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CAM102 Microbiology > Antibacterials > Flashcards

Antibacterials Flashcards

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Biology 101 flashcards
1
Q

Sterilise

A

To kill all microbes

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2
Q

Sanitise

A

To kill most microbes

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3
Q

Aseptic

A

Absence of microbes

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4
Q

Disinfectant

A

o Non-selective chemical for killing microbes
o Unsuitable for use on living tissue
o High concentrations required
o E.g. sodium hypochlorite

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5
Q

Antiseptic

A

o Non-selective chemical for killing microbes
o Appropriate for use on living tissue, usually skin
o High concentrations required
o E.g. betadine

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6
Q

Antibiotics

A

o Target particular pathways
o Pathways are unique to bacteria or group of bacteria
o Very small concentrations required
o For use on or in living tissues

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7
Q

Broad spectrum antibiotics

A

Effective against many bacterial groups

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8
Q

Narrow spectrum antibiotics

A

Effective against only a few bacterial groups

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9
Q

Bactericidal antibiotics

A

Kill bacteria

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10
Q

Bacteriostatic antibiotics

A

Inhibit growth of microbes, immune system kills.

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11
Q

Complication in the definition of bactericidal and bacteriostatic.

A

Decreasing concentration: bactericidal becomes bacteriostatic.
Increasing concentration: bacteriostatic becomes bacteriocidal.

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12
Q

Prophylactic therapy

A
  • Before the infection risk occurs e.g. surgery
  • Antimicrobial choice based on known or likely pathogen
  • Use only if: there is evidence for effectiveness or an infection is disasterous
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13
Q

Empirical therapy

A

• Best guess
• Use only when:
o Bacterial infections are very likely
o Treatment has substantial benefit
o ID, sensitivity unknown
• Use narrowest spectrum antibiotic for most likely pathogen
• First obtain specimens for MC&S testing
• Change to directed therapy when laboratory results are available.

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14
Q

Directed therapy

A

• Antimicrobial therapy with evidence from laboratory testing
o Microbial pathogen has been identified
o Antimicrobial sensitivity has been determined
• Then choose the antimicrobial that is:
o Most effective
o Least toxic
o Narrowest spectrum
• Directed therapy is the most desirable antimicrobial therapy

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15
Q

The antimicrobial creed

A

Microbiology guides therapy wherever possible
Indications should be evidence-based
Narrowest spectrum required
Dosage appropriate to the site and type of infection
Minimise duration of therapy
Ensure monotherapy in most situations

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16
Q

Oral antimicrobial administration

A
  • Preferred
  • Less serious adverse effects
  • Cheaper products
  • Lower costs to administer
  • Just as ‘powerful’ as injections
  • Drugs must have good oral bioavailability
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17
Q

Parenteral antimicrobial administration

A

• When oral administration is ineffective
o Poor oral bioavailability
o Swallowing difficulties
o Absorption problems (e.g. vomiting, diarrhoea)
o Higher concentrations are required than possible oral route
o Time critical (rare)
• Reassess daily and convert to oral ASAP

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18
Q

Topical antimicrobial administration

A
  • Use only when effectiveness is proven

* Antimicrobial different from oral and parenteral types, for avoidance of resistance

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19
Q

Adverse effects

A

• All microbials can cause adverse effects
• Adverse effects are usually mild, self-limiting
• Adverse effects more likely in:
o Elderly
o Patients with renal or hepatic impairment

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20
Q

Antimicrobial hypersensitivity (allergy)

A
  • Very commonly reported, esp. to penicillin
  • 5 to 10% of patients
  • But often vague details, inaccurate
  • Usually from parenteral administration
  • True anaphylaxis in 0.01% to 0.04% of courses of penicillin
  • 10% of anaphylaxis fatal
21
Q

When can a patient be given allergy causing antibiotics?

A
  • The antibiotics is clearly the most effective
  • Patient is carefully observed
  • Patient undergoes desensitisation therapy
22
Q

Multi-drug resistant bacteria

A 
o	Myobacterium tuberculosis 
o	Staphylococcus aureus
o	Enterococcus
o	Enterics (E. coli, Klebsiella, Enterobacter) 
o	Pseudomonas aeruginosa
23
Q

Antibiotic resistant mechanisms

A
  • Enzymes that degrade antibiotics e.g. beta-lactamases
  • Decreased inner cell membrane permeability
  • Decreased outer membrane permeability
  • Efflux pumps removing antibiotic from inside cells
  • Alteration of the binding site e.g. MRSA
24
Q

How to bacteria gain resistance genes?

A

• Inherent (natural) e.g. many Gram-negs to penicillin
• Vertical gene transfer
o Mutations after selection pressure of antibiotics
o Then transferred ‘vertically’ to progeny
• Horizontal gene transfer
o Genes transferred to related bacteria
o Mechanisms

25
Q

Horizontal gene transfer mechanisms

A

• Conjugation
o Related bacteria in direct contact
o Plasmid (ring of DNA) containing the gene transferred
o Main mechanisms of antibiotic resistance transfer
• Transformation
o DNA from external environment (dead bacteria) taken up
• Transduction
o Bacteriophages transfer DNA between closely related bacteria

26
Q

Research into new antibiotics

A 
•	To overcome problems with resistance?
•	Previously much research.
•	Now very limited.
•	Only one new antibiotic (Lipopeptides) with a novel mechanism of activity discovered in past 50 years.
•	Not a good business:
o	Resistance develops too quickly
o	We expect antibiotics to be cheap
27
Q

Overcoming antimicrobial resistance

A 
•	Change how we prescribe antibiotics
o	Prescribe only when absolutely necessary
o	Narrowest spectrum
o	Directed therapy when possible
o	Monotherapy
o	Correct dose
o	Only as long as necessary
o	Discuss antibiotic resistance with patients
o	Antimicrobial stewardship
28
Q

Antimicrobial sterwardship

A
  • Co-ordinated interventions designed to improve the appropriate use of antimicrobial therapy
  • All healthcare facilities in Australia now require to demonstrate they have an effective Antimicrobial Stewardship program.
29
Q

RHH Antimicrobial stewardship

A

o Antimicrobials must be prescribed in accordance with the current version of Therapeutic Guidelines Antibiotic or local guidelines, where appropriate.
o Patient’s medication chart shows for all prescriptions:
 Dose, frequency and route
 Indication
 Proposed duration with a review date or stop date documented
o Classification of antimicrobials
 Class A: unrestricted
 Class B: approval required
 Class C: higher level approval required

30
Q

Antibiotic sensitivity testing

A

• Patient specimens sent to the laboratory
o Blood
o Urine
o Swabs
o Aspirates
• Microscopy, culture and sensitivity (MC&S) requested
• If pathogen is isolated:
o Tested for sensitivity to a variety of antibiotics
o Tested for appropriate antibiotic concentration if required

31
Q

Antibiotic sensitivity testing methods

A

Agar disc diffusion, Broth dilution assay, Epsilometer (E) test

32
Q

Agar disc diffusion

A

o Make a ‘lawn’ of bacteria on agar plate
o Stamp with antibiotic impregnated discs
o Incubate then measure zones of inhibition (MM)
o Compare zones of inhibition with predetermined ‘break points’
o Inhibition zone > breakpoint: sensitive (S)
o Inhibition zone < breakpoint: resistant (R)
o Qualitative only: result shows sensitive or resistant only

33
Q

Broth dilution assay

A

o For when treatment concentration is required
 Appropriate antibiotic already known
 Make antibiotic dilution series
 Add test bacteria and growth medium
 Incubate. Cloudiness shows growth.
 MIC = lowest antibiotic concentration with no growth
o For minimum bactericidal concentrations (MBC):
 Plate out concentration with no growth, incubate
 MBC = lowest concentration with no growth

34
Q

Epsilometer (E) Test

A

o For when a treatment concentration is required
o E test strips: antibiotic concentration gradient on plastic strip
o Make a ‘lawn’ of bacteria on again plate
o Place E test strips for different antibiotics on bacterial lawn
o Incubate
o Intersection of clearing zone with scale shows minimum inhibitory concentrations (MIC)
o Ensure antibiotic concentration in the blood is at least the MIC

35
Q

Beta-lactams

A

• Most widely used group
• Cabapenams, cephalosporins, monobactams, penicillins
• All have beta-lactam ring structure
• Well tolerated (unless hypersensitive)
• Interfere with cell wall synthesis
• Mechnisms of activity
o Target Penicillin Binding Proteins (PBPs)
o PBPs are enzymes that catalyse the cross-linking of peptidoglycan in bacterial cell walls
o Beta-lactam antibiotics bind to and inactivate PBPs
o Cross0linking of peptidoglycans is inhibited
o Peptidoglycan precursors accumulate in cell
o Autolysis signal
o Cells die

36
Q

Aminoglycosides

A
  • Very effective against gram-negatives
  • Aerobes and facultative anaerobes only
  • Potential serious side effects
  • Binds to bacterial ribosomes
  • Bacteria fail to make proteins – death
  • E.g. gentamcin, tobramycin, amikacin streptomycin, paromycin, neomycin, framycetin
37
Q

Chloramphenicol

A
  • Very effective, broad spectrum
  • Binds to ribosomes – inhibit protein synthesis
  • Potential serious side effects
  • Systemic use only if no alternative
  • Mainly topical use: eye and ear infections
  • Chloramphenicol only
38
Q

Daptomycin

A
  • Effective against gram-positives only
  • Attaches to and disrupts bacterial cell membrane
  • Alternative t glycopeptides
  • Skin and soft tissue infections
  • S. aureus bacteraemia
  • Daptomycin only
39
Q

Glycopeptides

A
  • Effective against gram-positives only
  • Inhibit cell wall synthesis, like beta-lactams
  • Bind to precursor peptidoglycan units inside cells
  • Prevents formation of peptidoglycan chains and prevents peptidoglycan chains cross linking
  • No cell wall formed, new cells die
  • E.g. vancomycin, teicoplanin
40
Q

Lincosamides

A
  • Effective on gram-positive aerobes and anaerobes
  • Bind to ribosomes, inhibit protein synthesis
  • Significant adverse effects
  • Only use if non others appropriate
  • Clindamycin and lincomyin only
41
Q

Macrolides

A
  • Wide spectrum activity, except gram-negative rods
  • Binds to ribosomes, inhibiting protein synthesis
  • Binding is reversible: bacteriostatic only
  • Erythromycin, azithromycin, clarithromycin
42
Q

Nitroimidazoles

A
  • Bacteria and protozoa: anaerobes only
  • Damage to microbial DNA
  • Metronidazole, tinidazole only
43
Q

Oxazolidonones

A
  • Excellent against antibiotic resistant gram-positives
  • Reserved for antibiotic resistant staphylococcal, streptococcal and enterococcal infections
  • Binds to ribosomes, inhibiting protein synthesis
  • Some potential for adverse reactions
  • Linezolid only
44
Q

Polymyxins

A
  • Gram-negative rods
  • Insert into bacterial outer membrane
  • Increase cell permeability – death
  • Potential serious side effects
  • Mainly used externally
  • Polymixin B, polymyxin E (colistin)
45
Q

Quinolones

A
  • Very widely used
  • Excellent activity against aerobic gram-negatives
  • Extended spectrum types are effective against gram-positives, intracellular bacteria and anaerobes
  • Inhibit DNA replication and repair
  • Ciprofloxacin, moxifloxacin, norfloxacin, ofloxacin
46
Q

Rifamycins

A
  • Gram-positives only, especially staph., strep.
  • Effective against Myobacterium tuberculosis
  • Inhibits RNA synthesis – no proteins made
  • Combination use only – resistance develops rapidly
  • Rifampin and rifabutin only
47
Q

Streptogramins

A
  • Gram-positives only: reserved for vancomycin resistant Staphylococcus, Enterococcus infections
  • Bind to ribosomes – inhibit protein synthesis
  • Synergistic combination: quinupristin-dalfopristin
  • Pristinamycin is effective against Gram-negatives as well as Gram-positives
48
Q

Sulfonamides and Trimethoprim

A
  • Broad spectrum
  • Potential serious side effects
  • Only for serious infections: MRSA, L. monocytogenes
  • Inhibit folate synthesis
  • Sulfamethoxazole-trimethoprim
  • Very effective synergistic combination
49
Q

Tetracyclines

A
  • Broad spectrum. Also Plasmodium
  • Reasonably safe
  • Bind to ribosomes – protein synthesis inhibited
  • Binding is reversible – bacteriostatic only
  • Doxycycline, minocycline, tigecycline

CAM102 Microbiology (4 decks)

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