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CGIER II > CGIER 22 - Antibiotics > Flashcards

CGIER 22 - Antibiotics Flashcards

1
Q

Bacteria vs Human Cells

A
  • Prokaryotes
  • Some similar structures to humans like cytoplasm and ribosomes
  • Cyclic DNA
  • No nucleus
  • Single cell
  • Cell Wall
  • Some have flagella for movement
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2
Q

Group of Bacteria Based on Shape

A

Rod-shaped = bacilli
Spherical = coccus
Spiral shaped = sprillum/spirochetes

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3
Q

Human body can have near to _____ bacteria

A

10^14 (comparison to 10^13 human cells)
Bacteria are most abundant organisms on earth - tens of thousands of species identified

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4
Q

Commensal Bacteria

A
  • Normal body flora
  • Bacteria which occur on parts of the body exposed to external environment (nose, mouth, skin, GI tract)
  • Commensal relationship : one (commensal) benefits, other neither benefits nor suffers
    e.g. buffalo neither benefits nor suffers, bird benefits from sitting on it
    bird can become parasitic if it starts poking buffalo
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5
Q

Staphylococcus epidermis

A
  • Example of commensal bacteria
  • Nonpathogenic
  • May play a protective role in their host as normal flora (may be a pathogen in hospital environment)
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6
Q

Commensal Bacteria prevent pathogenic bacteria invading the body by:

A
  • Competition for nutrients
  • Secreting chemicals against them
  • Stimulating immune system
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7
Q

Commensal Bacteria also benefit the host by:

A

Providing vitamins or eliminating toxins
- Bacteria in the gut make vit K2 from K1 in leafy green vegetables
- Use of senna (herb) to drive gut motility, broken down to anthracenes, stimulant laxatives

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8
Q

Commensal -> Pathogenic Bacteria

A

Commensal bacteria can become pathogenic if colonize wounds/internal organs to cause infection and disease
Only 10-100 pathogenic bacteria need to enter our body to cause infection
= Opportunistic pathogen
Can also spread through the bloodstream and infect distant organs

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9
Q

Bacteria vs Virus

A
  • Antibiotics used primarily to fight bacterial infection, not active against viruses
  • Bacteria 1000 nm, cell wall, cell structures
  • Virus 20-400 nm, DNA/RNA enclosed in protein coat
  • Viral infections much more common than bacterial infections
  • Colds/most coughs/sore throats caused by viruses
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10
Q

Pathogenic Bacteria

A
  • Cause disease, attacks weak immune system
  • Haemophilus influenzae does not cause the flu
  • Bacterial infection can cause meningitis = HiB (H i type B)
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11
Q

Bacterial Diseases

A

e.g.
Food poisoning (Salmonella)
Sore throat
Pulmonary infections
Urinary tract infection
Dental caries (Strep mutans)
Colon cancer (Strep bovis)

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12
Q

Staphylococcus aureus

A
  • 50% of population carry on skin and nasal mucosa
  • Act as a pathogen with different potential site of infection
  • Most common source of infection in wounds, abscesses, boils
  • Usually localized, but if spreads most lethal form of septicemia may result
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13
Q

Pathogenesis of Bacterial Infection
(chain of events leading to disease development)

A
  • Toxigenicity
    bacteria produce toxins which damage specific tissue of the host
    e.g. food poisoning, cholera
  • Invasiveness
    multiply rapidly at site of infection
    overwhelm hosts defense mechanism
    e.g. pneumonia, tuberculosis
  • Secondary infection
    bacteria invade bloodstream to set up new sites of infection
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14
Q

Sources of Bacteria

A
  • Contamination of food/water
    e.g. cholera, typhoid
  • Air-borne
    nasal spray (sneeze), cough (mucous)
    e.g. anthrax, chickenpox, measles, TB
  • Contact
    bacteria transmitted through physical contact with contaminated surfaces
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15
Q

Antibiotics

A
  • Antibacterial or antifungal
  • Natural or synthetic chemicals
  • Antibiotic natural products produced by both bacteria and fungi (majority from single group of bacteria called actinomycetes), produced by microorganisms to compete against other microorganisms for space/nutrients
  • Vast majority of antibiotics in clinical use are natural products/derivates, modified = semi-synthetic
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16
Q

Bacteriostatic Antibiotics

A

Inhibits growth of bacteria
e.g. macrolides, chloramphenicol
Curve plateaus (number of bacteria does not increase)

17
Q

Bactericidal Antibiotics

A

Inhibits survival of bacteria
e.g. penicillin, cephalosporin
Curve becomes negative slope (number of bacteria decreases)

18
Q

Most used bacterias

A
  • Beta-lactams (resistance will be higher becauase more promiment)
  • Fluoroquinolones
  • Macrolides
  • Tetracyclines
  • Aminoglycosides
  • Glycopeptides
19
Q

Classes of Antibiotics

A
  • Inhibition cell wall synthesis
    e.g. penicillin, bacitracin, cephalosporin, vancomycin
  • Inhibition of protein synthesis
    e.g. tetracycline, erythromcin, streptomycin, chloramphenicol
  • Inhibition of DNA/RNA precursor synthesis
    e.g. rifamycin (transcription), quinolones (DNA rep)
  • Inhibition of DNA/RNA
  • Disruption of membrane function
    e.g. polymyxin

PABA - para-amino benzoic acid
Substrate for folic acid synthesis, coenzyme in the synthesis of purines & pyrimidines

20
Q

Lactam

A

Cyclic amide

21
Q

Lactone

A

Cyclic ester

22
Q

Inhibitors of Cell Wall Synthesis

A

1) beta-Lactams
(cyclic amide = lactam ring; N attached to beta-carbon)
- penicillins
- cephalosporins

2) Glycopeptides
(sugar-protein)
e.g. vancomycin

23
Q

Inhibitors of Protein Synthesis

A

1) Macrolides
(macrocyclic lactone ring - cyclic ester - 14-16 C, sugar based substituents)
e.g. erythromycin

2) Tetracyclines
(naphthacene core)

3) Amino glycosides
(sugar units)
e.g. tobramycin

24
Q

Inhibitors of DNA/RNA (precursor) synthesis

A

1) Inhibitors of DNA/RNA precursor synthesis
- Sulfa drugs (sulfonamides)
e.g. sulfamethoxazole

2) Inhibitors of DNA/RNA synthesis
- Quinolones (fluoro-quinolones)
e.g. ciprofloxacin

25
Q

Mechanisms of Antibiotic Resistance

A
  • Pump out antibiotic
  • Modify target of antibiotic
  • Destroy/neutralize antibiotic warhead

Other mechanisms (e.g. permeability barrier through mutation of outer membrane porins which control entry of molecules into bacterial cell)

26
Q
  1. Efflux Protein Pumps
A

Eject antibiotics from inside the cell even before they have an effect

27
Q
  1. Mutation of genes encoding targets
A
  • enzymes modifying targets
  • incoming antibiotic cannot identify the target, effect is lost

e.g. altered penicillin-binding proteins, altered DNA gyrase, altered rRNA

28
Q
  1. Destroying antibiotic itself
A

bacterial enzymes modify the antibiotics themselves
e.g. B-lactamase, Aminoglycoside-modifying enzymes

29
Q

Antibiotic Resistance

A

Ability of bacteria to protect themselves against the effects of an antiobiotics
- No antibiotics for which resistance does not exist
- Some bacteria can be resistant to virtually every available antibiotic

30
Q

Resistance genes can be transmitted

A
  • Vertical Transfer = from a bacterium to its progeny, e.g. mutations in chromosomal genes
  • Horizontal Transfer = between bacteria of different/same genera, e.g. genes on mobile genetic elements such as plasmids
31
Q

Origins of Resistance

A

1) Large number, short generation time
2) Genetic versatility
3) Horizontal gene transfer

32
Q

1) Large Number, Exponential growth of Bacteria

A

Bacteria can double their number in 20 mins

33
Q

Bacteria growth conditions are never ideal because of

A
  • lack of O2 and nutrients
  • waste build-up
34
Q

2) Genetic Versatility

A
  • oldest and most abundant organisms
  • adapt quickly to their environments
35
Q

Extremophiles

A

Can live in almost any conditions of pH, temp, pressure
e.g. Thiobacillus concretivorans lives in sulphuric acid strong enough to dissolve metal
e.g. Micrococcus radiophillus found in waste tanks of nuclear reactors

36
Q

3) Genetic Mutations

A
  • 1 error in 10^7 during bacterial DNA rep
  • 1 out of every 3 genes can be mutated
  • Mutation can confer resistance to an applied antiobiotic (non-mutant bacteria killed, mutant grows), can occur in a matter of days
  • Resistant bacterium is able to pass on resistance gene to other bacteria, even from different genera

CGIER II (3 decks)

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