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Medicine Phase 2a > Microbiology 4 - Antibiotics, Inflammation and other > Flashcards

Microbiology 4 - Antibiotics, Inflammation and other Flashcards

1
Q

Regarding antimicrobial resistance, which is true?

a) it is spread by plasmid mediate gene transfer
b) spontaneous gene mutations do not occur
c) MRSA refers to vancomycin resistant S. aureus
d) Only Mereopenem is effective against all gram negative bacteria

A

c) MRSA refers to vancomycin resistant S. aureus

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2
Q

*Antimicrobials. Which pairing is incorrect?
S. pyogenes : can use penicillin
Meropenem : a carbapenem
Glycopeptides : use for MRSA
Co-amoxiclav : contains a Beta-lactamase inhibitor
Cefuroxime : a macrolide

A

Cefuroxime : a macrolide

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3
Q

A 21 year old complains of myalgia, sore throat and tiredness. He is febrile and has an enlarged spleen. Which is the best answer?

a) He has sepsis and needs broad spectrum antimicrobial therapy with cefotaxime
b) A charcoal throat swab will confirm the diagnosis
c) Finding atypical lymphocytes on a blood film and a positive EBV IgM in serum would be consistent
d) PCR on a viral throat swab will confirm the diagnosis
e) This is a viral upper respiratory tract infection and doesn’t warrant investigation or antimicrobial therapy

A

c) Finding atypical lymphocytes on a blood film and a positive EBV IgM in serum would be consistent

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4
Q 
Which of these does NOT feature in the definition of Sepsis?
Temperature >38.3oC or <36oC
Heart rate >90
Systolic blood pressure >130
White Cell count >12
Hypoxia
A

Systolic blood pressure >130

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5
Q

Describe features of sepsis

A

Temperature >38.3oC or <36oC
Heart rate >90
White Cell count >12
Hypoxia

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6
Q 
Infection control: which is False? The five steps of hand hygiene are to wash hands:
Before contact with patient
Before bodily fluid exposure
Before aseptic procedures
After contact with patient surroundings
After patient contact
A

Before bodily fluid exposure

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7
Q

What is the single most effective method of preventing cross infection?

A

Hand hygiene

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8
Q

What are the broadest spectrum beta-lactam antibiotics available?

A

Carbapenems

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9
Q

What are CPEs

A

Coliforms - standard gut germs

Carbapenemase Producing Enterobacteriaceae

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10
Q

Give examples of CPEs

A

E.coli
Klebsiella
Serratia
Enterobacter

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11
Q

Where do CPEs colonise?

A

Large bowel
Skin below waist
Moist sites

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12
Q

CPEs are the most common cause of what infections?

A

UTI

Intra-abdominal infections

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13
Q

What are infections less commonly caused by CPEs?

A

Respiratory tract infection

Skin and soft tissue infection

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14
Q

True or false:
In the past, the vast majority of these germs were susceptible to the antibiotics that we currently use with gram positive infection

A

False

is all true except its gram negative infection

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15
Q

What are Carbapenems?

A

(type of) Broad spectrum Beta-Lactams

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16
Q

What can Carbapenems be used for?

A

(moved from being rarely used last resort antibiotics to) Frequently used second-line agents and even first-line therapy for patients with severe sepsis as resistance of gram NEGATIVES or agents like cephalosporins and piperacillin-tazobactam

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17
Q

What is a HCAI

A

Health care associated infection

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18
Q

How many HCAIs are there in England per year

A

300,000

Estimated deaths per yr:
Primarily attributable - 5,000 (1% of all deaths)
Substantial contribution - 15000 (3% of all deaths)

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19
Q

What is the yearly cost to the NHS of HCAI

A

£1 bil

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20
Q

What law states infection control?

A

Health Act 2006

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21
Q

Define infect(ion)

A

affect a person, organism etc with a disease-causing organism

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22
Q

What are routes of transmission of infections in hospital and what can be done to stop transmission via these routes?

A

Environment – Design, Cleaning, Isolation
Patient – Isolation, antimicrobial stewardship
Staff – barrier precautions, isolation, hand-washing

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23
Q

What are 3 classes of Carbapenemase

A

Class A serine beta-lactamases
Class B metallo-beta-lactamases
Class D

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24
Q

Give example of Class A, B and D Carbapenemase

A

A - KPC
B - NDM-1, IMP or VIM
D - OXA variants

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25
Q

True or False:

Most strains are not susceptible to flucloxacillin (and other beta-lactams e.g. cephalosporins, carbapenems, meticillin)

A

False

Most strains are susceptible to flucloxacillin (and other beta-lactams e.g. cephalosporins, carbapenems, meticillin)

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26
Q

True or False:
Protective Equipment must be worn by all staff, whatever their role or grade, when there is a risk of contamination to the person or their clothing
Eg Gloves, Aprons etc

A

True

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27
Q

What is endogenous infection?

A

Infection of a patient by there own flora

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28
Q

How can you reduce endogenous infection risk?

A

Good nutrition and hydration
Antisepsis/skin prep where indicated
Control underlying disease (drain pus)
Remove lines and catheters as soon as clinically possible
Reduce antibiotic pressure as much as clinically possible e.g. short courses, narrow spectrum

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29
Q

Define antimicrobial

A

Agents produced by micro-organisms that kill or inhibit the growth of other micro-organisms in high-dilution

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30
Q

What was the first antibiotic?

A

Penicillin

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31
Q

Define antibiotic

A

Molecules that work by binding to a target site on bacteria that affect biochemical reaction(s) crucial to survival of bacteria

(Crucial binding site varies between antimicrobial class)

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32
Q

Give examples of 4 antibiotics

A 
Beta Lactam Glycopeptides
Metronidazole
Rifampicin
Fluroquinolones
Sulphonamides
Trimethoprim
Aminoglycosides, Tetracyclines, Macrolides &amp; Chloramphenicol
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33
Q

*Give examples of Beta Lactam Glycopeptides

A

Penicillins

Cephalosporins

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34
Q

*How do Beta Lactam Glycopeptides (e.g. penicilllins and cephalosporins) work?

A

These bind to bacterial cell wall and result in the inhibition of cell wall synthesis e.g. penicillin binding proteins on bacteria surface

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35
Q

Which antibiotics interfere with nucleic acid synthesis or function

A

Metronidazole

Rifampicin

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36
Q

How do Fluroquinolones affect bacteria

A

Inhibit DNA gyrase

essential for bacterial DNA replication

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37
Q

What types of antibiotics inhibit ribosomal activity and protein synthesis?

A

Aminoglycosides
Tetracyclines
Macrolides
Chloramphenicol

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38
Q

How do Sulphonamides affect bacteria?

A

Inhibit folate synthesis - required for bacteria to grow since folic acid cannot cross bacteria cell wall

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39
Q

How does inhibited folate synthesis affect bacteria

A

Folate required for bacteria to grow since folic acid cannot cross bacterial cell wall

40
Q

What other antibiotic inhibits folate synthesis of bacteria, other than Sulphonamides

A

Trimethoprim

41
Q

State 2 categories of antibiotics

A

Bacteriostatic

Bactericidal

42
Q

What is meant by an antibiotic being Bacteriostatic

A

Prevents growth of bacteria but does not necessarily kill it.
e.g. they inhibit protein synthesis, DNA replication or metabolism
(Kill >90% in 18-24 hours)

43
Q

What is meant by an antibiotic being Bactericidal

A

These agents kill the bacteria.
Generally this is done by inhibiting cell wall synthesis
(Kill >99% in 18-24 hours)

44
Q

Where would a bactericidal antibiotic be useful?

A

If there is poor penetration

e.g. endocarditis or difficult to treat infections or need to eradicate infection quickly e.g. meningitis

45
Q

Give example of bactericidal antibiotic

A

Beta Lactams

46
Q

*What is a Beta Lactam

A

Class of broad-spectrum antibiotics, consisting of all antibiotic agents that contain a beta-lactam ring in their molecular structures. This includes penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems.

47
Q

Give examples of Beta Lactams

A

amoxicillin
ampicillin
piperacillin
ticarcillin

48
Q

What is MIC

A

Minimal Inhibitory Concentration
(useful but may not always be best)
(for antibiotic dosage)

49
Q

What 2 major determinants of the antibacterial effects

A

Concentration and Time

The drug must not only attach to its binding target but also must occupy an adequate number of binding sites, which is related to its concentration within the microorganism.

To work effectively, the antimicrobial should remain at the binding site for a sufficient period of time in order for the metabolic processes of the bacteria to be sufficiently inhibited.

50
Q

What is concentration dependent killing

A

Important: How high the concentration is above the MIC (‘Knockout punch’)

51
Q

Give examples of drugs that use concentration dependent killing mechanism

A

Aminoglycosides

Quinolones

52
Q

What is time dependent killing

A

Sustained killing

Key parameter is time that serum concentrations remain above the MIC during the dosing interval.

53
Q

Give examples of drugs that use time dependent killing mechanism

A

Beta-lactams
Clindamycin
Macrolides
Oxazolidinones (linezolid)

54
Q

Give examples of Macrolides

A

Erythromycin

Diathromycin

55
Q

The antimicrobial/antibiotic must reach and stay at the site of bacterial infection. Is this affects by Pharmaco-Kinetics or Dynamics?

A

Pharmacokinetics

56
Q

What are pharmacokinetics of a drug?

A

Movement of a drug from its administration site to the place of its pharmacologic activity and its elimination from the body:

  • Release from the dosage form
  • Absorption from the site of administration into the bloodstream
  • Distribution to various parts of the body, including the site of action
  • Rate of elimination from the body via metabolism (liver) or excretion (kidney) of unchanged drug
57
Q

What needs to be considered when administering antibiotics to patient, regarding the site of infection?

A

Which antibiotics will penetrate that site?
What is the pH of the site?
Is the antibiotics lipid soluble?

58
Q

What needs to be considered when administering antibiotics to patient, regarding what antibiotics are safe for the patient?

A 
Intolerance, allergy and anaphylaxis 
Side effects
Age
Renal &amp; liver function
Pregnancy and breast feeding
Drug interactions
Risk of CLOSTRIDIUM DIFFICILE
59
Q

What is Clostridium Difficile?

A

Antibiotic induced diarrhoea

60
Q

Name antibiotics that can result in Clostridium difficile

A 
In general ANY antibiotic that begins with the letter C can result in clostridium difficile:
• Ciprofloxacin
• Clindamycin
• Cephalosporins
• Co-amoxiclav (augmentin)
• Carbapanems e.g. meropenem
61
Q

True or False:

Flucloxacillin can be used to treat Staphylococcus Aureus

A

True

62
Q

How do bacteria resist antibiotics?

A

Target site mutation
Destruction/Inactivation of antibiotic
Prevention of antibiotic entry
Remove antibiotic from bacterium

63
Q

Give example of Target Site Mutation causing bacteria to be resistant to antibiotic

A
  • Flucloxacillin (or methicillin) is no longer able to bind penicillin binding protein of Staphylococci in MRSA
  • Wall components change in enterococci and reduce vancomycin binding - vancomycin-resistant enterococci
64
Q

Give example of Destruction/Inactivation of antibiotic causing bacteria to be resistant to antibiotic

A
  • Beta lactam ring of penicillins and cephalosporins can be hydrolysed by bacterial enzyme ‘beta lactamase’ meaning they are unable to bind to penicillin binding proteins and inhibit cell wall synthesis
  • Staphylococci produce penicillinase so penicillin (but not flucloxacillin) is inactivated
65
Q

Give example of ‘Prevention of antibiotic entry’ causing bacteria to be resistant to antibiotic

A

Bacteria modifies its bacterial membrane porin channel size, numbers or selectivity

66
Q

Give example of ‘Remove Antibiotic From Bacterium’ causing bacteria to be resistant to antibiotic

A

Proteins in bacterial membranes can act as an export or Efflux pump so the Antibiotic is Pumped Out of the Bacteria/microbe resulting in Reduced levels and thus Effect of Antibiotic On Bacteria/microbe:

  • S.aureus or S.pnuemoniae resistance to fluroquinolones
  • Enterobacteriacae resistance to tetracyclines
67
Q

Give examples of intrinsic natural resistance of a bacteria to antibiotic developing

A
  • Aerobic bacteria are Unable to reduce Metronidazole to its active form thus the antibiotic is harmless to them
  • Anaerobic bacteria Lack oxidative metabolism required to uptake Aminoglycosides
  • Vancomycin is Not taken up by Gram negative bacteria - it cannot penetrate their outer membrane since its too large

(all subpopulation of a species will be equally resistant)

68
Q

Why cant Vancomycin work on Gram Negative bacteria?

A

Not taken up by gram -ve bacteria as cannot penetrate the outer membrane (too large)

69
Q

Give example of antibiotic group or individual that is unable to affect:
Aerobic bateria

A

Metronidazole

unable to reduce this into active form

70
Q

Give example of antibiotic group or individual that is unable to affect:
Anaerobic bateria

A

Aminoglycosides

lack oxidative metabolism required to uptake this

71
Q

How can bacteria develop acquired resistance to a bacteria?

A

Spontaneous gene mutation

Horizontal Gene Transfer

72
Q

What is acquired resistance? (bacteria to antibiotic)

A

A bacterium which was previously susceptible obtains the ability to
resist the activity of a particular antibiotic

73
Q

Describe how spontaneous gene mutation causes antimicrobial resistance

A
  • New nucleotide base pair
  • Change in amino acid sequence
  • Change to enzyme or cell structure
  • Reduced affinity or activity of antibiotic
74
Q

What are 3 methods of Horizontal gene transfer?

A

Conjugation
Transduction
Transformation

75
Q

Horizontal Gene Transfer: What is meant by Conjugation?

A

Sharing of extra chromosomal plasmids

76
Q

Horizontal Gene Transfer: What is meant by Transduction?

A

Insertion of plasmid genetic material by bacteriophages (viral vector)

77
Q

Horizontal Gene Transfer: What is meant by Transformation?

A

Picking up naked genetic material

78
Q

Give examples of clinically relevant Gram Positive Antibiotic Resistant bacteria

A

Methicillin resistant Staphylococcus Aureus (MRSA)

Vancomycin-resistant enterococci (VRE)

79
Q

MRSA - how did this arise?

A

Staphylococcal casette cromosomi mec (SCCmec) contains resistance gene mecA
Gene encodes penicillin-binding protein 2a (PBP2a) that does not bind penicillin i.e. resistance

Confers resistance to all B-lactam antibiotics in addition to methicillin

80
Q

VRE - how did this arise?

A

Plasmid mediated acquisition of gene encoding altered amino acid on peptide chain preventing vancomycin binding.

81
Q

What promotes VRE development

A

use of cephalosporin

82
Q

Give examples of clinically relevant Gram Negative Antibiotic Resistant bacteria

A

Beta-lactamases
ESBL (Extended spectrum B-lactamases)
AmpC B-lactamase resistance

83
Q

What are Beta-lactamases

A

Enzymes that hydrolyse penicillins

84
Q

*Give examples of Beta-lactamases

A

TEM-1 in E.coli, H. influenzae and N. gonorrhoea

SHV-1 in K. pneumoniae

85
Q

How can we counter Beta-lactamases

A

Beta-lactamase inhibitors

Given alongside antibiotics

86
Q

*Why are ESBL (Extended spectrum b lactamases) worse than Beta-lactamases?

A

ESBL have further mutation at active site means it can destroy more than just penicillin or amoxycillin

87
Q

What antibiotics can be inactivated by ESBL?

A

Penicillins
Amoxycillin
Cephalosporins e.g. cefuroxime, cefalexin,
cefotaxime
Combination antibiotics such as co-amoxiclav and tazocin

88
Q

Describe resistance of AmpC B-lactamase

A

Broad spectrum penicillin, cephalosporine and monobactam resistance

B-lactamase inhibitor resistant in bacteria such as Citrobacter spp. and Enterobacter spp.

89
Q

*How can we treat AmpC B-lactamase resistance

A

Quinolones or Trimethoprim but may require carbapenam treatment or agents such as fosfomycin or temocillin (use for UTIs and chest infections)

90
Q

What are antibiotics used for?

A

Treatment

Prophylaxis e.g. Preventing post-surgical infection or specific indications in cases of Endocarditis or Post-splenectomy

91
Q

What are antibiotic classes?

A 
Beta-lactams
Penicillins
(B-lactamase inhibitors)
Cephalosporins
Monobactams
Carbapenems
Glycopeptides
Macrolides
Lincosamides
Tetracyclines
Aminoglycosides
Oxazolidinones
Quinolones
Metronidazole
Trimethoprim
92
Q

Where do Beta Lactams target

A

Bacterial cell wall

93
Q

*Give examples of Beta-Lactams

A
  • Penicillins
  • Cephalosporins
  • Carbapenems
  • Combinations (B lactam inhibitor/B lactam)
94
Q

When would you have contra-indications of Beta-Lactams

A

People who have NAY type of penicillin allergy

Use with caution if patient has no true IgE mediated/severe allergy

95
Q

*True or False:
MRSA has flucloxacillin resistance and its thus RESISTANT TO ALL BETA LACTAMS e.g. cephalosporins, pip/tazobactam and carbapenems

A

True

96
Q

*Give examples of Penicillins

A

Benzylpenicillin/Penicillin G - IV
Phenoxymethylpenicillin/Pen V - Oral
Amoxicillin - IV & Oral
Flucloxacillin - IV & Oral

97
Q

Describe activity of Benzylpenicillin/Penicillin G

A

Streptococci e.g Strep. pneumoniae and Beta Hameolytic Streps (A,B,C,G)
Laos other gram +ve bacteria including clostridia

Medicine Phase 2a (22 decks)

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