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Phase 2a Medicine > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Define ‘pathogen’.

A

Organism that causes, or is capable of causing, disease

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2
Q

Define ‘commensal’

A

Organism which colonises the host, but causes no disease in normal circumstances.

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3
Q

What is an ‘opportunist pathogen’.

A

Microbe that only cases disease if host defences are compromised.

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4
Q

Define ‘virulence / pathogenicity’.

A

The degree to which a given organism is pathogenic, and any strategy used to achieve this.

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5
Q

Define ‘asymptomatic carriage’.

A

When a pathogen is carried harmlessly at a tissue site where it causes no disease.

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6
Q

Name nine tests / stains used to identify bacteria.

A
  1. Gram stain
  2. Ziehl-Neesen stain
  3. Catalase test
  4. Coagulase test
  5. Haemolysis test
  6. Optochin test
  7. Oxidase test
  8. Macconkey agar
  9. XLD agar

REMEMBER: Gay Zoologists Can Cum Heavily Over My Orange Xylophone

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7
Q

What are the two families of bacteria?

What is the difference?

A
  • Gram positive - single membrane

- Gram negative - double membrane

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8
Q

What does gram staining differentiate between?

A

Gram positive and gram negative bacteria

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9
Q

Describe the process of gram staining.

A
  1. Apply primary stain (e.g. crystal violet) to heat fixed bacteria
  2. Add iodine, which binds to crystal violet and helps fix it to cell wall
  3. Decolourise with ethanol or acetone
  4. Counterstain with safranin
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10
Q

What is the result of the gram stain test for gram negative and gram positive bacteria? Explain why.

A

Gram negative = pink
- Decolouriser INTERACTS with lipids, and cells lose their outer LPS membrane and CV-I complexes, thus appear pink

Gram positive = purple
- Decolouriser DEHYDRATES cell wall, and CV-I complex gets trapped in multi-layered peptidoglycan, resulting in purple appearance

REMEMBER: gram Negative = piNk

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11
Q

What does Ziehl-Neesen differentiate between?

A

Acid-fast bacilli and non-acid fast bacilli

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12
Q

What family of bacteria does Ziehl-Neesen identify? Why?

A

Mycobacteria, because they are acid-fast bacilli

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13
Q

What are the results for the Ziehl-Neesen stain?

A

Acid-fast bacilli = red (e.g. mycobacteria)

Non-acid fast bacilli = blue (e.g. E.coli)

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14
Q

What does the catalase test differentiate between?

A

Staphylococcus and streptococcus bacteria

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15
Q

How do you carry out the catalase test?

A

Add H2O2 to bacteria and observe if there is bubbling

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16
Q

What is the result if you do a catalase test on staphylococcus and streptococcus?

A

Staphylococcus are catalase POSITIVE so you see BUBBLING

Streptococcus are catalase NEGATIVE so there is NO REACTION

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17
Q

What is coagulase?

What produces it?

A

An enzyme produced by Staphylococcus aureus that converts soluble fibrinogen to insoluble fibrin

Other staphylococci do NOT produce coagulase

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18
Q

What are the results of the coagulase test?

A

Staphylococcus aureus is coagulase POSITIVE so you see clumping

Other staphylococci are coagulase NEGATIVE so there is no clumping

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19
Q

What is haemolysis?

A

The ability of bacteria to break down red blood cells in blood agar

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20
Q

What does haemolysis require?

A

Haemolysin

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21
Q

What is the result of alpha haemolysis in the haemolysis test?

A

An indistinct zone of partial destruction of RBCs appears around the colony, often accompanied by an opaque green/brown discolouration of the medium

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22
Q

Which bacteria are alpha haemolytic?

A
  • Streptococcus pneumoniae
  • Many oral streptococci (viridians streptococci)
  • S.intermedius
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23
Q

What are viridians streptococci and what can they cause?

A

Collective name for oral streptococci

They can cause serious pathology e.g. infective endocarditis

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24
Q

What is the result of beta haemolysis in the haemolysis test?

A

A clear, colourless zone appears around the colonies, in which the RBCs have undergone complete lysis

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25
Q

Which bacteria are beta haemolytic?

A
  • Streptococci pyogenes
  • Streptococci agalactiae
  • Many other streptococci
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26
Q

Can bacteria other than streptococci be beta haemolytic?

A

Yes, S.aureus and Listeria monocytogenes are both beta haemolytic

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27
Q

If you conduct the haemolysis test on Streptococci and Staphylococcus, but they both appear beta haemolytic;

  1. Which staphylococcus bacteria is it?
  2. How do you differentiate?
A
  1. S.aureus - beta haemolytic staphylococci

2. Coagulase test - staphylococci are coagulase positive, streptococci are coagulase negative

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28
Q

What is the result of gamma haemolysis in the haemolysis test?

A

No change, bacteria are non-haemolytic

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29
Q

What does the optochin test differentiate between?

What do you observe?

A

Streptococcus pneumoniae and Streptococcus mitis

A clear zone is seen around S.pneumoniae as it is susceptible to optochin, but S.mitis is uninhibited as it is resistant

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30
Q

Describe the process of the optochin test.

A

Place an optochin soaked disc on agar and observe bacterial growth

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31
Q

What is seen with alpha haemolytic bacteria in the optochin test?

A

They are resistant to optochin so there will be growth around the disc

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32
Q

What does the oxidase test test for?

A

Tests if a micro-organism contain cytochrome oxidase, an enzyme in the bacterial ETC

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33
Q

What does an oxidase positive test mean?

A

Bacteria are definitely AEROBIC

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34
Q

What does a negative oxidase test mean?

A

Bacteria are either aerobic or anaerobic

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35
Q

Name four oxidase positive bacteria.

A
  • P.aeruginosa
  • V.cholerae
  • Campylobacter (e.g. C.jejuni)
  • Helicobacter
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36
Q

Which type of bacteria grow on Macconkey agar?

A

Gram-negative bacilli

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37
Q

What does Macconkey agar differentiate between?

What are the results?

A

Differentiated between lactose-fermenting and non-lactose fermenting G-ve bacilli

Lactose-fermenting = pink/red
Non-lactose fermenting = white/transparent

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38
Q

Why does the Macconkey agar turn pink/red with lactose-fermenting G-ve bacilli?

A

It contains a pH indicator, so bacteria which ferment lactose produce acid, which alters the pH

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39
Q

Why can’t G+ve bacteria grow on Macconkey agar?

What else can’t grow on it?

A

Bile salts present inhibit G+ve bacteria, and inhibit swarming of G-ve bacteria Proteus spp.

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40
Q

Give three examples of bacteria which would turn Macconkey agar red/pink.

A
  • E.coli
  • Klebsiella pneumoniae
  • Enterobacter spp.
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41
Q

Give two bacteria which would cause the Macconkey agar to appear white/transparent.

A
  • Salmonella spp.

- Shigella spp.

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42
Q

What does XLD agar differentiate between?

A

Salmonella and Shigella

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43
Q

What is observed in the XLD agar test?

A 
Salmonella = red/pink colonies with black spots
Shigella = red/pink colonies
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44
Q

Name three genera of Gram positive cocci.

A
  • Staphylococci
  • Streptococci
  • Enterococci
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45
Q

Name two genera of Gram negative cocci.

A
  • Neisseria

- Moraxella

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46
Q

Name four genera of Gram positive bacilli.

A
  • Bacillus
  • Clostridia
  • Corynebacteria
  • Listeria monocytogenes
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47
Q

Name six genera of Gram negative bacilli.

A
  • E.coli
  • Campylobacter
  • Pseudomonas
  • Salmonella
  • Shigella
  • Proteus
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48
Q

What is the bacterial capsule?

What can it do?

A

A polymer of sugar that protects bacteria from host immune system

It can inhibit parts of the innate immune system

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49
Q

What is the bacterial cell wall made of?

A

Phospholipids

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50
Q

What makes bacteria prokaryotes?

A

The absence of a nuclear membrane

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51
Q

What is a plasmid?

A

A circular loop of DNA, often containing genes for antibiotic resistance

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52
Q

Which enzyme is present in bacterial cytoplasm?

A

RNA polymerase

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53
Q

What is cell envelope like in G+ve bacteria?

A
  • Single cytoplasmic membrane
  • Large amount of peptidoglycan on outer surface
  • No endotoxin (lipopolysaccharide)
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54
Q

What is the cell envelope like in G-ve bacteria?

A
  • Double membrane; inner and outer
  • Less peptidoglycan; between the membranes
  • Outer membrane has lipopolysaccharide (endotoxin) which the immune system reacts to
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55
Q

What do antibiotics target in G-ve bacteria?

A

Peptidoglycan between cell envelope membranes

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56
Q

Which mucosal surfaces are vulnerable to bacterial colonisation?

A
  • Nasal cavity
  • Larynx
  • Stomach
  • Colon
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57
Q

What is a spore? How do you destroy one?

A

A hardy capsule which bacteria can store themselves inside

They need to be autoclaved to be destroyed

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58
Q

What temperature limits can bacteria survive within?

A

-80ºc to 80ºc

120ºc for spores

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59
Q

What pH limits can bacteria survive within?

A

4-9

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60
Q

How long can bacteria survive in water / desiccation?

A

2hrs - 3m

50yrs for spores

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61
Q

How do you measure growth of bacteria?

A

Shine a light through them and measure absorption

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62
Q

How do bacteria divide?

A

Binary fission

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63
Q

What are the four phases of a bacterial growth curve?

Explain them.

A
  1. Lag phase - bacteria are taking in nutrients needed to divide and multiply
  2. Log phase - bacteria grow exponentially until they run out of nutrients
  3. Stationary phase - nutrients run out so bacteria can no longer divide
  4. Death phase - bacteria die without nutrients
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64
Q

What is an endotoxin?

A

A component of the outer membrane of G-ve bacteria - LIPOPOLYSACCHARIDE

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65
Q

How does an endotoxin trigger an immune response?

A

Host immune system will recognise toxin and initiate immune response called ENDOTOXIC SHOCK

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66
Q

Is endotoxic shock specific or non-specific?

A

Non-specific

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67
Q

What happens if you subject an endotoxin to heat?

A

It is stable

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68
Q

Which type of bacteria mainly produce endotoxins?

A

Gram negative

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69
Q

Can an endotoxin be converted into a toxoid?

A

No

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70
Q

Which bacteria secrete exotoxins?

A

Gram positive and gram negative

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71
Q

What are exotoxins?

A

Proteins

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72
Q

What is the action of the immune system to exotoxins?

A

Specific

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73
Q

What effect do botulism and tetanus have on the nervous system?

A

Botulism - inhibits nervous system

Tetanus - stimulates nervous system

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74
Q

What happens to exotoxins if you expose them to heat?

A

They denature

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75
Q

T/F: Exotoxins can be converted to toxoids.

A

True

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76
Q

What is transcription?

A

RNA polymerase acts on the bacterial chromosome to form mRNA

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77
Q

What is translation?

A

Occurs at 30s/50s ribosome to produce proteins

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78
Q

What sort of mutations can occur on the bacterial chromosome?

A
  • Base substitutions
  • Deletions
  • Insertions
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79
Q

Why can mutations cause antibiotics to be ineffective?

A

Protein coded for is altered by mutation, meaning it is no longer susceptible to the antibiotic

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80
Q

Name three ways bacteria transfer genes.

A
  1. Transformation
  2. Transduction
  3. Conjugation
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81
Q

What is transformation?

A

The genetic alteration of a bacterial cell via the uptake of an exogenous substance (e.g. via plasmid)

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82
Q

What is transduction?

A

Process by which foreign DNA is introduced into a bacteria via vector or virus (e.g. bacteriophage)

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83
Q

What is conjugation?

A

The transfer of genetic material between bacterial cells by direct cell-to-cell contact (e.g. via pilus)

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84
Q

Where will you normally find staphylococcus?

A

On the nose and skin

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85
Q

How many species are there of staph?

A

At least 40

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86
Q

Why might a patient with a S.aureus infection present with shoulder pain?

A

Referred pain from osteomyelitis in cervical spine vertebrae (C6 & C7)

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87
Q

What is the preferred method of imagine for osteomyelitis?

A

MRI scan

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88
Q

What is the standard treatment for S.aureus infection?

A

Flucloxacillin for 3 months

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89
Q

What does the coagulase test reveal about S.aureus?

A

It’s coagulase positive

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90
Q

How is S.aureus spread?

A

Aerosol and tough (e.g. coughing and breathing)

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91
Q

Which antibiotics is MRSA resistant to?

A
  • B-lactams
  • Gentamicin
  • Erythromycin
  • Tetracycline
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92
Q

What are the four virulence factors S.aureus has?

A
  • Pore-forming toxins
  • Proteases
  • Toxic shock syndrome toxin
  • Protein A
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93
Q

How does S.aureus use pore-forming toxins to cause disease?

A
  • PVL toxin produced caused haemorrhage pneumonia

- Alpha-haemolysin induces apoptosis (at low levels) and necrosis (at high levels)

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94
Q

How does S.aureus use proteases to cause disease?

A

Produces exfoliatin, which attacks desmosomes between skin cells, which causes scalded skin syndrome

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95
Q

How does S.aureus cause disease using toxic shock syndrome toxin?

A

Stimulates cytokine release, triggering an inflammatory response and tissue damage

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96
Q

How does S.aureus use protein A to cause disease?

A

Uses protein A, a surface protein, to cause immunoglobulins to bind in the wrong orientation to antigens

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97
Q

Which conditions are associated with S.aureus infections?

A
  • Wound infections
  • Abscesses
  • Osteomyelitis
  • Scalded skin syndrome
  • TSS
  • Food poisoning
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98
Q

Give three examples of coagulase negative staphylococci.

A
  • S.epidermis
  • S.saprophyticus
  • Acute cystitis
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99
Q

What sort of bacteria is S.epidermis and where does it tend to infect?

A

Opportunistic bacteria, causing infections in prosthetic limbs and catheters

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100
Q

What are the 3 classifications of streptococci?

A
  • Haemolysis
  • Lancefield typing
  • Biochemical properties
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101
Q

Give an example of an alpha haemolytic streptococcus.

A

S.intermedius

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102
Q

Give an example of a beta haemolytic streptococcus.

A

S.pyogenes

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103
Q

Give an example of a gamma haemolytic streptococcus.

A

S.mutans

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104
Q

Explain the Lancefield typing classification.

A

A method of grouping coagulase negative and catalase negative bacteria based on the bacterial carbohydrate cell surface antigens

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105
Q

What does S.pyogenes cause?

A
  • Wound infections (e.g. cellulitis)
  • Tonsillitis & pharyngitis
  • Otitis media
  • Scarlet fever
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106
Q

What are the complications of a S.pyogenes infection?

A
  • Rheumatic fever
  • Glomerulonephritis
  • Immunologically mediated complications
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107
Q

How does S.pyogenes stimulate an immunologically-mediated complication?

A

It produces erythrogenic toxin which is a super antigen, meaning it gives rise to an exaggerated immunological response and increased circulating cytokine levels

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108
Q

How do you assess the risk of a S.pyogenes infection:

A

Anti-streptolysin O titre

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109
Q

What are the pathogenic factors associated with S.pyogenes?

A

Secretion of…

  • Hyaluronidase - spreading
  • Streptokinase - clot degradation
  • C5a peptidase - reduces chemotaxis
  • Streptolysin O & S toxin - binds cholesterol
  • Erythrogenic toxin - exaggerated response

Surface factors…

  • Hyaluronic acid capsule - protection
  • M protein - encourages complement degradation
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110
Q

What might the clinical presentation look like in a patient with a S.pneumoniae infection?

A
  • Heavy smoker with nasal congestion and fever
  • Cough and severe chest pain 2 days later
  • Rust-coloured sputum
  • Chest X-ray showing consolidation
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111
Q

Where might you find normal commensal of S.pneumoniae? How much of the population have this?

A

30% of population have commensal in the oro-pharynx

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112
Q

What can S.pyogenes cause?

A
  • Pneumonia
  • Otisis media
  • Sinusitis
  • Meningitis
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113
Q

What factors can pre-dispose you to a S.pyogenes infection?

A
  • Impaired mucus trapping (e.g. viral infection)
  • Hypogammagloninaemia
  • Asplenia
  • Diabetes
  • Renal disease
  • Sickle cell disease
  • <2yrs
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114
Q

Why can asplenia make you pre-disposed to S.pyogenes?

A

Spleen produces tuftsin, which enhances phagocytosis. Therefore without a spleen, this is impaired and the host is susceptible to infection.

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115
Q

What are the pathogenic factors of S.pyogenes?

A
  • Polysaccharide capsule - anti-phagocytic and there are 84 types, 61 of which are unvaccinated against
  • Teichoic acid - binds to choline receptors
  • Peptidoglycan - protects bacteria
  • Pneumolysin cytotoxin - pore-forming
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116
Q

What are viridans streptococci?

A

Collective name for oral streptococci

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117
Q

What type of haemolysis do viridans streptococci show?

A

Alpha and gamma haemolysis

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118
Q

Which type of viridans streptococci are responsible for infective endocarditis?

A
  • S.sanguinis

- S.oralis

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119
Q

Which group of viridans streptococci are the most pathogenic?
Which bacteria are in this group?

A

Milleri group;

  • S.intermedius
  • S.anginosis
  • S.constellatus
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120
Q

What do the milleri group cause?

A

Deep organ abscesses, e.g. in brain and liver

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121
Q

What is a common presentation for a corynebacterium diptheriae infection?

A
  • Child with severe sore throat
  • Fever & malaise for 2 days
  • Lymphadenophathy in neck
  • Rapid breathing
  • Thick greyish membrane on tonsils
  • Swab shows G+ve bacilli
  • Treat with antitoxin and erythromycin
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122
Q

How does corynebacterium diptheriae spread?

Explain the spread

A

Droplet spread

Caused by production of a toxin which inhibits protein synthesis

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123
Q

What is the prevention for corynebacterium diptheriae infection?

A

Vaccination with toxoid

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124
Q

Describe the structure of a lipopolysaccharide.

A

Lipid A - toxic portion that is anchored in the outer leaflet of the outer membrane

Core (R) antigen - short chain of sugars

Somatic (O) antigen - highly antigenic repeating chain of oligosaccharides

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125
Q

What are coliforms?

A

Bacteria that are normally found in the environment and in human faeces

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126
Q

What can you use to differentiate between lactose fermenting and non-lactose fermenting bacteria?

A

Macconkey agar

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127
Q

E.coli are commensal enterobacteria. What does this mean?

A

They are present in the host, but don’t cause disease in normal circumstances

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128
Q

What does ‘facultative’ mean?

What does ‘facultative anaerobe’ mean?

A

Facultative = is able to

Facultative anaerobe = able to respire aerobically and anaerobically

129
Q

How do E.coli move about?

A

Flagella

130
Q

What infections are caused by pathogenic strains of E.coli?

A
  • Wound infections
  • Cystitis
  • Gastroenteritis
  • Traveller’s diarrhoea
  • Bacteraemia
  • Meningitis (in infants)
131
Q

What do pathogenic and commensal serotypes / strains of E.coli have in common?

A

They all share a common ‘core’ genome

132
Q

What is the difference between pathogenic E.coli and commensal E.coli?

A

Pathogenic E.coli contain blocks of genes not found in commensal E.coli

133
Q

How do E.coli become pathogenic?

A

They acquire their pathogenicity by mating with other bacteria and acquiring their blocks of genes

134
Q

What are the pathogenic factors for E.coli causing traveller’s diarrhoea?

A
  • Strain is enterotoxigenic E.coli (ETEC)
  • Have pili, which enable it to adhere to tissue of SI
  • When it adheres to SI tissue, it releases a labile toxin that alters the role of the Gs protein on the GI cell surface
  • This means it can no longer stimulate adenyl cyclase, resulting in more Cl- being released into GI lumen
  • Causes watery diarrhoea
135
Q

Which other enterobacteria is closely related to E.coli?

A

Shigella

136
Q

What are the four main species shigella?

A
  • S.dysenteriae
  • S.flexneri
  • S.boydii
  • S.sonnei
137
Q

Shigella damages the intestinal mucosa, which results in…

A
  • Acute infection of LI

- Painful diarrhoea, often with blood and mucus within it

138
Q

Describe the pathogenesis of shigella infections

A
  • Acid-tolerant, so survive the stomach acid
  • Infective dose = 100 (very low)
  • Spread from person-to-person or via contaminated water / food
  • Target microfold (M) cells for transport across the GI epithelium
  • Cross epithelial cell layer, and are engulfed by macrophages
  • Induce apoptosis in macrophages, causing release of free radicals, resulting in inflammatory response and cell damage
  • Release shiga toxin which disrupts protein synthesis, causing necrosis
139
Q

Where are microfold (M) cells found?

A
  • In gut-associated lymphoid tissue (GALT) in Peyer’s patches
  • In mucosa-associated lymphoid tissue (MALT)
140
Q

Briefly describe the action of the shiga toxin

A
  • Disrupts protein synthesis, which can cause necrosis

- Targets the kidney, resulting in haemolytic uraemia syndrome

141
Q

What are the two main species of salmonella?

A
  • S.enterica

- S.bongori

142
Q

Which species of salmonella is responsible for salmonellosis?

A

S.enterica

143
Q

What is salmonellosis?

A

Any infections caused with salmonella

144
Q

How do you catch S.bongori?

A

Contact with reptiles

145
Q

Which three infections are caused by salmonella?

A
  • Gastroenteritis
  • Enteric fever (typhoid)
  • Bacteraemia
146
Q

Describe the clinical presentation of gastroenteritis.

A
  • Frequent cause of food poisoning from milk and poultry
  • 6-36 hour incubation
  • Resolves in a week
  • Localised infection
147
Q

Describe the clinical presentation of enteric fever.

A
  • Systemic disease
  • Caused by Salmonella type and Salmonella paratyphi
  • Spread: faecal-oral
  • Results in fever, headache, diarrhoea & dry cough
  • Splenomegaly and hepatomegaly
148
Q

Describe the pathogenesis of (general) salmonellosis.

A
  • Ingestion of contaminated water / food
  • High infective dose
  • Salmonella mediates its endocytosis across gut lumen
149
Q

Describe the pathogenesis of salmonellosis in gastroenteritis.

A
  • Bacteria presence results in chemokine release and neutrophil recruitment
  • Results in neutrophil-induced tissue injury due to inflammatory response
  • Fluid and electrolyte loss due to cell damage, resulting in diarrhoea
  • Eventual inflammation / necrosis of gut mucosa
150
Q

Describe the pathogenesis of salmonellosis in enteric fever.

A
  • Migrates to the basolateral membrane of cells in the intestinal lumen (Peyer’s patch)
  • Causes inflammation, ulceration and diarrhoea
  • Little damage to gut mucosa initially
  • Bacteria is engulfed and survives, then spreads systemically via lymph nodes
  • Enters bloodstream via thoracic duct, the multiplies in macrophages of liver, spleen, and bone marrow
  • Results in septicaemia and massive fever
  • Spreads to gall bladders from liver, where person can be a carrier for 1yr-lifetime
151
Q

Is Klebsiella pneumoniae opportunistic or not?

A

Opportunistic

152
Q

Which nosocomial infections does Klebsiella pneumoniae cause?

A
  • Pneumonia
  • Bloodstream infections
  • Wound / surgical site infections
  • Meningitis
153
Q

How do Vibrio cholerae respire?

A

They are facultative anaerobes

154
Q

Describe the structure of vibrio cholerae?

A

Curved bacilli with single polar flagellum

155
Q

What does vibrio cholerae cause?

A

Cholera

156
Q

How is vibrio cholerae transmitted?

A

Faecal-oral route

157
Q

Does vibrio cholerae have a high or low ID?

A

High, it is sensitive to acid so requires a lot to pass through the stomach

158
Q

What is the incubation time for V.cholerae?

A

5 hours - it multiplies in the SI

159
Q

What is the main symptom of a V.cholerae infection?

A

Voluminous “rice-water” stools

160
Q

Why can cholera cause death?

A

Causes patients to lose 20L fluid a day plus electrolytes, causing dehydration and death

161
Q

How are the majority of cholera patients treated?

A

80% treated with oral rehydration

162
Q

What are the virulence determinants of V.cholerae?

A
  • Pilli, for colonissation

- Cholera toxin (acts in the same way as E.coli labile toxin)

163
Q

How does the cholera toxin cause its harmful effects?

A
  • Results in uncontrolled cAMP production
  • Which causes activation of protein kinases
  • Which causes modification of ion transporter
  • Therefore there is loss of Cl- and Na+

= H₂O loss

164
Q

What localised acute infections can pseudomonas aeruginosa cause?

A
  • Burns / surgical wound infections
  • UTIs (catheters)
  • Keratitis
165
Q

Who tends to get acute systemic infections caused by P.aeruginosa?

A

Neutropenic patients (e.g. leukaemia, chemotherapy, AIDs, etc)

166
Q

What is the leading cause of nosocomial pneumonia in ICU patients?

A

Pseudomonas aeruginosa

167
Q

Who tends to get chronic infections caused by P.aeruginosa? Why?

A

Cystic fibrosis patients

They have poor functioning Cl- transporters meaning they have dehydrated lung mucus, which is the perfect environment for bacteria to grow

168
Q

Why is P.aeruginosa hard to eradicate in cystic fibrosis patients?

A

It’s antibiotic resistant

169
Q

Where is commensal haemophilus influenzae found?

A

Nasopharyngeal carriage in 25-80% of the population

170
Q

What can haemophilus influenzae cause in under 5 year olds? How?

A

If haemophilus influenzae crosses the BBB, it causes meningitis

171
Q

What can H.influenzae cause?

A
  • Meningitis (<5yrs)
  • Bronchopneumonia
  • Epiglottitis, sinusitis, otitis media
  • Bacteraemia
  • Lung infections (CF/COPD patients)
172
Q

What does ‘fastidious’ mean?

A

Specific requirements for survival

173
Q

What is the only medium H.influenzae can grow on?

Why?

A

Chocolate agar - blood agar heated to 80ºc to allow release of haem by RBCs

174
Q

What does H.influenzae need to grow?

A

Haem

175
Q

How does H.influenzae move around?

A

It doesn’t - it’s non-motile

176
Q

What are the virulence determinants for H.influenzae

A
  • Pilli - adherence to epithelial cells and mucin
  • Capsule (invasive strains only)
  • LPS - causes inflammation
177
Q

Name two beta-proteobacteria.

A
  • Bordetella pertussis

- Neisseria

178
Q

What bacteria causes whooping cough?

A

Bordetella pertussis

179
Q

How is B.pertussis transmitted?

A

Via aerosol

180
Q

What is the clinical presentation of whooping cough?

A
  • Non-specific flu-like symptoms

- Paroxysmal coughing - cough followed by inhalation resulting in whooping sound

181
Q

What can whooping cough lead to?

A

Sub-conjunctival haemorrhage

182
Q

Describe the structure of Neisseria.

A

Non-flagellated diplococci

183
Q

What are the two important species of neisseria?

A
  • N.meningitidis

- N.gonorrhoeae

184
Q

Where can you find neisseria bacteria during an infection?

A
  • Polymorphonuclear lymphocytes of CSF

- Urethral discharge

185
Q

Where can you find asymptomatic N.meningitidis in 5-10% of the population?

A

Nasopharynx

186
Q

How is N.meningitidis transmitted?

A

Via aerosol transmission

187
Q

Describe the pathogenesis of N.meningitidis.

A

Crosses nasopharyngeal epithelium and enters bloodstream

188
Q

What happens if low or high numbers of N.meningitidis enter the blood stream?

A

Low numbers: asymptomatic bacteraemia

High numbers: septicaemia

189
Q

How do you get meningitis from N.meningitidis?

A

If it crosses the BBB and colonises in the subarachnoid space

190
Q

What is the mortality risk if you are septicaemic with N.meningitidis?

A

Very high risk of mortality

191
Q

What are the virulence determinants of N.mengitidis?

A
  • Capsule (non-capsulated in nasopharynx, capsulated is anti-phagocytic)
  • Pilli - promote colonisation and cell invasion
  • LPS - cytokine cascade and inflammatory response which leads to sepsis
192
Q

How is N.gonorrhoeae transmitted?

A

Person to person

193
Q

What does gonorrhoea cause?

A
  • Urethritis

- Infection of fallopian tubes (if bacteria ascends)

194
Q

Is N.gonorrhoeae capsulated or non-capsulated?

A

Non-capsulated

195
Q

Give two examples of campylobacter.

A
  • C.jejuni

- C.coli

196
Q

Does campylobacter have a high or low infectious dose?

A

Low

197
Q

How do you get campylobacter infections?

A
  • Undercooked poultry

- Unpasteurised milk

198
Q

What symptoms do you get with a campylobacter infection?

A

Mild-severe diarrhoea with blood

  • Self-limiting within a week
199
Q

What are the virulence factors of campylobacter?

A
  • Invasins

- Cytolethal distending toxin

200
Q

How do campylobacter invasins work?

A

Invade ill and colonic epithelial cells, causing local acute inflammatory response

201
Q

How does cytolethal distending toxin (CDT) cause disease?

A

Arrests cell cycle, meaning target cells swell and lyse

202
Q

Give two examples of e-proteobacteria.

A
  • Campylobacter

- Helicobacter pylori

203
Q

Describe the shape of H.pylori.

A

Spiral shaped

204
Q

What percent of the population is H.pylori present in?

A

50% - only a fraction will develop the disease

205
Q

What can H.pylori lead to?

A
  • Gastritis

- Peptic ulcers

206
Q

What is the virulence factor of H.pylori?

A

Urease - hydrolyses urea to generate ammonia to act as a buffer to gastric acid

207
Q

Describe the two developmental stages in the growth cycle of chlamydia.

A
  1. Elementary bodies (EBs) - DORMANT
    - infectious
    - enter cell through endocytosis
    - prevent phagosome fusion
  2. Reticulate bodies (RBs) - ACTIVE and FRAGILE
    - replicative
    - non-infectious
208
Q

What happens if Chlamydia trachomatis spreads to the uterus / ovaries?

A

Pelvic inflammatory disease

209
Q

What infections can chlamydia trachomatis cause?

A
  • Conjunctivitis

- Trachoma (blindness)

210
Q

What are the most common G-ve bacteria responsible for respiratory tract infections?

A
  • Bordetella pertussis

- Haemophilus influenzae

211
Q

What are the most common G-ve bacteria responsible for urinary tract infections?

A
  • Some E.coli strains

- Klebsiella pneumoniae

212
Q

What are the most common G-ve bacteria responsible for GI tract infections?

A
  • Vibrio cholerae
  • Shigella dysenteriae
  • Some E.coli strains
  • Campylobacter jejune
  • Helicobacter pylori
213
Q

What are the most common G-ve bacteria responsible for meningitis?

A
  • Neisseria meningitidis

- Haemophilus influenzae

214
Q

What are the most common G-ve bacteria responsible for STIs?

A
  • Klebsiella pneumoniae

- Chlamydia trachomatis

215
Q

What are the most common G-ve bacteria responsible for wound infections?

A
  • Pseudomonas aeruginosa

- Some E.coli strains

216
Q

Are fungi eukaryotic or prokaryotic? Why?

A

Eukaryotic - they have a nuclear membrane

217
Q

What is the cell wall of fungi made of?

A

Chitin

218
Q

What does ‘heterotrophic’ mean?

A

Get nutrients from what they are living on

219
Q

Which type of pathogen is heterotrophic?

A

Fungi

220
Q

How to fungi travel?

A

Growth or spore release

221
Q

What are yeast?

A

Small, single cell organisms that divide by budding

222
Q

What do moulds form?

A

Multicellular hyphae and spores

223
Q

What are dimorphic fungi?

A

Fungi which exist as yeasts and moulds, switching between the two when conditions suit

224
Q

Give an example of a dimorphic fungus and the conditions required for each form.

A

Coccidioides immitis

  • Mould at ambient temperatures
  • Yeast at body temperature
225
Q

Why do only a few fungi have an effect on humans?

A
  • Inability to grow at body temperature

- Cannot evade adaptive / innate immune response

226
Q

What is the burden of fungal disease on healthcare?

A

Enormous, since most will have at least one during their life

227
Q

Which three conditions can lead to fungal infections becoming life-threatening / invasive?

A
  • Immunocompromised patients
  • Post-surgical patients
  • Healthy hosts (only certain types of fungi)
228
Q

Which fungal diseases are life-threatening / invasive to immunocompromised patients?

A
  • Candida line infections
  • Pneumocystis
  • Invasive aspergillosis
229
Q

Which fungal diseases are life-threatening / invasive to post-surgical patients?

A

Intra-abdominal fungal infections

230
Q

Which fungal diseases are life-threatening / invasive to healthy hosts?

A
  • Fungal asthma

- Travel associated fungal infections

231
Q

What is the aim of antimicrobial drug therapy?

A

To achieve inhibitory levels of agent at site of infection, without host cell toxicity

232
Q

What does antimicrobial drug therapy need to be effective?

A

A molecule with selective toxicity for organism targets

233
Q

What does an antimicrobial drug molecule rely on to work?

A
  • Target does not exist in humans
  • Target is significantly different to human analogue
  • Drug is concentrated in organism cell with respect to humans
  • Organism has an increased permeability to the compound
  • Human cells are ‘rescued’ from toxicity by alternative metabolic pathways
234
Q

Why is selective toxicity easier to achieve with fungi than bacteria?

A

Fungi are eukaryotic cells, and are therefore more similar, thus harder to differentiate from human cells

235
Q

Describe fungal nucleus.

A
  • DNA/RNA synthesis and protein synthesis

- Similar to mammalian

236
Q

Which drug targets fungal nuclei?

A

Flucytosine

237
Q

Name four molecules within the cell wall of fungi.

A
  • Mannoproteins
  • B1,3-glucan
  • B1,6-glucan
  • Chitin
238
Q

Which drugs target cell walls in fungi?

A

Echinocandins

239
Q

What is the difference between human cell membranes and fungal cell membranes?

A

Humans’ contain cholesterol, fungi’s contain ergosterol

240
Q

Name six families of drugs used to fight fungal infections.

A
  • Polyenes
  • Allylamines
  • Azoles
  • Echinocandins
  • Pyrimidine
  • Grisan
241
Q

What is an example of a polyene drug?

A

Amphotericin B Nystatin

242
Q

What is the mechanism of action of polyenes?

A

Bind to sterols and destabilises cell membranes - pore forming compound

243
Q

What would you use polyenes for?

A

Systemic and topical fungal disease

244
Q

Why can polyenes be toxic to humans?

A

Although they have a 10x higher affinity for ergosterol than cholesterol, it can still be toxic in high doses

245
Q

What toxicity do polyenes cause in humans?

A
  • Nephrotoxicity (dose dependent, reversible)
  • Distal renal tubular acidosis (hypokalaemia)
  • Hyperkalaemia (if infused rapidly)
  • Infusion related chills, riggers, hypotension, and acute anaphylactoid reactions
246
Q

What is an example of an allylamine?

A

Terbinafine

247
Q

What is the mechanism of action for allylamines?

A

Inhibit ergosterol biosynthesis

Reversible inhibition of enzyme required for growth of fungus

248
Q

What can you use allylamines for?

A

Superficial infections, e.g. onychomycocis

249
Q

Are allylamines well absorbed or not?

A

They are well absorbed, but undergo extensive first phase metabolism, resulting in bioavailability of only 45%

250
Q

What are the main fungi allylamines are used against?

A
  • Candida

- Aspergillus

251
Q

What are the side effects of allylamines?

A
  • Taste disturbance

- Deranged LFTs

252
Q

Give some examples of azoles.

A
  • Clotrimazole (active against Candida)
  • Miconazole
  • Ketoconazole (active against Candida)
  • Fluconazole (active against Cryptococcus)
  • Itraconazole (active against Aspergillus and dimorphics)
  • Voriconazole
  • Posaconazole
253
Q

What is the mechanism of action for azoles?

A

Inhibit ergosterol biosynthesis

254
Q

What can you use azoles for?

A

Topical or systemic fungal diseases

255
Q

What are the side effects of azoles?

A
  • Transaminitis (elevated transaminases in liver)
  • Hepatitis
  • Alopecia (long term fluconazole)
  • GI: Nausea, abdominal pain, diarrhoea (common with itraconazole)
256
Q

What are the drug interactions for fluconazole?

A
  • Warfarin
  • Calcineurin inhibitors
  • Anxiolytics
257
Q

What are the drug interactions for itraconzaole?

A
  • Same as fluconazole
  • Steroids
  • Statins
258
Q

Give three examples of echinocandins.

A
  • Caspofungin
  • Anidulafungin
  • Micafungin
259
Q

What is the mechanism of action of echinocandins?

A

Inhibit the formation of cell wall glucan

260
Q

What can you use echinocandins for?

A

Systemic diseases

261
Q

Why can’t you use echinocandins for certain types of fungal infections?

A

Fungi genera that have little glucan in cell wall are relatively unaffected by echinocandins

262
Q

How are echinocandins best administered?

A

IV; they have poor oral bioavailability

263
Q

What is easier to culture from blood; fungi or bacteria?

A

Bacteria; blood cultures are only half as sensitive for fungi as for bacteria

264
Q

What is the best way to culture candida?

A

From tissue / fluids

But only if cultured properly and if these samples can be obtained

265
Q

Which drugs can you use on Candida?

A

Echinocandins and amphotericin B

266
Q

Which element of fungi can you identify from serum samples?

A

1,3 B-D glucan

267
Q

What is onychomycosis?

A

Very common fungal infection of the nail

268
Q

What is the most common cause of onychomycosis?

A

Trichophtyon rubrum

269
Q

What are the differential diagnoses for onychomycosis?

A
  • Psoriasis
  • Lichen planus
  • Trauma
  • Eczema
  • Malignant melanoma
270
Q

What are the treatment options of onychomycosis?

A
  • Topical amorolfine

- Systemic itraconazole or terbinafine

271
Q

What are the down sides to treatment of onychomycosis?

A
  • Takes ages

- High failure rate

272
Q

What is pneumocystis?

A

A form of pneumonia caused by a yeast-like fungus

273
Q

Who is vulnerable to develop pneumocystis?

A

Moderate-severe immunocompromised patients (esp. HIV, transplant, and steroids)

274
Q

What clinical presentation would make you think ‘pneumocystis’?

A

When a patient has hypoxia that is more severe than the CXR would suggest

ESPECIALLY with gradual onset or risk factors

275
Q

How do you treat pneumocystis?

A
  • Co-trimoxazole
  • Clindamycin
  • Pentamidine
  • Trimetrexate
276
Q

When is a person likely to become colonised by the fungus responsible for pneumocystis?

A

During early life

277
Q

What are the five mycobacteria of medical importance?

What do each of them cause?

A
  • M.tuberculosis - tuberculosis
  • M.leprae - leprosy
  • M.avium complex - disseminated infections in AIDs, and patients with chronic lung disease
  • M.kansasii - chronic lung infections
  • M.marinum - fish tank granuloma
  • M.ulcerans - Buruli ulcer
278
Q

Are mycobacteria aerobic or anaerobic?

A

Aerobic

279
Q

What can you not use to destain mycobacteria?

A
  • Acid

- Alcohol

280
Q

Tuberculosis can cause meningitis. True or false?

A

True

281
Q

Are mycobacteria resistance to phagolysosomal killing?

A

Yes

282
Q

Describe the cell wall of mycobacteria.

A
  • High content of high molecular weight lipids
  • Weakly gram-positive or colourless
  • Contains lipoarabinomannan and mycolic acids - make up strong waxy cell wall which is hard for immune system to damage
  • Survives inside macrophages and low pH environments
283
Q

Why is it difficult to stain mycobacteria?

A

High lipid content with mycolic acids in cell wall makes Mycobacteria resistant to gram stain

284
Q

How long does it take to generate one new generation of mycobacteria?

A

15-20 hours (compared to 1 hour for common bacteria)

285
Q

Why does slow growth of mycobacteria affect antibiotic efficacy?

A

It is more difficult for antibiotics to target division phase of mycobacteria

286
Q

Who initially identified tuberculosis?

A

Robert Koch

287
Q

What are the four Koch postulates?

A
  1. Bacteria should be found in all people with disease
  2. Bacteria should be isolated from the infected lesions in people with disease
  3. A pure culture inoculated into a susceptible person should produce symptoms of the disease
  4. The same bacteria should be isolated from the intentionally infected individual
288
Q

What stain should you use to identify mycobacteria?

What is the result of a positive test?

A

Ziehl-Neesen stain - pink/red stain for acid-fast mycobacteria

289
Q

What method of identification is used to quickly diagnose TB in TB endemic countries?

A

Nucleic acid detection

  • PCR amplifies TB DNA
290
Q

What happens when a macrophage phagocytoses mycobacteria?

A
  • Mycobacteria are engulfed into phagosome, which forms a phagolysosome
  • Bacteria has adapted to withstand phagolysosomal killing and escape into the cytosol
291
Q

Describe the immune response to mycobacteria.

A
  1. Macophages phagocytose mycobacteria
  2. Acidification and degradation of mycobacteria by proteases results in generation of antigens for presentation to T cells
292
Q

Effective immunity to mycobacteria requires…

A

CD4 T-cells which generate interferon gamma. This helps activate intracellular killing by macrophages

293
Q

What do macrophages release when they phagocytose mycobacteria?

A

IL-12

294
Q

How does IL-12 aid the immune response to mycobacteria?

A

It stimulates the generation of T helper cells and interferon gamma release

295
Q

Name two genetic defects that increase susceptibility to mycobacterial infection.

A

Defects in…

  • interferon gamma / IL-12 receptors
  • elements of their signalling pathways
296
Q

What are granuloma?

A

Lesions that arise in response to trying to contain mycobacteria

297
Q

How do granuloma affect macrophages?

A

They stimulate macrophages to become epithelioid cells

298
Q

What is a ‘langhans giant cell’?

A

Multinucleate cells formed of fused macrophages

299
Q

Which cells are able to infiltrate granuloma?

A

Cytotoxic CD8 T-cells

300
Q

What can happen to central tissue in a granuloma?

A

It can necrotise and form a caveating granuloma

  • In the lung, this can cause a cavity
301
Q

How does the formation of a granuloma affect the mycobacteria within it?

A

Granuloma prevents nutrients from entering, thereby starving the mycobacteria. TB goes into dormant state, but can reactivate when conditions are optimal

302
Q

The highly immunogenic nature of mycobacterial lipids stimulate T-cell responses ___ weeks after exposure to M.tuberculosis

A

3-9 weeks

303
Q

What are the positive effects of mycobacterial lipids stimulating an immune response?

A
  • Macrophage killing of mycobacteria
  • Containment of infection
  • Formation of tissue granuloma
304
Q

What are the negative effects of mycobacterial lipids stimulating an immune response?

A
  • Hypersensitivity reaction (type 4), with skin lesions, eye lesions, and joint swelling
305
Q

How can you measure the reactivity of T-cells to mycobacterial lipids?

A

Tuberculin skin test or interferon gamma release assays

306
Q

What is the tuberculin skin test?

A

Intradermal injection of purified protein derivatives, inducing swelling and redness

307
Q

What are IGRAs? Describe them.

A

Interferon gamma release assay

  • Use antigens specific to M.tuberculosis to distinguish between this and BCG vaccine / environmental mycobacteria
  • IGRAs demonstrate exposure to M.tuberculosis but NOT active infection
308
Q

What are the four principles of mycobacteria treatment?

A
  1. Prolonged treatment (6 months) - slowly replicating bacteria
  2. Different populations of bacteria, in different locations (intracellular and extracellular), with different pH
  3. Resistance may emerge so use multi-drug combinations to target all populations and mutants
  4. Compliance is essential - directly observe treatment for many patient groups
309
Q

What is the standard therapy for tuberculosis?

A
  • Isoniazid (INH), Rifampicin (RIF), Pyrazinamide (PZA), and Ethambutol (ETH) for two months
  • Isoniazid and rifampicin for a further four months
310
Q

What is the treatment for tuberculosis if resistance develops?

A
  • Fluroquinolones
  • Injectable agents (e.g. streptomycin, cyclosporine, and capreomycin)
  • Prothionamide
311
Q

What are the side effects of anti-tuberculous drugs?

A
  • Hepatotoxicity (isoniazid, rifampicin, pyrazinamide)
  • Peripheral neuropathy (isoniazid) - give vitamin B6 to prevent
  • Optic neuritis (ethambutol)
312
Q

Describe primary tuberculosis.

A
  • Bacilli settle in lung apex and form granulomas

- Bacilli taken in by lymphatics to hilar lymph nodes

313
Q

What is a ‘primary complex’ in primary tuberculosis?

A

Granuloma + lymphatics + lymph nodes = primary complex

314
Q

Why do tuberculous bacilli settle in apex of lungs?

A

More air and less blood supply, thus fewer defending white cells

315
Q

Describe latent tuberculosis

A
  • Cell mediated immune (CMI) response from T-cells
  • Primary infection is maintained by CMI persists
  • No clinical disease (normal CXR)
  • Detectable CMI to TB on tuberculin skin test / IGRA
316
Q

Describe pulmonary tuberculosis

A
  • Could occur immediately following primary disease (post-primary) or after latent reactivation
  • CMI response from T-cells
  • Necrosis in lesion
  • Caseous material coughed up leaving cavity
  • TB may spread
  • CMI and caseation in lesion results in cavity
317
Q

How does TB spread from the lungs to other parts of the body?

A

Bacilli spreads from lung apex to hilar lymph nodes, and then to anywhere else

318
Q

What can a spread of TB cause?

A
  • TB meningitis
  • Miliary TB (widespread dissemination and tiny spotted lesions all over lungs and elsewhere)
  • Pleural TB
  • Bone and joint TB
  • Genitourinary TB

Phase 2a Medicine (5 decks)

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