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CP - JL > Core Microbiology - Part 1 > Flashcards

Core Microbiology - Part 1 Flashcards

1
Q

What do bacteriostatic antibiotics do

A

inhibit bacterial growth e.g. protein synthesis inhibitors

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2
Q

What is MIC

A

The minimum concentration of an antibiotic at which VISIBLE growth is inhibited

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3
Q

What is synergism?

A

Activity of two microbial together is greater than seperately e.g. B lactams/aminoglycosides for streptococcal endocarditis

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4
Q

What is selective toxicity?

A

choosing targets that are not present or are significantly different to the human host

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5
Q

Antibiotic targets

A

Call wall, DNA synthesis, RNA synthesis, plasma membrane, protein synthesis

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6
Q

Major component of cell wall

A

Peptidoglycan

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7
Q

Peptidoglycan structure

A

NAM cross linked by NAG

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8
Q

Why is the cell wall a good antibiotic target?

A

Not present in humans

Constantly remodelled

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9
Q

What are the 2 cell wall synthesis inhibitor groups

A

B-lactams

Glycopeptides

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10
Q

What are the B-Lactam antibitoics

A

Contain the B-lactam ring (C-C-C-N)

Target cell wall synthesis

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11
Q

What is the B-lactam ring a structural analogue of?

A

The D-alanyl D-alanine residue that hang of N

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12
Q

How do B-lactam antibitoics word

A

Interferes with function of penicillin binding proteins as trans peptidase enzymes are involved in the cross linking of peptidoglycan

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13
Q

4 group of beta lactam antibiotics

A

Penicillins - narrow
Carbapenems - broad
Cephalosporins - v broad
Monobactams - gram -ve activity only

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14
Q

What are glycopeptides

A

Large molecules that bind directly to terminal D-alanylD-alanine on NAM
Inhibit transpeptidases and peptidoglycan crosslinking
They inhibit cell wall synthesis

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15
Q

What do glycopeptides act on

A

gram +ve activity only as unable to penetrate the second outer layer in gram -ve bacteria

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16
Q

What ribosomes are used in bacteria protein synthesis

A

70S (have 50S and 30S subunits)

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17
Q

Name the groups of protein synthesis inhibitors

A 
Aminoglycosides
Macrolides, Lincosamids, Streptogramins (MLS)
Tetracyclines
Oxazolidunones
Mupirocin and Fusidic Acid
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18
Q

How do aminoglycosides work

A

bind to 30S subunit

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19
Q

How do MLS work

A

bind to 50S subunit –> blocks exit tunnel of ribosome preventing protein elongations

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20
Q

How do Tetracylines work

A

Bind to 30S sub unit

Interferes with tRNA and rRNA binding hence prevents RNA translation

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21
Q

How to oxazolidinone work

A

Bind to 50S subunit –> inhibit assembly of the initiation complex!

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22
Q

Name the DNA Synthesis INhibitors

A

Trimethoprim and Sulphonamides

Quinolone and fluoroquinlones

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23
Q

What is folate acid a precursor to

A

Purine synthesis

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24
Q

How does trimethoprim work

A

Dihydrofolate reductase inhibior

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25
Q

How does sulphonamides work

A

Dihydropteroate synthetase inhbitor

But toxicity and resistance

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26
Q

What do fluorquinolones and quinolones act via

A

DNA gyrase andn topoisomerase IV

These are involved in the remodelling of the DNA

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27
Q

How do RNA synthesis inhibitors work?

A

RNA polymerase inhibitor –> Prevent the synthesis of mRNA

Rifampicin

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28
Q

Name the 2 plasma membrane agents

A

Collision (gram -Ve activity only) - fairly toxic

Daptomycin (Gram +ve activity only)

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29
Q

How does daptomycin work

A

Cyclic lipo-peptides

Lipphilic tail enters the cell membrane

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30
Q

Main adverse effects of aminoglycosides

A

Reversible renal impairment
Irreversible Ototoxicity
TDM indicated

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31
Q

Main adverse affects ofo B-lactams

A

Allergic reactions

Steven Johnson syndrome is a severe skin reaction

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32
Q

Main adverse effects of Linezolid

A

Bone marrow depression

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33
Q

What is safe to use with a mild penicillin allergy

A

Cephalosporins and carbapenems

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34
Q

What is safe to use with any penicillin allergy

A

Aztreonam but be careful if allergic to ceftazidime due to similar side chains

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35
Q

What is the % of C.diff in normal flora

A

20%

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36
Q

What are the four common precipitating factors before C.Diff

A

Co-amoxiclav
Cephalosprins
Ciprofloxacin
Clindamycin

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37
Q

What do we use to treat CSF infections

A

Beta lactase –> good availability in the presence of inflammation
Amino glycosides and vancomycin have poor availability

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38
Q

What do we use to treat Urine infections

A

Trimmethoprim and beta lactams have good availabiility

MLS have poor availability

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39
Q

What does concentration dependent mean

A

Determinant of bacterial killing is the factor by which the concentration exceeds the MIC

Inhibit intermittently to achieve high peaks

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40
Q

What does time dependent mean

A

Main determinant of killing is the amount of time the antibiotic concentration exceeds the MIC

Administer frequently to maintain high levels

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41
Q

Why use combination therapy?

A

Increases efficacy
Provide broad spectrum
Reduce resistance

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42
Q

What is the post antibiotic era1

A

the term used to describe the time after widespread antibiotic resistance

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43
Q

What is RMSA resistant to

A

Penicillin

Penicillinase conveys the resistance

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44
Q

What is CPE

A

Carbapenemase producing eneterbactericaea

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45
Q

What are enterebacteriaceae resistant to

A

amoxicillin, ciprofloxacin, gentamicin, carbapenems

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46
Q

what are ESBL

A

Extended spectrum beta lactamase producing enterebactericaeae

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47
Q

What is sensitivity testing used for

A

Allows for the transition from empiric to targeted antibiotics
Basic principle to measure zone of inhibition of antibiotic

Liquid media provides more accurate measure of MIC

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48
Q

What do we have determine about the MIC in sensitivity testing

A

If the MIC is above a predetermined breakpoint level i.e. high enough to kill the organism and sustained in the body for long enough using practicable dosing regimes

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49
Q

Limitation of sensitivity testing

A

Correlation between antimicrobial sensitivity and clinical response is not absolute

Certain organisms are clinically resistant despite being effective invitro

50
Q

What resistance gene is expressed in vivo in response to beta lactam antibitoics in eneterbactericaea infections

A

Amp-C Beta lactamase gene in enterobactericaea

51
Q

Resistance mechanisms

A 
No target
Reduced permeability
Altered target
Over expression of target
Enzyme degradation of antibiotic
Efflux pump to expel the drug
52
Q

What infection do we suspect after surgery if still not getting better despite broad spectrum antibiotics

A

Candida

53
Q

What is vancomycin impermeable to?

A

The outer layer on gram -ve bacteria

54
Q

What is the uptake of aminoglycosides dependent on?

A

An oxygen dependent active transport (hence doesn’t work on anaerobes)

55
Q

Why is MRSA resistant to penicillin

A

Altered penicillin binding protein (encoded for by the MecA gene)

56
Q

Why is VRE resistant to vancomycin

A

Altered peptide sequence in gram +ve bacteria
D-ala D-ala to D-ala D-lac
Reduces vancomycin binding 1000 fold

57
Q

What degrades pencillins and cephalosporins

A

B-lactamases (produced by ESBLs and NDM-1)

58
Q

How do efflux pumps convert resistance?

A

Drug expelled before antibiotic can interact with the target

Occurs with multiple antibiotics especially in gram -ves

59
Q

What are resistance genes coded in

A

Plasmids

60
Q

What enables the horizontal transfer of resistance

A

Transposons and intergrons

61
Q

How to avoid problems with antibiotics

A

Only use when necessary
Use most narrow spectrum available
Use combination therapy if indicated
be willing to consult books and expert sources for information

62
Q

Acute viral infections

A

mumps, hep A, influenza, measles

63
Q

Acute viral infections have what type of genetic material

A

DNA

64
Q

Chronic viral infections have what type of genetic material

A

RNA

65
Q

Chronic latent viral infections

A

HSV, cytomegalovirus

66
Q

Chronic persistent viral infections

A

HIV, Hep B, Hep C

67
Q

Structure of cirus

A

Nucleic Acid
Protein Coat
With or without envelope
They are obligate intracellular parasties

68
Q

What are LTR

A

Long terminal repeats essential for incorporating virus into the genome

69
Q

Virus replication

A

Attachment, cell entry, uncaring, early proteins produced and viral enzymes, replication, late transcription/translation produces structural enzymes, virus assembly, virus release

70
Q

Polymerases in eukrayotes and DNA viruses

A

DNA to DNA

DNA to RNa

71
Q

polymerases in RNA viruses

A

RNA to RNA

72
Q

Polymerases in retroviruses

A

RNA to DNA

73
Q

What is Azidothymidine (AZT)

A

Anti-cancer drug also inhibits HIV replication

NRTI - inhibits reverse transcriptase

74
Q

2 types of NRTIS

A 
Pyrimidine analogus (zidoviduine and lamivudine)
Purine analogues (abacavir and tenofovir)
75
Q

Why ae NRTIs also effective against HBV

A

as it also contains the reverse transcriptase enzymes

76
Q

What are protease inhibitors

A

Act as aspartate protease inhibitor in HIV

77
Q

What does ritonavir do?

A

Helps boost the level of other protease inhibitors

78
Q

Newer HIV drugs

A

Fusion inhibitors –> stop viruses fusing with membrane (enfuvritide)
Chemokine receptor agonists (prevent HIV entering the cell) e.g. Maraviroc (CCR-5)

79
Q

What is HAART

A

Highly active retroviral treatment

80
Q

What does HAART consist of

A

2 NRTI’s and 1 NNRTI or Protease inhibitor

81
Q

When do we give HAART

A

When CD4 count start to fall and taken life long

But problems with liver toxicity

82
Q

What mutation results in lamivudine resistance

A

M184V mutation

83
Q

What can cure people with HIV

A

CCR5 delta 32 allelle!

84
Q

Treatment of Hep C

A

Interferons and ribvirin

85
Q

2 type of fungi

A

Moulds/filamentous or yeast

86
Q

How do moulds/filmentous divide

A

By spores - have hairy micellium

87
Q

How do yeasts divide

A

by budding - produce buttery colonies

88
Q

What type of fungi cause disease in humans

A

only micro

89
Q

Cryptococcus and candida are what type of fungi

A

yeast

90
Q

athletes foot is what type of fungi

A

filamentous

91
Q

Where is ergosterol found

A

fungal cell membranes

92
Q

what does ergosterol do?

A

Regulates membrane permeability –> required for normal growth and function of cells

93
Q

What are B-1,3, glucans

A

Large polymers of UDP glucose not in human cells

Forms fibrous netweorks on the inner surface of cell walls

94
Q

What synthesizes B-1,3 glucans

A

B-1,3,-glucan synthase

95
Q

What are the 4 anti fungal classes

A

Polyenes
Allyamines
Azoles
Echinocandins

96
Q

How do polyenes work

A

Associate with ergosterol – > form pore-like aggregates in cell membrane
Loss of membrane integrity and leakage of potassium causing cell death

97
Q

Range of amphotericin B

A

Most fungi of medical importance

98
Q

Problems of amphotericin B

A

Allergic reactions and nephrotoxicity! hence made lipid associated amphotericin B to reduce nephotoxicity!

99
Q

Amphotericin B administration

A

Paraenterally

100
Q

Nyastin Use

A

Superifical infections –> oral/vanginal candidiasis as too toxic for systemic use

101
Q

How do allyamines work

A

Inhibit squalene epoxidase preventing ergosterol synthesis

102
Q

Allyamines adverse effects

A

Liver toxicity they are broad spectrum though

103
Q

Allyamines use

A

Dermatophyte infections –> topical or systemic for tinea captious and onychomycosis

104
Q

How do azoles work

A

Lanesterole demethylase inhibitos

105
Q

Types of azoles

A

Imidazole - 2 nitrogen atoms, toxic so rarely used

Triazoles - 3 nitrogen atoms, less toxic

106
Q

Activity of azoles

A

Essestially broad for fungi

107
Q

What does fluconazole now have activity against

A

aspergillus

108
Q

Adverse affects of azoles

A

Hepatotoxicity

Drug interaction –> inhibits cytochrome P450 enzymes

109
Q

Use of imidazoles

A

Superficial infections and candidiases

110
Q

Triazole uses

A

Systemic infections
Aspergilliosis
Candidiasis (fluconazole)

111
Q

How do echinocandins work

A

B-1,3, glucan synthase inhibitos cause abnromal cell wall

112
Q

What do echinocandins work on

A

Aspergillum and candida BUT misses mouulds and cryptooccus

Has minimal side effects

113
Q

Use of echinocandins

A

Systemic infections

114
Q

What is 5-fluorocytosine

A

A synthetic analogue of cytosine

115
Q

How does 5-flurocytosine enter fungal cells

A

Using cytosine premise enzyme

116
Q

How foes 5-fluorocytosine work

A

Converted to 5-fluorouracil and 5-fluorodeoxyuridine monophosphate

Inhibits RNA/protein syntehss and DNA synthesis

117
Q

5-fluorocytosine spectrum of activity

A

Candida and cryptococcus

118
Q

Adverse effects of 5-fluorocytosine

A

Bone marrow suppression –> 5-fluorouracil is an anticancer drug

119
Q

Treatment of cryptoccus

A

Amphotericin B and 5-flurorcytosine

120
Q

How does griseofulvin work

A

Inhibits fungal mitosis

Treats dermatophytes with mental adverse effects

121
Q

Use of griseofulvin

A

Treats dermatophyte infections in children that require systemic treatment

122
Q

What drugs require TDM

A

Itraconazole
5-fluorocytosine
Voriconazole

CP - JL (14 decks)

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