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Clinical Pathology > 1) Core Microbiology > Flashcards

1) Core Microbiology Flashcards

1
Q

Define “Antibiotics”

A

Chemical products of microbes that inhibit or kill other organisms. Important to remember that they are not man-made

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2
Q

Define “Antimicrobial agents” (antibacterial, antifungal, antiviral)

A

1) Antibiotics
2) Synthetic compounds with a similar effect to antibiotics
3) Semi-synthetic compounds (modified from antibiotics. May have different antimicrobial activity/spectrum, pharmacological properties or toxicity

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3
Q

Define “Bacteristatic”

A

Method of antibiotic function that inhibits bacterial growth by e.g. inhibiting protein synthesis in the microbe. This causes it to die secondarily to the effect of the antibiotic, not directly

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4
Q

Define “Bactericidal”

A

Method of antibiotic function that directly kills the bacteria e.g. Cell wall-active agents

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5
Q

Define “Minimum Inhibitory Concentration (MIC)”

A

Minimum concentration of an antibiotic at which visible growth of a bacterium is inhibited. The smaller the value the more active the antibiotic substance is

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6
Q

Define “Synergism”

A

Activity of two antimicrobials given together is greater than the sum of their activity if given separately

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7
Q

What is a clinical example of synergism?

A

β-lactam/aminoglycoside combination therapy of Streptococcal Endocarditis

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8
Q

Define “Antagonism”

A

One antimicrobial agent diminishes the effect of the other

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9
Q

Define “Indifference”

A

Activity of one antimicrobial agent is unaffected by the addition of another agent

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10
Q

2 examples of antibacterial mechanisms?

A

1) Inhibition of a critical process in bacterial cells

2) Selective toxicity (target not present or significantly different in human host)

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11
Q

5 antibiotic targets?

A

1) Cell wall
2) Protein synthesis
3) DNA synthesis
4) RNA synthesis
5) Plasma membrane

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12
Q

What is the major component of bacterial cell walls?

A

Peptidoglycan

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13
Q

Why is peptidoglycan a good antibiotic target for human use?

A

Human cells don’t have a cell wall so is ideal for selective toxicity

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14
Q

2 features of peptidoglycan?

A

1) Both gram +ve and -ve

2) Made of a polymer of 2 glucose derivatives: N-acetyl muramic acid (NAM) and N-acetyl glucosamine (NAG)

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15
Q

Which 2 glucose derivatives make up peptidoglycan, the major component of bacterial cell walls?

A

1) N-acteyl muramic acid (NAM)

2) N-acetyl glucosamine (NAG)

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16
Q

4 types of cell wall synthesis inhibitors? The first 2 are the main ones

A

1) β-lactams (penicillins)
2) Glycopeptides
3) Cycloserine (anti-tuberculosis agent)
4) Fosfomycin (not available in the UK)

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17
Q

Which group of drugs were the first true antibiotics used in clinical practice?

A

β-lactams. The drug was benzylpenicillin. They have now become the more widely prescribed of the antibacterial antibiotics

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18
Q

What is common about all β-lactam antibiotics?

A

All contain a β-lactam ring. This is a 4 membered ring structure (C-C-C-N) and forms a structural analogue of D-alanyl-D-alanine

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19
Q

How do β-lactams work?

A

Interfere with the function of “penicillin binding proteins”. These are transpeptidase enzymes involved in the peptidoglycan synthesis and maintenance

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20
Q

What was the first oral penicillin?

A

Phenoxymethyl penicillin

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21
Q

What was the first penicillin used against members of the family enterobacteriaceae?

A

Ampicillin. This can only be delivered parenterally. The oral equivalent is amoxycillin

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22
Q

3 examples of penicillin type β-lactam antibiotics?

A

1) Amoxicillin (bold)
2) Benzylpenicillin
3) Flucloxacillin (staph. aureus)

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23
Q

Describe the spectrum of penicillin type β-lactam antibiotics?

A

Relatively narrow

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24
Q

2 examples of cephalosporin type β-lactam antibiotics?

A

1) Cefuroxime (bold)

2) Ceftazidime

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25
Q

Describe the spectrum of cephalosporin type β-lactam antibiotics?

A

Broad. Cover gram -ve well

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26
Q

2 examples of carbapenem type β-lactam antibiotics?

A

1) Meropenem

2) Imipenem

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27
Q

Describe the spectrum of carbapenem type β-lactam antibiotics?

A

Extremely broad. Cover both gram +ve and -ve.

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28
Q

1 example of monobactam type β-lactam antibiotics?

A

Aztreonam

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29
Q

Aztreonam is not a widely used antibiotic, but what is 1 example of when it is used?

A

Patients with a penicillin allergy

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30
Q

2 examples of glycopeptide antibiotics?

A

1) Vancomycin (bold)

2) Teicoplanin

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31
Q

How do glycopeptide antibiotics work?

A

Bind directly to terminal D-alanyl-D-alanine on NAM pentapeptides. This inhibits the binding of transpeptidases onto this area, causing peptidoglycan cross-linking to cease

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32
Q

What type of gram activity do glycopeptides have?

A

Gram +ve, so they are unable to penetrate gram -ve outer membrane porins

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33
Q

How does protein synthesis in bacteria occur? (Recap)

A

At the ribosome. 2 ribonucleoprotein complexes (50S and 30S) combine to form the 70S initiation complex. mRNA in the 30S, tRNA in the 50S etc.

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34
Q

What do Aminoglycosides, Macrolides, Lincosamides, Streptogramins (MLS), Tetracyclines and Oxazolinones all have in common?

A

They are all groups of antibiotics that inhibit protein synthesis in the bacterial cell

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35
Q

2 examples of aminoglycosides?

A

1) Gentamicin (bold)

2) Amikacin

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36
Q

How do aminoglycosides work?

A

Bind to the 30S ribosomal subunit, although this mechanism is not fully understood

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37
Q

Why do you need to be careful when administering gentamicin in patients with gram -ve sepsis?

A

It can cause AKI

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38
Q

2 examples of Macrolides, Lincosamides, Streptogramins (MLS)

A

1) Erythromycin (bold)

2) Clindamycin (bold)

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39
Q

How do Macrolides, Lincosamides, Streptogramins (MLS) type protein synthesis inhibitors work?

A

Bind to the exit tunnel of the 50S ribosomal subunit, inhibiting protein elongation

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40
Q

How does tetracycline work?

A

Binds to 30S ribosomal subunit, inhibiting RNA translation by interfering with the binding of tRNA to rRNA

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41
Q

1 example of oxazolidinone type protein synthesis inhibitors?

A

Linezolid (bold)

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42
Q

How does linezolid work?

A

Inhibits the initiation of protein synthesis by inhibiting the assembly of the initiation complex. May bind to 50S or 70S

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43
Q

What do trimethoprim (bold), sulphonamides, quinolone and fluoroquinolone all have in common?

A

They are antibiotics that act by inhibiting DNA synthesis

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44
Q

What types of DNA synthesis inhibitors work by inhibiting folate synthesis?

A

Trimethoprim and sulphonamides.

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45
Q

What is the specific enzyme involved in bacterial DNA synthesis that trimethoprim targets?

A

Dihydrofolate reductase. It is often used in the treatment of UTI’s

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46
Q

What is the specific enzyme involved in bacterial DNA synthesis that sulfonamide targets?

A

Dihydropteroate synthetase

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47
Q

What is the name given to the combination treatment of trimethoprim and sulfonamide?

A

Co-trimoxazole. It is used to treat:

1) Some protozoal infections
2) infections caused by Pneumocystis jirovecii
3) Resistant bacterial infections

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48
Q

How do quinolone and fluoroquinolones work?

A

Inhibit one of or both DNA gyrase and topoisomerase IV enzymes. These are involved in the remodelling of DNA during DNA replication

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49
Q

3 examples of quinolone and fluoroquinolones?

A

1) Nalidixic acid
2) Ciprofloxacin (bold)
3) Levofloxacin

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50
Q

What is rifampicin?

A

RNA synthesis inhibitor

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51
Q

How does rifampicin work?

A

Inhibits RNA polymerase, preventing the synthesis of mRNA

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52
Q

What is rifampicin used for?

A

Antituberculosis therapy. Staph. aureus is resistant to this so it is only ever used in combination with another antibiotic

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53
Q

2 examples of plasma membrane antibiotic agents?

A

1) Colistin

2) Daptomycin

54
Q

Either colistin or daptomycin work against gram +ves, and the other against gram -ves. Which is which?

A 
Colistin = gram -ves
Daptomycin = gram +ves
55
Q

When is colistin used?

A

As a last resort antibiotic when the bacteria is resistant to everything else. Some cases of collision resistant bacteria have been found in China though. Oh dear

56
Q

Name some adverse effects that people experience to all drugs

A 
Nausea
Vomiting
Headache
Skin rashes
(Acute) Infusion reactions
Allergic reastions
57
Q

Name 3 adverse effects of antibiotic use

A

1) Generation of antibiotic resistance
2) Fungal infection from superficial and invasive candidiasis
3) Clostridium difficile infection

58
Q

What adverse effects do people experience from ahminoglycosides?

A

1) Reversible renal impairment on accumulation

2) Irreversible ototoxicity

59
Q

What is the main problem people experience from β-lactams?

A

Allergic reactions. 1-10% of people get some kind of generalised rash, while around 0.01% experience anaphylaxis

60
Q

What is the main adverse reaction people have to linezolid?

A

Bone marrow depression

61
Q

What is safe to use in patients with a non severe penicillin allergy?

A

Cephalosporins and carbapenems

62
Q

What is safe to use in patients with any penicillin allergy?

A

Aztreonam

63
Q

What clinical features of C. difficile infection account for it transmissibility?

A

Enterotoxin and spore production

64
Q

What strain of C. difficile infection causes more severe disease?

A

Hypervirulent strain 027

65
Q

What 4 C’s describe common precipitating antibiotics used to treat C. difficile infection?

A

1) Co-amoxiclav (amoxicilin-clavulanate)
2) Cephalosporins
3) Ciprofloxacin
4) Clindamycin

66
Q

What is the general strategy behind antibiotic use?

A

As the level of knowledge of infecting organism(s) increases, the antimicrobial spectrum of agent(s) used should decrease

67
Q

After starting a patient on an antibiotic, how long should they be left before reviewing this antibiotic?

A

48 hours. At this stage they should be stopped if there is no evidence of infection, switched from IV to oral, changed based on need of spectrum or just continued.

68
Q

What is flucloxacillin used to treat?

A

Staphylococcus aureus (not MRSA) infection

69
Q

What is benzylpenicillin used to treat?

A

Streptococcus pyogenes infection

70
Q

What are cephalosporins used to treat?

A

Gram-negative bacilli infection

71
Q

What group should cephalosporins be avoided by?

A

Elderly patients

72
Q

What type of organism is metronidazole used to remove?

A

Anaerobes

73
Q

What is vancomycin used to treat?

A

Gram positive infection, including MRSA

74
Q

What antibiotic is used to treat most bacteria?

A

Meropenem

75
Q

3 reasons why antibiotics are combined?

A

1) Increase efficacy
2) Provide adequately broad spectrum e.g. polymicrobial infection or empiric treatment of sepsis
3) Reduce resistance

76
Q

Define “Antibiotic era”

A

Term used to describe the time since the widespread availability of antibiotics to treat infection

77
Q

Define “Post-antibiotic era”

A

Term used to describe the time after widespread antibiotic resistance has reduced the availability of antibiotics to treat infection

78
Q

What is the clinical problem relating to using antibiotics clinically?

A

Organisms become resistant to antibiotics traditionally used to treat them over time

79
Q

6 cases of antibiotic resistance?

A

1) Meticillin-resistant staphylococcus aureus (MRSA)
2) Vancomycin/glycopeptide-resistant enterococci (VRE/GRE)
3) Extended-spectrum β-lactamase-producing enterobacteriaceae (ESBL)
4) NDM-1 producing Gram-negative bacilli
5) Multi-drug resistant tuburculosis (MDR-TB)
6) Extremely-drug resistant tuberculosis (XDR-TB)

80
Q

What does empiric treatment of infection mean?

A

Based on experience. A clinically educated guess due to the absence of perfect information

81
Q

What does targeted treatment of infection mean?

A

Based on evidence. Tests have been performed and the organism causing the infection has been discovered so specific antibiotics are used to treat it

82
Q

How does antibiotic resistance affect empiric therapy of infection?

A

1) Risk of under-treatment

2) Risk of excessively broad-spectrum treatment

83
Q

How does antibiotic resistance affect targeted treatment of infection?

A

Requires alternative which may be:

1) Expensive
2) Last line
3) Toxic

84
Q

4 reasons for sensitivity testing?

A

1) Enable transition from empiric to targeted therapy
2) Explain treatment failures
3) Provide alternatives for antibiotics that have tried an failed
4) Provide alternative oral antibiotics when IV is no longer required

85
Q

Describe the basic principle of sensitivity testing?

A
  • Culture the micro-organism in the presence of several antimicrobial agents
  • Determine whether MIC is above the breakpoint level (basically high enough to kill organism) for each antibiotic by measuring the radius of the “zone of inhibition”
86
Q

3 limitations of sensitivity testing?

A

1) Infection may not have been caused by the organism that has been tested
2) Correlation between antimicrobial sensitivity and clinical response is not absolute, only more likely to respond to antimicrobial with larger zone of of inhibition
3) Certain organisms are “clinically resistant” to antimicrobial agents

87
Q

As a general rule, antibiotic + target = cell death. 6 basic principle to do with this that bacteria exploits to become resistant to antibiotics?

A

1) No target = no effect
2) Reduced permeability = antibiotic can’t get in
3) Altered target = no effect
4) Over expression of the target = effect diluted
5) Enzymatic degradation = antibiotic destroyed
6) Efflux pump = antibiotic expelled from cell

88
Q

Common clinical example of absent target causing antibiotics not to work?

A

Treatment failure may be because the infection is non-bacterial e.g. fungal or viral

89
Q

2 examples of reduced permeability aiding antibiotic resistance?

A

1) Gram -ve bacteria have an outer membrane that is impermeable to vancomycin
2) Uptake of gentamicin requires and oxygen dependent active transport mechanism so cannot occur in anaerobes

90
Q

2 examples of target alteration to bring about antibiotic resistance?

A

1) MRSA has an altered PBP2 protein that does not bind β-lactams e.g. flucloxacillin
2) Altered peptide sequence in Gram-positive peptidoglycan (D-ala D-ala –> D-ala D-lac) reduces the binding of vancomycin (VRE) by 1000x

91
Q

3 examples of antibiotic-modifying enzymes made by bacterial cells that degrade antibiotic chemicals?

A

1) β-lactamases break down penicillins and cephalosporins
2) Aminoglycoside modifying enzymes break down gentamicin
3) Chloramphenicol acetyltransferase breaks down chloramphenicol

92
Q

1 example of drug efflux as a method of producing antimicrobial resistance?

A

Antifungal triazoles are removed from candida spp. cells

93
Q

What are many resistance mechanisms encoded by?

A

Single genes

94
Q

What are resistance genes encoded in?

A

Plasmids

95
Q

Can resistance genes be transmitted within a species?

A

Yes, and also between different bacterial species by bacterial conjugation. This speeds up resistance as one species may produce a resistance gene and then pass it onto a different species

96
Q

Name 2 things that enable horizontal transfer of resistance?

A

Transposons and integrons

97
Q

What is horizontal transfer of resistance?

A

DNA sequences designed to be transferred from plasmid to plasmid or plasmid to chromosome

98
Q

What is vertical transfer of resistance?

A

Chromosomal or plasmid-borne resistance is transferred to daughter cells on bacterial cell division

99
Q

Describe the pathway of how antibiotic exposure leads to antibiotic resistance?

A
  • Sensitive strains exposed to antibiotics at sub-lethal concentrations
  • Chance of survival will be enhanced by development of resistance
  • Resistant strain will out-compere sensitive strains
  • Resistance passed on by vertical transfer
  • Mixture of sensitive and resistant strains exposed to antibiotic
100
Q

4 ways to avoid problems with antibiotics?

A

1) Never use an antibiotic unless absolutely necessary
2) Always use the most “narrow-spectrum” agent available
3) Use combination therapy if indicated
4) Be willing to consult expert information sources

101
Q

What part of the globe has by far the most new cases of HIV per year?

A

Sub-Saharan Africa: 2.3 million total new cases in 2012, 1.6 million of these were here

102
Q

What are the 3 groups of pathogenesis of virus infections?

A

1) Acute infection
2) Chronic latent infection
3) Chronic persistent infection

103
Q

What is the most common pathogenesis of virus infection?

A

Acute infection

104
Q

What is a key distinguishing factor between the physical makeup of acute infections vs. chronic infections?

A

Viruses containing RNA tend to cause acute infection, whereas those made up of DNA tend to cause chronic infection. The exception to this rule if HIV, which acts using RNA reverse transcriptase so contains RNA

105
Q

4 examples of acute virus infections?

A

1) Influenza
2) Measles
3) Mumps
4) Hepatitis A

106
Q

2 examples of chronic latent virus infections?

A

1) Herpes simplex

2) Cytomegalovirus

107
Q

3 examples of chronic persistent virus infections?

A

1) HIV
2) Hepatitis B
3) Hepatitis C

108
Q

How do chronic latent infections present clinically?

A

In most of the population they don’t. However in some people they occasionally get flare ups of symptoms rather than always presenting symptoms.

109
Q

3 things that make up a virus?

A

1) Nucleic acid (either DNA or RNA)
2) Protein (structural coat and non-structural enzymes)
3) Lipid envelope (not present in all)

110
Q

In what part of the body would viruses not tend to have a lipid envelope and why?

A

GI tract. Acidic conditions would rupture the envelope, damaging the virus

111
Q

Describe how viruses enter a host cell an replicate?

A
  • Attaches to the cell via a receptor
  • Enters cell
  • Virus is uncoated
  • Early proteins e.g. viral enzymes are produced
  • These are then replicated
  • Late proteins e.g. viral structural proteins are assembled
  • Virus is assembled
  • Virus is released
112
Q

What part of the virus life cycle can be targeted for anti-viral activity?

A

Viral enzymes. These are vital for virus replication but are unique to viruses

113
Q

Where are DNA –> DNA polymerases often found?

A

Eukaryotes and DNA viruses

114
Q

Where are DNA –> RNA polymerases often found?

A

Eukaryotes and DNA viruses

115
Q

Where are RNA –> RNA polymerases often found?

A

RNA viruses

116
Q

Where are RNA –> DNA polymerases often found?

A

Retroviruses e.g. HIV and Hepatits B virus

117
Q

(Recap) What is the basic structure of a mono-nucleotide?

A

Base, ribose sugar and a phosphate group

118
Q

What does NRTI stand for?

A

Nucleoside Reverse Transcriptase Inhibitor

119
Q

What was one of the first NRTI’s?

A

AZT (azidothymidine)

120
Q

What was azidothymidine first used for and why is it no longer used for this?

A

Developed originally as an anti-cancer drug. However it was found to be toxic against healthy cells as well

121
Q

What are the major differences between the different NRTI’s?

A

The differences in base analogues. Either made from purines (adenine and guanidine) or pyrimidines (cytosine and thymidine)

122
Q

1 example of a thymidine analogue NRTI’s?

A

Zidovudine

123
Q

1 example of a cytosine analogue NRTI’s?

A

Lamivudine

124
Q

2 examples of purine analogue (i.e. adenine and guanidine) NRTI’s?

A

1) Abacavir

2) Tenofovir

125
Q

What NRTI’s can be used to treat Hepatitis B virus as well as HIV and should be used in regime in the case of dual infection?

A

Lamividine and Tenofovir

126
Q

2 examples of NNRTI’s (Non-Nucleotide Revere Transcriptase Inhibitors)?

A

1) Efavirenz

2) Nevirpine

127
Q

7 examples of protease inhibitors?

A

1) Atazanavir
2) Darunavir
3) Fospamprenavir
4) Lopinavir
5) Nelfinavir
6) Ritonavir*
7) Saquinavir

128
Q

How can you recognise a protease inhibitor by its name?

A

All of them seem to end in “-navir”

129
Q

What are 3 groups of newer drugs used in the treatment of HIV?

A

1) Fusion inhibitors - prevent the binding of the virus to the cell
2) Intergrase inhibitors - block the integration of the HIV virus into the CD4 of the host cell
3) Chemokine receptor antagonists

130
Q

1 example of a fusion inhibitor used to treat HIV?

A

Enfuviritide

131
Q

1 example of an integrase inhibitor used to treat HIV?

A

Raltegravir

132
Q

1 example of a chemokine receptor antagonist used to treat HIV?

A

Maraviroc

Clinical Pathology (13 decks)

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