
A
  • Poor selective toxicity because bacteria and eukaryotes have similar nucleic acid synthesis pathways – but still very useful agents
  • quinolones and fluoroquinolones (synthetic drugs)
  • rifampin/rifampicin
41
Q
A
42
Q

rifampin/rifampicin

A
  • cidal
  • inhibits RNA polymerase: blocks mRNA synthesis
  • rifampicin
  • narrow, used for TB, leprosy, and some Gm-ves
43
Q
  1. Cell membrane disruption
A
  • Poor selective toxicity as bacterial and human membranes are very similar in
    structure
  • polymyxins
44
Q

polymyxins characteristics

A
  • cidal
  • Disrupt plasma membrane, detergent-like activity
  • polymyxin B, polymyxin E = colistin
  • Narrow, topical use for Gm-ve’s e.g. Ps. aeruginosa Colistin is drug of last resort for multiply-antibiotic-resistant Gm-ve’s
45
Q

polymyxins tox and fact

A
  • High toxicity, kidney damage, neurotoxicity * Drugs of last resort for some multi-resistant Gram negative bacteria e.g. Ps. aeruginosa, Klebsiella pneumoniae
46
Q
  1. Metabolic antagonists/antimetabolites info
A
  • structurally similar to enzyme substrate, so compete with metabolite
  • block enzyme activity, thus block a metabolic pathway
  • can have good selective toxicity as host lacks pathway, or host enzyme differs from bacterial enzyme
  • sulfonamides (sulfa drugs)
  • trimethoprim (synthetic drug)
47
Q

Sulfonamides (sulfa drugs)

A
  • static
  • inhibit folic acid synthesis by competing with pABA
  • sulfanilamide, sulfamethoxazole
  • broad
48
Q

trimethoprim (synthetic drug)

A
  • static
  • inhibits folic acid synthesis by inhibiting enzyme DHF reductase
  • trimethoprim (often used in combination with a sulfonamide as synergistic* )
  • broad, Tp/Su= Cotrimoxazole combination is widely used

MICR (18 decks)

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