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Medical Microbiology > Section 1- Antimicrobial Agents > Flashcards

Section 1- Antimicrobial Agents Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

Mechanisms of antimicrobial action

A

Selective toxicity=key; only inhibit bacteria
Most antimicrobials are antibacterial
Fewer to treat eukaryotic infections (fungi, protozoa); don’t want to hurt host
Even fewer antiviral (use host material)

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2
Q

Ideal antimicrobial agent

A 
Readily available
Inexpensive
Chemically stable (doesn't expire)
Easily administered (oral)
Nontoxic and nonallergenic
Selectively toxic for many pathogens
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3
Q

Selective inhibition/toxicity

A

Harm microorganisms but not host

Due to differences in structure and metabolic pathways

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4
Q

Broad spectrum antibiotics

A

Effective against many pathogens
Ex: tetracycline
Con: can kill friendly bacteria

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5
Q

Narrow spectrum antibiotics

A

Effective against very few pathogens

Ex: penicillin

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6
Q

Bactericidal

A

Kill bacteria
Not very common
Used when host defense mechanisms are impaired (immunocompromised)
Required in endocarditis, meningitis, kidney infection, etc.
Leaks LPS into bloodstream, which is BAD

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7
Q

Bacteriostatic

A

More common
Inhibit bacterial growth
Used when host defense mechanisms are intact
Used in many infectious diseases

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8
Q

5 major sites antimicrobials target

A 
Cell wall
Cell membrane
Ribosomes
Metabolic pathways (unique to microbe)
DNA/nucleic acid metabolism
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9
Q

Inhibition of cell wall synthesis

A

Inhibit peptidoglycan synthesis by preventing cross-linking of NAM subunits
Cell walls weaken and eventually lyse
Effective only when bacterial cells are growing
No effect on plant or animal cells (no peptidoglycan)
Most prominent antibiotics in this group are Beta-lactam antibiotics
Also Vancomycin, Isoniazid, and ethambutol

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10
Q

Beta-lactam antibiotics

A

Inhibit cell wall synthesis
Functional groups are beta-lactam rings (be able to recognize)
Bind to transpeptidase enzymes that cross link NAMs and disrupt
“-cillins” and “ceph-“
Ex: Penicillin, Cephalosporins, Imipenem
**NOT effective against mycoplasmas (no cell wall)

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11
Q

Vancomycin

A

Interferes with Alanine-Alanine bridges that link NAMs in peptidoglycan of Gram (+) bacteria
Binds directly to peptide bonds
Used sparingly, expensive

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12
Q

Isoniazid and ethambutol

A

Disrupt formation of arabinogalactan-mycolic acid (waxy outer layer) in mycobacterial species
Ex: Tuburculosis

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13
Q

Penicillins

A

All end in “-cillin”
Primarily effective against Gram(+)
HOWEVER, Ampicillin and Amoxicillin effective against (+) and (-) (used in UTI, Salmonellosis, Listeria monocytogenes, and group A streptococcal infections)
Adverse effects=Allergic reactions and anaphylactic shock (hyperimmune responses)

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14
Q

Cephalosporins

A

3-4 different generations
1st generation effective against Gram(+) and streptococci
2nd generation sort of effective against (+), (-), and streptococci
3rd generation effective against (-) and streptococci

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15
Q

Disruption of Cytoplasmic Membrane

A

Some drugs become incorporated into cytoplasmic membrane and damage its integrity
Ex: Amphotericin B (polyene)

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16
Q

Amphotericin B (polyene)

A

Attaches to ergosterol (only in fungi) found in fungal membranes
Creates channel
Humans somewhat susceptible to drug b/c cholesterol similar to ergosterol; causes nephrotoxicity
Bacteria lack sterols and are not susceptible

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17
Q

Inhibition of Protein Synthesis

A

Ribosomes differ between eukaryotes and prokaryotes
Drugs can selectively target translation
Human mitochondria have 70S ribosomes, like prokaryotes, and can be harmed by these drugs
Anti-ribosomal antibiotics impair ribosomes by binding to one of the subunits
Ribosomes are essential for translation of mRNA to proteins
No translation=no protein synthesis=no growth
Examples: CLEan TAG

18
Q

Prokaryote vs Eukaryote ribosomes

A

Eu: 80S (40S and 60S)
Pro: 70S (30S and 50S)
S= mobility measure

19
Q

CLEan TAG

A 
CLEan= Chloramphenicol, Lincomycin, Erythromycin-->inhibit 50S
TAG= Tetracycline, Aminoglycosides-->inhibit 30S
20
Q

Chloramphenicol

A

Crosses blood-brain barrier
First choice in brain abscess caused by Staphylococcus aureus or meningitis
Adverse effects: bone marrow suppression, aplastic anemia, grey baby syndrome, leukemia

21
Q

Lincomycin

A

Aka Clindamycin
Used in anaerobic and severe aerobic infections
Ex: TSS
Adverse effect: pseudomembranous colitis (caused by C. diff) because good bacteria are inhibited and C. diff increases

22
Q

Erythromycin

A

Macrolide antibiotic
Similar to Azithromycin and Clarithromycin
Effective against (+) and some (-) like Mycoplasma pneuoniae and legionella pneumophila
Adverse effects: GI disturbances (nausea, vomiting, abdominal pain, diarrhea)

23
Q

Tetracycline

A

Has 4 rings
Used to treat: acne vulgaris, non-gonococcal urethritis, rocky mountain spotted fever, Lyme disease
Good for intracellular infections
Adverse effects: Stains developing teeth, inactivated by Calcium (can’t take with milk or yogurt), photosensitive, drug induced lupus and hepatitis

24
Q

Aminoglycosides

A

Ex: Amikacin, Gentamicin, Kanamycin, Tobramicin, Neomycin, Streptomycin
Used to treat severe Gram (-) infections and tuburculosis
Adverse effects: Nephrotoxicity (kidney failure), Ototoxicity (hearing loss)

25
Q

Inhibition of Metabolic Pathways

A

When differences exist between metabolic processes of host and pathogen
Ex: Sulfonamides and Trimethoprim; inhibit enzymes involved in synthesis of bacterial folic acid
Humans can’t make folic acid themselves, so don’t have this pathway and human metabolism is unaffected
Without folic acid, bacterial cell can’t divide because it helps make DNA and RNA

26
Q

Trimethoprim/Sulfamethoxazole

A

Used to treat otitis media (ear infections), UTIs, Prophylaxis, and treatment of Pneumocytisis jiroveci pnemonia in AIDS patients
Adverse effects: rash, Stevens-Johnson syndrome (SJS) that can progress to Toxic epidermal necrolysis (TEN)

27
Q

Inhibition of Nucleic Acid Synthesis

A

Several drugs function by blocking DNA replication or mRNA transcription
Only slight differences between prokaryotic and eukaryotic DNA
Drugs often affect both
Inhibition of Viral vs. Bacterial Nucleic Acid Synthesis

28
Q

Inhibition of Viral Nucleic Acid Synthesis

A

Create nucleotide analogs that insert and distort shapes of nucleic acid molecules; prevents further replication, txn, and tln
Most often used against viruses b/c viral DNA polymerases are more likely to incorporate the analogs and viral nucleic acid synthesis is faster than host cell’s
Ex: Acyclovir, AZT, Lamivudine
Also effective against rapidly dividing cancer cells

29
Q

Inhibition of Bacterial Nucleic Acid Synthesis

A

DNA supercoiling prevented
Quinolones and fluoroquinolones inhibit prokaryotic DNA gyrase (that supercoils DNA)
Little effect on eukaryotes or viruses
Ex: Ciprofloxacin, Norfloxacin, Levofloxacin
Other drugs bind to and inhibit action of RNA polymerase during txn (No RNA=no replication)
Ex: Rifamycin, Rifampicin (“Rif” group)

30
Q

2 classes of resistance mechanisms

A

Genetic and Non-genetic

31
Q

Non-genetic mechanisms of resistance

A

Inaccessibility to drugs (drug can’t reach; abscess, TB lesion)
Stationary phase (no cell wall being actively made; insusceptible to inhibitors of cell wall synthesis)
Protoplasts and spheroplasts (no cell wall material; insusceptible to inhibitors of cell wall synthesis)
Biofilms (gelatinous layer protects bacteria; they are less accessible)

32
Q

Genetic mechanisms of resistance

A

Chromosome-mediated (due to spontaneous mutation in target molecule or in drug uptake system)
*Bacteria only have 1 chromosome, so 100% of offspring affected
or
Plasmid-mediated (transferred via conjugation with pili; multidrug resistance; common in gram (-) rods)

33
Q

End result of genetically conferred resistance

A

Production of drug-inactivating enzymes
Modification of target structures
Alteration of membrane permeability

34
Q

Resistance to Beta-Lactams

A

Gram (+) and (-) both produce B-lactamase (penicillinase)
Both also alter the transpeptidase enzyme
Gram (-) can also alter porins

35
Q

Clavulanic acid

A

Blocks the action of B-lactamase
Not itself an antibiotic, but when combined with amoxicillin (a B-lactam), it allows amoxicillin to remain active
Amoxicillin + Clavulanic acid= Augmentin

36
Q

2 main antibiotic susceptibility testing methods

A

Dilution method and Disc Diffusion method

37
Q

Dilution method

A 
Prepare 2 fold [antibiotic] dilutions
Add 1/2 million bacterial cells per tube
Incubate overnight
Check for turbidity
Establish MIC
38
Q

Minimum Inhibitory Concentration (MIC)

A

Lowest concentration of a drug that prevents the bacterial growth (no turbidity)
First clear tube

39
Q

Kirby-Bauer Disc Diffusion method

A

Seed agar plates with bacteria in question
Place antibiotic discs over seeded plate
Incubate overnight
Measure inhibition zones
Relate results to zones given in interpretive chart
**Inverse relationship between MICs and zone diameters

40
Q

Therapeutic Index

A

=Max Safely Achievable Level / MIC
Penicillin TI= 800; good
Aminoglycosides TI= 10; bad
High=more effective

Medical Microbiology (5 decks)

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