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Medical Microbiology > Antibiotics > Flashcards

Antibiotics Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

What are antibiotics?

A

Natural products of fungi and bacteria - soil dwellers

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2
Q

What is the effect of antibiotics on bacteria?

A
  • natural antagonism and selective advantage

- kill or inhibit growth of other microorganisms

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3
Q

How are antibiotics produced?

A

Most derived from natural products by fermentation, then modified chemically

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4
Q

Why are antibiotics chemically modified?

A

↑ pharmacological properties

↑ antimicrobial effect

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5
Q

Name an example of totally synthetic antibiotics

A

Totally synthetic - e.g. sulphonamides

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6
Q

What allows the selective toxicity in antibiotics?

A
  • Differences in structure and metabolic pathways between host + pathogen
  • Harm microorganisms, not host
  • Target in microbe, not host (if possible)
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7
Q

When s selective toxicity an issue for antibiotics?

A
  • Difficult for viruses (intracellular), fungi + parasites

- Variation between microbes

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8
Q

Describe the therapeutic margin of antibiotics

A 
Active dose (MIC)  Vs. Toxic effect
Narrow for toxic drugs e.g. aminoglycosides, vancomycin ototoxic, nephrotoxic
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9
Q

What is the effect of antibiotics on microbial antagonism?

A

Maintains flora - complex interactions
Competition between flora

Limits growth of competitors and PATHOGENS

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10
Q

Describe the consequences of antibiotics on microbial antagonism

A

Some antibiotics disrupt ecosystem; Loss of flora → bacterial or pathogen overgrowth
e.g. Antibiotic Associated Colitis

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11
Q

Which antibiotics can cause antibiotic associated collitis?

A

Clindamycin
Broad-spectrum lactams
Fluoroquinolones
> Cause pseudomembranous colitis

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12
Q

How much of the normal gut flora does C.difficile compose?

A

Clostridium difficile (part of normal flora of 3% of population)

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13
Q

What is pseudomembranous colitis?

A

Pseudomembranous colitis: Clostridium difficile overgrowth

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14
Q

What are the symptoms of pseudomembranous colitis?

A

Ulcerations – inflammation
Severe diarrhoea due to inability to absorb water
Serious hospital cross-infection risks

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15
Q

How is bacterial clearance achieved?

A

Antibiotic + immunity → bacterial clearance

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16
Q

Who classifies as an immunosuppressed patient?

A
  • Cancer chemotherapy
  • Transplantations
  • Myeloma, leukaemias
  • HIV w/ low CD4
  • Neutropenics
  • Asplenics
  • Renal disease
  • Diabetes
  • Alcoholics,
  • Babies, elderly
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17
Q

How are antibiotics classified?

A
  • Type of activity
  • Structure
  • Target site for activity
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18
Q

What are bactericidal antibiotics?

A

Kill bacteria
Used when host defense mechanisms are impaired

Required in endocarditis, kidney infection

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19
Q

What are bacteriostatic antibiotics?

A

Inhibit bacteria
Used when host defense mechanisms are intact

Used in many infectious diseases

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20
Q

What are broad spectrum antibiotics?

A

Effective against many types

Example: Cefotaxime

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21
Q

What are narrow spectrum antibiotics?

A

Effective against very few types

Example: Penicillin G

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22
Q

How can the same antibiotic family be used to treat different types of bacteria?

A

3 different drugs; cephalosporins (penicillin)

Chemically modified to give different biological properties (1/2/3rd gen) to treat

  • Gram -ve E.coli
  • Gram +ve Streptococci (pneumoniae)
  • Gram +ve staphylococcus
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23
Q

Why do we use different antibiotics for Gram +/-ve bacteria?

A

Have different structures so require different mechanisms of action to overcome

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24
Q

How are antibiotic families classed?

A

Antibiotics are classified in families based on their structures

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25
Q

What is the significance of antibiotic families?

A

Important to know for:

  • Drug resistance
  • Classification
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26
Q

How do families of antibiotics work?

A

Structural mimics of natural substrates for enzymes
e.g. - β-lactams

Penicillins and cephalosporins contain β-lactam rings ∴ are informally called β-lactams

27
Q

How do bacteria become resistant to β-lactams ?

A

Some bacteria develop β-lactamase enzymes that degrade the β-lactam structure making these antibiotics non-functional in treatment

28
Q

How does bacterial structure effect antibiotic selective toxicity?

A

There are many targets for selective toxicity

Bacteria have complex multimeric structures with complex metabolisms

Structures only in bacteria are good antibiotic targets

29
Q

What are the bacteria targets for common antibiotics?

A
  • Cell wall synthesis
  • Free radicals
  • DNA/RNA processing
  • Protein synthesis
  • Cell membrane
  • Folic acid synthesis
30
Q

Give examples of cell wall synthesis antibiotics

A

Cell wall synthesis antibiotics e.g: (β-lactams) and Vancomycin (kept in reserve to treat MRSA)
Very potent

31
Q

Name examples of protein synthesis inhbiitors

A

Erythromycin, chloramphenicol (eye drops, topical drug v. toxic not given IV)

32
Q

Explain the selective toxicity of protein synthesis inhibitors

A

Bind to different ribosomal subunits; can inhibit bacterial ribosomes without inhibiting eukaryotic ribosomes - safe; good selective toxicity

33
Q

How do DNA / RNA processing antibiotics work?

A

Inhibit DNA replication / RNA production - these mechanisms differ ∴ provides selective toxicity to enzymes involved

34
Q

What is DNA gyrase?

A

DNA gyrase is a topoisomerase (different to eukaryotes) responsible for (un)coiling during DNA replication

35
Q

Give examples of DNA/RNA processing antibiotics and their roles

A

Rifampin
- key drug against TB, targets DNA-directed RNA Pol producing mRNA

Quinolones
(e.g. ciprofloxacin etc.) v. potent DNA Gyrase inhibitors

36
Q

Describe the selective toxicity of folic acid synthesis antibiotics

A

Bacteria synthesise their own folic acids

V. good selective target as humans don’t contain folic acid producing enzymes

37
Q

How do folic acid synthesis antibiotics work?

A

Antibiotics inhibit folic acid production causing bacteria to lack of co-factors for vital chemical reactions

38
Q

Give an example of a useful cell membrane antibiotic

A

E.coli gram -ve bac. that cause UTIs are resistant to almost every antibiotic except for colistin
However colistin is v. toxic; only used when necessary

39
Q

Describe the selectivity of free radical antibiotics

A

Antibiotics that generate free radicals have multiple targets throughout bacterial cell e.g. metronidazole (fights anaerobes)

40
Q

What is peptidoglycan?

A

A crosslinking structure of peptides and polysaccharides

41
Q

Describe the outer structure of a Gram +ve bacteria

A

Massive peptidoglycan structure on top of bacteria membrane

Multiple other cell wall components e.g. teichoic and lipoteichoic acids - equivalent of exotoxin LPS

42
Q

How do cell wall synthesis antibiotics work?

A

Antibiotics (β-lactams) that inhibit cell wall synthesis, target enzymes that form peptidoglycan

43
Q

Describe the Gram-ve bacteria outer layers

A

Gram -ve also have peptidoglycan but it resides in the periplasmic space with an outer membrane - impermeability barrier; only way nutrients, ions etc. get through is via porins

44
Q

Why are some antibiotics useless on gram -ve bacteria?

A

Many antibiotics can’t be used on gram -ve bacteria as they can’t infiltrate the impermeable outer membrane barrier

45
Q

How is peptidoglycan formed?

A

This structure is put together by a series of enzyme reactions

46
Q

Why does each bacteria have a different peptidoglycan structure?

A

Different bacteria have varying peptidoglycan structures ∴ the enzymes forming them have slightly different specificities

47
Q

Describe the structure of a general peptidoglycan

A

Composed of (penta) polypeptides that are crosslinked to hold a matrix with long polysaccharide (n acetylglucosamine) chains together

48
Q

Outline the process of peptidoglycan formation

A
  1. Peptidoglycan precursor: disaccharide w/ 5 peptides
    and terminal D-ala-D-ala isomers (D-alanines)
  2. Precursor transported across cytoplasmic membrane
    by linking to lipid transport molecule
  3. Precursor joins pentameric a.a. structure
  4. Cell wall transcarboxypeptidases polymerise by
    recognising + cleaving terminal D-ala’s
  5. Terminal D-ala linked to end of pentapeptide
  6. Pentapeptide linked to next monomer’s D-ala which
    also has terminal D-ala cleaved
49
Q

What is the significance of the peptidoglycan D-ala-D-ala terminus?

A

D-ala-D-ala required for crosslinking to occur and are specific to peptidoglycan synthesis in bacteria

50
Q

How do some antibiotics inhibit peptidoglycan formation?

A

Certain antibiotics (cycloserine) block terminal D-ala’s production

Others prevent precursor transport

51
Q

What enzyme provides β-lactams selective toxicity against peptidoglycan formation?

A

Trans-carboxypeptidases are good antibiotic targets of β-lactams as not present in human cells - specific to bacteria

52
Q

How does vancomycin inhibit cell wall synthesis?

A

Vancomycin recognises D-ala-D-ala and binds to it, preventing peptidoglycan formation

53
Q

What is a PBP?

A

Penicillin binding proteins (crosslinking enzymes)

synthesise peptidoglycans and competitively bind to cephalosporins + penicillins etc.

54
Q

How do β-lactams cause their effect?

A

When β-lactams administered, they have to cross the porin and bind + inhibit the PBP

55
Q

What is the effect of a successful β-lactam?

A

If able to target PBP, the antibiotic can prevent bacteria from crosslinking, causing an autolytic response

56
Q

Outline features of the folic acid synthesis inhibitors

A

Combinations are synergistic and bactericidal

  • Gram +ve and G-ve
  • Nocardia + toxoplasma
  • UTI
  • Broad spectrum
57
Q

How do sulfonamides inhibit folic acid synthesis in bacteria?

A

Sulfonamides (antibiotics- competitive inhibitor) inhibit dihydropteroate synthetase enzyme that is specific to bacteria

Structure almost identical to PABA (recursor) of tetrahydrofolic acid

58
Q

Outline how folic acid synthesis inhibitors provide selective toxicity

A

Humans ingest in diet Dihydrofolic acid (Vit.b9)

Humans have dihydrofolate reductase enzyme ; converts dihydrofolic acid (vit.b9) → tetrahydrofolic acid -completely different to bacterial enzyme ∴ trimethoprim (antibiotic) has little effect against host enzyme but high affinity against bacterial enzyme

59
Q

Describe the use of antibiotics

A
  • Treatment of bacterial infections
  • Prophylaxis
  • Inappropriate use; viral sore throats; patient pressure
60
Q

Outline how antibiotics are used for prophylaxis

A
  • close contacts of transmissible infections
  • Decreased carriage rates
    (↑ ~80% in outbreaks) e.g. meningitis
  • prevention of infection e.g. tuberculosis
  • peri-operative cover for gut surgery
  • people with ↑ susceptibility to infection
61
Q

How are community infections treated?

A

Community infections often treated orally by GP

62
Q

How are serious infections treated?

A

Hospitalisation - systemic treatment

e.g. i/v rapid delivery, high [blood]
often unable to take oral – vomiting, unconscious,
poor gut absorption due to trauma

63
Q

How are topical infections treated?

A

conjunctivitis, superficial skin infections, burns, antiseptic creams, heavy metal ointments

64
Q

What does antibacterial MIC dose depend upon?

A
  • Age, weight, renal + LFT of patient and infection severity
  • Susceptibility organism
  • Antibiotic properties i.e. MIC

Medical Microbiology (15 decks)

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