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PVS > Microbiology 2 > Flashcards

Microbiology 2 Flashcards

1
Q

List the protein synthesis targeting antibiotics

A
  • Aminoglycosides
  • Nitrofurans
  • tetracyclines
  • Chloramphenicol
  • Macrolides
  • Lincosamides
  • Pleuromutilins
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2
Q

List the bacteriocidal protein synthesis targeting antibiotics

A
  • Aminoglycosides (streptomycin, neomycin)

- Nitrofurans

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3
Q

List the bacteriostatic protein synthesis targeting antibiotics

A
  • Tetracyclines (oxytetracyline, doxycycline)
  • Chloramphenicol
  • Macrolides (erythromycin, tylosin)
  • Lincosamides
  • Pleuromutilins
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4
Q

Compare eukaryotic and bacterial ribosomes

A
  • Eukaryote has 80s: 40s and 60s subunits

- Prokaryote has 70s : 30s and 50s subunits

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5
Q

What is the mechanism of resistance against ribosome targeting antibiotics?

A
  • intrinsic:Ribosome sequence alterations leading to alterations in binding sites for drug
  • Extrinsic: Acquisition of degradative enzymes that modify the drug
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6
Q

Describe the structure of nitrofurans

A

Furan ring with nitro group is the defining structural feature

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7
Q

Describe the mechanism of action of nitrofurans

A
  • Unique

- Reduced by bacterial flavoproteins to reactive intermediates that inhibit bacterial ribosomes and other macromolecules

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8
Q

Describe the mechanism of action of aminoglycosides

A

Bind 30s subunit and affect number of steps in protein synthesis, leading to non-functional proteins
- Irreversibl inhibition

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9
Q

Describe the activity and pharmacology of aminoglycosides

A
  • Gram -ve
  • Not absorbed orally
  • Poor tissue penetration (hydrophilic)
  • Eliminated by renal filtration
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10
Q

Describe the mechanism of action of tetracyclines

A
  • Enter cell by active process, bind to receptors on 30s subunit
  • Block tRNA attachment
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11
Q

Describe the activity and pharmacology of tetracyclines

A
  • Many Gram -ve and +ve
  • Atypical bacteria e.g. Ricketssia, Borellia, Chlamydia, Mycoplasma
  • Can be absorbed orally but varies in group
  • Dairy and ant-acids impair use
  • Concentrate in liver, significant biliary secretion
  • Can cause GIT imbalances
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12
Q

Describe the mechanisms of action of chloramphenicol

A

Binds 50s subunit, prevents linking of amino acids to growing peptides

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13
Q

Describe the activity and pharmacology of chloramphenicol

A
  • Broad spectrum
  • Clinically ineffective against Chlamydia
  • Good distribution incl CNS and eye
  • Banned from use in food animals
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14
Q

Describe the mechanism of action of macrolides

A

Block 50s activity

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15
Q

Describe the activity and pharmacology of macrolides

A
  • Active against Gram +ve nad anaerobic bacteria
  • High lipid solubility, good distribution
  • Bacteriostatic, but erythromycin can kill at high concentrations
  • Chromosomal resistance can develop
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16
Q

Describe the mechanism of action of lincosamides

A

Bind 50s subunit and block peptidyl transferase activity

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17
Q

Describe the activity and pharmacology of lincosamides

A

Primarily Gram +ve but some -ve

  • Basic, lipid soluble
  • Wide distribution in body
  • Facultative aanaerobic bacteria are intrisincally resistant due to methylation of 50S binding site
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18
Q

Describe the toxic effects of lincosamides

A

Serious fatal diarrhoea in horses, rabbits, guinea pigs and other herbivores, can cause problems in cattle. Caused by rapid bacterial overgrowth

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19
Q

List the DNA disruption and RNA synthesis targeting classifications

A
  • Nucleic acid targeting
  • Non-ribosome blocking of protein synthesis
  • DNA precursor affecting
  • DNA packaging
  • DNA destruction
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20
Q

List the antibiotics that affect DNA in some way

A
  • Sulphonamide/trimethoprim
  • Quinolones, novobiocin
  • Nitroimidazoles
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21
Q

Name the antibiotic that affects RNA synthesis

A

Rifampicin

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22
Q

Describe the mechanism of action of sulphonamides/trimethoprim

A
  • Affect nucleotide synthesis
  • Competitive inhibitors of dihydropteroate synthase
  • Cell lacks dihydrofolate synthesis which is required for DNA synthesis
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23
Q

How does sulphonamide exert its action?

A

Similar structure to PABA, substitutes it in the synthesis of dihydrofolate

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24
Q

How does trimethoprim exert its action?

A

Inhibits dihydrofolate reductase preventing production of THF and thus the production of nucleotides

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25
Q

Why are sulphonamide and trimethoprim used together?

A

Some production of DHF can still occur where sulphonamide is used alone, addition of trimethoprim prevents conversion of this to THF and then nucleotide

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26
Q

Describe the mechanism of action of quinolones

A
  • Inhibits DNA gyrase activity, needed for supercoiling of DNA to be packaged in bacteria
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27
Q

How can resistance to quinolones develop?

A

Single point mutation

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28
Q

Describe the pharmacokinetics of quinolones

A
  • Low activity on gut anaerobes
  • Rapid oral absorption (poor in ruminants)
  • Excretion via urine after partial metabolism in liver
  • Large volume of distribution
  • Good penetration into CSF, bronchial secretions, bone, cartilage, prostatic tissues
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29
Q

Give an example of a side effect of quinolones

A

Cartilage erosion in horses

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30
Q

Describe the mechanism of action of nitroimidazoles

A
  • Reduction products of imidazole group are reactive with DNA
  • Cause DNA strand breaks
  • Require reduction environment so ineffective on aerobic bacteria
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31
Q

Name members of the fluoroquinolone group

A
  • Nalidixic acid
  • Erofloxacin
  • Neomycin
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32
Q

Describe the spectrum of activity of nitroimidazoles

A
  • Effective only on anaerobes

- Some Gram +ve, all Gram -ve

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33
Q

Describe the pharmacokinetics of nitroimidazoles

A
  • Absorbed rapidly after oral admin
  • Wide distribution (lipophilic)
  • Will cross placenta and into milk
  • Functional in abscesses
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34
Q

List the adverse effects of nitroimidazoles

A
  • Carcinogenic and mutagenic
  • Hepatotoxicity
  • Neurotoxicity including seizures
  • Ataxia
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35
Q

Describe the spectrum of activity of pleuromutlins

A

Mainly Gram +ve, moderate against some fastidious Gram -ve bacilli, Mycoplasma and Campylobacter, inactiva against Enterobacteriaceae

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36
Q

Define narrow spectrum of activity

A

Few bacterial groups targeted, usually only effective on Gram +ve bacteria

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37
Q

What are potential outcomes of combined antibacterial therapy?

A
  • Additive effect (purely summative)
  • Synergistic effect
  • Indifference
  • Antagonistic effect
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38
Q

Give an example of where combined antibacterial therapy may have an antagonistic effect

A

Combination of bacteriostatic drug with a bacteriocidal drug

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39
Q

List the potential mechanisms of antibiotic resistance

A
  • Modification/breakdown of drug
  • Efflux
  • Reduced permeability
  • Modified pathways
  • Altered target site
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40
Q

Explain how efflux pumps lead to antibacterial resistance

A
  • Pumps on bacteria, reduce intracellular concentration of the antibiotic
  • Not inhibiting every component of the cell
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41
Q

Explain how bacteria may be able to modify/breakdown a drug before it enters the cell

A

Secretion of enzymes into the cytoplasm or out of the cell, altering the structure of the antibiotic and thus preventing function

42
Q

List the ways in which genetic make up of bacteria can change

A
  • New genes (insertion, inheritance on plasmids)
  • Loss of genes (deletions)
  • Modification of function by genes by deletion, inheritance or point mutation
  • Modification of promotors leading to altered expression (point mutations)
43
Q

Explain transferable acquired resistance in bacteria

A
  • Based on genetic transfer through plasmids

- Transposons can hop between chromosomes and plasmids

44
Q

Define intrinsic resistance

A

Innate ability of group to resist activity of a particular antimicrobial agent through inherent structure or functional characteristics which allow tolerance of the drug (e.g. lack or altered target)

45
Q

Define acquired resistance

A

When a microorganism obtains the ability to resist the activity of a drug, allowing alteration of drug, alteration of target, or provides bypass mechanism

46
Q

Give examples of intrinsic resistance

A
  • Poor permeability due to outer membrane (Gram-ve intrinsically resistant to vancomycin)
  • Target different to other genera (e.g. Enterococci resistant to cephalosporins, have low affinity for enterococal PBPs)
  • Lack target (e.g. Gram +ve bacteria are resistant to LPS targeting antibiotics e.g polymyxin)
47
Q

Describe acquired resistance through mutation

A
  • Common
  • Ribosome, or ribosomal proteins, such that the antibiotic does not bind target
  • Mutation of DNA gyrase so it tolerates fluoroquinolones
48
Q

Give examples of acquired resistance genes

A
  • beta-lactamases
  • Aminoglycoside modifying enzymes
  • Alternate targets MRSA (add variant of target)
  • Efflux systems (new gene, or upregulation of existing)
49
Q

Describe the alternate target resistance of MRSP

A
  • have mecA gene, encodes alternate penicillin binding protein (PBP2a)
  • Low affinity for beta lactam
  • Outcome is strains which can tolerate most of beta-lactam antibiotics, as anitbiotic only binds PBP1 not PBP2a
50
Q

Describe resistance to vancomycin via the modification of the cell wall

A
  • Production of altered peptidoglycans
  • Method of vancomycin resistance in enterococci
  • Alteration of terminal amino acid residues of NAM/NAG-peptide subunits
  • Mediated by van genes found on transposon
  • van gene can be transferred via plasmids
51
Q

Describe the resistance to antibiotic by efflux

A
  • New genes or upregulation of existing
  • Antibiotic efflux transporters classified into 5 superfamilies based on amino acid sequence and energy source used to export substrates
  • All transport groups of compounds with similar chemical properties so may lead to cross-resistance
52
Q

Name the 5 superfamilies of bacterial antibiotic efflux transporters

A
  • Major facilitator superfamily (MFS)
  • ATP- binding cassette superfamily (ABC)
  • Small multidrug resistance family (SMR)
  • Resistance -nodulation-cell-division superfamily (RND)
  • Multi-antimicrobial extrusion protein family (MATE)
53
Q

List the antibiotics and other agents exported by the major facilitator superfamily transporters

A
  • Tetracycline, fluoroquinolones, erythromycin, lincosamides, rifampicin, chloramphenicol, aminoglycosides
  • QACs, basic dyes, phosphonium ions
54
Q

List the antibiotics and other agents exported by the resistance-nodulation-cell division superfamily transporter

A
  • Tetracyclines, fluoroquinolones, erythromycin, rifampicin, beta-lactams,fusidic acid, chloramphenicol, aminoglycosides
  • Basic dyes, detergents, fatty acids
55
Q

List the antibiotics and other agents exported by the small multidrug resistance family transporters

A
  • Tetracycline, erythromycin, sulfadiazine

- QACs, antiseptics, tratrphynly compounds, phosphonium, ethidium

56
Q

List the antibiotics and other agents exported by the ATP-binding cassette superfamily transporter

A
  • Tetracycline, fluoroquinolones, erythromycin, rifampicin, macrolides, beta-lactams, fusidic acid, chloramphenicol, aminoglycosides
  • Ionophors, ethidium, akaloids, phospholipids
57
Q

List the antibiotics and other agents exported by the mutli antimicrobial extrusion protein superfamily transporters

A
  • Tetracycline, fluoroquinolones, erythromycin, rifampicin, chloramphenicol, beta-lactams, fusidic acid, aminoglycosides
  • Dyes
58
Q

What are the major mechanisms of resistance against beta-lactams?

A

Cleavage by beta-lactamases

- Altered PBPs, aternate PBPs

59
Q

What are the major mechanisms of resistance against aminoglycosides

A
  • Enzymatic modification
  • Efflux
  • Ribosomal mutations
  • 165 rRNA methylation
60
Q

What are the major mechanisms of resistance against quinolones?

A
  • Efflux
  • Modification
  • Target mutations
61
Q

What are the major mechanisms of resistance against vancomycin?

A
  • Altered cell walls

- Efflux

62
Q

What is the major mechanism of resistance against rifampicin?

A

Altered beta-subunit of RNA polymerase

63
Q

What are the major mecahnisms of resistance against antibioics that inihibit cell wall synthesis (e.g. streptogramins such as virginiamycins, quinupristin, dalfopristin)

A

Enzymatic cleavage, modification, efflux

64
Q

Name some bacterial antibiotic susceptibility tests

A
  • Dilution test (for MIC)
  • Kirby-Bauer Disc diffusion
  • E strip diffusion (rapid simple MIC)
65
Q

Explain the principles of the Kirby-Bauer resistance test

A
  • Assessment of the diffusion gradient around an antibacterial disc
  • Measure, compare ot known values
  • Allows establishment of susceptibility and MIC
66
Q

Describe the use of Evaluator (E) strips in assessing bacterial resistance

A
  • Strip has gradient of antibiotic content
  • Compaire amount of bacterial growth with demarkation on strip
  • Allows determination of susceptibility and MIC
67
Q

Outline the interpretation of a disc diffusion and dilution assays

A
  • Resistant = small inhibitory zone on disc diffusion and high MIC by dilution
  • Susceptible = very large inhibitory zone on disc diffusion and low MIC by dilution
68
Q

Outline how resistance can spread

A
  • Selective pressure leading to survival of resistant bacteria
  • Eventually end up with fully resistant populations
69
Q

What is multi-drug resistance?

A
  • Acquired non-susceptibiltiy to at least one agent in 3 or more categories
  • Antimicrobial category list based on clinical break points for drugs that are listed for use against that organism
70
Q

What is XDR?

A
  • Extensively drug resistant

- Acquired non-susceptibility to at least one agent in all but 2 or fewer antimicrobial categories

71
Q

What is PDR?

A
  • Pan-drug resistant

- Acquired non-susceptibility to all agents in all antimicrobial categories

72
Q

How can MDR, XDR and PDR develop?

A
  • Plasmid transfer of resistance
  • Cassettes and transposable elements allowing increased mobility of complex collections of genes to express resistances and ability to hop in chromosomes and plasmids between
  • TN3 transposon gene
  • Plasmid conjugation
  • Transduction (bacteriophage)
  • Transformation (uptake of naked DNA from environment)
73
Q

Explain how the TN3 transposon gene can lead to the transfer of resistance between bacteria

A
  • Genes are on mobile elements
  • Taken up by other bacteria
  • Selected for and maintained
  • Big problem for lots of Gram -ve
74
Q

When may prophylactic treatment with antibiotics be advantageous?

A

When started within 3 hours of contamination

75
Q

What are the disadvantages of prophylactic antibiotic use?

A
  • Toxicity
  • Encouragement of drug resistance
  • Residues in food animals
  • Cost
76
Q

Give examples of deleterious use of antibiotic prophylaxis

A
  • Growth promotion with fluoroquinolones increases resistant pathogens
  • Neomycin used in calves predisposes to diarrhoea
  • Tetracyclines given to feedlot calves increases mortality
  • Inter-uterine treatment e.g. neomycin to prevent post-partum metritis may affect fertility
77
Q

Give examples of prophylactic antibiotic use

A
  • Feedlot pneumonia of calves on arrival
  • Leptospira in cows (remove carriers)
  • Strangles in horses (treat at risk horses, quarantine)
  • Broilers at known risk of colibacillocis or chronic respiratory disease
78
Q

Outline where antimicrobial combination therapy may be used

A
  • Mixed bacterial infections
  • Therapy in severe conditions where aetiology unknown
  • Treating life threatening cases prior to susceptibility data
  • Treating unusual pathogens incl. Mycobacterium
  • Syntergistic effects e.g. sulphonamide and trimethoprim
79
Q

Give examples of adjunctive therapy that may be used with antimicrobials

A
  • Fluids
  • Surgery
  • Drugs to improve effectiveness e.g. modifying urine pH
  • Glucocorticoid treatment to reduce trauma while drugs act (but also leads to immune suppression)
80
Q

What is the importance of the MIC in clinical use?

A
  • Need to reach MBC, as only reaching MIC may allow overgrowth of resistant bacteria
  • Need to maintain this for particular period of time with most drugs
81
Q

When should culture and sensitivity be carried out?

A

Always, in order to prescribe specific drug for specific pathogen

82
Q

What is an important consideration when giving antibiotics to ruminants?

A

Cannot be administered orally as will knock out the rumen microflora

83
Q

Give the points of the 7 point plan for responsible use of antimicrobials in veterinary practice

A
  • Work with clients to avoid need for antimicrobials
  • Avoid inappropriate use
  • Choose right drug for right bug
  • Monitor antimicrobial sensitivity
  • Minimise use
  • record and justify deviation from protocols
  • Report suspected treatment failure to the VMD
84
Q

What is a potential consequence of antimicrobial resistance through veterinary use?

A

May also have resistance in the human variant

85
Q

Explain how vets can work with clients to avoid the need for antimicrobials

A
  • Inform owners about benefits of regular health checks, educate on antibiotic use
  • Use symptomatic relief or topical preparations where possible
  • Use integrated disease programmes, biosecurity, monitoring of health status for early intervention, environmental modification to reduce infection risk
  • Vaccination where possible
  • Isolate infected animals
  • Improve animal health and welfare
86
Q

Explain how vets can avoid inappropriate use of antimicrobials

A
  • Use for bacterial infections
  • Restrict use to ill or at-risk animals
  • Advise clients on correct administration of products and completion of course
  • Avoid underdosing (consider formulation and site that needs dosing)
87
Q

Explain how to choose the “right drug for the right bug”

A
  • Identify likely target organisms and predict susceptibility
  • Create practice based protocols for common infections based on clinical judgement and up to date knowledge
  • Know how antimicrobials work and their pharmcodynamics
  • Use as narrow spectrum as possible
  • Have idea of pathogen likely prior to culture and sensitivity by using in house smears and microscopy
88
Q

Explain the monitoring of antimicrobial sensitivity

A
  • Must be determined so can implement change in treatment where necessary
  • Monitor bacterial culture and sensitivity trends
89
Q

Explain how to antimicrobial use can be minimised

A
  • Use only when necessary, and evidence that usage will reduce morbidity/mortality
  • Regularly assess antimicrobial use and develop written protocols for appropriate use
  • Use alongside strict aseptic techniques and written practice guidelines
90
Q

Explain the recording and justification of deviations from antimicrobial protocol

A
  • Must be able to justify choice and dose

- Accurate records allow evaluation of outcome of therapeutic regimens

91
Q

Explain the reporting of suspected treatment failure of antimicrobials to the VMD

A
  • May be first indication of resistance

- report through Suspected Adverse Reaction Surveillance Scheme (SARSS)

92
Q

Explain what is meant by narrow spectrum antibiotics

A
  • Only treat specific groups of bacteria
  • Gram +ve or Gram -ve
  • or Gram +ve with some Gram -ve
  • Anaerobic or aerobic
93
Q

Explain what is meant by broad spectrum antibiotics

A
  • Treat wide range of bacteria
  • Often active against Mycoplasmas
  • Gram +ve and Gram -ve
94
Q

Which antimicrobials can be used to treat Gram +ve bacteria?

A
  • Beta-lactams e.g. penicillin, cloxacillin, 1st gen cephalosporins
  • Macrolides e.g. erythromycin, tylosin
  • Lincomycin, tiamulin, novobiocin
95
Q

Which antimicrobials can be used to treat Gram -ve bacteria

A
  • Aminoglycosides (e.g. dihydrostreptomycin, framycetin, kanamycin, neomycin, streptomycin, gentamycin)
  • Septinomycin, apramycin
96
Q

Which antimicrobials can be considered broad spectrum?

A
  • Beta-lactams except penicillin
  • Sulphonamides
  • Tetracyclines
  • Fluoroquinolones (protected group)
97
Q

What factors may affect the choice of antimicrobial?

A
  • Pathogen to be treated
  • Age of animal
  • Pregnancy status
  • Concurrent disease
  • Immune status of patient
  • Food or not food animal
  • Licensing
  • Toxicity and side effects
  • Practical considerations e.g.practice stock
98
Q

Why could efflux systems allow resistance to multiple antibiotics while an enzyme to degrade an antibiotic may only lead to resistance to that group?

A

Efflux is non-specific and leads to reduced intracellular concentrations of that antimicrobial. Enzymes need to be specific to that antibiotic and so can only provide resistance to that one drug

99
Q

What is clavulanic acid?

A

A beta-lactamase inhibitor that allows the functioning of beta-lactam antibiotics where there is resistance to beta-lactam alone

100
Q

What are the risks associated with antimicrobial resistance in commensals?

A

May be opportunistic pathogens and may be reservoirs for plasmid transfer of resistance genes

101
Q

Describe fusidic acid

A
  • Protein synthesis inhibitor preventing turnover of elongation factor G
  • Resistance via: alterations in ribosomal structure or drug, chromosomal mutation
  • Bacteriostatic
  • Effective for Gram +ve

PVS (23 decks)

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