Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MBChB Year 3 > Week 6 - Clinical Microbiology 1 > Flashcards

Week 6 - Clinical Microbiology 1 Flashcards

1
Q

Describe the bacterial structure?

A
  • Cell membrane
  • Peptidoglycan cell wall (thicker in gram positives)
  • Outer membrane
  • Periplasm
  • Positive/negative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List the 4 antibiotic targets?

A
  1. Cell wall peptidoglycan
  2. Metabolism
  3. DNA
  4. Ribosome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 2 different ways that an antibiotic can act?

A
  1. Bactericidal

2. Bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe Bactericidal antibiotic action?

A
  • Achieve sterilisation of the infected site by directly killing bacteria
  • Lysis of bacteria can lead to release of toxins & inflammatory material
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe Bacteriostatic antibiotic action?

A
  • Suppresses growth but does not directly sterilise infected site
  • Requires additional factors to clear bacteria- immune mediated killing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the antibiotic spectrum?

A
  • Spectrum refers to the range of bacterial species effectively treated by the antibiotic
  • Antibiotic spectrum can vary widely even within the same antibiotic class
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the antibiotic spectrum of Meropenem?

A
  • Active against almost all gram positive & gram negative species.
  • Resistance is rare except for MRSA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the antibiotic spectrum of

Benzyl-penicillin?

A
  • Highly active against streptococci

- Most other disease causing bacteria are resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe Broad Spectrum antibiotics?

A

Treat most causes of infection but also have a substantial effect on colonising bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe Narrow Spectrum antibiotics?

A
  • Useful only where the cause of the infection is well defined
  • Have a much more limited effect on colonising bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give 5 examples of gram negative bacteria?

A
  1. Pseudomonas
  2. Haemophilus
  3. Neisseria
  4. Other coliforms
  5. E. coli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give 3 examples of gram positive bacteria?

A
  1. Streptococcus
  2. Enterococcus
  3. Staphylococcus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give 2 examples of anaerobes bacteria?

A
  1. Clostridium

2. Bacteroides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 3 uses of antibiotics?

A
  1. Guided therapy
  2. Empirical therapy
  3. Prophylactic therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe Guided therapy antibiotic use?

A

Depends on identifying cause of infection & selecting agent based on sensitivity testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe Empirical therapy antibiotic use?

A
  • Best (educated) guess therapy based on
    clinical/epidemiological acumen
  • Used when therapy cannot wait for culture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe Prophylactic therapy antibiotic use?

A

Preventing infection before it begins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What 2 harms does antibiotic disruption of bacterial flora lead to?

A
  1. Overgrowth with yeasts- thrush

2. Overgrowth of bowel- diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What 2 things is antibiotic use negatively associated with?

A
  1. Development of C. difficile colitis

2. Future colonisation & infection with resistant organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How could you compromise in antibiotic guided therapy?

A
  • Use antibiotic which has limited action to the bacteria causing infection
  • If possible limit penetration to site of infection
  • Achieve clinical cure with as little impact on colonisation and resistance as possible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What type of antibiotic is best for guided therapy?

A

Narrow spectrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What type of antibiotic is best for empirical therapy?

A

Broad spectrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the 4 classes of β-Lactam Antibiotics?

A
  1. Penicillins
  2. Cephalosporins
  3. Carbapenems
  4. Monobactams
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the antibiotic combination in Augmentin/Co-amoxiclav?

A

Amoxicillin/clavulanic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the antibiotic combination in Tazocin?

A

Piperacillin/tazobactam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

List the 6 common β-Lactam Antibiotics?

A
  1. Benzylpenicillin
  2. Flucloxacillin
  3. Amoxicillin
  4. Ceftriaxone
  5. Meropenem
  6. Aztreonam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the Mechanism of action of β-Lactam Antibiotics?

A
  • β-lactam motif analogue of branching structure of peptidoglycan
  • Inhibits cross linking of cell wall peptidoglycan
  • Causes lysis of bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What type of antibiotic are β-Lactam Antibiotics?

A

Bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are Beta-lactamases?

A

Enzymes that lyse & inactivate beta-lactam drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What 2 things commonly secrete Beta-lactamases?

A

Gram negatives & S.aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What can Beta-lactamases lead to?

A

Confer high level resistance to antibiotic: Total antibiotic failure is likely to result

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How are most β-Lactam Antibiotics administered & why?

A
  • Most β-lactams poorly absorbed from GI tract: IV

- Some can be effective orally: amoxicillin, flucloxacillin. Vomiting limits dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How are β-Lactam Antibiotics secreted?

A

Usually unchanged in urine, some also via bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the half life of β-Lactam Antibiotics?

A

Half life varies enormously: Benzylpenicillin ≈ 1 hour Ceftriaxone ≈ 8 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the 4 types of adverse effects seen with β-Lactam Antibiotics?

A
  1. GI toxicity
  2. Hypersensitivity
  3. Infection
  4. Miscellaneous rare reactions (seizures, haemolysis, leukopenia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

List the 3 GI toxicity effects of β-Lactam Antibiotics?

A
  1. Nausea & vomiting
  2. Diarrhoea
  3. Cholestasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

List the 3 hypersensitivity effects of β-Lactam Antibiotics?

A
  1. Type 1 Urticaria, anaphylaxis
  2. Type 4 Mild to severe dermatology
  3. Interstitial nephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

List the 3 infection effects of β-Lactam Antibiotics?

A
  1. Candidiasis: Oral Vulvovaginal
  2. Clostridium difficile infection
  3. Selection of resistant bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe the common Type I hypersensitivity allergic reaction to antibiotics?

A
  • Most patients develop an urticarial rash
  • Anaphylaxis is the most feared complication
  • Cross reaction between classes is variable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the 3 factors associated with reported hypersensitivity syndrome?

A
  1. Non allergic
  2. Gastrointestinal symptoms
  3. Therapeutic failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Describe penicillin cross reactivity?

A

Patients allergic to a penicillin will usually be allergic to other penicillins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe how penicillin cross reactivity can be managed with other antibiotic classes?

A
  • Penicillin allergy may be safely managed with other β-lactams
  • Particularly important if patient presents with life- threatening infection (esp. meningitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the 3 common penicillins?

A
  1. Benzyl-penicillin
  2. Amoxicillin
  3. Flucloxacillin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the common Cephalosporins?

A

Ceftriaxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the common Carbapenems?

A

Meropenem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the common Monobactams?

A

Aztreonam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the 2 common β-lactam/β-lactamase inhibitor combinations?

A
  1. Co-amoxiclav

2. Piperacillin/tazobactam = tazocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe how Benzylpenicillin is administered?

A
  • Administered IV
  • There is an oral agent (Penicillin V) but not often
    used
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is Benzylpenicillin used for?

A

1st choice antibiotic for serious streptococcal infection (i.e. erysipelas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Benzylpenicillin is a ______ spectrum agent?

A

Narrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What 2 bacterias is Benzylpenicillin very effective against?

A
  1. Streptococcus

2. Neisseria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is Amoxicillin?

A

Semi-synthetic penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is Amoxicillin used for?

A
  • Increased activity against gram negative organisms (resistance)
  • More orally bioavailable than natural penicillins
  • Treatment of a wide range of infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the 3 bacterias that Amoxicillin is very effective against?

A
  1. Streptococcus
  2. Enterococcus
  3. Neisseria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is Flucloxacillin?

A

Synthetic penicillin developed to be resistant to beta-lactamase produced by staphylococci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the 2 bacterias that Flucloxacillin is very effective against?

A
  1. Staphylococcus aureus (not MRSA)

2. Streptococci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is Flucloxacillin NOT effective against?

A

No activity at all against gram negative organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the route for Flucloxacillin?

A

Orally but nausea limits dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are Beta-lactamase inhibitors administered with & why?

A
  • Penicillin antibiotic

- Greatly broadens spectrum of penicillins against Gram negatives & S. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are 2 Beta-lactamase inhibitors?

A
  1. Clavulanic acid

2. Tazobactam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the 5 bacterias that Co-amoxiclav is effective against?

A
  1. Streptococcus
  2. Enterococcus
  3. Staphylococcus (not MRSA)
  4. Neisseria
  5. Haemophilus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the 5 bacterias that Benzylpenicillin is NOT effective against?

A
  1. Bacteroides
  2. Staphylococcus
  3. Other coliforms
  4. Haemophilus
  5. Pseudomonas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are Cephalosporins effective against?

A

Good activity against Gram positives & Gram negatives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is more susceptible to beta-lactamases: Cephalosporins or penicillins?

A

Penicillins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Describe the multiple generations of cephalosporins?

A
  • Gram negative spectrum increases with each generation
  • Some loss of Gram positive activity
  • Recent introduction of MRSA active cephalosporins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the 5 bacterias that Ceftriaxone are effective against?

A
  1. Streptococcus
  2. Staphylococcus (not MRSA)
  3. E. coli
  4. Neisseria
  5. Haemophilus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the 2 bacterias that Ceftriaxone are NOT effective against?

A
  1. Enterococcus

2. Pseudomonas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are Carbapenems?

A

Ultra-broad spectrum beta- lactam antibiotics developed during search for beta-lactamase inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Describe what Carbapenems are effective/resistant against?

A
  • Excellent spectrum of activity against Gram positive & Gram negative
  • No activity against MRSA
  • Resistant to beta-lactamases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the 2 ultra broad spectrum antibiotics?

A
  1. Meropenem

2. Tazocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the only member of the monobactam class of antibiotics?

A

Aztreonam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Describe Monobactams?

A

Beta-lactam antibiotic but no cross reactivity to penicillins so can be given to those with penicillin allergy (except anaphylaxis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

How are Monobactams administered?

A

Only given IV, no oral absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the 4 bacterias that Aztreonam is effective against?

A
  1. E. coli
  2. Neisseria
  3. Haemophilus
  4. Pseudomonas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the 5 bacterias that Aztreonam are NOT effective against?

A
  1. Staphylococcus (not MRSA)
  2. Enterococcus
  3. Streptococcus
  4. Clostridium
  5. Bacteroides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How does Vancomycin work?

A
  • Inhibits cell wall formation in Gram positives only

- Not dependent on PBP binding so effective against resistant organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the route for administering Vancomycin?

A
  • Not absorbed from GI tract so IV

- Oral route only for C. diff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

How common is Vancomycin resistance?

A

Occurs but is uncommon (esp. Staph)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is Vancomycins half life?

A

Long half-life so loading doses usually given

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the main clinical issue with Vancomycin?

A

Underdosing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Describe the 4 factors of toxicity with Vancomycin?

A
  1. Nephrotoxicity-more likely with higher doses
  2. Red-man syndrome if injected too rapidly
  3. Ototoxicity (rare)
  4. Therapeutic drug monitoring undertaken (narrow therapeutic index)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is Red-man syndrome?

A
  • Anaphylactoid reaction

- Very rare now infusion rates slow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the most effective antibiotic to treat cellulitis?

A

Flucloxacillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What antibiotic is effective against MRSA?

A

Vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Why are beta-lactams the most important class of antibiotics?

A
  • Wide spectrum of activity
  • Excellent efficacy
  • Low toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the 5 most common infectious causes of death in low-income countries?

A
  1. Lower respiratory infections
  2. HIV/AIDS
  3. Diarrhoeal diseases
  4. Malaria
  5. Tuberculosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

List the 6 antibiotic resistant infectious diseases?

A
  1. MRSA = Methicillin-resistant Staphylococcus aureus
  2. VRSA = Vancomycin-resistant Staphylococcus aureus
  3. ESBLs = Extended spectrum beta-lactamase
  4. CPEs = Carbapenemase Producing Enterobacteriaceae
  5. MDRTB = Multidrug-resistant TB
  6. HIV = Human immunodeficiency viruses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the 7 multifactorial reasons behind the increase in infectious diseases/resistance?

A
  1. New patterns of travel (air) & trade (food)
  2. Developments in agricultural practices/animal husbandry
  3. Sexual behaviour
  4. Medical interventions/developments in technology
  5. Increasing populations at extremes of age
  6. Over/unnecessary use of antibiotics
  7. The breakdown of economic, social & political systems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What infectious disease is a common cause of death in high income countries?

A

Lower respiratory tract infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the 2nd most common reason for empirical antibiotic therapy?

A

UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Describe the occurrence and effects HAI have?

A
  • Increased morbidity, mortality, use of investigations, use of antibiotics, length of stay
  • Decreased throughput
  • 􏰎Costs NHS in Scotland approx. £200 million per year
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is the 2nd most common cause of death after cardiovascular disease?

A

Sepsis (70% community acquired)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are the 8 resistance mechanism?

A
  1. Loss of porins
  2. Beta-lactamases in periplasmic space
  3. Overexpression of transmembrane efflux pump
  4. Antibiotic-modifying enzymes
  5. Target mutations
  6. Ribosomal mutation or modification
  7. Mutations in lipopolysaccharide structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is Carbapenem-resistant K. pneumonia susceptible to?

A
  1. Colistin
  2. Tigecycline
  3. Gentamicin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the 3 critical bacterias that need new antibiotics?

A
  1. Acinetobacter baumannii, carbapenem-resistant
  2. Pseudomonas aeruginosa, carbapenem-resistant
  3. Enterobacteriaceae, carbapenem-resistant, ESBL-producing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are the 4 big challenges facing antibiotic development in the 21st century?

A
  1. New antibiotics are needed to combat resistance
  2. New antibiotics are reserved to guard against resistance
  3. It can take in excess of 10 years from discovery to launch
  4. Est. to cost $1billion to bring a new drug to market
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What are the 4 targets for antibiotics?

A
  1. Cell wall biosynthesis
  2. Protein biosynthesis
  3. DNA & RNA replication
  4. Folate metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What are the 3 types of antibiotics that inhibit the 50S Ribosomal Subunit?

A
  1. Macrolides
  2. Clindamycin
  3. Chloramphenicol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Give 3 examples of Macrolides?

A
  1. Erythromycin
  2. Clarithromycin
  3. Azithromycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What are the 2 types of antibiotics that inhibit the 30S Ribosomal Subunit?

A
  1. Aminoglycosides (Gentamicin)

2. Tetracyclines (Doxycycline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What are macrolides effective against?

A
  • Good spectrum of activity against Gram positives & respiratory gram negatives
  • Active against Legionella, Mycoplasma & Chlamydia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

How are Macrolides administered?

A

Oral even in severe infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are the 5 bacterias that Clarithromycin is effective against?

A
  1. Streptococcus
  2. Staphylococcus
  3. Neisseria
  4. Haemophilus
  5. “Atypicals”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What are the 5 “Atypicals” that Clarithromycin is effective against?

A
  1. Legionella
  2. Mycoplasma
  3. Coxiella
  4. Chlamydia
  5. Chlamydophila
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What are the 3 adverse effects associated with Macrolides?

A
  1. Diarrhoea & Vomiting
  2. QT prolongation
  3. Hearing loss with long term use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are the 3 drugs that interact with Macrolides (esp. Clarithromycin)?

A
  1. Simvastatin- Avoid co-prescription, Temporarily stop simvastatin
  2. Atorvastatin
  3. Warfarin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Why should Macrolides only be used in relatively non-severe infections?

A

Resistance among “typical” pathogens is relatively common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is Clindamycin similar to in terms of mechanism of action & absorption?

A

Macrolides (oral)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the 2 key differences of Clindamycin compared to Macrolides?

A
  1. No action against aerobic Gram negatives or
    “atypicals”
  2. Excellent activity against anaerobes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What is Clindamycin highly effective at?

A

Stopping exotoxin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What are 2 gram positive toxin mediated diseases that Clindamycin is used to treat?

A
  1. Toxic shock syndrome

2. Necrotising fasciitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What are the 4 bacterias that Clindamycin is effective against?

A
  1. Bacteroides
  2. Clostridium
  3. Streptococcus
  4. Staphylococcus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What is Clindamycin particularly effective against?

A

Anaerobes, which means its particularly effective at disrupting colonic flora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What is Clindamycin notorious for causing?

A

C. difficile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Describe C. Differgic antibiotics?

A
  • Antibiotics dramatically alter the colonic flora
  • C. difficile commonly colonises the human colon
  • Forms spores which can be difficult to eradiacate from hospitals
  • Has developed resistance to common antibiotic classes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What are the 4C’s which cause C. diff?

A
  1. Clindamycin
  2. Co-amoxiclav
  3. Cephalosporins
  4. Ciprofloxacin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Describe Chloramphenicol?

A
  • Inhibits 50S ribosome
  • Excellent broad spectrum of activity
  • Toxic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What are the 3 side effects of Chloramphenicol’s toxicity?

A
  1. Bone marrow suppression
  2. Aplastic anaemia
  3. Optic neuritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What are the 2 modern uses of Chloramphenicol?

A
  1. Topical therapy to eyes

2. Bacterial meningitis with beta-lactam allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What are the 2 mechanisms of action for Gentamicin (Aminoglycosides)?

A
  1. Reversibly binds to the 30S ribosome (bacteriostatic)

2. Poorly understood action on the cell membrane (bactericidal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

List the 3 side effects of Aminoglycosides toxicity?

A
  1. Nephrotoxicity
  2. Ototoxicity- hearing loss, loss of balance, oscillopsia
  3. Neuromuscular blockade (usually only significant in myaesthenia gravis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Describe the once-daily dosing of Aminoglycosides?

A
  • Give high initial dose
  • Leave long dosing interval (24-48hrs) to minimise toxicity
  • Measure trough level to ensure drug not accumulating
  • Give for 3 days only
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

List the 4 bacteria that Gentamicin is effective against?

A
  1. Pseudomonas
  2. Staphylococcus
  3. E. coli
  4. Other coliforms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Describe Tetracyclines?

A
  • Similar spectrum of activity to macrolides
  • Also active against “atypical” organisms
  • Relatively non-toxic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Why should Tetracyclines not be used for children & pregnant women?

A
  1. Bone abnormalities

2. Tooth discolouration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What are the 5 bacterias that Doxycycline is effective against?

A
  1. Streptococcus
  2. Staphylococcus
  3. Neisseria
  4. Haemophilus
  5. “Atypicals”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

List the 5 “Atypicals” that Doxycycline is effective against?

A
  1. Rickettsia
  2. Mycoplasma
  3. Coxiella
  4. Chlamydia
  5. Chlamydophila
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What are 2 types of antibiotics that work by inhibiting DNA Repair & Replication?

A
  1. Quinolones (Ciprofloxacin & Levofloxacin)

2. Rifampicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What are Quinolones?

A

Broad spectrum, bactericidal antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Describe Ciprofloxacin (Quinolones) & its uses?

A
  • Good against Gram negatives, weaker against Gram positives

- Commonly used in UTI/abdominal infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Describe Levofloxacin (Quinolones) & its uses?

A
  • Sacrifices some Gram negative activity for stronger Gram positive action
  • Respiratory tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What is the route of administering Quinolones?

A

Excellent oral bioavailability: can use oral dosing even in severe infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

List the 3 side effects of Quinolones toxicity?

A
  1. Gastrointestinal toxicity
  2. QT prolongation
  3. Tendonitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What are 2 other therapeutic problems with Quinolones?

A
  1. Resistance emerging on therapy/tendon damage

2. C. diff infection (esp. in North America)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What are the 6 bacterias that Quinolones are effective against?

A
  1. E. coli
  2. Other coliforms
  3. Neisseria
  4. Haemophilus
  5. Pseudomonas
  6. Atypicals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

List the 5 “Atypicals” that Ciprofloxacin & Levofloxacin are effective against?

A
  1. Legionella
  2. Mycoplasma
  3. Coxiella
  4. Chlamydia
  5. Chlamydophila
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What are the 3 bacterias that Levofloxacin is effective against?

A
  1. Streptococcus
  2. Staphylococcus
  3. “Atypicals”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What are the 2 indications for Rifampicin in the UK?

A
  1. Tuberculosis (in combination therapy)

2. In addition to another antibiotic in serious Gram positive infection (esp. Staph. aureus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What are the 2 Rifampicin interactions?

A
  1. Rifampicin is a potent CYP450 enzyme inducer

2. Most drugs that undergo hepatic metabolism affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What are the 3 problems with Tuberculosis?

A
  1. Slow growing
  2. High bacterial burden
  3. Limited access of drugs to granuloma (no vascular
    supply)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What are the 2 solutions to Tuberculosis?

A
  1. Prolonged courses of therapy (usually 6 months)

2. Combination therapy to prevent resistance & kill growing and resting organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What are the 4 standard short course drugs used too treat Tuberculosis?

A
  1. Isoniazid
  2. Rifampicin
  3. Ethambutol
  4. Pyrazinamide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Describe Isoniazid & what it causes?

A
  • Bactericidal to fast growing mycobacteria

- Causes hepatotoxicity, peripheral neuropathy, B3 deficiency prevented with pyridoxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Describe Rifampicin & what it causes?

A
  • Bactericidal against slowly replicating organisms in necrotic foci
  • Liver, bone marrow & renal toxicity relatively uncommon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Describe Ethambutol & what it causes?

A
  • Bacteriostatic against slow growing mycobacteria

- Principle toxicity is optic neuritis, watch for loss of colour vision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Describe Pyrazinamide & what it causes?

A
  • Bactericidal, even against slow growing mycobacteria intracellularly
  • Principle toxicity is hepatitis, also causes arthralgia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

What does inhibition of the folate metabolism pathway lead to?

A

Impaired nucleotide synthesis & therefore impaired DNA replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Describe Trimethoprim?

A
  • Orally administered

- Good range of action against Gram positive & Gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What is Trimethoprim limited to use in?

A

Uncomplicated UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Describe the 3 factors of Trimethoprim’s toxicity?

A
  • Elevation of serum creatinine
  • Elevation of serum K+, problematic in patients with chronic renal impairment
  • Rash & GI disturbance relatively uncommon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What is Co-trimoxazole?

A

Trimethoprim / Sulfamethoxazole combination antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What are the 2 side effects of Co-trimoxazole toxicity?

A
  1. Bone marrow suppression

2. Stevens Johnson Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

What are the 2 advantages of Co-trimoxazole?

A
  1. Used in certain uncommon infections by specialists

2. Pneumocystis jirovecii pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What is the mechanism of action of Metronidazole?

A
  • Enters by passive diffusion & produces free radicals

- Effective against most anaerobic bacteria (not actinomyces)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What is Metronidazole often added to?

A

Therapy in intra-abdominal infections, esp abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What are the 2 side effects of Metronidazole?

A
  • Unpleasant reaction with alcohol

- Peripheral neuropathy with long term use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What is an Uncomplicated UTI (cystitis)?

A
  • Lower urinary tract symptoms

- Absence of sepsis or evidence of upper tract involvement (pyelonephritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Describe the treatment of an Uncomplicated UTI (cystitis)?

A
  • Treatment only needs to sterilise urine, no need for systemic activity
  • Low risk infection so can often wait for culture results
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Describe Trimethoprim’s effect in lower UTI treatment?

A
  • 1st line agent
  • Avoid in 1st trimester of pregancy
  • Penetrates well into prostate so good choice for men
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Describe Nitrofuratoin’s effect in lower UTI treatment?

A
  • Excellent, broad spectrum of activity
  • Concentrated in urine so no effect on other tissues
  • Failure to concentrate in urine in renal failure
  • Relatively non-toxic in short courses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What is the toxic side effect of Nitrofuratoin with long term use?

A

Pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What is the principle bacterial cause of a UTI?

A

E. coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What antibiotic would you use for a woman with an uncomplicated UTI & no past medical history or systemic symptoms?

A

Trimethoprim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What antibiotic would you use for a women with a complicated UTI?

A

Ciprofloxacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What 2 possible antibiotic would you use for a women with a UTI & is severely unwell?

A
  1. Amoxicillin

2. Gentamicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What are 3 antibiotics that are thought to be safe in pregnancy?

A
  1. Most beta-lactams
  2. Macrolides
  3. Anti-tuberculants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What are 5 antibiotics that are NOT thought to be safe in pregnancy?

A
  1. Tetracyclines- Bone/tooth abnormalities
  2. Trimethoprim- Neural tube defects (1st Tri)
  3. Nitrofurantoin- Haemolytic anaemic (3rd Tri)
  4. Aminoglycosides- Ototoxicity (2nd/3rd Tri)
  5. Quinolones- Bone/joint abnormalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

Describe Inherently resistant antibiotics?

A

Lack a pathway or target which a drug interacts with, or the drug is unable to gain access to the target

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Describe antibiotics with Acquired resistance?

A

Drug which was previously sensitive has gained some genetic material encoding for resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What are 2 examples of inherent resistance antibiotics?

A
  1. Vancomycin against Gram negative bacteria

2. Metronidazole against aerobic bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What are the 4 ways main that antibiotics can develop resistance?

A
  1. Enzymes inactivate/modify antimicrobials (beta-lactamases)
  2. Change drug target so that antibiotic no longer has any effect
  3. Decreasing cell permeability to the drug (decreased porins), so the conc required to be effective is not achieved
  4. Bacteria export the drug from inside the cell (multi-drug resistance efflux pump)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What are the 4 main ways that a bacterial cell can become resistant to antibiotics?

A
  1. Chromosomal mutation
  2. Acquisition of a mobile piece of DNA (plasmid, integron or transposon)
  3. DNA uptake can also occur through transformation (only certain types of bacteria)
  4. Pieces of DNA can be transferred between bacteria by viruses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

What is vertical gene transfer?

A

Genetic information passed from parent cell to progeny via binary fission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

What is horizontal gene transfer?

A

Genes transferred other than through traditional reproduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What is horizontal & vertical gene transfer the primary reason for?

A

Antibiotic resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What happens once a mutation coding for antibiotic resistance has occurred in a cell?

A

Transfer this mutation to all their progeny (vertical transmission)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

What is treatment of infections with 2 drugs acting in different ways based on?

A

Principle that if a mutation occurs in 1 drug target the other drug will still kill the organism, this is because we don’t yet know the sensitivity of the organism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Give an example for when an infection is treated with 2 drugs?

A

Pseudomonas infection with tazocin & gentamicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Describe bacterial conjugation?

A
  • Requires cell to cell contact between 2 bacteria (don’t need to be same species)
  • Small pieces of DNA called plasmids are transferred
  • Horizontal gene transfer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What 2 things can be transferred in bacterial conjugation?

A
  1. Antibiotic resistance

2. Ability to use new metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What are plasmids?

A

Pieces of circular double stranded DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What 2 things can be carried on plasmids?

A
  1. Genetic information (resistance to antibiotics, allow themselves to replicate, heavy metals, UV light)
  2. Genes which encode pili, mediate adherence & toxins (genes of interest to host cell)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What are the 2 ways plasmids can exist?

A
  1. Free within the cell

2. Integrated into the host chromosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

What are plasmids important in?

A

Horizontal gene transfer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

What are plasmids capable of doing?

A

Replicating themselves independently of the bacterial chromosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

Where are plasmids found in?

A

Gram positives & Gram negatives & several different types of plasmids can exist within a single cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

What are 4 factors which make plasmids a very effective way of spreading resistance?

A
  1. Multiply in high numbers
  2. High rate of cell to cell transfer
  3. Can be picked up by different species
  4. Carry genes for resistance to several drugs at once
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What does the most common resistance information carried on plasmids relate to?

A

Enzymes which break antibiotics down or modifications to membrane drug transport systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

What is transduction?

A

Small pieces of DNA are transferred between bacteria (usually same species) by a virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

What are Bacteriophages?

A

Viruses which infect bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

How is transduction different to conjugation/transformation?

A
  • Unlike conjugation it does not require the cells to touch

- Unlike transformation its unaffected by DNAses in the bacterium environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

What is released when bacteria die & what happens to it?

A
  • Some naked DNA is released into the surrounding environment
  • Some bacteria are capable of taking naked DNA up & inserting it into their chromosome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

What happens if the naked DNA released by a dead bacteria inserts into a coding region for penicillin binding protein?

A

Change in the penicillin binding protein meaning that it can still cross link the peptidoglycan precursors to form the cell wall but has a reduced affinity for beta-lactam antibiotics such as penicillin which will then no longer kill the bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

What has been seen clinically for the process of naked DNA inserting into a coding region?

A

Some strains of Strep pneumoniae have become resistant to penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

What is transformation a mechanism of?

A

Horizontal gene transfer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

What makes a successful resistance mutation?

A

The balance between the fitness cost & the selection pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

What happens in an environment without a selective pressure?

A

Slower growing mutants will be outgrown by their wildtype colleagues & will slowly die away

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

What does the time taken for bacteria to grown mutations depend on?

A

Significance of the fitness cost associated with that mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

What can sometimes develop in the mutated bacteria to compensate for the fitness cost?

A

Other mutations may develop which allow the mutated bacteria to compete with wild type colleagues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

What is 1 area that we can really influence the development of antibiotic resistance?

A

Selection pressure (changing culture of antibiotics —> resistance mutations less likely to persist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

Describe the timeline of resistance in Staphylococcus aureus?

A
  1. Penicillin introduced
  2. Penicillin resistant strains detected
  3. Methicillin introduced
  4. Methicillin resistant strains detected (MRSA)
  5. Increasing use of vancomycin
  6. Vancomycin intermediate strains detected
  7. Vancomycin resistant strains detected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

Describe MRSA?

A

Strains are resistant to all Beta-lactams except some very new cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

What is the gene that codes for MRSA resistance?

A

MecA gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

What is the purpose of the penicillin binding protein?

A

Mediate the cross linking in the peptidoglycan which makes up the bacterial cell wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

What does the MecA gene cause?

A

Decreased affinity, which allows the bacteria to continue to produce cell wall even in high concentrations of the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

What is a major risk factor for MRSA?

A

Nursing home care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

What would the 1st line antibiotic be for cellulitis?

A

Flucloxacillin

208
Q

Where does MRSA live in the human body?

A

Moist areas

209
Q

Describe an MRSA screen?

A

Swab of the nose & perineum

210
Q

What are the 3 common gut commensals?

A
  1. E. coli
  2. Klebsiella
  3. Enterobacter
211
Q

What are coliforms?

A

Group of bacteria which live in the gut of humans & animals

212
Q

What are E. coli, Klebsiella & Enterobacter causes of?

A

Infections such as UTI, intra-abdominal sepsis & hospital acquired pneumonia (HAP)

213
Q

What are 4 antibiotics commonly used to treat resistance in coliforms?

A
  1. Penicillins (amoxicillin)
  2. Quinolones (ciprofloxacin)
  3. Cephalosporins
  4. Aminoglycosides (gentamicin)
214
Q

What are the 2 side rings in the beta-lactam structure?

A
  1. Beta-lactam ring

2. Thiozolidine ring

215
Q

What is resistance to beta-lactam antibiotics mediated by?

A

Family of antibiotic degrading enzymes called Beta-lactamases which hydrolyse the beta-lactam ring

216
Q

Describe the beta-lactamase inhibitors: Clavulanate & Tazobactam?

A
  • Compounds which have only weak antibacterial activity but which mainly act by binding the beta-lactamase
  • Thus allowing the beta-lactam to continue to act
217
Q

What are Extended Spectrum Beta-Lactamases (ESBLs) usually?

A

Plasmid encoded

218
Q

Describe Extended Spectrum Beta-Lactamases (ESBLs)?

A

Enzymes which are able to hydrolyse the beta-lactam ring of not only penicillins but also cephalosporins

219
Q

What are the 4 treatment options for Extended Spectrum Beta-Lactamases (ESBLs)?

A
  1. Ciprofloxacin
  2. Temocillin
  3. Gentamicin
  4. Meropenem
220
Q

What do bacteria carrying ESBLs often also carry?

A

Resistance genes for other commonly used antibiotics so they can be quite difficult to treat & some situations Meropenem is one of the few options

221
Q

What type of ESBL is the most widely spread in the UK?

A

CTX-M

222
Q

What are carbapenemases?

A

A group of enzymes which are capable of hydrolysing Meropenem

223
Q

What is another common mechanism for carbapenem resistance?

A

Combination of porin loss & increased production of a type of betalactamas enzyme known as AmpC

224
Q

Regarding selection pressure, what happens when we use more Meropenem?

A

More likely that resistant mutants will survive

225
Q

What are 4 reasons as to why Meropenem is being used more over the last 8 years?

A
  1. Changes to testing of tazocin
  2. Increased ESBL rates
  3. Avoidance of cephalosporins so tazocin is used more readily & patients failing on tazocin are moved to meropenem quickly
226
Q

How can we avoid meropenem resistant mutants surviving?

A

Use Carbapenem sparing agents ie. Gentamicin & Temocillin

227
Q

Why is the emergence of Klebsiella isolates resistant to carbepenems (such as meropenem) incredibly concerning?

A

These antibiotics are often the last option for treatment of multidrug resistant strains & if the resistance spreads we will have problems with infections that can’t be treated

228
Q

What 2 other areas of medicine will be effected without effective antibiotics?

A
  1. Complex surgery

2. Bone marrow transplants

229
Q

What bacteria is a master of antimicrobial resistance?

A

Pseudomonas aeruginosa

230
Q

Describe the 3 factors which make Pseudomonas aeruginosa antimicrobial resistant?

A
  1. Multiple other modifying enzymes
  2. Porin down regulations
  3. 4 efflux pumps (1 is always expressed, the other can be unregulated in response to stressors)
231
Q

What are the 3 non-genetic mechanisms of resistance?

A
  1. Protected environment (abscess)
  2. Resting stage
  3. Presence of a foreign body
232
Q

Why can surgery in some situations be the best cure for an infection?

A
  • When the body detects infection it can attempt to isolate it in 1 area i.e. abscess
  • This provides the bacteria with an environment protected from antibiotics
233
Q

Describe how “Resting stage” can lead to antibiotic resistance?

A

Bacteria which are not dividing i.e. ‘resting state’ are less susceptible to cell wall inhibiting agents such as penicillins & cephalosporins

234
Q

Why are such long courses of anti-tuberculous drugs required?

A
  • The bacteria is at “resting stage” and therefore resistant to antibiotics
  • Slow growing dormat tubercule bacilli
235
Q

List 2 reasons as to why the presence of a foreign body can lead to apparent resistance?

A
  1. Immune system is not as effective & removal of bacteria is often a team effort between antibiotics & the immune system
  2. Biofilm
236
Q

What is the biofilm sometimes called?

A

Slime layer

237
Q

What 2 prosthetic materials have biofilm on their surfaces?

A
  1. Indwelling lines

2. Prosthetic joints

238
Q

Describe a biofilm?

A

Complex bacterial community with channels for diffusion of water, oxygen & nutrients

239
Q

List the 3 ways that a biofilm can lead to resistance?

A
  1. Close proximity of bacteria facilitates gene exchange including exchange of resistance determinants
  2. Channels for diffusion of nutrients are sometimes too small for antibiotics
  3. Bottom of biofilm nutrients penetrate in smaller amounts & so the bacteria replicate slower making them less susceptible to cell wall agents
240
Q

Why does using short courses of antibiotics prevent spread of antibiotic resistance?

A

The remainder of our commensal flora is exposed to selection pressure for a shorter period of time

241
Q

What are 2 new antibiotic options that we could use instead of meropenem so to reduce resistance?

A

Aztreonam & Temocillin

242
Q

What is the largest use of antibiotics worldwide?

A

Promoting the growth of livestock animals

243
Q

What are the 4 main mechanisms of antibiotic resistance?

A
  1. Target change
  2. Inactivation
  3. Decreased entry
  4. Increased exit
244
Q

Describe target change in Streptococcus pneumonia & MRSA?

A

Penicillin binding protein is altered such that it has a decreased affinity for the drug so peptidoglycan cross linking is not prevented

245
Q

Give 3 examples of when drug inactivation can be seen?

A
  1. Beta-lactamases
  2. ESBLs
  3. Carbapenemases in coliforms
246
Q

When can you see antibiotic resistance in the form of decreased entry?

A

Coliforms which can be carbapenem resistant through a combination of AMPC & porin loss

247
Q

What are 3 conventional pathogens?

A
  1. Endogenous flora
  2. Hospital acquired
  3. Environmental organisms
248
Q

What are 2 opportunistic pathogens?

A
  1. Coagulase-negative staphylococci (CoNS)

2. Aspergillus

249
Q

What 6 medical interventions have led to an increasing population of often profoundly immunocompromised patients?

A
  1. Improved survival at extremes of life
  2. Improved cancer treatment
  3. Developments in transplant techniques
  4. Developments in intensive care
  5. Management of chronic inflammatory conditions
  6. Steroids
250
Q

Give 4 reasons why the prevention & treatment of infection in immunocompromised hosts not that straightforward?

A
  1. Basic patterns are recognizable but organisms are unpredictable
  2. Isolated deficiencies are rare
  3. Malfunction of 1 part often influences another
  4. Underlying diseases & their treatment affect a range of mechanisms
251
Q

What is neutropaenia defined as?

A

Neutrophils <0.5 x 109/L or <1.0 x 109/L & falling

252
Q

What 2 things does cytotoxic chemotherapy therapeutic irradiation (TBI) cause?

A
  1. Decreased proliferation of haemopoietic progenitor cells

2. Depletion of marrow reserves

253
Q

What is an important risk factor for infection?

A

Neutropaenia (risk increases with degree, duration & rate of fall)

254
Q

What 3 ways does cytotoxic drugs, irradiation & steroids effect neutrophil function?

A
  1. Decrease chemotaxis
  2. Decrease phagocytic activity
  3. Decrease intracellular killing
255
Q

List 4 gram positive cocci pathogens that effect neutrophil function?

A
  1. Staph. aureus
  2. Coagulase negative staphylococci
  3. Viridans streptococci (mitis, oralis)
  4. Enterococci (faecalis, faecium)
256
Q

List 2 anaerobe pathogens that effect neutrophil function?

A
  1. Bacteriodes spp.

2. Clostridia spp.

257
Q

List 4 gram negative bacilli pathogens that effect neutrophil function?

A
  1. E. coli
  2. Pseudomonas aeruginosa
  3. Klebsiella pneumoniae
  4. Enterobacter spp.
258
Q

List 2 fungi pathogens that effect neutrophil function?

A
  1. Candida spp.

2. Aspergillus spp.

259
Q

Describe Chronic Granulomatous Disease?

A
  • Inherited disorder
  • X linked most common
  • Defect in gene coding for NADPH oxidase
260
Q

What 2 things does a defect in gene coding for NADPH oxidase result in?

A
  1. Deficient production of oxygen radicals

2. Defective intracellular killing

261
Q

What are the signs/symptoms of Chronic Granulomatous Disease?

A
  • Recurrent bacterial & fungal infections –> abscesses lung, lymph nodes, skin
  • Inflammatory responses with widespread granuloma formation
262
Q

List the 3 common pulmonary infections which can occur in Chronic Granulomatous Disease?

A
  1. Aspergillus spp.
  2. Staph. aureus
  3. Nocardia spp.
263
Q

List 7 things which suppress cellular immunity?

A
  1. DiGeorge syndrome (primary deficiency, rare)
  2. Malignant lymphoma
  3. Cytotoxic chemotherapy
  4. Extensive irradiation
  5. Immunosuppressive drugs
  6. Allogeneic stem cell transplantation especially if GVHD
  7. Infections
264
Q

List 6 immunosuppressive drugs which effect cellular immunity?

A
  1. Corticosteroids
  2. Cyclosporin (used in organ rejection)
  3. Tacrolimus
  4. Alemtuzumab (anti-CD52 monoclonal)
  5. Rituximab (anti-CD20 monoclonal)
  6. Purine analogues ie. fludarabine
265
Q

List 5 infections which suppress cellular immunity?

A
  1. HIV
  2. Mycobacterial infections
  3. Measles
  4. EBV
  5. CMV
266
Q

List 3 things which suppress humeral immunity?

A
  1. Bruton agammaglobulinaemia (primary, rare)
  2. Antibody production decreases in lymphoproliferative disorders (CLL, multiple myeloma)
  3. Intensive radiotherapy & chemotherapy
267
Q

In what type of cancer is the humeral immunity usually preserved?

A

Acute leukaemia

268
Q

What does Intensive radiotherapy & chemotherapy ultimately cause?

A

Hypogammaglobulinaemia

269
Q

What do splenic macrophages do?

A

Eliminate non-opsonized microbes ie. encapsulated bacteria

270
Q

What is the site of primary immunoglobulin response?

A

Spleen

271
Q

List 3 infections which can cause Humoral deficiency/ splenectomy/ hyposplenism?

A
  1. Strep. pneumoniae
  2. Haemophilus influenzae type b
  3. Neisseria meningitidis
272
Q

What are the 3 principle barriers against microbial invasion?

A
  1. Skin
  2. Conjunctivae
  3. Mucous membranes- gut, respiratory tract, GU tract
273
Q

List the 5 factors of skin which make it a physical barrier against microbial invasion?

A
  1. Desquamates
  2. Dry
  3. pH = 5-6
  4. Temp = 5oC lower
  5. Secretory IgA in sweat
274
Q

What 2 things may impair the integrity of skin?

A
  1. Chemotherapy

2. Irradiation

275
Q

What happens when the mucosal barrier is injured via chemotherapy & irradiation?

A

GI lymphoid tissue responds with inflammatory response = Mucositis

276
Q

What are the 4 signs & symptoms of Mucositis?

A
  1. Pain
  2. Dysphagia
  3. Xerostomia (dry mouth)
  4. Ulceration
277
Q

What does Mucositis lead to?

A

Impairment of GI function & alterations in permeability –> Altered nutritional status

278
Q

What 4 things alter the gut microbiome?

A
  1. H2 antagonists
  2. PPIs
  3. Antibiotics
  4. Diarrhoea
279
Q

What factors equal severe nutritional deficiency?

A

<75% ideal body weight OR Rapid weight loss +

Hypoalbuminaemia

280
Q

What 4 things can cause impaired nutritional status?

A
  1. Anorexia
  2. Nausea & vomiting
  3. Mucositis
  4. Metabolic derangements
281
Q

What does iron deficiency reduce?

A

Microbicidal capacity of neutrophils & T cell function

282
Q

What may cause local organ dysfunction?

A

Tumours (obstruction –> infection)

283
Q

What organ is particularly susceptible to tumours causing organ dysfunction?

A

Lungs

284
Q

What are 2 signs of CNS tumours/spinal cord compression?

A
  1. Loss of cough/ swallow reflex

2. Incomplete bladder emptying

285
Q

What 2 concurrent illnesses can cause organ dysfunction?

A
  1. Stress- reduced T cell function

2. Diabetes mellitus- reduced opsonization, chemotaxis

286
Q

What were the 2 first solid organ transplants?

A
  1. Kidney

2. Pancreas

287
Q

What solid organ transplant has the highest % of graft survival?

A

Kidney from living donor (95% 1yr, 89% 3yr)

288
Q

What solid organ transplant has the lowest % of graft survival?

A

Lung (82% 1yr, 65% 3yr)

289
Q

What are 6 general principles of decreasing the chances of infection in solid organ transplants?

A
  1. Optimal tissue typing
  2. Donor evaluation
  3. Organ procurement
  4. Surgical technique
  5. Tailored immunosuppressive regimen
  6. Prevention of infection
290
Q

What % of liver transplants have an infection-related mortality?

A

23% (highest)

291
Q

List the 4 general principles of infection in solid organ transplants?

A
  1. Potential aetiology is diverse- community acquired bacterial & viral infections, opportunistic infections
  2. Pulmonary infection can progress rapidly
  3. Inflammatory responses are impaired
  4. Diagnosis is often difficult- radiology, histology, serology, molecular methods
292
Q

Describe the empirical therapy for infections in solid organ transplants?

A

Early diagnosis & prompt, aggressive Radiotherapy (toxicites/interactions common)

293
Q

What should you focus on in infections with solid organ transplants?

A

Prevention- anti-bacterial, fungal, viral prophylaxis

294
Q

What 2 solid organ infections would you use pre-emptive therapy?

A
  1. CMV

2. Fungal infection

295
Q

What is the risk of infection following solid organ transplant related to?

A

Relationship between epidemiological exposure & net state of immunosuppression

296
Q

List 7 community-acquired pathogens responsible for solid organ transplant infections?

A
  1. Bacteria- pneumococcus, listeria, salmonella, legionella

2. Viruses- influenza, parainfuenza, RSV

297
Q

When are nosocomial infections in solid organ transplant common?

A

Early post transplant & if ventilated or prolonged length of stay

298
Q

Give 3 examples of nosocomial infections in solid organ transplant?

A
  1. Resistant gram +ve & gram -ve bacteria
  2. Clostridium difficile associated disease (CDAD)
  3. Fungi
299
Q

List 3 latent donor-derived infections following solid organ transplant?

A
  1. TB
  2. Syphilis
  3. Viruses (HIV, Hepatitis B, CMV)
300
Q

List 4 active blood stream infections at procurement following solid organ transplant?

A
  1. Staphylococci
  2. Pneumococci
  3. Salmonella
  4. E. coli
301
Q

List 2 reactivated infections which can occur following solid organ transplant?

A
  1. M. tuberculosis

2. Viruses: HSV, VZV, CMV

302
Q

List 2 opportunistic pathogens which can occur following solid organ transplant?

A
  1. Aspergillus

2. Pneumocystis

303
Q

What are the 4 types of Allogeneic stem cell transplants?

A
  1. Syngeneic
  2. Related
  3. Unrelated
  4. Haploidentical
304
Q

What are the 3 types of stem cells?

A
  1. Bone marrow
  2. Peripheral Blood Stem Cell (PBSC)
  3. Cord blood
305
Q

What are the 3 immune system defects associated with engraftment?

A
  1. Neutropaenia
  2. Lymphopaenia
  3. Hypogammaglobulinaemia
306
Q

What are the 6 transplant related factors associated with engraftment?

A
  1. Mucositis
  2. Veno-occlusive disease (VOD)
  3. Central catheter
  4. Thrombocytopaenia
  5. Acute GVHD
  6. Chronic GVHD
307
Q

What are the 8 high incidence infections associated with engraftment?

A
  1. HSV
  2. Adenovirus
  3. Candida
  4. CMV
  5. VZV
  6. Late/early aspergillus
  7. Viridans streps
  8. Coag neg staph
308
Q

What are the 3 low incidence infections associated with engraftment?

A
  1. Encapsulated bacteria
  2. Pneumocystis
  3. Toxoplasma
309
Q

What are 2/3 episodes of febrile neutropenia in cancer patients due to?

A

Infection

  • Endogenous
  • Exogenous (community, nosocomial)
310
Q

List the 6 non-infectious causes of febrile neutropaenia?

A
  1. Malignancy
  2. Chemotherapy
  3. Transfusion
  4. Antibiotics
  5. Colony stimulating factors
  6. Allergies
311
Q

What does neutropaenic fever equal?

A

Infection until proven otherwise

312
Q

List 7 possible sites of infection in febrile neutropaenic patients with haematological malignancy & how common these are (%)?

A
  1. Bloodstream- 46.5%
  2. Mouth & pharynx- 18.5%
  3. Skin & soft tissues- 14%
  4. Respiratory tract- 11%
  5. Gastrointestinal tract- 6%
  6. Urinary tract- 2%
  7. Other sites- 1%
313
Q

What are the 7 most common Gram positive aerobic bacteria in neutropaenic cancer patients?

A
  1. Coagulase negative staphylococci
  2. Staphylococcus aureus
  3. Viridans streptococci
  4. Other streptococci (S. pyogenes, S. pneumoniae)
  5. Enterococcus spp.
  6. Bacillus spp.
  7. Listeria monocytogenes
314
Q

What are the 6 most common Gram negative aerobic bacteria in neutropaenic cancer patients?

A
  1. Escherichia coli
  2. Klebsiella spp.
  3. Pseudomonas spp.
  4. Proteus
  5. Enterobacter
  6. Serratia spp.
315
Q

What are the 3 most common Anaerobic bacteria in neutropaenic cancer patients?

A
  1. Bacteroides spp.
  2. Clostridium spp.
  3. Fusobacterium spp.
316
Q

What are the 3 most common Fungi in neutropaenic cancer patients?

A
  1. Candida spp.
  2. Aspergillus spp.
  3. Pneumocystis jirovecii
317
Q

What are the 4 most common viruses in neutropaenic cancer patients?

A
  1. HSV
  2. VZV
  3. Influenza
  4. RSV
318
Q

What is a fever?

A

Pyrexia OR Hypothermia (temperature > 38oC OR < 36oC)

319
Q

What is SIRS (systemic inflammatory response)?

A

Sweats, chills, rigors, malaise, tachypnoea >20/minute, tachycardia >90bpm,
hypotension (patients may appear well perfused despite hypotension)

320
Q

What is sepsis?

A

Evidence of infection (including SIRS) + Organ dysfunction i.e. ≥ 1 of hypotension, confusion or tachypnoea (Resp Rate ≥22/minute)

321
Q

What is septic shock?

A

Sepsis induced hypotension requiring inotropic support or hypotension that is unresponsive (within 1hr) to adequate fluid resuscitation i.e. systolic BP <90mmHg or a reduction of >40mmHg from baseline

322
Q

What is Neutropenic sepsis OR febrile neutropaenia?

A
  • Neutrophil count < 0.5, or < 1 if recent chemotherapy (usually within 10 days but can persist for up to 21 days)
    +
  • Fever/Hypothermia or SIRS or SEPSIS/Septic shock
323
Q

Describe the immediate clinical management of infections in the immunocompromised?

A
  • Neutropaenic sepsis is a MEDICAL EMERGENCY
  • Do not await confirmation of neutropaenia in patients who are haemodynamically compromised
  • Assess within 15 minutes of presentation
324
Q

What do you assess sepsis severity using?

A

NEWS

325
Q

When should you institute sepsis 6?

A

Within 1hr of SEPSIS recognition

326
Q

What is the treatment for someone with (standard risk) NEWS <5 & NOT allergic to penicillin/beta-lactam?

A
  • Piperacillin/tazobactam 4.5g IV 6hy

- No routine gentamicin

327
Q

What is the treatment for someone with (standard risk) NEWS <5 with an allergy to penicillin/beta-lactam?

A
  • Vancomycin IV + Ciprofloxacin 400mg IV 12hy OR
  • Aztreonam 2g IV 6hy
  • Consider gentamicin
    (based on local epidemiology)
328
Q

What is the treatment for someone with (high risk) Septic shock or NEWS >5 & NO allergy to penicillin/beta-lactam?

A
  • Piperacillin/tazobactam 4.5g IV 6hy +
  • Gentamicin
    (based on local epidemiology)
329
Q

What is the treatment for someone with (high risk) Septic shock or NEWS >5 & an allergy to penicillin/beta-lactam?

A
  • Vancomycin IV + Ciprofloxacin 400mg IV 12hy OR

- Aztreonam 2g IV 6hy + Gentamicin (based on local epidemiology)

330
Q

In Acute leukaemia/ Allogeneic STC patients with sepsis requiring inotropic support or septic shock, what antibiotics should you consider?

A

Meropenem 1g 8hy + aminoglycoside

331
Q

What antibiotic should you add if you suspect skin or soft tissue infection?

A

Vancomycin

332
Q

What antibiotic should you add if you suspect atypical pneumonia?

A

Clarithromycin

333
Q

What antibiotic should you use if there is a previous/known ESBL infection/carrier?

A

Meropenem

334
Q

What is the 6 part chain of infection?

A
  1. Infectious agent
  2. Reservoirs
  3. Portal of exit
  4. Means of transmission
  5. Portal of entry
  6. Susceptible host
335
Q

List 3 reservoirs for infection?

A
  1. Environment
  2. Animals
  3. Humans (symptomatic/asymptomatic, carriers)
336
Q

What are 3 means of infection prevention?

A
  1. Water control
  2. Rodent control
  3. Isolation
337
Q

What is the portal of exit for TB?

A

Respiratory tract

338
Q

What is the portal of exit for Salmonella?

A

Faeces

339
Q

What is the portal of exit for Norovirus?

A

Vomit

340
Q

What is the portal of exit for Blood borne viruses?

A

Cuts & injuries

341
Q

What is the portal of exit for Enterovirus?

A

Conjunctival secretions

342
Q

What are the 2 direct modes of transmission of infection?

A
  1. Direct contact

2. Droplet spread

343
Q

What are the 3 indirect modes of transmission of infection?

A
  1. Airborne
  2. Vehicle borne (food water fomites)
  3. Vectorborne (mechanical or biologic)
344
Q

Give 4 examples of infection portal of entry?

A
  1. Respiratory tract
  2. Mucous membranes
  3. Skin- non-intact
  4. Mouth (faecal-oral)
345
Q

List the 10 standard hospital precautions of infection prevention/control?

A
  1. Assess patients for infection risk & ensure they are cared for in a safe place
  2. Good hand hygiene
  3. Cover nose & mouth when coughing/ sneezing
  4. Suitable personal protective equipment
  5. Keep reusable care equipment clean & well maintained
  6. Keep care environment clean & tidy
  7. Safely handle used linen
  8. Safely clean up blood & body fluid spills
  9. Safely dispose of household & care activity waste
  10. Take corrective action if injured/exposed to blood & body fluids
346
Q

What outbreak was linked to artificial nails in a neonatal intensive care unit?

A

Extended-spectrum beta-lactamase-producing Klebsiella pneumoniae

347
Q

What are the 4 infective contact transmission based precautions?

A
  1. Isolation
  2. Cleaning
  3. Gloves
  4. Apron
348
Q

What are the 2 infective droplet transmission based precautions?

A
  1. Surgical mask

2. Eye protection

349
Q

What 7 factors make for a susceptible host?

A
  1. New host
  2. Immune status
  3. Vaccination
  4. Prophylaxis
  5. Nutrition
  6. Treatment of immuno-suppressive
  7. Protective isolation
350
Q

What are the 6 strategies for a hospital acquired infection (HAI)?

A
  1. Isolation
  2. Screening
  3. Cohorting
  4. Standard & transmission based precautions
  5. Surveillence
  6. Antimicrobial stewardship
351
Q

Describe the 9 procedures in an aseptic technique?

A
  1. Reduce activity in area
  2. Keep exposure of susceptible site to a minimum
  3. Check sterile packs for evidence of damage or moisture
  4. Ensure all fluids materials in date
  5. Do not re-using single use items
  6. Hand decontamination
  7. Use disposable apron
  8. Use sterile gloves.
  9. Appropriate waste disposal
352
Q

Describe the maintenance of a central venous catheter (CVC)?

A
  • Aseptic access technique
  • Daily site review
  • Remove CVC at earliest opportunity
353
Q

What has “Matching Michigan” resulted in?

A

60% reduction in central line-associated bloodstream infection (CLABSIs)

354
Q

Describe how antimicrobial resistance is ancient?

A
  • Diverse collection of genes encoding resistance to β-lactam, tetracycline & glycopeptides
  • Resistance is a natural phenomenon predating modern antibiotic use
355
Q

What are the 2 key factors in antibiotics driving resistance?

A

Course duration x No. of courses

356
Q

What 2 penicillins are narrow spectrum?

A

Benzylpenicillin & phenoxymethylpenicillin

357
Q

What 2 penicillins are moderate/broad spectrum?

A

Flucloxacillin & Amoxicillin

358
Q

What is an example of a broad spectrum combination penicillin?

A

Amoxicillin-clavulanate / Co-amoxiclav (Augmentin®)

359
Q

What is the problem with broad spectrum antibiotics?

A

Collateral damage

360
Q

List the 4 individual effects that collateral antibiotic damage causes?

A
  1. Antibiotic resistance
  2. Drug reaction / toxicity / interactions
  3. Diarrhoea (clostridium difficile)
  4. Vascular site infection (S.aureus bacteraemia)
361
Q

List the 2 population effects that collateral antibiotic damage causes?

A
  1. Antibiotic resistance

2. Clostridium difficile

362
Q

What correlates with rise in C. diff infection?

A

Increase in broad spectrum antibiotics (Cephalosporins)

363
Q

What 5 countries have the highest % of E. coli resistant to Cephalosporins?

A
  1. India
  2. China
  3. Kenya
  4. Ghana
  5. Mexico
364
Q

How much higher is the risk of death in patients infected with a resistant bug instead of a sensitive bug?

A

2x more likely with resistant bug

365
Q

What 3 things does the antibiotic guardian state for reducing antimicrobial resistance?

A
  1. Value Antibiotics
  2. Prescribe & Support prescribing as responsibly as we can
  3. Preserve most Valuable Agents for our most complex infections
366
Q

What is Antimicrobial Stewardship?

A

Programme to ensure safe & appropriate use of antibiotics

367
Q

List the 5 aims of Antimicrobial Stewardship?

A
  1. Optimize outcome
  2. Minimise unintended consequences
  3. Reduce AMR & C. Difficile
  4. Patient at centre of prescription decision making
  5. Hospital & community
368
Q

List 5 ways that Antimicrobial Stewardship is achieved through?

A
  1. Monitoring/ surveillance
  2. Guidelines/protocols
  3. Specific restrictions (reporting/antibiotics)
  4. Specific interventions
  5. Multidisciplinary working
369
Q

Describe how to work out the volume of antibiotic prescribing?

A
  • Measured through pharmacy records (not per individual)
  • Stratified for antibiotic type (defined daily dose)
  • Adjusted for population size (e.g. per 1000 population/ per admission/ occupied bed day)
370
Q

What are the 5 key components of antimicrobial stewardship?

A
  1. Appropriate for target population (primary vs secondary, specialist vs generalist, national vs local adaptation)
  2. Decision support - when to avoid/use antibiotics
  3. Appropriate investigations to support management
  4. Takes into account epidemiology of infection including AMR
  5. Availability/ cost
371
Q

List the 3 investigations that you could do in primary care to support antibiotic prescription?

A
  1. CRP, Near patient testing (“Strep test”)
  2. Urinalysis only if symptoms & failed on prior prescription
  3. Only “swab” infected- limited value as reflects commensal bacteria (MRSA)
372
Q

What is the empirical guidance in primary care?

A
  • Diagnosis often “syndromic”
  • Limited potential to support with investigations
  • Viral vs Bacterial (?Self limiting) vs No infection
  • Electronic prescribing
373
Q

How can you optimise lab diagnosis in the antimicrobial stewardship programme?

A

Sampling, testing & minimisation of “over diagnosis”

374
Q

What is the purpose of lab restricted reporting of sensitivities?

A

Reduce use of inappropriate agents

375
Q

What are the 6 steps to antibiotic prescribing?

A
  1. Is an antibiotic required?
  2. Which antibiotic?
  3. How should it be administered (severity)?
  4. Adjunctive measures?
  5. How long?
  6. REVIEW
376
Q

Give 5 examples of when NOT to prescribe an antibiotic?

A
  1. Viral + Self limiting bacterial RTIs
  2. Asymptomatic bacteruria, uncomplicated cystitis
  3. Ingrowing toe nails
  4. Varicose eczema
  5. Systemic inflammatory response due to cancer, ischaemia, inflammation
377
Q

How effective is the use of antibiotics in lower respiratory tract infections?

A

No better than placebo in primary care

378
Q

What are the 3 different types of urinary tract infections?

A
  1. Asymptomatic bacteruria
  2. Uncomplicated UTI (cystitis)
  3. Catheter-associated UTI
379
Q

How common is an Asymptomatic bacteruria (UTI) & how would you treat it?

A
  • 40% of elderly women

- Confirm urinary symptoms: If not don’t treat!

380
Q

How common is an Uncomplicated UTI (cystitis) & how would you treat it?

A
  • 30% of cystitis is culture negative
  • NSAIDs may be as effective as antibiotics
  • Consider delayed antibiotics
381
Q

How common is an Catheter-associated UTI & how would you treat it?

A
  • Remove catheter

- Treat if symptoms / sepsis

382
Q

What are the 4 non-antibiotic measures that can be applied in primary care for infections?

A
  1. Reassurance/explanation- Printed information
  2. Symptomatic measures: fluids, analgesia
  3. Delayed script
  4. Review date- “safety netting”
383
Q

What are the 5 symptoms/signs of infection?

A

Fever, sweats, rigors, shivers and shakes

384
Q

What are the 4 localised symptoms/signs of a bacterial infection?

A
  1. Dysuria & frequency
  2. Dyspnoea, cough + green/ brown sputum, crepitations
  3. Erythema, heat, swelling
  4. Sore throat with exudate & adenopathy
385
Q

Describe the choice of antibiotic in a non severe infection (community or hospital)?

A
  • Use narrow spectrum agents
  • Lower respiratory tract: Amoxicillin or Doxycycline
  • Lower UTI: Trimethoprim or Nitrofurantoin
  • Mild Cellulitis: Flucloxacillin or doxycycline
386
Q

Describe the choice of antibiotic in a severe/life threatening infection?

A
  • Usually IV combination (Beta lactam + Gentamicin) initially
  • Use of protected antibiotic if risk of multi-drug resistance
  • Prompt (<1 hour) admin
387
Q

What type of antibiotics can increase the risk of Clostridium difficile?

A

Any antibiotic of prolonged duration

388
Q

Give 2 examples of rapidly progressive/immediately life-threatening infections?

A
  1. Organ dysfunction = sepsis

2. Deep seated/ involving vital organs- bacteraemia, CNS, cardiovascular, graft related

389
Q

How should you assess the severity of infection in primary care?

A

Rapid admission to hospital + consider pre-hospital treatment

390
Q

How should you assess a severe systemic infection of unknown source in secondary care?

A
  • Urgent blood cultures then IV antimicrobial therapy within 1hr
  • Chest X-ray & consider other imaging/lab investigations
391
Q

When in a severe systemic infection of unknown source would you cover for S. aureus?

A

If healthcare associated, recent hospitalisation, post-op wound/ line related, IVDU

392
Q

When in a severe systemic infection of unknown source would you cover for an MRSA infection?

A

Recent MRSA carrier or previous infection

393
Q

When in a severe systemic infection of unknown source would you cover for a severe Streptococcal infection?

A

Pharyngitis/ erythroderma/ hypotension

394
Q

What antibiotics would you give for a severe systemic infection of unknown source?

A

IV Amoxicillin 2g 6hrly + IV Gentamicin (max 3-4days)

395
Q

What antibiotic would you add for a severe systemic infection if S. aureus was suspected?

A

ADD IV Flucloxacillin 2g 6hrly

396
Q

What antibiotics would you give for a severe systemic infection if MRSA was suspected or patient has a true penicillin/beta-lactam allergy?

A

IV Vancomycin + IV Gentamicin (max 3-4 days)

397
Q

What antibiotics would you add for a severe systemic infection if streptococcal infection was suspected?

A

ADD IV Clindamycin 600mg 6 hrly, duration reviewed with response/micro results at 72hrs

398
Q

Describe the potency of Gentamicin?

A

Bacteriocidal + protein synthesis inhibition (Primarily anti Gram negative)

399
Q

How would you use Gentamicin?

A

Empirically & short term, avoid >4 days, needs therapeutic drug monitoring

400
Q

What are 2 areas that have toxic side effects of Gentamicin?

A

Renal & 8th cranial nerve (vestibulocochlear nerve)

401
Q

How would you review antibiotics in primary care?

A

“Safety netting”or review to assess response

402
Q

How would you review antibiotics in secondary care?

A
  • Clinical, micro results
  • De-escalate: Simplify or Switch or Stop
  • Review IV daily : IVOST
  • Document (3 day) review
  • Record Specific Duration of treatment
  • Consider Specialist input & Source Control
403
Q

What does IVOST stand for?

A

IV to Oral switch therapy

404
Q

What are 3 antimicrobial Stewardship Organisational

Aspects?

A
  1. Good clinical practice (all prescribers, all HCWs)
  2. Organisational priority
  3. Dedicated Team with expertise in infection
    management, prescribing surveillance &
    quality improvement
405
Q

Describe the dedicated infection team?

A
  • Infection specialist(s), Clinical Pharmacist
  • Multi-disciplinary clinical network & committee
  • Management engagement & IPC coordination
  • Clinical Governance & patient safety
406
Q

Describe restrictive antimicrobial stewardship intervention?

A

Short term benefits including reduction in resistance

407
Q

Describe persuasive antimicrobial stewardship intervention?

A

Longer term benefits through behaviour change

408
Q

What 2 Antimicrobial Stewardship Interventions result in a reduced mortality?

A
  1. Guideline adherence (empirical guideline & de-escalation)
  2. Infectious disease Physician consultation in Staphylococcus aureus bacteremia
409
Q

What 4 things are reduced when you apply AMS and reduce total antibiotic use in primary care?

A
  1. Clostridium difficile
  2. MRSA
  3. Gram negative bacteraemia mortality
  4. AMR in Gram negative bacteraemia
410
Q

What are the 2 main human factors effecting antibiotic resistance?

A
  1. Knowledge & experience- perception of resistance, misconception that spectrum of activity (efficacy), lack of confidence in diagnosis, fear of failure
  2. Prescribing culture- peer practice, hierarchy, speed of escalation of treatment, brand familiarity, fear of litigation
411
Q

What are the 4 key factors of realistic medicine to optimise use & outcome?

A
  1. Reduce variation in prescribing practice
  2. Reduce waste (over prescribing, redundancy)
  3. Reduce harm (C. diff, AMR, penicillin allergy, toxicity)
  4. Personalised/Individualise (risk based treatment)
412
Q

What are 4 factors for minimising antibiotic collateral damage?

A
  1. Importance of selecting the right antibiotic
  2. Restrict broad spectrum agents
  3. Knowing when antibiotics not required
  4. Promotion of shorter course therapy
413
Q

What are 30% of cystitis?

A

Culture negative

414
Q

What antibiotics would you prescribe for an uncomplicated UTI?

A
  • Trimethoprim/ Nitrofurantoin in lower UTI

- 3 days (women) or 7 days (men)

415
Q

What do 40% of elderly women have?

A

Asymptomatic bacteruria

416
Q

What are the likely bugs that you should cover when treating a UTI?

A

Gram negative coliforms

417
Q

How would you treat an upper UTI/Pyelonephritis,SEPSIS?

A

Gentamicin with oral switch (7 days total)

418
Q

How is sepsis quantified?

A
  • Increase in Sequential Organ Failure Assessment (SOFA) score of ≥ 2 for the organ in question
    OR
  • “Quick SOFA” = Confusion or Hypotension or Tachypnoea
419
Q

What is a high qSOFA score associated with?

A

High mortality

420
Q

What is sepsis 6/BUFALO?

A
  1. Perform Blood cultures (other bacteriology)
  2. Broad spectrum antibiotics
  3. Oxygen to achieve target saturation
  4. Measure Lactate & Hb
  5. IV fluids
  6. Monitor urinary output hourly
421
Q

What is an immediate penicillin allergy?

A

<1 hr, type 1 hypersensitivity reaction

422
Q

What is a delayed penicillin allergy?

A
  • Blistering rash & systemic illness

- Type IV hypersensitivity

423
Q

What % of penicillin allergies aren’t actually an allergy?

A

80%

424
Q

What 4 things is mislabelling of a penicillin allergy associated with?

A
  1. Increased treatment cost
  2. Admission length
  3. AMR
  4. Poor outcomes
425
Q

Give 8 indications for IV antibiotic therapy?

A
  1. Sepsis syndrome, SIRs or rapidly progressing infection
  2. Infective endocarditis
  3. CNS infection
  4. Bacteraemia (S. aureus)
  5. Osteomyelitis (initially)
  6. Mod-severe skin & soft tissue infection
  7. Infection & oral route compromised
  8. No oral formulation of antibiotic available
426
Q

What 3 bugs can cause cellulitis?

A
  1. Usually GAS (group A beta-hemolytic Strep) or groups B, C or G
  2. Staphylcoccous aureus
  3. Gram negatives uncommon
427
Q

What antibiotic would you give for cellulitis?

A

Flucloxacillin

  • oral 5 days if mild
  • IV- (IVOST) if mod-severe 7-10 days
428
Q

What antibiotics would you give in very severe cellulitis?

A

Add IV Clindamycin & Gentamicin to flucloxacillin therapy

429
Q

What 3 bugs can cause necrotising fasciitis?

A
  1. Usually GAS (group A beta-hemolytic Strep) or groups B, C. G
  2. Staphylcoccous aureus
  3. Gram negatives rarely
430
Q

Describe necrotising fasciitis?

A
  • Pain out with appearance
  • Masked by NSAIDs
  • Rapidly progressive with multi-organ failure
431
Q

What is the EAGLE effect associated with necrotising fasciitis?

A
  • Static growth phase with excess toxin production

- Beta lactams not effective

432
Q

What are the 2 treatments for necrotising fasciitis?

A
  1. Surgery

2. Immunoglobulin

433
Q

What are 3 bugs presenting with gram positive cocci on blood culture at 24hrs?

A
  1. Staphylococcus aureus
  2. Staphylococcus epidermidis
  3. Meticillin resistant or sensitive
434
Q

How would you investigate & treat S. aureus bacteraemia?

A
  • Find & remove source of infection: vascular, bone/joint, prosthetic, cardiac
  • ECHO (endocarditis) & other treatment for underlying source (eg spinal infection)
  • Repeat BCs after 48-96 hours of effective IV antibiotics
435
Q

What antibiotic would you give for a S. aureus bacteraemia?

A

Flucloxacillin 2g 6 hourly, ≥2 weeks

436
Q

What would you give a S. aureus bacteraemia patient with a true penicillin allergy?

A

Vancomycin as per guidance/calculator, ≥2 weeks

437
Q

When would you do a transoesophageal echocardiography (TOE) for a bacteraemia?

A
  1. Persistent fever or no improvement or further positive blood cultures
  2. Negative transthoracic echocardiogram (TTE) if PV or if endocarditis is still suspected
438
Q

When would you give antibiotics in an exacerbation of COPD?

A

Purulent (green) sputum

439
Q

What does yellow sputum mean?

A

Asthma

440
Q

What antibiotics would you give in an exacerbation of COPD?

A

Amoxicillin or Doxycycline, use shortest duration

441
Q

What are the 2 risk factors for Clindamycin?

A
  1. Substrate & inhibitor of CYP3A4

2. QTc prolongation

442
Q

Give 3 drugs which interact with Clindamycin?

A
  1. Simvastatin
  2. Fluconazole
  3. Citalopram
443
Q

What has gentamicin got a low risk of?

A

C. Diff infection

444
Q

What should you do to avoid kidney infection & CNVIII toxicity with gentamicin?

A

Limit to 72hrs & switch to alternate IV or oral agent, stop at earliest signs as it may be irreversible

445
Q

What are the 3 most common types of illnesses that travellers get?

A
  1. Gastrointestinal diagnoses
  2. Febrile illness
  3. Dermatological diagnosis
446
Q

List the 6 most common bacterial causes of travellers diarrhoea?

A
  1. Enterotoxigenic E.coli
  2. Enteroaggregative E.coli
  3. Campylobacter sp
  4. Salmonella sp
  5. Shigella sp
  6. C.difficile
447
Q

List the 3 most common viral causes of travellers diarrhoea?

A
  1. Norovirus
  2. Rotavirus
  3. Enteric adenovirus
448
Q

List the 6 most common parasitic causes of travellers diarrhoea?

A
  1. Giardia
  2. Cryptosporidium
  3. Cyclospora
  4. Microsporidia
  5. Isospora
  6. Entamoeba histolytica
449
Q

Describe the clinical manifestations of travellers diarrhoea?

A
  1. Often day 4 to 14 travel

2. Self limiting: 1-5 days, 8-15% last >1 week

450
Q

List the 4 symptoms (ETEC) of travellers diarrhoea?

A
  1. Anorexia, malaise & abdominal cramps
  2. Watery diarrhoea (no blood)
  3. Fever, nausea & vomiting
  4. “colitic symptoms”- salmonella/shigella etc
451
Q

List the 4 management plans for travellers diarrhoea?

A
  1. Fluid replacement
  2. Antibiotics (reduce duration by 24hrs)- Quinolones, Azithromycin
  3. Antimotility agents (caution)
  4. Investigation for other causes
452
Q

What is the most common & most concerning problems with travellers diarrhoea?

A
  • Most common: diarrhoea

- Most concerning: undifferentiated fever

453
Q

List the 2 types of mosquitoes which can cause travellers diarrhoea?

A
  1. Aedes

2. Anopheline

454
Q

Describe how the Aedes mosquito infects travellers?

A
  • Dengue fever
  • Female mosquito
  • Bites in the morning
455
Q

Describe how the Anopheline mosquito infects travellers?

A
  • Malaria

- Bites from dusk –> dawn

456
Q

What are the 3 ways to physically avoid mosquito bites?

A
  1. Indoors- AC, screens
  2. Impregnated netting- permethrin, “tucked in”, “mosquito free”
  3. Clothing- cover up, spray/soak
457
Q

How often should you reapply 30% deet?

A

Every 3-4hrs

458
Q

Describe the epidemiology of malaria?

A
  • 27-48% hospitalised returning travellers
  • Most common cause fever in travellers from sub
    saharan Africa
  • Diagnosis initially missed up to 59% cases
459
Q

What is the incubation period for P.falciparum?

A

7-14 days

460
Q

What is the incubation period for P.vivax?

A

12-17 days

461
Q

What is the incubation period for P.ovale?

A

15-18 days

462
Q

What is the incubation period for P.malaria?

A

18-40 days (>1yr)

463
Q

What are the 3 ways to diagnose Malaria?

A
  1. Antigen testing (common)
  2. Blood films (thick & thin)
  3. PCR
464
Q

List the 8 clinical features of malaria?

A
  1. Fever
  2. Malaise
  3. Headache
  4. Myalgia
  5. Diarrhoea
  6. Anaemia
  7. Jaundice
  8. Renal impairment
465
Q

List the 8 clinical features of severe malaria?

A
  1. Parasitaemia >2%
  2. Cerebral malaria
  3. Severe anaemia
  4. Renal failure
  5. Shock
  6. DIC
  7. Acidosis
  8. Pulmonary oedema
466
Q

What are the 2 forms of treatment for Malaria?

A
  1. Artemether compounds e.g. Riamet

2. Quinine & Doxycycline

467
Q

What are the 2 ways to prevent malaria?

A
  1. Bite avoidance

2. Chemoprophylaxis

468
Q

List the 3 types of Malarial chemoprophylaxis?

A
  1. Mefloquine- Once weekly, Psychiatric side effects
  2. Doxycycline- Daily, Photosensitisation
  3. Malarone- Minimal side effects, Cost
469
Q

What are the 2 types of enteric fevers?

A
  1. S. typhi

2. S. paratyphi

470
Q

Describe Typhoid?

A
  • Human reservoir only (no animal reservoir): Human to human

- ↑ innoculum = shorter incubation period/↑ attack rate

471
Q

Describe the pathogenesis of Typhoid?

A

Contaminated food/water –> effects liver, spleen & lymph nodes –> eventually bacteraemic

472
Q

What is the incubation period for Typhoid?

A

5-21 days

473
Q

What 4 factors influence Typhoids incubation period?

A
  1. Age
  2. Gastric acidity
  3. Immune status
  4. Infectious load
474
Q

List the clinical features of Typhoid?

A
  1. Fever
  2. Myalgia
  3. Headache
  4. Cough
  5. Abdo pain
  6. Constipation
  7. Diarrhoea
475
Q

What 2 things can Typhoid lead to?

A
  1. Septic shock

2. Death

476
Q

List the 4 GI symptoms associated with Typhoid?

A
  1. Diarrhoea v Constipation: 50:50, Diarrhoea more common in children
  2. Abdominal pain
  3. Rectal bleeding
  4. Bowel perforation: Hyperplasia Peyer’s patches
477
Q

List the 4 other symptoms associated with Typhoid?

A
  1. Neurological: headache, enteric encephalopathy
  2. Bacteraemia: metastatic infection
  3. Relative bradycardia
  4. Rose spots
478
Q

Describe enteric encephalopathy associated with Typhoid?

A
  • Altered consciousness/confusion
  • Increased mortality
  • Steroids
479
Q

What 4 ways do you diagnose Typhoid?

A
  1. Travel history- Area visited, Food & drink, pre travel vaccination/advice
  2. Blood culture- 60-80% positive
  3. Stool culture- 30% positive
  4. Serology- Poor sensitivity/specificity
480
Q

What are the 3 treatments for Typhoid?

A
  1. Quinolones- Most effective agents, Resistance!
  2. Cephalosporins- Empirical therapy, Longer courses (14 days)
  3. Azithromycin- Very good activity with increasing evidence, Lack of evidence in severe disease, Oral option
481
Q

What is the incubation period of Dengue fever?

A

5-14 days

482
Q

List the 9 clinical features associated with “Breakbone fever” in Dengue fever?

A
  1. Headache
  2. Fever
  3. Retro-orbital pain
  4. Arthralgia/myalgia
  5. Rash
  6. Cough
  7. Sore throat
  8. Nausea
  9. Diarrhoea
483
Q

List the 3 laboratory features in Dengue fever?

A
  1. Leucopenia
  2. Thrombocytopenia
  3. Transaminitis
484
Q

How do you treat Dengue fever?

A
  • Symptomatic

- No cure

485
Q

What is the definition of Dengue Haemorrhagic fever?

A
  • ↑vascular permeability
  • Thrombocytopenia
  • Fever
  • Bleeding
486
Q

List the 7 possible causes of viral haemorrhagic fever?

A
  1. Lassa
  2. Ebola/Marburg
  3. Crimean-Congo haemorrhagic fever
  4. SAVHFs
  5. Rift Valley Fever
  6. Dengue hemorrhagic fever
  7. Yellow fever
487
Q

Describe the exposure of viral haemorrhagic fever?

A
  • Rural > Urban

- Nosocomial

488
Q

Describe the clinical presentation/development of viral haemorrhagic fever?

A

Exposure –> Non specific febrile illness –> Haemorrhagic manifestations –> Sepsis syndrome/shock –> Death

489
Q

What is the incubation period for viral haemorrhagic fever?

A

Upto 21 days

490
Q

In what 3 stages of disease can you treat viral haemorrhagic fever?

A
  1. Non specific febrile illness
  2. Haemorrhagic manifestations
  3. Sepsis syndrome/shock
491
Q

How would you treat viral haemorrhagic fever?

A
  • Supportive
  • Correct coagulopathy/anaemia
  • Ribavirin
492
Q

What are 3 factors to consider when trying to diagnose travellers diarrhoea?

A
  1. Non travel related infection
  2. Some prediction from area visited
  3. Visit to malarious area = malaria until proven otherwise
493
Q

List 7 crucial history questions you would ask when suspecting travellers diarrhoea?

A
  1. Where were they?
  2. For how long?
  3. What was purpose of visit?
  4. What did they get up to when there?
  5. Any pre travel vaccines/prophylaxis?
  6. How long are they back for?
  7. How long have they been unwell for?
494
Q

What is the clinical assessment tool used to help identify at risk patients with community acquired pneumonia?

A

CURB-65 score for pneumonia severity

495
Q

What are the 5 clinical criteria that the CURB-65 score for pneumonia severity is based on?

A
  1. Mental status/confusion
  2. Urea > 7mmol/L
  3. Respiratory rate >30
  4. Systolic BP <90 mmHg or diastolic BP <60 mmHg
  5. Age >65
496
Q

Name the 4 most common bacterial causes of community acquired pneumonia?

A
  1. Steptococcus pneumonia
  2. Haemophilus influenzae
  3. Staphylococcus aureus
  4. Group A streptococci
497
Q

Name the 3 most common atypical causes of community acquired pneumonia?

A
  1. Legionella spp.
  2. Mycoplasma pneumoniae
  3. Chlamydia pneumoniae
498
Q

Name the 3 most common respiratory viruses causing community acquired pneumonia?

A
  1. Influenza A & B viruses
  2. Parainfluenza viruses
  3. Respiratory syncytial virus
499
Q

What are 4 additional clinical/microbiological information that would be important when suspecting community acquire pneumonia?

A
  1. Travel history- epidemic pathogen exposures, potential antimicrobial resistance
  2. Previous (recent) antibiotic therapy
  3. Previous microbiology culture results
  4. Drug allergies/intolerances
500
Q

What are the 5 specific samples that you would take for severe community acquired pneumonia?

A
  1. Respiratory samples- Routine Microbiology culture, Viral PCR (Gargle/throat swab can also be sent)
  2. Urine specimen for Legionella pneumophila urinary antigen testing (Serotype 1 only)
  3. PCR for Legionella species
  4. Blood culture
  5. MRSA Screen
501
Q

What empirical antibiotics would you prescribe for severe community acquired pneumonia?

A

IV amoxicillin or IV co-amoxiclav with Clarithromycin

502
Q

What empirical antibiotics would you prescribe for community acquired pneumonia with true penicillin/beta-lactam allergy?

A

Levofloxacin (IV only if oral route compromised)

503
Q

What are 2 other legionella infections?

A
  1. Pontiac fever

2. Extrapulmonary Legionella disease

504
Q

Describe Pontiac fever?

A
  • Acute, self-limiting febrile illness

- Symptoms: nonspecific & include fever, headache, myalgia, nausea, vomiting & diarrhoea

505
Q

Describe Extrapulmonary Legionella disease?

A
  • Rare & can occur as a complication of Legionella pneumonia
  • Seen in immunocompromised
  • Manifestations: abscesses, septic arthritis, myocarditis, pericarditis, peritonitis & meningitis
506
Q

What should always be considered in any patient presenting with pneumonia?

A

Legionella infection

507
Q

What is Legionella infection associated with?

A

Contamination of water supplies in large facilities such as hospitals, hotels or apartment buildings

508
Q

What are the 4 patient risk factors for Legionella infection?

A
  1. Old age
  2. Smoking
  3. Chronic lung, cardiovascular or renal disease
  4. Immunocompromised
509
Q

What is the gold standard test for a Legionella infection?

A

Culture or PCR

510
Q

What are the 4 most commonly identified bacterial causes of acute epiglottitis?

A
  1. Haemophilus influenzae
  2. Streptococcus pneumoniae
  3. Staphylococcus aureus
  4. Beta-haemolytic streptococci: Groups A, B, C, F, G
511
Q

What empirical antibiotics would you prescribe for acute epiglottitis?

A

IV Ceftriaxone with Clindamycin

512
Q

What oral antibiotic would be appropriate for the treatment of an invasive Group A streptococcal infection/acute epiglottitis?

A

Clindamycin

513
Q

What is GAS (invasive streptococcus pyogenes infection)?

A

Gram positive cocci that causes a wide range of infections

514
Q

List the virulence factors possessed by GAS (invasive streptococcus pyogenes infection)?

A

Streptolysins, DNases, Exotoxins, Streptococcal super-antigens

515
Q

List the 9 clinical manifestations of GAS (invasive streptococcus pyogenes infection)?

A
  1. Skin & soft tissue infection
  2. Necrotising fasciitis
  3. Myositis
  4. Septic arthritis
  5. Pharyngitis & RTI
  6. Postpartum endometritis
  7. Puerperal sepsis
  8. Meningitis
  9. Toxic shock syndrome
516
Q

What is the best treatment for GAS (invasive streptococcus pyogenes infection) when there is clinical evidence of shock?

A

Bacteriostatic antibiotics (such as clindamycin, linezolid) are superior to bactericidal antibiotics (such as beta-lactams)

517
Q

GAS is inherently susceptible to ________?

A

Penicillin

MBChB Year 3 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions