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PVS > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What is the function of bacterial replication?

A

To avoid elimination

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2
Q

What is required in order for pathogens to replicate?

A
  • Tolerate host environment
  • Evade host defences
  • Compete successfully for nutrition
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3
Q

What is the O-antigen?

A

LPS on gram-ve bacteria

- Binds to TLR4 and leads to toxic shock

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4
Q

What is the bacterial capsule and what are its functions?

A
  • Composed of protein subunits
  • May allow better penetration through mucosa, adhesion to cells, avoidance of phagocytosis and inhibition of complemetnt
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5
Q

What is the function of bacterial Fc binding proteins?

A

Prevent interactions with Fc-receptors on phagocytes and so prevent phagocytosis

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6
Q

What are leukotoxins?

A

Toxins produced by pathogens that remove WBCs especially phagocytes

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7
Q

Which organism inhibits the phagolysosome?

A

Salmonella

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8
Q

Which organism is able to escape the phagolysosome?

A

Listeria

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9
Q

What are the consequences of caogulases?

A
  • Clot blood
  • Lead to damage to blood vessles
  • If antibiotic goes through circulatory system will be inhibited
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10
Q

How may infection of a susceptible host with a pathogen occur?

A
  • Entry through damaged epithelium leading to tissue invasion
  • Adhrence to skin/mucous membranes
  • engulfment by phagocyte cells on mucus membranes and survival of the pathogen in the phagocyte and transfer in tissues
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11
Q

List the factors that contribute to the ability to clear disease?

A
  • Pathogen involved
  • Immune suppression/modified physiology
  • Site of infection
  • Breaching of defensive barrier by accident or deliberately
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12
Q

Define persistent infection

A

Form of chronic, commonly involve silent and productive/clinical stages

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13
Q

Define latent infection

A

Overlaps with persistent, dormant until conditions are favourable for the pathogen

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14
Q

Define carrier state of infection

A

Infection present but does not suffer any symptoms, however can still spread disease

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15
Q

Describe the structure of Gram -ve bacteria

A
  • Cytoplasmic membrane, thin cell wall, outer cytoplasmic membrane
  • Outer membrane has lipopolysaccharides (LPS)
  • Peptidoglycan can also trigger TLR, TLR4
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16
Q

Describe the structure of Gram +ve bacteria

A
  • Single cytoplasmic membrane, thick cell wall, often have capsule
  • Peptidoglycans in cell wall
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17
Q

Describe the structure of acid fast bacteria

A
  • Similar to Gram +ve
  • Cytoplasmic membrane, thick cell wall
  • Mycolic acids in cell wall preventing penetration of disinfectants etc
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18
Q

Describe the structure of Mycoplasmas

A
  • Single membrane, poor morphology, no cell wall
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19
Q

What are the sources of endo and exotoxins?

A
  • Exo: living Gram +ve and -ve bacteria

- Endo: lysed Gram -ve bacteria

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20
Q

Where are endo and exotoxins found?

A
  • Exo: released from the cell

- Endo: part of the cell

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21
Q

What is the chemical composition of exo and endotoxins?

A
  • Exo: protein

- Endo: lipopolysaccharide

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22
Q

What is the heat sensitivity of exo and endotoxins?

A
  • Exo: liable (60-80C)

- Endo: stable (250C)

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23
Q

Describe the immune reactions to exo and endotoxins

A
  • Exo: strong

- Endo: weak

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24
Q

Is conversion to toxoids possible for exo or endotoxins?

A
  • Exo: yes

- Endo: no

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25
Q

Are exo or endotoxins pyretic?

A
  • Exo: no

- Endo: yes

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26
Q

Describe the enzymatic activity of exo and endotoxins

A
  • Exo: mostly enzymatic activity

- Endo: no enzymatic activity

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27
Q

What is the molecular weight of exo and endotoxins?

A
  • Exo: 10KDa

- Endo: 50-1000KDa

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28
Q

Compare the denaturing of exo and endotoxins

A
  • Exo: on boiling, can get denatured

- Endo: cannot be denatured on boiling

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29
Q

Compare the specificity of exo and endotoxins

A
  • Exo: specific to a particular bacterial strain

- Endo: non specific

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30
Q

Describe the antigenicity of exo and endotoxins

A
  • Exo: high

- Endo: poor

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31
Q

Give examples of exotoxin producing bacteria

A
  • Staph aureus
  • Bacillus cereus
  • Sterp pyogenes
  • Vibrio cholera
  • Bacillus anthracis
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32
Q

Give examples of endotoxin producing bacteria

A
  • E. coli
  • Salmonella typhi
  • Shigella
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33
Q

Briefly describe the key features of Bacillus anthracis and Clostridium spp

A
  • Spore forming
  • Gram +ve
  • Visualised using malachite green staining
  • Heat needed to penetrate into spore cortex
  • Spores resistant to disinfectants and heat
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34
Q

Give the stages of viral infection

A
  • Acquisition
  • Binding of receptor on cell and infection of cell
  • Replication of proteins
  • Release of more virus from cell
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35
Q

Define antibiotics

A

Low molecular weight microbial metabolites which can kill or inhibit the growth of susceptible bacteria

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36
Q

Define bactericidal

A

Kills the organism

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37
Q

Define bacteriostatic

A

Temporarily inhibits the growth of the organism

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38
Q

What is meant by the “magic bullet”?

A

Single drug that is able to clear infection/pathogens without affecting the host cells

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39
Q

Give examples of differences between bacterial and eukaryotic cells

A
  • Ribosome structure

- Bacterial cell walls

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40
Q

What is the consequence of a drug target that is similar to host biology?

A

More undesired interactions

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41
Q

Give an example of how killing a pathogen may lead to adverse effects

A
  • Gram -ve bacteria release lipid-A as they die

- This can cause sepsis/toxic shock

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42
Q

Give examples of adverse reactions to antimicrobials

A
  • Direct host toxicity
  • Toxic interference with other drugs
  • Interferences with protective host flora
  • Tissue necrosis at injection site
  • Impairment of host immune function
  • Hypersensitivity
  • Enzyme induction/inhibition
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43
Q

Give examples of side effects from antimicrobials

A
  • Nephrotoxicity (aminoglycosides)
  • Neurotoxicity
  • Tendon damage (quinolones)
  • Liver disturbances (rifampicins)
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44
Q

Outline the secondary effects due to rifampicin

A
  • Metabolised by liver, induces P450 pathway
  • Increases rate of metabolism of many other drugs normally cleared by the liver
  • Can cause redness of body fluids
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45
Q

Give examples of possible side effects due to rifampicin specifically

A
  • Hepatotoxicity
  • Respiratory
  • Cutaneous (flushing, pruritus, rash, redness, watering of eyes)
  • Abdominal (nausea, vomiting, abdominal cramps +/- diarrheoa)
  • Flu-like symptoms (chills, fever, headache, arthralgia, malaise)
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46
Q

List the potential routes for antimicrobial administration

A
  • IV
  • Oral
  • IM
  • Per rectum
  • Topical
  • Nebulised (sprays for lungs)
47
Q

Why is oral administration of antimicrobials contraindicated in ruminants?

A

Will destroy the rumen microflora

48
Q

What is meant by time dependent activity?

A

Time exposed more significant than the concentration, time that serum concentration exceeds the MIC

49
Q

Describe concentration dependent activity antimicrobials

A
  • Concentration increase leads to killing increase
  • Requires high concentration at drug binding site in order to be effective
  • Maintaining this level between doses may not be beneficial
50
Q

What physiochemical features facilitate penetration into cells?

A
  • Highly lipophilic

- Low ionisation

51
Q

Give examples of acidic (polar) antibiotics with low lipophilicity

A
  • Penicillin
  • Cephalosporins
  • Beta-lactamase- inhibitors
52
Q

Give examples of basic antibiotics with low lipophilicity

A
  • Polymyxins

- Aminoglycosides (gentamycin, spectinomycin, tobramycin, streptomycin, amikacin)

53
Q

Describe the tissue distribution characterstics of polar antibiotics with low lipophilicity

A
  • Do not readily penetrate intact natural body barriers
  • Effective concentration in CSF, milk, other transcellular fluids not always achieved
  • Adequate concentrations may be achieved in joints, pleural and peritoneal fluids
  • Penetration may be aided by acute inflammation
54
Q

Name a weak- acid antibiotic drug of moderate to high lipophilicity

A

Sulphonamide

55
Q

Give examples of weak-basic antibiotic drugs with moderate to high lipophilicity

A
  • Trimethoprim
  • Lincosamides (lincomycin, clindamycin)
  • Macrolides (erythromycin, tylosin, spiramycin, tilmicosin)
56
Q

Give examples of amphoteric antibiotic drugs with moderate to high lipophilicity

A

Tetracyclines (tetracycline, chlortetracycline, oxytetracycline)

57
Q

Give examples of highly lipophilic, low ionisation antibiotics

A
  • Chloramphenicol
  • Fluoroquinolones (enfrloxacin, norfloxacin, ciprofloxacin)
  • Lipophilic tetracyclines
  • Metronidazole
  • Rifampicin
58
Q

Describe the tissue distribution characteristics of antibiotics with moderate to high lipophilicity

A
  • Cross cellular membranes more readily than polar, enter transcellular fluids to greater extent
  • Some trapping may occur (some ionisation)
  • Penetrations of CSF and ocular fluids affected by plasma proteins binding as well as lipophilicyt
59
Q

Describe the tissue distribution characteristics of highly lipophilic, low ionisation antibiotics

A
  • Cross cellular barriers easily
  • Penetrate into difficult transcellular fluids e.g. prostatic fluid and bronchial secretions
  • All penetrate into CSF except tetracyclines and rifampicin
  • All penetrate into intracellular fluids
60
Q

What natural barriers exist in the host that may prevent penetration of antibiotics into tissues?

A
  • BBB, poor penetration so require high doses to reach brain

- Lesions and pathologies may have poor perfusion and so poor drug delivery

61
Q

When is the use of a bactericidal antibiotic indicated?

A

Where infections cannot be controlled by or eradicated by host mechanisms

62
Q

When is the use of bacteriostatic antibiotics indicated?

A

Where the animal is healthy otherwise and only need to control the infection to allow the host to regain control

63
Q

What is required in order for bacteriocidal antibiotics to function?

A

Bacterial growth, hence cannot be used in conjunction with bacteriostatics

64
Q

Why might bacteriostatic drugs be ineffective?

A
  • Nature/site of infection e.g. endocarditis (site)

- Host immunosuppression e.g. cat with existing feline leukaemia infection

65
Q

Which antibiotics stem from Bacillus spp?

A
  • Colistin (polymyxin E)
  • Polymyxin B
  • Bacitracin
66
Q

Which organism is the source of the largest number of antibiotics?

A
  • Streptomyces spp
  • Source of: Streptomycin, tetracycline, Neomycin, Rifamycin, Vancomycin, Linicomycin, Eyrthromycin, Kanamycin, Amphoteracin B, Chloramphenicol
67
Q

Which antimicrobials stemp from Penicillium spp (fungi)?

A
  • Penicillin G

- Griseofulvin (anti-fungal)

68
Q

Which antibiotic stems from Cephalosporium spp.?

A

Cephalosporins

69
Q

What control methods other than antibiotics should be used?

A
  • Prevention (vaccination, biosecurity, infection control plans)
  • Removal of infected animals, euthanasia of infected animals to prevent spread of untreatable conditions
70
Q

What are the goals of antimicrobial therapy?

A
  • Eliminate infections without toxicity in the host

- Prevent infections in situations where the risk is high

71
Q

What is MIC?

A

Minimum inhibitory concentration

- the concentration required at a site of infection to achieve bacterial inhibition

72
Q

What is MBC?

A

Minimum bactericidal concentration

- the concentration required at a site of infection to kill the bacteria

73
Q

What factors may affect the ability to achieve the required concentrations of antimicrobials?

A
  • Pharmacological properties where antimicrobials distribute
  • Elimination from the host (method and rate)
  • MIC/MBCs achievable depending on area and drug
  • Bacterial resistance mechanisms may increase MIC/MBC to unachievable amounts
74
Q

What is required in order for an antimicrobial to be effective?

A
  • Distribution to the right site
  • Be above MIC/MBC
  • Come into contact with the organisms
75
Q

Outline how E. coli may respond differently to antibiotic treatment depending on site of infection

A
  • If in abscess and growing anaerobically, are more resistant
  • Do not express oxidative transport systems in anaerobic conditions
  • Reduces entry of antibiotic into the bacterial cell
76
Q

Give examples of how location of pathogens may affect antibiotic efficacy

A
  • Intracellular organisms not affected by extracellular drugs
  • Milk proteins may bind to antibiotics
  • Local pH may reduce disassociation of some antibiotics and reduce distribution
  • Poor blood supply and good epithelial barriers may reduce drug access
77
Q

List factors that may restrict access of, or concentration of antimicrobials to site of infection

A
  • Abscess formation, pus
  • Foreign bodies
  • Oedema fluid
  • Factors that may bind the drug
78
Q

What are MRLs?

A

Maximum Residue Levels

79
Q

What is the significance of MRLs?

A
  • Restrictions on use of antimicrobials in food producing animals as residues may enter food
  • With-holding periods before animal or products can enter food chain
  • Differs for different drugs
80
Q

List factors that affect the MRL

A
  • Drug persistence profile
  • Drug dosing schedule
  • Route of dose (e.g. oral vs injection into tissue)
81
Q

List the classifications of antibiotics

A
  • Inhibition of protein synthesis
  • Inhibition of cell membrane function
  • Inhibition of cell wall synthesis
  • Interference with other pathways
  • Inhibition of DNA dependent RNA polymerase
  • Disruption of DNA structure
82
Q

Briefly describe the bacterial cell wall structure

A
  • Peptidoglycan unique to bacteria (good target)
  • Polymer of sugars and amino acids forming mesh-like cell wall
  • Sugars form alternating residues of beta-(1,4) linked N-acetylglucosamine N-acetylmuramic
  • N-acteylmuramic acid cross linked by peptide chains of 3-5 amino acids
  • Peptidoglycan serves structural role, counteracts osmotic pressure of cytoplasm
83
Q

What do beta lactam antibiotics target?

A

Penicillin binding protein (transpeptidase) which stops peptide cross links in cell wall

84
Q

What do peptide antibiotics target?

A

Directly interact with cell wall D-Ala-D-Ala moieties

Prevent synthesis of NAG/NAM polymers

85
Q

What do bacitracin antibiotics target?

A

Cyclic peptides that interfere with dephosphorylation of isoprenyl carriers for cell wall synthesis

86
Q

What do teixobactin antibiotics target?

A

Bind to highly conserved motif of lipid II (precursor of peptidoglycan) and lipid III (precursor of cell wall teichoic acid)
- NB, recent, not commercial yet

87
Q

List the antibiotics that come under the wall targeting group

A
  • Beta-lactams
  • Peptide antibiotics (glycopeptides, vancomycin)
  • Bacitracin
  • Teixobactin
88
Q

Compare the activity of beta-lactam antibiotics in Gram +ve and Gram -ve bacteria

A
  • Direct access to cell wall in Gram +ve bacteria

- Require porin to get to wall through outer membrane of Gram -ve bacteria

89
Q

Describe the mechanism of action of beta-lactam antibiotics

A
  • Binds to cell receptors PBP (penicillin binding protein)
  • Inhibits transpeptidation of cell wall peptidoglycan, damaging integrity of binding proteins
  • Peptide precursors accumulate
  • This triggers autolysin activity (needed to weaken bonds to allow cell growth)
  • Positive pressure on weakened cell wall leads to cell lysis
90
Q

What is the mechanism of resistance to beta-lactam antibiotics?

A

Mutation in transpeptidase (PBP) or presence of beta-lactamases that degrade beta-lactams

91
Q

What are the 2 structural forms of beta-lactams?

A

Penicillin

Cephalosporins

92
Q

Describe penicillin

A
  • Organic acids
  • Ionised in serum so spread well in ECF, poor at crossing membranes
  • 3 groups: narrow spectrum, penicillinase stable, braod spectrum
  • Low resistance in Gram +ve bacteria
  • Polar hydrophilic molecules, circulate in blood and ECF without entering cells, short half lives, large molecules, largely excreted in urine
93
Q

Name the narrow spectrum penicillins

A
  • Penicillin-G (benzylpenicillin-G)

- Penicillin-V (phenoxmethyl-penicillin)

94
Q

Name the penicillinase stable penicillins

A
  • Methicillin

- Cloaxacillin

95
Q

What are the penicillinase stable penicillins resistant to?

A

S. aureus beta-lactamase

96
Q

Name the broad spectrum penicillins

A
  • Ampicillin

- Carbenicillin

97
Q

Describe cephalospporins

A
  • Beta-lactam ring attached to 6-membered dihydrothiazine ring
  • Resistant to beta-lactamase produced by Staphylococcus
  • Used on patients hypersensitive to penicillin
  • 3rd and 4th generaition are protected
98
Q

What group of bacteria are resistant to cephalosporin?

A

Extended Spectrum Beta-lactamases

99
Q

Describe the mechanisms of action of bacitracin

A
  • Interferes with dephosphorylation of isoprenyl pyrophosphate carrier (bactophenol)
  • Bactophenol is carrier molecule that transports components of peptidoglycan cell wall across inner membrane
  • If inhibited, cannot build cell wall
100
Q

Describe the structure of bacitracin

A
  • Cyclic polypeptide based agent

- Cyclic structure with long chain attached

101
Q

Describe the spectrum of activity of bacitracin

A
  • Narrow

- Gram +ve bacteria only

102
Q

Give an example of a side effect of bacitracin

A
  • Nephrotoxicity when used systemically

- Limited to use topical and ophthalmic preparations

103
Q

Outline the use of vancomycin

A
  • Protected group under good antimicrobial stewardship

- Last line of defence in multiple resistant staphylococcal infections

104
Q

List the membrane targeting antibiotics

A
  • Polypeptides (polymyxins, Colistin)

- Cationic peptides (newer, e.g. PEptivet)

105
Q

What are the consequences of disruption of bacterial cell membrane integrity?

A
  • Leakage of essential ions
  • Removal of proton motive force
  • Damage to cytoplasmic conditions
  • Significant disruption of cell homeostasis
106
Q

Describe the structure of polymyxins

A

Cyclic peptide with long hydrophobic tail

107
Q

Describe the mechanism of action of polymyxins

A
  • Act on Gram -ve bacteria
  • Disrupt bacterial cell membrane by interacting with its phospholipids
  • Interact with LPS on Gram -ve outer membrane
108
Q

Describe the use of polymyxins

A
  • Voluntary ban of vet use

- Resistance develops by mutation of LPS, inheritable

109
Q

Describe the administration of polymyxins

A
  • Pooly absorbed from GI tract, given by injection
  • Some nephrotoxicity with systemic use
  • Well tolerated if topical
110
Q

Describe the pharmacokinetics of polymyxins

A
  • Bind moderately to plasma proteins
  • Bind extensively to muscle
  • Diffuse poorly
  • Slow excretion by glomerular filtration
111
Q

Describe the spectrum of activity of antimicrobial peptides

A
  • Broad
  • Active against clinically relevant antibiotic-resistant strains
  • Gram -ve and Gram +ve
112
Q

Describe the mechanism of action of antimicrobial peptides

A
  • Small peptides, insert into membrane and disrupt
  • Gram -ve: peptide fist interacts with LPS on outer membrane, permeabilised allowing peptide to be captured inside
  • Gram +ve: peptide attracted to techoic acid and other anionic groups found externally on peptidoglycan layer
113
Q

What facilitates the intrinsic resistance of eukaryotic cells to antimicrobial peptides?

A
  • High content of zwitterionic phospholipids and cholesterol

- These are absent in bacteria

PVS (23 decks)

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