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PHASE 2A > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Define pathogen

A

An organism that can cause disease

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2
Q

Define Commensal

A

An organism that colonises a host but does not normally cause disease

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3
Q

Define opportunistic pathogen

A

Microbe that only causes disease if host defences are compromised

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4
Q

Define Virulence/pathogenicity

A

The degree to which an organism is pathogenic

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5
Q

Define Asymptomatic carriage

A

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

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6
Q

What is the morphological classification of bacteria?

A
  1. Cocci (balls)

2. Bacilli (rods)

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7
Q

How can cocci exist?

A

Single
Diplo
Cluster
Chain

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8
Q

How can bacilli exist?

A

Single
Chain
Curved (vibrio)
Spiral (spirochete)

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9
Q

Name 2 forms of bacterial toxins

A
  1. Endotoxin

2. Exotoxin

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10
Q

What is an endotoxin?

A

Component of outer membrane of bacteria –> Gram NEGATIVE LPS

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11
Q

What is an exotoxin?

A

Secreted proteins from Gram Positive and Negative bacteria

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12
Q

What type of bacteria can’t be cultures on artificial media?

A

Obligate intracellular bacteria

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13
Q

Name 3 types of obligate intracellular bacteria

A
  1. Rickettsia
  2. Chlamydia
  3. Coxiella
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14
Q

Name a bacteria with no cell wall

A

Mycoplasma pneumoniae

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15
Q

Name 3 types of bacteria that grow as filaments

A
  1. Actinomyces
  2. Nocardia
  3. Streptomyces
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16
Q

Name 3 types of spirochetes bacteria

A
  1. Leptospira
  2. Treponema
  3. Borrelia
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17
Q

Describe the process of Gram staining

A
  1. Apply crystal violet stain
  2. Add iodide - binds to cell wall
  3. Decolourise with ethanol
  4. Counterstain with pink safranin
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18
Q

What colour is Gram Positive bacteria on gram staining?

A

Purple/blue - ethanol dehydrates cell wall

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19
Q

What colour is Gram Negative bacteria on gram staining?

A

Pink/red - ethanol degrades LPS

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20
Q

Name 4 Gram Positive tests

A
  1. Catalase test
  2. Coagulase test
  3. Haemolysis test
  4. Optochin test
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21
Q

What is the mechanism of action of the catalase test?

A

Flavoproteins reduce O2 ro H2O2

H2O2 then reacts with the catalase

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22
Q

What Gram positive bacteria are catalase positive?

A

Staphylococci

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23
Q

What Gram positive bacteria are catalase negative?

A

Streptococci

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24
Q

What is the mechanism of the coagulase test?

A

Coagulase activates prothrombin
Caused fibrinogen to be converted to fibrin
Fibrin clop formation around bacteria

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25
Q

What Gram positive bacteria are coagulase positive?

A

Staphylococcus aureus

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26
Q

What Gram positive bacteria are coagulase negative?

A

Staphylococci except Staphylococcus aureus = S. epidermis and S. saphrphyticus

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27
Q

How does a haemolysis test work?

A

Streptococci express haemolysis –> breakdown RBC in blood agar

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28
Q

What group of bacteria is the haemolysis test used to distinguish between?

A

Streptococci

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29
Q

What group of bacteria is the coagulase test used to distinguish between?

A

Staphylococci

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30
Q

What are the 3 outcomes of a haemolysis test?

A

Alpha haemolysis - partial lysis
Beta haemolysis - complete lysis
Gamma hameolysis - no lysis

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31
Q

What colour does the agar go with alpha haemolysis?

A

Green –> H2O2 oxidises haemoglobin

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32
Q

What colour does the agar go with beta haemolysis?

A

Clear –> RBC lysis occurs

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33
Q

Give an example of a alpha haemolytic strep

A

S. pneumoniae

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34
Q

Give an example of a beta haemolytic strep

A

S. pyogenes

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35
Q

Give an example of a gamma haemolytic strep

A

S. bovis

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36
Q

What is the optochin test a test for?

A

It is an alpha haemolytic strep test to distinguish between Strep. pneumoniae and Strep. viridians

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37
Q

Give an example of a optochin sensitive strep

A

Strep. pneumoniae

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38
Q

Give an example of a optochin resistant strep

A

Strep. viridians

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39
Q

Name 2 aerobic cocci gram positive bacterias

A
  1. Staphylococcus

2. Streptococcus

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40
Q

Name an anaerobic cocci gram positive bacteria

A

Peprostreptococcus

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41
Q

Name 3 aerobic bacilli gram positive bacterias

A
  1. Corynebacterium (diphtheriae)
  2. Listeria
  3. Bacillus (anthracis)
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42
Q

Name an anaerobic bacilli gram positive bacteria

A

Clostridium (botulinum, tetani, difficile, perfringens)

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43
Q

Name 3 Gram negative tests

A
  1. MacConkey agar
  2. CLED media
  3. Oxidase test
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44
Q

What is the MacConkey agar test selective for gram negative cultures?

A

Bile salts inhibit gram positive growth

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45
Q

What are the 2 outcomes of a MacConkey agar plate?

A

Lactose postive

Lactose negative

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46
Q

What happens to the agar with a lactose positive test?

A

Bacteria can metabolise lactose so it generates lactase and lowers the pH producing red stain

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47
Q

Name a lactose positive gram negative bacterias

A

Enterobacteriaceae

E.g. E. coli or Klebsiella

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48
Q

Name 4 lactose negative gram negative bacterias

A

Shigella
Salmonella
Pseudomonas
Proteus

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49
Q

What happens in a CLED media test

A

Lactose fermenters stain yellow –> used for urinary pathogens

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50
Q

What does the oxidase test determine?

A

If an organism contains cytochrome oxidase or indophenol oxidase

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51
Q

Name 3 oxidase positive organisms

A

Pseudomonas
Vibrio
Neisseria

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52
Q

Name an aerobic cocci gram negative bacteria

A

Neisseria (meningitidis, gonorrhoea)

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53
Q

Name an anaerobic cocci gram negative bacteria

A

Veilonella

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54
Q

Name 4 oxidase positive aerobic bacilli gram negative bacteria

A

Vibtio
Helicobacter
Campylobacter
Pseudomanas

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55
Q

Name 4 paryobacteria aerobic bacilli gram negative bacteria

A

Haemophilius
Brucella
Bordetella
Pasteurella

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56
Q

Name 5 coliform aerobic bacilli gram negative bacteria

A 
Escherichia
Klebsiella
Salmonella
Shigella
Citrobacter
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57
Q

Name an anaerobic bacilli gram negative organism

A

Bacteroides

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58
Q

Name 4 features of the cell membrane structure of a gram positive bacteria

A
  1. Outer capsule
  2. Lots of peptidoglycan
  3. Lipoteichoic acid
  4. Inner membrane
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59
Q

Give 4 features of S. aureus

A

Staphylococcus bacteria
Coagulase +ve
Commensal in nose and skin
Spread by aerosol and touch

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60
Q

Name 4 virulence factors of S. aureus

A
  1. Pore forming toxins
  2. Proteases
  3. Toxic Shock Syndrome toxin - stimulates cytokine release
  4. Protein A - surface protein which binds to Ig’s in wrong orientation
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61
Q

Name 4 pyogenic associated conditions with S. aureus

A

Wound infections
Hospital Acquired Pneumonia
Septicaemia
Osteomyelitis

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62
Q

Name 3 toxin mediated condition associated with S. aureus

A

Scaled skin syndrome
Toxic Shock Syndrome
Food poisoning

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63
Q

What is the full name of S. aureus

A

Methicillin-resistant Staphylococcus aureus (MRSA)

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64
Q

What is MRSA resistant to?

A

Beta lactams
Erythromycin
Gentamycin
Tetracyclines

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65
Q

What infections are often associated with S. epidermidis?

A

Opportunistic infections often due to prostheses and catheters

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66
Q

Name a virulence factor of S. epidermidis

A

Forms persistent biofilms

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67
Q

What does S. saprophyticus cause?

A

Acute cystitis

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68
Q

Name 2 virulence factors of S. saprophyticus

A

Haemagglutinin - adhesion

Urease - formation of kidney stones

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69
Q

Name 3 ways to classify Streptococci bacteria

A
  1. Haemolysis
  2. Sero-grouping (Lancefield grouping A-H and K-V)
  3. Biochemical properties
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70
Q

What is sero-grouping?

A

Method of grouping catalase negative and coagulase negative bacteria based on bacterial carbohydrate cell surface antigens

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71
Q

Name a Group A streptococci bacteria

A

S. pyogenes

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72
Q

Name a Group B streptococci bacteria

A

S. agalactiae

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73
Q

Give 3 features of S. pneumoniae

A

Alpha haemolytic Strep
Optochin sensitive
Oropharyngeal commensal

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74
Q

Name 2 endotoxin virulence factors for S. pneumoniae

A
  1. Antiphagocytic capsule

2. Inflammatory wall components

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75
Q

Name an exotoxin virulence factor for S. pneumoniae

A

Pore forming toxin (pneumolysin)

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76
Q

Name 4 conditions associated with S. pneumoniae

A

Pneumonia
Otitis media
Sinusitis
Meningitis

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77
Q

Give 2 features of Viridans Sterptococci

A

Optochin resistant

Collective name for oral strep

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78
Q

What is the most virulent viridians strep?

A

Milleri group - S. intermedium, S. angionsus, S. constellatus

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79
Q

Name 3 conditions associated with viridian’s strep

A
  1. Dental caries
  2. Infective endocarditis
  3. Abscesses
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80
Q

Give 2 features of S. pyogenes

A

Beta haemolytic strep

Lancefield group A

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81
Q

Name 5 conditions associated with S. pyogenes

A 
Cellulitis 
Tonsillitis/pharyngitis
Otitis media
Impetigo
Scarlet fever
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82
Q

Name 2 endotoxin virulence factors of S. pyogenes

A

Capsule

M surface protein - degrades complement

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83
Q

Name 2 exotoxin virulence factors of S. pyogenes

A

Enzymes

Toxins - exaggerate immune response

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84
Q

Name a gram positive bacilli bacteria

A

Corynebacterium diphtheriae

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85
Q

How does corynebacterium diphtheriae cause diphtheria?

A

Droplet spread causes diphtheria - grey throat patches

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86
Q

Name a virulence factor of Corynebacterium diphtheriae

A

Toxin inhibits protein synthesis

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87
Q

How can Corynebacterium diphtheriae be prevented?

A

Toxoid vaccination

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88
Q

Name 4 features of the cell membrane structure of a gram negative bacteria

A
  1. Lipopolysaccharide (LPS)
  2. Outer membrane
  3. Small amount of peptidoglycan
  4. Inner membrane
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89
Q

What is lipopolysaccharide?

A 
Forms the outer leaflet of the outer membrane lipid biller 
Made of 3 parts:
1. Lipid A- toxic part
2. Core R antigen 
3. Somatic O antigen - highly antigenic
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90
Q

Name 2 classes of virulence factors for gram negative bacteria

A

Colonisation factors

Toxins/effectors

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91
Q

Name 4 colonisation virulence factors for gram negative bacteria

A

Adhesins
Invasins
Nutrine acquisition
Defence

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92
Q

Name toxin/effector virulence factors for gram negative bacteria

A

Usually secreted protein –> damage and subversion

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93
Q

Give features of Proteobacteria

A

Gram Negative bacteria
Rod shaped
Facultatively anaerobic motile bacilli

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94
Q

Name the 3 main types of enterobacteria

A

Escherichia coli (E. coli)
Salmonella
Shigella

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95
Q

How can enterobacteria be catergorsied?

A

By cell surface antigens - K (cell capsule), H (flagellum) and O (LPS antigen)

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96
Q

Which enterobacteria are motile?

A

E. coli and salmonella

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97
Q

Which enterobacteria are non-motile?

A

Shigella

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98
Q

Give features of E. coli

A

Gram negative bacteria
Enterobacteria (coliform)
Commensals
Peritrichous flagella

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99
Q

Name 7 conditions associated with E. coli

A 
Wound infections 
UTI's 
Gastroenteritis 
Travellers' diarrhoea 
Bacteraemia 
Meningitis in infants
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100
Q

Name 6 pathogenic strains of E. coli

A
  1. Entero-toxigenic (ETEC)
  2. Entero-pathogenic (EPEC)
  3. Entero-haemorrhagic (EHEC)
  4. Entero-invasive (EIEC)
  5. Entero-aggregative (EAEC)
  6. Uro-pathogenic (UPEC)
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101
Q

Where does Entero-toxigenic E.coli work and what does it cause?

A

Acts in small intestine causing secretory diarrhoea

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102
Q

Where does Entero-pathogenic E.coli work and what does it cause?

A

Acts in small intestine causing watery diarrhoea (<1 year)

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103
Q

Where does Entero-haemorrhagic E.coli work and what does it cause?

A

Acts in large intestine and causes bloody diarrhoea and Hemolytic uremic syndrome (HUS) - food borne

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104
Q

Where does Entero-invasive E.coli work and what does it cause?

A

Acts in large intestine causing blood diarrhoea/dysentery (children)

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105
Q

Where does Entero-aggregative E.coli work and what does it cause?

A

Acts in large intestine causing chronic diarrhoea (children)

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106
Q

Where does Uro-pathogenic E.coli work and what does it cause?

A

Acts in urinary tract causing UTI’s (women)

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107
Q

What are the virulence facts for entero-toxigenic E. coli?

A

Toxin and pili

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108
Q

What are the virulence facts for entero-pathogenic E. coli?

A

Pedestal formation

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109
Q

What are the virulence facts for entero-haemorrhagic E. coli?

A

Pedestal formation and Shiva-Like toxin

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110
Q

What are the virulence facts for entero-invasive E. coli?

A

Invasins –> inflammatoin/ulceration

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111
Q

What are the virulence facts for entero-aggregative E. coli?

A

Pili and cytotoxin = shorter villi and mucus production

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112
Q

What are the virulence facts for uro-pathogenic E. coli?

A

Haemolysin = inflammation

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113
Q

Explain the pathogenic mechanism for enter-toxigenic E.coli

A

Heat labile toxin enters the epithelial cell and causes G protein modification (Gs)
Adenylate cyclase activated locked in ON state
Increase cAMP production –> binds to protein kinase A and phosphorylates the CFTR transporter
Loss of CL and H2O = diarrhoea

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114
Q

Explain the pathogenic mechanism for entero-pathogenic and entero-haemorrhagic E.coli (pedestal formation)

A

Pathogen adheres to microvilli with pathogenic pili
Type 3 Secretion System acts like syringe
Injects toxins into epithelial cell which rearranges actin and disrupts tight junctions and ion activity (diarrhoea)
Microvilli reform into pedestals holding pathogen

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115
Q

What is Shigellosis?

A

Diseases caused by shigella bacteria

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116
Q

Explain the pathology of shigella

A

Invasins –> inflammatoin/ulceration
AND
Shiga-liek toxin

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117
Q

Name a virulence factor for shigella

A

Shiga toxin –> interferes with protein synthesis - stops translation

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118
Q

Explain the pathogenesis of shigella

A

Low infective dose (acid tolerant) - transferred in contaminated food/water or person-to-person
Enter gut muscle by invading M cells in GALT –> phagocytksed –> released during apoptosis
Shiga toxin damages epithelium leading to inflammation
Bacteria then free to infect adjacent cells

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119
Q

Name the symptoms of shigella

A

Severe bloody diarrhoea
Frequent small volume still
Self-;limiting

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120
Q

Name a complication associated with shigella

A

Shiga toxin targets kidneys leading to renal failure/Hemolytic uremic syndrome (HUS)

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121
Q

Name the main species of Salmonella

A

S. enterica

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122
Q

Name 2 types of salmonellosis caused by S. enterica

A 
Gastroenteritis (food poisoning) 
Enteric fever (typhoid)
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123
Q

Explain the pathogenesis of S. enterica

A

Ingestion of contaminated food/water (high infective dose)
Invades small intestine epithelium leading to inflammatory response
Salmonella movement
- Transcytosed to basolateral membrane – phagocytosed in submucosa
- Survival and replication within macrophage –> disseminated around body through lymphatics –> typhoid

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124
Q

Give the features of Proteus mirabillis

A

Gram negative bacilli enterobacteria
Differentiates into an elongated hyperflagellated form
Opportunistic infection - UTI –> bacteraemia
Virulence factor = urease

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125
Q

Give the features of Klebsiella penumoniae

A

Gram negative bacilli enterobacteria
Typical CAP pathogen
Opportunistic, nosocomiali infections

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126
Q

What conditions can Klebsiella penumoniae lead to?

A 
Colonisation of GIT and oropharynx is benign but can lead to:
UTI
Pneumonia
Surgical wound infections 
Bacteraemia
Sepsis
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127
Q

Give the features of Yersinia

A

Gram negative bacilli enterobacteria
Y. enterocolitica = ileum localised
Y. pestis = bubonic plague

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128
Q

Give the features of Vibrio cholerae

A

Gram negative bacteria
Facultative anaerobe
Curved rods with a single polar flagellum

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129
Q

Explain the pathogenesis of Vibrio cholerae

A

Tansmissiong through faecal contaminated food/water and uncooked shellfish - high infective dose
5 day incubation period in small intestine
Voluminous watery stool

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130
Q

Name 2 virulence factors of Vibrio cholerae

A

Pili - colonisation

Cholera toxin - causes increase in cAMP production so mass loss of Cl- and H2O

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131
Q

What are the symptoms and treatment for Vibrio cholerae

A

Rice water stools that can lead to hypovolaemic shock - can lose 2-L of fluid / day
Treated by oral rehydration therapy

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132
Q

Give the features of Pseumdomonas aeruginosa

A

Gram negative bacilli
Ubiquitous, free-living aerobe
Motile and opportunistic

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133
Q

Name the infections associated with Pseumdomonas aeruginosa

A

Local - burns, surgery, catheters
Systemic - neutropenic patients (leukaemia, chemo, ADIS)
ICU - ventilators (HAP)
Chronic - CF

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134
Q

Name 3 virulence factors of Pseumdomonas aeruginosa

A

Twitching motility
Pili
Multiple toxins - inhibit protein synthesis and interfere with cell signalling or cause cell death or damage

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135
Q

Give the features of Haemophilus influenzae

A

Gram negative bacteria

Human parasite mainly carried nasopharyngeally

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136
Q

Name 6 conditions associated with Haemophilus influenzae

A 
Meningitis 
Pneumonia 
Sinusitis
Epiglottitis 
Bacteraemia 
Otitis media
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137
Q

Name 3 virulence factors of Haemophilus influenzae

A
  1. Pili - adherence
  2. Penetrating capsule - invasive stain are encapsulated, can penetrate nasopharyngeal epithelium and are resistance to phagocytosis and the complement system
  3. LPS - inflammation and also resistant to complement
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138
Q

What conditions are associated with Legionalla pneumophila?

A

Legionnaires disease (atypical pneumonia) in immunocompromised

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139
Q

Where is Legionalla pneumophila present?

A

In man-made aquatic environment - air conditioning, water towers and replicate within freshwater protozoa

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140
Q

Explain the pathogenesis of Legionalla pneumophila

A

Pathogen infects Pathogen infects alveolar macrophages –> avoids destruction and replicates
Releases pro-inflammatory signals –> neutrophil influx into lungs

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141
Q

What condition is associated with Bordetella pertussis

A

Pertussis (whooping cough)

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142
Q

Explain the pathogenesis of Bordetella pertussis

A

Aerosol transmission - low infective dose so highly contagious
7 day flu symptoms leading to paroxysmal cough

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143
Q

Name 2 virulence factors of Bordetella pertussis

A
  1. Pertussis toxin - increase cAMP production due to G-protein in locked OFF state (so prevents inhibitor of cAMP)
  2. Adenylate cyclase-haemolysin toxin - increase in cAMP production
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144
Q

Give the features of Nisseria

A

Gram negative bacteria
Non-flagellated diplococci
Fastidious
Humans only known reservoir

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145
Q

Name 2 form of Nisseria

A
  1. N. meningitidis

2. N. gonorrhoea

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146
Q

Explain the pathogenesis of N. meningitidis

A

Aerosol transmission

Crosses nasopharyngeal epithelium and enters blood

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147
Q

Name 3 conditions associated with N. meningitidis

A
  1. Bacteraemia
  2. Septicaemia
  3. Meningitis (crosses BBB)
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148
Q

Name 3 virulence factors of N. meningitidis

A
  1. Anti-phagocytic capsule
  2. Pili - colonises
  3. LPS - cytokine cascade and sepsis
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149
Q

Explain the pathogenesis of N. gonorrhoea

A

Sexual transmission - STD

Can be asymptomatic

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150
Q

Name 6 conditions associated with N. gonorrhoea

A
  1. Urethritis
  2. Salpingitis
  3. Proctitis
  4. Gingivitis
  5. Pharyngitis
  6. Babies infected by mum - Conjunctivitis
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151
Q

Name 2 virulence factors of N. gonorrhoea

A

Twitching motility

LPS - inflammatory response and serum resistance

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152
Q

Give the features of Campylobacter

A

Gram negative proteobacteria
Spiral rods
Unipolar or bipolar flagella
Low infective dose

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153
Q

Name 2 types of Campylobacter

A

C. jejune

C. coli

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154
Q

What is Campylobacter the most common cause of?

A

Food poisoning - self limiting bloody diarrhoea (often with blood lasting a week)

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155
Q

Give the features of Helicobacter pylori

A

Gram negative proteobacteria
Microaerophilic (requires CO2)
Spiral shaped
Tuft of polar flagella

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156
Q

Name 2 conditions Helicobacter pylori is associated with

A
  1. Gastritis

2. Peptic ulcer disease

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157
Q

Name a virulence factor of Helicobacter pylori

A

Urease –> ammonia = gastric acid buffer

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158
Q

Give the key features of bacteriodes

A

Gram negative bacteria
Non motile rods
Most abundant commensal
Opportunistic infections = anaerobic

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159
Q

Give the key features of Chlamydia

A

Obligate intracellular parasites
Very small
Non motile

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160
Q

How many phases are in the growth cycle of Chlamydia?

A

2 - Elementary bodies and Reticulate bodies

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161
Q

When are the elementary bodies of Chlamydia present?

A

Infectious stage

Enter cell through endocytosis and inhibits phagosome function

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162
Q

When are the reticulate bodies of Chlamydia present?

A

Non infectious stage

Intracellular replication using nutrients form host cell

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163
Q

Name the 3 most important types of Chlamydia

A
  1. C. trachomatis
  2. C. penumoniae
  3. C. psittaci
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164
Q

What is C. trachomatis and what does it cause?

A

Most common form of STD
Infects epithelial cell fo mucous membrane s of urethra and vagina
Causes conjunctivitis (hand-to-eye transmission)

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165
Q

What is C. pneumoniae?

A

An atypical CAP pathogen

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166
Q

What does C. psittaci cause?

A

Severe pneumonia

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167
Q

Give the key features of spirochetes

A

Gram negative bacteria
Long, slender, helical and highly flexible
Most are free-living and on-pathogenic

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168
Q

How do spirochetes move?

A

In a corkscrew movement due to end-flaggelum between outer membrane and peptidoglycan

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169
Q

Name 3 spirochetes

A
  1. Borrelia burgdorferi - Lyme disease
  2. Leptospira interrogates - zoonosis
  3. Treponema pallidum - syphilis
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170
Q

What is Lyme disease and how does it spread?

A

Tick-bourne, 30-40 flagella
Causes bullseye rash and flu like symptoms
Infection spreads through extracellular matrix and move through the bloodstream and lymphatics to other organs

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171
Q

How do you get zoonosis and what are the symptoms?

A

Animal urine contact with mucous membrane

Flu like symptoms –> Weil’s disease (severe)

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172
Q

How many stages of syphilis are there?

A

3 stages - Primary, secondary and tertiary

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173
Q

What happens in the primary stage of syphilis?

A

Localised infection that is highly infectious

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174
Q

What happens in the secondary stage of syphilis?

A 
Systemic infection (skin, lymph nodes, joints, vessels) 
Highly transmissible
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175
Q

What happens in the tertiary stage of Syphilis?

A

Granuloma in soft tissue leading to cardio and near syphilis
Occurs several years post-infection
Non-infectious form

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176
Q

How can you treat Syphilis?

A

Flucloxacillin

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177
Q

Give the key features of Fungi structure

A

Eukaryotic with chitinous cell wall

Moves through spore production - air and water Can be yeast or mould

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178
Q

What is yeast?

A

Small single celled organism that divides by budding

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179
Q

What is mould?

A

Forms multicellular hyphae and spores

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180
Q

Why can only certain types of fungi cause human infection?

A

Inability to grow at 37 degrees

Innate and adaptive immunity

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181
Q

Name the 3 main genera if human fungal infections

A
  1. Ascomycota
  2. Basidiomycota
  3. Mucormycota aka zygomycetes
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182
Q

Give some examples of fungi that are part of the Ascomycota genera

A 
Aspergillus
Pneumocystis 
Candida
Fusarium 
Scedosporium 
Dermatophytes
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183
Q

Give some examples of fungi that are part of the Basidiomycota genera

A

Cryptococcus

Trichosporon

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184
Q

What 3 things can you do to diagnose fungal diseases?

A
  1. Microscopy and histology
  2. Culture
  3. Molecular methods and serology
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185
Q

What is the basis of good antimicrobial treatment for fungi diseases?

A

Inhibitory levels of agent at infection site without host cell toxicity
Drug should concentrate in target cell/target molecule not present in host

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186
Q

Name 2 fungal molecular characteristics

A

Hard to find - eukaryotes

Molecules

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187
Q

Name 4 fungal molecules

A
  1. Ergosterol (plasma membrane)
  2. Mannoproteins
  3. Glucan
  4. Chitin (cell wall)
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188
Q

Name 4 treatments that can used for fungal diseases

A
  1. Polyenes
  2. Allylamines
  3. Azoles
  4. Echinocandins
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189
Q

How do polyenes work against fungal diseases?

A

Fungicidal - pore formation in ergosterol cell membrane

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190
Q

Name a side effect of polyenes as treatment for final disease

A

Nephrotoxicity (affects cholesterol)

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191
Q

Name a polyene

A

Amphotericin

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192
Q

How do allylamines work to treat fungal diseases?

A

Fungicidal - inhibits ergosterol pathway step

Extensive distribution to skin (poorly perfused) - dermatophyte treatment

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193
Q

Name a Allylamine

A

Terbinafine

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194
Q

How do azoles work to treat fungal diseases?

A

Fungistatic - dose dependent ergosterol synthesis inhibitors

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195
Q

Name 4 long term side effect of using azoles to treat fungal disease

A
  1. Alopecia
  2. GI problems
  3. Hepatitis
  4. Resistance
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196
Q

Name 4 azoles and what they treat

A
  1. Fluconazole - candida, crypto coccus
  2. Itraconazole - degree of mould activity - aspergillum, fusarium and dimorphic (often used for dermatophytes)
  3. Voriconazole - improved activity against moulds - treats invasive aspergillosis
  4. Posaconazole - some activity against zygomycetes
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197
Q

How to echinocandins work to treat fungal diseases?

A

Inhibit gluten synthesis
Fungicidal (yeast)
Fungistatic (mould)

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198
Q

Why are echinocandins the treatment of choice in severe or resistant disease?

A

Few side effects or interactions

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199
Q

In what patients are you most likely to see Pneumocystis Pneumonia?

A

Immunocompromised - HIV, organ transplant, haematology

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200
Q

What do you use to treat Pneumocystis Pneumonia?

A

Co-trimoxazole

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201
Q

Define virus

A

An infectious, obligate intracellular parasite compromising genetic material (DNA or RNA) surrounded by a protein coat and /or a membrane

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202
Q

What is a virion?

A

A virus when it’s not inside an infected cell

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203
Q

Give the 3 key features of virion structure

A
  1. Lipid envelope with spike projections
  2. Protein cashed
  3. Nucleic acid (RNA or DNA) and vision associated polymerase
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204
Q

What shapes can viruses exist as?

A

Helical
Icosahedral
Complex

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205
Q

What size do human viruses range from and to?

A

20-260 nm in diameter

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206
Q

Name the 6 stages of viral replication

A
  1. Attachment
  2. Cell entry
  3. Interaction with host cell
  4. Replication
  5. Assembly
  6. Release
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207
Q

What happens in the first stage of viral replication (attachment)?

A

Cell/viral receptor interaction

E.g. gp120 and CD4 in HIV

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208
Q

What happens in the second stage of viral replication (cell entry)?

A

Central viral core (nucleic acid and proteins) enter cell

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209
Q

What makes up the central viral core?

A

Nucleic acid and proteins

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210
Q

What happens in the third stage of viral replication (interaction with host cell)?

A

Use cell material for replications and evade host defence

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211
Q

What happens in the fourth stage of viral replication (replication)?

A

New viral components produced in nucleus/cytoplasm

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212
Q

What does the translation of viral mRNA produce?

A

Structural proteins
Viral genome
Non-Structural proteins - e.g. enzymes

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213
Q

Where does the fifth stage of viral replication (assembly) occur?

A

Occurs in different places depending on the virus
Nucleus = Herpes
Cytoplasm = Poliovirus
Cell membrane = HIV

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214
Q

What happens in the last stage of viral replication (release)?

A

Cell lysis (rhinovirus) or exocytosis from cell (HIV and influenza)

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215
Q

Name 5 ways in which viruses can cause disease

A
  1. Direct host cell destruction
  2. Modification of host cell function/structure
  3. Over-reactive host response
  4. Cell proliferation and immortalisation
  5. Cell defence evasion
216
Q

Name 3 viruses that use direct host cell destruction to cause viral disease

A
  1. Influenza
  2. Poliovirus
  3. HIV
217
Q

Name 2 viruses that use Modification of host cell function/structure to cause viral disease

A
  1. HIV

2. Rotavirus

218
Q

Name 2 viruses that use an over-reactive host response to cause viral disease

A
  1. Hep B and C

2. HIV

219
Q

Name a virus that uses cell proliferation and immortalisation to cause viral disease

220
Q

Name 3 ways in which cell defence evasion can be used to cause viral disease

A
  1. Cellular level
  2. Molecular level
  3. Host defence modulation
221
Q

Name 2 ways of cellular level cell defence evasion that cause viral disease

A

Latency - Herpesviridae

Persistance - Measles

222
Q

What are the benefits of persistence in causing viral disease?

A

Direct cell to cell spread
Avoids random release into environments
Spreads quicker
Avoids the immune system

223
Q

Name 3 ways of Molecular level cell defence evasion that cause viral disease

A
  1. Antigenic variability - flu and HIV
  2. Presentation of host cell apoptosis - Herpesviridae
  3. Down-regulation of interferon and ochre intracellular host defence proteins
224
Q

Explain the pathogenesis of the rotavirus infection

A
  1. Acid resistant rotavirus invades jejunal epithelial cells causing villi and microvilli atrophy
  2. SA and enzyme concentration is reduced
  3. No sugar absorption causing hyper-osmosis
  4. Diarrhoea occurs
225
Q

Explain the pathogenesis of Hepatitis B infection

A
  1. HBV infection causes antibody and CTL response
  2. Hepatocyte destruction (liver damage) occurs
  3. Steady state reached between hepatocyte destruction and viral replication – no spread
226
Q

Explain the pathogenesis of Cervical carcinoma development

A
  1. HPV infects suprabasal layer of genital tract and replicates as mucosal cells move up
  2. HPV and host cell genome integration causing Rb and p53 suppression (control growth and proliferation)
  3. Carcinogenesis occurs due to excessive cell growth and proliferation
227
Q

Why is the range of clinical syndromes due to issues so large?

A

Viruses have:
Different host cell and tissues that they can infect
Different methods of interaction with the host cell

228
Q

Define Infectivity

A

Ability to become established in host (adherence and immune evasion)

229
Q

Define Virulence

A

Ability to cause disease when established

230
Q

Define Invasiveness

A

Ability to penetrate mucous surfaces to reach sterile sites

231
Q

Define Microbiome

A

Described the totality of microorganisms, their genetic elements and their environmental interaction in an environment

232
Q

Why do viruses need rapid cell entry?

A

As free virus in the blood stream is easily neutralised by the immune response

233
Q

Name 2 types of response to viral infection

A
  1. Humoral response

2. Cell mediated response

234
Q

What antibodies are involved in the humeral response to viral infections and how do they respond?

A

IgA - blocks viral binding so unable to inject genetic material
IgM - aids agglutination
Complement and GB antibody - opsonisation and cell lysis and neutralise toxins

235
Q

What cells are involved in the cell mediated response to viral infections and how do they respond?

A

Interferon - prevents infection in non infected cells through antiviral action (induces antiviral protein DAI on nearby non infected cells)
Cytotoxic T lymphocytes - directly kill infected cells
Natural killer cells and macrophages - activates antibody-dependent cell destruction

236
Q

What is most viral infection cell damage caused by?

A

The immune response

237
Q

Viruses may cause direct cell cytotoxicity. Name 4 examples

A
  1. Influenza virus to respiratory epithelium
  2. Varicella rooster virus to skin cells
  3. Yellow fever virus to liver cells
  4. HIV to CD4 T-cells
238
Q

Name 4 ways in which viruses can cause host defence evasion

A
  1. Antigenic variation - rhinovirus, HIV, influenza
  2. HSV glycoprotein binds to C3b - inhibits classical and alternate complement
  3. Immune suppression - MMR, EBV, HIV
  4. EBV blocks action of DAI - Adenovirus
239
Q

Why does influenza have antigenic variability?

A

Changes in haemagglutinin and Neuraminidase give coat variability

240
Q

How can bacterial infections enter their host?

A

Through GI or GU tracts

Or skin/mucous membrane wounds

241
Q

What response is initiated is the is a low number/virulence of bacteria?

A

Phagocytes are active

242
Q

What response is initiated is the is a high number/virulence of bacteria?

A

Cell mediated immunity response

243
Q

What response is initiated when extracellular bacteria is involved?

A

Antibody response

244
Q

What response is initiated when intracellular bacteria is involved?

A

Cellular response

245
Q

Name 3 ways in which bacteria compete with the host cell and colonising flora

A
  1. Sequestering nutrients
  2. Using novel metabolic pathways
  3. Out-competing other microorganisms
246
Q

Name 2 types of bacterial colonisation factors

A
  1. Adhesins

2. Biofilms

247
Q

How do adhesins help bacteria colonise?

A

Help bacteria bind to mucosal surfaces

248
Q

Name 3 types of adhesins

A
  1. Fimbriae and pili filamentous proteins - E.g. Neisseria gonorrhoeae
  2. Lipid - E.g. lipid trichroic acid of Streptococcus pyogenes
  3. Glycosaminoglycans of Chlamydia sp.
249
Q

How do biofilms help bacteria colonise?

A

Bacteria can stick together on a surface by secreting extracellular polymeric substance of protein, polysaccharides and DNA - help protect against antimicrobials
E.g. S. aureus and Streptococcus mutans

250
Q

How are antibodies involved in the immune response against bacterial infections?

A

Antibodies - neutralise toxins and block host cell attachment (IgA)
Complement - cell lysis, opsonisation and proliferation prevention

251
Q

Describe a delayed type 4 hypersensitivity reaction

A 
Intracellular infection (TB) --> Tdth cells stimulated --> influx of inflammatory cells
Second contact --> Tdth secretes IFN, TNF, IL --> macrophage recruitment
Prolonged DTH = continuous macrophage activation --> granuloma formation --> lytic enzymes cause tissue damage
252
Q

Name 5 ways in which bacterial infection evade host defences

A
  1. Resist phagocytosis - polysaccharide capsule, M protein, phagolysosome escape
  2. Protease lyses IgA
  3. Antigenic variation
  4. Pili = movement
  5. Adhesins
253
Q

What immune response occurs when protozoa infections are in the blood?

A

Humoral immunity

254
Q

What immune response occurs when protozoa infections are in the tissue?

A

Cell mediated immunity

255
Q

Name 3 ways in which protozoa evade host defences

A
  1. Surface antigen variability
  2. Intracellular phase
  3. Shed outer coat
256
Q

Immune response is not sufficient to kill worms. Name 3 other processes that occur that can kill worms

A
  1. IgE and IgG produced
  2. IL5 released - eosinophil production
  3. IL3 - mast cell growth
    Eosinophil basic protein is toxic to worms
257
Q

Name 2 ways in which worms evade host defences

A
  1. Decreased antigen expression by adult worms

2. Glycolipid/glycoprotein coat is hot derived so not perceived as foreign to the immune system

258
Q

Give the key features of protozoa

A

Single cell eukaryotes
Membrane bound nucleus
Eat food by phagocytosis and digest it in intracellular vacuoles

259
Q

Name the 4 types of protozoa

A
  1. Flagellates (flagella)
  2. Sporozoans (non-motile)
  3. Amoebae (pseudopodia)
  4. Ciliates (cilia)
260
Q

Give 4 examples of flagellates protozoa

A
  1. Trypanosoma
  2. Trichromonas vaginalis
  3. Leishmania
  4. Giardia Lamblia
261
Q

Give 2 examples of Sporozoans protozoa

A
  1. Plasmodium

2. Taxoplasma gondii

262
Q

Give an example of Amboebae protozoa

A

Entamoeba histolytica

263
Q

Give an example of Ciliates protozoa

A

Balatidium coli

264
Q

Give the main features of Entamoeba histolytica

A

Amboebae protozoa
Faecal-oral transmission
Colonise in the gut in humans
Causes severe dysenteric illness

265
Q

How does Entamoeba histolytica cause severe dysenteric illness and how is it treated?

A

Cysts ingested and travel to small intestine
Release trophozoites which go to large intestine
Local invasion of intestinal wall
Can spread through the blood to liver, brain and lungs
Treatment = Metronidazole

266
Q

Name the 2 types of Trypanosomiasis

A

African - ‘sleeping sickness’

American - Chagas disease

267
Q

Give the main features of African Trypanosomiasis (type of protozoa, cause by, found)

A

Flagellate protozoa

Caused by Trypanosoma Bruce gambiense (west/central) and rhodesiense (east)

268
Q

Give the 5 symptoms African Trypanosomiasis

A
  1. Fever
  2. Headaches
  3. Extreme fatigue
  4. Joint pains
  5. CNS symptoms (personality change)
269
Q

Give the main features of American Trypanosomiasis (type of protozoa, caused by, vector, found)

A

Flagellate protozoa
Caused by Trypanosoma cruzi
Vector = triatomine bug
Seen in Central/South America

270
Q

Name 5 early symptoms and 3 late symptoms of American Trypanosomiasis

A 
Early:
1. Fever
2. Headache 
3. Lymphadenopathy 
4. Chagoma
5. Romana's sign 
Late:
1. Cardiac manifestation 
2. Megaoesophagus 
3. Megacolon
271
Q

Give the key features of Leishmaniasis (type of protozoa, caused by, vector..)

A 
Flagellate protozoa 
Caused by Leishmania spp
Vector = female sand fly 
Disease of poverty 
3 types
272
Q

Name the 3 types of Leishmaniasis protozoa and briefly describe each one

A
  1. Cutaneous leishmaniasis - ulcers on exposed parts of body, creates issues with social rejection and scarring
  2. Mucocutaneous - lesions that can cause destruction to mucous membranes o the nose, mouth and throat and can lead to recurrent pneumonia and sepsis
  3. Visceral - ‘Kala Azar’ - affects the internal organs, characterised by irregular bouts of fever, weight loss, swelling of spleen and liver and anaemia
273
Q

Give the transmission, symptoms, diagnosis and treatment of Giardia lamblia

A

Flagellate protozoa
Faeco-oral transmission
Diagnosis by still microscopy
Treatment = metronidazole

274
Q

Give the transmission, symptoms and treatment of Trichomonas vaginalis

A

Flagellate protozoa
Sexually transmitted
Usually asymptomatic but can have dysuria and yellow frothy discharge
Treatment = metronidazole

275
Q

Which people are more prone to Balantidium coli and what symptoms do they acquire?

A

Ciliates protozoa
Mainly in the immunocompromised
Causes severe diarrhoea and/or ulceration of colon

276
Q

Give the 4 key features of Sporozoans

A

No locomotory extension
All species are parasitic
Most are intracellular parasites
Reproduce by multiple fission

277
Q

Give the key features of Cryptosporidiosis (type of protozoa, caused by, transmission, symptoms, diagnosis)

A 
Sporozoan protozoa 
Caused by cryptosporidium spp 
Transmission via contaminated food/water
Symptoms = watery diarrhoea, vomiting, fever and fatigue 
Oocytes seen in stool sample
278
Q

Give the key features of Toxoplasmosis (type of protozoa, caused by, transmission, symptoms)

A

Sporozoan protozoa
Caused by toxoplasma gondii
Transmission via contaminated food/water or feline faeces
Can cause disseminated disease, toxoplasma encephalitis, chorizorentinitis

279
Q

Name the 5 types of disease causing plasmodium (malaria)

A
  1. falciparum
  2. ovale
  3. vivax
  4. malariae
  5. knowlesi (rare)
280
Q

Give 4 reasons why malaria is increasing worldwide

A
  1. Increasing resistance of parasite to antimalarials
  2. Increasing resistance of mosquito to insecticides
  3. Ecological and climate changes
  4. Increase travel to endemic areas
281
Q

What is the vector of malaria?

A

Female anopheles mosquito around stagnant water

282
Q

What are the 4 stages of a female anopheles mosquito?

A
  1. Human stage - exo-erythrocytic
  2. Hypnozoite stage (only in vale and vivax)
  3. Human Stage - endo-erythritic
  4. Mosquito (vector) stage
283
Q

Briefly explain the exo-erythrocytic stage of the malaria lifecycle

A
  1. Mosquito injects sporozoites during feeding - infect liver hepatocytes
  2. Sporozoites replicate –> schizont formation
  3. Schizont ruptures –> merozoites enter bloodstream
284
Q

Briefly explain the Hypnozoite stage of the malaria lifecycle

A

Only oval and vivax

Lie dormant in liver and reactivate week to years later

285
Q

Explain the endo-erythrocytic stage of the malaria lifecycle

A
  1. Merozoites infect RBC –> immature trophozoites
  2. Immature trophozoites (ring) mature
  3. EITHER:
    a) Trophozoite –> schizont formation –> ruptures and merozoites released infecting other RBCS
    b) Trophozoite –> gametocyte –> ingested by mosquito during meal
286
Q

Explain the mosquito (vector) stage of the malaria lifecycle

A
  1. Macrogametocyte –> ookinete –> oocyst

2. Oocyst ruptures releasing sporozoites which travel to salivary gland of mosquito

287
Q

Which stage of the malaria lifecycle gives rise to the clinical manifestations?

A

Endo-erythrocytic stage

288
Q

Name 7 clinical features of malaria

A
  1. Fever
  2. Chills and sweats
  3. Headache
  4. Myaligia
  5. Fatigue
  6. Nausea
  7. Diarrhoea
  8. Abdominal pain
289
Q

Why are clinical features seen?

A

Due to pro inflammatory cytokines (TNF and IL) being released when haemolysis occurs

290
Q

Give 4 signs of malaria

A
  1. Anaemia
  2. Jaundice
  3. Hepatosplenomegaly
  4. Haemoglobinuria
291
Q

How is malaria diagnosed?

A 
Anaemia 
Low platelets 
Hyperbilirubinemia 
Thick and thin blood films - 3 times in 24 hours
Light microscopy
292
Q

Why are both a thick and thin blood film taken?

A 
Thick = shows you malaria is present 
Thin = identification of morphological features - type, parasite count
293
Q

How high does the parasite count have to be for malaria to be considered severe?

294
Q

What is the treatment for Complicated falciparum malaria?

A

IV artesunate (quinine and doxycycline)

295
Q

What is the treatment for Normal falciparum malaria?

A

Oral raiment OR oral quinine and doxycycline

296
Q

What is the treatment for non-falciparum malaria?

A

Oral chloroquine

297
Q

What other treatment should be provided with the vivid and oval strains of malaria and why?

A

Primaquine for hypnozoite clearance - gets rid of the dormant stage so there is no relapse

298
Q

Name 6 types of extra treatment of malaria for supportive measures

A
  1. Cerebral: antiepileptics
  2. ARDS: oxygen, diuretics, ventilation
  3. Renal failure: fluids, dialysis
  4. Sepsis: broad spectrum antibiotics
  5. Bleeding/Anaemia: blood products
  6. Exchange transfusion if huge parasite burden
299
Q

Which malaria strain causes the most malaria related deaths?

A

P. falciparum

300
Q

Explain the pathophysiology behind P. falciparum

A
  1. Infected RBC’s display specific membrane proteins which can adhere to adhesion molecules expressed in small blood vessels (cytoadhereance) –> triggers coagulation by thrombin and increases vascular permeability
  2. Small vessels become obstructed by clumps of RBCs
301
Q

What are the consequences of cytoadherence and accumulation of RBCs?

A

Blocks brain and lung microcirculation causing hypoxia in tissues and cause cerebral malaria

302
Q

Give 6 clinical features seen in adults from P. falciparum

A
  1. Coma
  2. Adult respiratory distress syndrome (ARDS)
  3. Hypoglycaemia (especially in pregnancy)
  4. Renal failure
  5. Shock
  6. Blackwater fever
303
Q

Give 6 clinical features seen in children from P. falciparum

A
  1. Tachypnoea
  2. Acidosis
  3. Anaemia
  4. Hypoglycaemia
  5. Raised intracranial pressure
  6. Convulsions (60-80%)
304
Q

Give 2 definitions of antibiotic

A

Molecule that binds to bacteria target site and effects reactions critical to bacterial survival
Agents produced by microorganism that kill o inhibit the growth of other microorganisms in high dilution

305
Q

What do antimicrobials include?

A 
Antifungal 
Antibacterial 
Antihelminthic
Antiprotozoal
Antiviral
306
Q

What parts of a cell can antibiotics act on?

A

Cell wall synthesis
Nucleic Acid synthesis
Protein synthesis

307
Q

What do beta lactams act on?

A

They bind covalently to peptidoglycan PBP which inhibits cell wall synthesis leading to cell lysis

308
Q

Name 4 groups of beta lactams

A
  1. Penicillins
  2. Cephalosporins
  3. Carbapenems
  4. Monobactams
309
Q

How do antibiotics metronidazole and rifampicin work?

A

Interfere with nucleic acid synthesis and function

310
Q

How do Fluoroquinolone antibiotics work?

A

Inhibit DNA gyrase

311
Q

How do Sulphonamides and trimethoprim antibiotics work?

A

Inhibit folate synthesis and carbon unit metabolism

312
Q

What types of antibiotics inhibit ribosomal activity and protein synthesis?

A 
Macrolides
Tetracyclines
Aminoglycoside (gentamicin) 
Chloramphenicol
Lincosamides
313
Q

What do bacteriostatic antibiotics do?

A

Inhibit bacterial growth by inhibiting protein syntheses, DNA replication and metabolism
Also reduce exotoxin production and endotoxin surge less likely from gram -ve bacteria

314
Q

What do bactericidal antibiotics do?

A

Inhibit cell wall synthesis causing death of bacteria

315
Q

Are beta lactams bacteriostatic or bactericidal?

A

Bactericidal

316
Q

When are bactericidal antibiotics very useful?

A

Poor tissue penetration (e.g. Endocarditis)
Difficult to treat infections (e.g. TB)
Need to eradicate infection quickly (e.g. meningitis)

317
Q

What is required for a bacteriostatic antibiotics to work?

A

Minimum inhibitory concentration (MIC) MIC:MBC ratio >4

318
Q

What is required for bactericidal antibiotics to work?

A

Minimum bactericidal concentration (MBC)

319
Q

What are the major determinants of anti-bacterial effects?

A

Concentration of drug occupying binding sites

Time the antibiotic remains on binding site

320
Q

What does concentration dependent killing depend on?

A

The height of concentration above the minimum inhibitory concentration (MIC)
Peak concentration/MIC ratio

321
Q

What does time dependent killing depend on?

A

On time the concentration stays above the minimum inhibitory concentration for
t>MIC

322
Q

Give an example of an antibiotic group that uses concentration dependent killing

A

Aminoglycosides

323
Q

Give 2 examples of a antibiotic groups that uses time dependent killing

A

Beta lactams

Macrolides

324
Q

What does the antibiotic depend on to reach and stay at the site of bacterial infection?

A

Pharmacokinetics

325
Q

Name 4 mechanisms of antibiotic resistance

A
  1. Change in antibiotic target
  2. Destroy or inactivate antibiotic
  3. Prevent antibiotic access
  4. Remove antibiotic from bacteria
326
Q

Explain the change in antibiotic target mechanism of antibiotic resistance and give an example

A

Changes molecular configuration at antibiotic binding site or masks it
Flucloxacillin is no longer able to bind to PBP of Staphylococci in MRSA

327
Q

Give 2 examples of the destroy/inactivate antibiotic mechanism of antibiotic resistance

A
  1. Beta lactamase hydrolyses beta lactam ring so it can no longer bind to PBP
  2. Staph producing penicillinase so penicillin but flucloxacillin is inactivated
328
Q

Explain the preventing antibiotic access mechanism of antibiotic resistance

A

Modify membrane channels - size, number and selectivity

329
Q

Give 2 examples of the preventing antibiotic access mechanism of antibiotic resistance

A
  1. Gram -ve bacteria against aminoglycosides

2. Pseudomonas aeruginosa against imipenem

330
Q

Explain the removal of antibiotic from bacteria mechanism of antibiotic resistance and give an example

A

Export pumps remove the antibiotic so the level of antibiotic is reduced

  1. S. aureus and S. pneumoniae resistant to fluoroquinolones
  2. Enterobacteriaceae resistance to tetracyclines
331
Q

By what 2 ways can antibiotic resistance develop?

A
  1. Intrinsic (naturally resistant)

2. Acquired

332
Q

Give 3 examples of intrinsic antibiotic resistance development

A
  1. Gram -ve outer membrane can’t be penetrated by vancomycin
  2. Enterococci PBP are not effectively bound by cephalosporins
  3. Aerobic bacteria enable to reduce metronidazole to its active form
333
Q

Name the 2 types of acquired antibiotic resistance that can occur

A
  1. Spontaneous mutation

2. Horizontal gene transfer

334
Q

How can acquired spontaneous mutation antibiotic resistance come about?

A
  1. New nucleotide base pair
  2. Change in aa sequence
  3. Change to enzymes to cell structure
  4. Reduced affinity or activity of antibiotic
    Cause altered enzyme function leading to reduced antibiotic effect
335
Q

Give and briefly explain the 3 types of horizontal gene transfer antibiotic resistance

A
  1. Conjugation - sharing of extra-chromosomal DNA plasmids (‘bacteria sex’)
  2. Transduction - insertion of DNA by bacteriophages
  3. Transformation - bacteria takes up free DNA
336
Q

Name 2 important gram +ve antibiotic resistant organisms

A
  1. Methicillin resistant Staphylococcus Aureus (MRSA)

2. Vancomycin Resistant Enterococci (VRE)

337
Q

How has MRSA gained antibiotic resistance?

A
  1. Staphylococcal cassette chromosome med (SSCmec) contains resistance gene mecA
  2. Encode penicillin-binding protein 2a (PBP2a) that does not bind to penicillin
  3. Confers resistance to beta lactam antibiotics as well as Methicillin
338
Q

How has VRE gained antibiotic resistance?

A

Plasmid mediated acquisition of gene encoding altered aa on peptide chain preventing vancomycin binding
Promoted by cephalosporin use

339
Q

Name 3 important gram -ve antibiotic resistant types

A
  1. b-lactamase enzymes hydrolysing penicillins
  2. Extended spectrum beta lactamase (ESBL)
  3. AmpC b-lactamase resistance
340
Q

Give 3 examples of b-lactamase enzymes hydrolysing penicillins

A

TEM-1 in E. coli, H. influenzae and N. gonorrhoea
SHV-1 in K. pneumoniae
CTX_M cephalosporinase in enterbacteriaceae

341
Q

What, typically, are b-lactamase enzymes hydrolysing penicillins sill sensitive to?

A

Beta-lactamase inhibitors

342
Q

What were formed to extend b-lactam resistance

A

Extended spectrum beta lactamase (ESBL) inhibitors due to a further mutation at active site

343
Q

What can extended spectrum beta lactamase inhibitors destroy or inactivate?

A

Penicillin
Amoxycillin
Cephalosporins
Combination antibiotics

344
Q

What is AmpC B-lactamase resistance?

A

Broad spectrum penicillin, cephalosporin and monobactam resistance

345
Q

What are carbapenems?

A

Beta lactams that are highly resistant to beta lactamse or cephalosporins = last resort antibiotic

346
Q

What can carbapenemases be produced by?

A

Carbapenemase reistant enterobacteria (CRE)

347
Q

What type and part of bacteria do beta lactam antibiotics target?

A

Gram +ve bacteria

Cell wall killers - target their thick peptidoglycan layer

348
Q

With what antibiotic are skin infections (Staph. aureus, Group A strep) treated?

A

Flucloxacillin (beta lactam)

349
Q

With what antibiotic are chest infections (Strep. penumoniae) treated?

A

PO penicillin V or IV benzylpenicillin (beta lactams)

350
Q

With what antibiotic are throat infections (Group A strep) treated?

A

PO penicillin V or IV benzylpenicillin (beta lactams)

351
Q

What family of antibiotics doe cephalosporin belong to and when is it very useful to use?

A

Part of the beta lactam familiy
Good for people with a penicillin allergy
Better for more resistant bugs
Able to get to hard to reach places

352
Q

Name 2 antibiotics that are glycopeptides

A
  1. Vanomyocin

2. Teicoplanin

353
Q

What type of bacteria do glycopeptides act on and what do they treat?

A

Act on cell walls of gram +ve bacteria

Used to treat MRSA and used if someone has a penicillin allergy

354
Q

Name 2 antibiotics that are marcolides

A
  1. Clarithromycin

2. Erythromycin

355
Q

What type of bacteria do Macrolides act on and what do they treat?

A

Inhibit protein synthesis of gram +ve bacteria (S. aureus and beta haemolytic strep) and atypical pneumonias
Used to treat cellulitis (if penicillin allergy), MRSA and severe/atypical pneumonia

356
Q

Name a Lincosamide antibiotic

A

Clindamycin

357
Q

What type of bacteria do lincosamides act on and what are they used to treat?

A

Inhibit protein synthesis of gram +ve bacteria and anaerobes

Used to treat cellulitis (if pen allergy) and necrotising fasciitis

358
Q

Name a tetracycline antibiotic

A

Doxycycline

359
Q

What type of bacteria do tetracyclines act on and what are they used to treat?

A

Inhibit protein synthesis
Broad spectrum but mainly act on gram +ve
Used to treat cellulitis 9if pen allergy), chest infections and pneumonia

360
Q

What types of infections are caused by gram -ve bacteria?

A 
Urine infections (E. coli, Klebsiella sp, Proteus sp.)
Gallbladder infections (E. coli, Klebsiella sp, Proteus sp.)
Abdominal infections (E. coli, Klebsiella sp, Proteus sp.)
Infectious diarrhoea (shigella, salmonella)
361
Q

What type of bacteria does Gentamicin act on and what is it used to treat?

A

Gram -ve and staphs (used synergistically to treat streps)

Used to treat UTIs and in infective endocarditis (synergistically)

362
Q

What is a disadvantage of Gentamicin?

A

Have to keep doing drug treating to ensure no nephrotoxicity
IV only

363
Q

Give an example of a Quinolone antibiotic

A

Ciprofloxacin

364
Q

What type of bacteria do Quinolone antibiotics act on and what is it used to treat?

A

Inhibit DNA synthesis of gram -ve bacteria

Used to treat UTIs, gallbladder and abdominal infections

365
Q

What type of bacteria does Trimethoprim act on and what is it used to treat?

A

It’s a folate antagonist and is bored spectrum but is mainly used for gram -ve bacteria
Used in the treatment of UTIs

366
Q

What type of bacteria does Nitrofurantoin act on and what is it used to treat?

A

Gram -ve and +ve bacteria

First line UTI treatment

367
Q

Name 7 types of mycobacteria and what conditions they are associated with

A
  1. M. tuberculosis - TB
  2. M. leprae - Leprosy
  3. M. avian complex (MAC) - infection in AIDS and chronic lung disease
  4. M. kansaii - chronic lung infection
  5. M. marina - fish tank granuloma
  6. M. ulcerans - Buruli ulcer
  7. M. fortuitous complex - skin and soft tissue infections
368
Q

Give the key features of mycobacteria

A 
Aerobic 
Non-Motile 
Non spore forming
Slow growing (15-20hrs)
Phagosome reistant 
Acid fast bacillus 
Weakly gram +ve or colourless
369
Q

What does the cell wall of mycobacteria contain?

A

Mycolic acids

Lipoarabinomannan

370
Q

How does the show growing nature of mycobacteria effect growth and response in humans?

A

Slow reproduction
Slow growthin humans - gradual onset of disease
Slow growth in culture
Slow response to treatment - 6 months minimum

371
Q

Why are mycobacteria resistant to gram stain?

A

The acid fast bacilli (AFB) have high lipid content with mycolic acids in the cell wall

372
Q

What stain is used for mycobacteria?

A

Ziehl-Neelson

373
Q

Explain how to do a ZIehl-Neelson stain

A

Carbol fuschin –> acid alcohol –> methylene blue

Need 10,000 AFB/ml

374
Q

What is a positive result for acid fast bacilli?

A

Red/pink stain

375
Q

Briefly explain the immunology of mycobacteria

A
  1. Phagocytosed by macrophage –> phagolysosome
  2. Withstand phagolysosomal killing and escape to the cytosol
  3. Hosts aim to kill AFB using microbicidal molecules and acidification aids digestion and degradation by proteases –> generation of antigens for presentation to T-cells (APC)
  4. CD4 T cells recognise APC –> generate IFN gamma –> activate intracellular killing by macrophages
  5. IL-12 released by macrophages which stimulates Th1 T cells and IFN gamma release
376
Q

What causes susceptibility to mycobacterial infection?

A

Genetic defects in IFN-g or IL-12 receptors or elements of their signaling pathways result in susceptibility to mycobacterial infection

377
Q

What is a granuloma(ta)?

A

Lesions that arise in a response that tried to contain mycobacteria (but also occurs in other infections and non-infectious processes)

378
Q

How are granulomas formed in repose to mycobacteria?

A

Highly stimulated macrophages –> epithelioid cells –> fuse = Langhans giant cells
Central tissue necrosis by cytotoxic CD8 T cells –> caseating granuloma –> cavity in tissues (TB = lungs)

379
Q

Name 2 types of leprosy

A
  1. Tuberculoid leprosy

2. Lepromatous leprosy

380
Q

What immune response is associated with Tuberculoid leprosy?

A

Th 1 CD4 T-cell response –> IFN and TNF release

381
Q

What does Tuberculoid leprosy cause?

A

Tissue hypersensitivity and granuloma leading to tissue damage

382
Q

What immune response is associated with Lepromatous leprosy?

A

Th2 CD4 T-cell response –> IL 4, 5, and 10 release

383
Q

What does Lepromatous leprosy cause?

A

Lesions full of bacilli and NO granuloma –> leads to skin lesions

384
Q

What are the polar responses with gradation between Tuberculoid and Lepromatous leprosy characterised by?

A

Too much immune response and so tissue injury or too little response with uncontrolled tissue damage by bacilli

385
Q

What is the treatment for mycobacteria?

A

Same as TB treatment - isoniazid, rifampicin, pyrazinamide, ethambutol

386
Q

What happens in primary TB?

A

Bacilli taken into lymphatic to hilarious lymph nodes of the lungs

387
Q

Briefly explain latent TB and what is seen with it

A

Cell mediated repose from T cell
primary infection contained but CMI persists
No clinical disease (normal CXR)
Detectable CMI to TB on tuberculin skin test

388
Q

Briefly explain Pulmonary TB

A
  1. Granuloma forms around bacilli that had settled in apex
  2. In apex of lung there is more air and less blood supply (fewer defending white cell to fight)
  3. CMI and necrosis in results in abscess of bacilli forming and caseous material coughed up leaving cavity
389
Q

When can pulmonary TB occur?

A

Can occur immediately following primary infections to after later reactivation

390
Q

What is the primary complex of TB compose of?

A

Granuloma, lymphatics and lymph nodes

391
Q

Where can TB spread to?

A

Genitourinary TB
Pleural TV
Bone and joint TB
TB meningitis

392
Q

What is the purpose of the Lancefield test?

A

To distinguish between different types of Beta-haemolytic bacterias according to antigens on their cell wall

393
Q

Where in the body would you find normal flora (commensals)?

A 
Mouth 
Skin
Vagina
Urethra
Large Intestine
394
Q

Name 7 sterile sites of the body (no colonising organisms)?

A 
Blood 
CSF
Pleural fluid 
Peritoneal cavity 
Joints
Urinary tract
Lower respiratory tract
395
Q

How could you detect whether an individual has had pervious exposure to TB?

A
  1. Tuberculin skin test (Mantoux)

2. Interferon gamma release assays

396
Q

Between what temperatures and what pH range can bacteria grow?

A

-80 to +80 degree Celsius

pH 4 to 8

397
Q

What are the 3 phases of bacterial growth?

A
  1. Lag phase
  2. Exponential phase
  3. Stationary phase
398
Q

Give 2 functions of pili

A
  1. Hep adhere to cell surfaces

2. Plasmid exchange

399
Q

What are plasmids?

A

Circular pieces of DNA that often carry genes for antibiotic resistance

400
Q

How would you describe the arrangement of staphylococci?

A

Clusters of cocci

401
Q

How would you describe the arrangement of streptococci?

A

Chains of cocci

402
Q

Describe the pathogenesis of gastroenteritis

A
  1. Endocytosis
  2. Chemokine release
  3. Neutrophil recruitment and migration
  4. Neutrophil induced tissue injury
  5. Fluid and electrolyte loss –> diarrhoea
403
Q

What are dimorphic fungi?

A

Fungi that can exist as both yeast and mould

These are yeast in tissues but mould in vitro

404
Q

Give 4 disadvantages of azoles

A
  1. High first pass metabolism, bioavailability = 45%
  2. ADRs can cause hepatitis
  3. Drug interactions dur to CYP450
  4. Resistance can develop
405
Q

What are he 5 ways in which viruses can evert host defences?

A
  1. Virus persistance or latency
  2. Down regulation of interferons
  3. Virus variability die to gene reassortment or mutation
  4. Prevention of host cell apoptosis
  5. Viral modulation of host defences
406
Q

What are retroviruses?

A

Viruses that are enveloped

407
Q

What genus does HIV belong to and what is the significance of this?

A

Lentiviruses - very slow with long incubation period

408
Q

Where did HIV 1 and 2 arise from?

A

SIV (simian immunodeficiency virus)
HIV 1 originally from chimpanzees
HIV 2 originally from sooty mangabey

409
Q

Name 3 HIV types

A

M (main) - split into clades
O (outlaying)
N (new)

410
Q

Give the 4 key features of HIV 1 structure

A
  1. Envelope with gp120 and gp41 (gp160)
  2. Matrix and p17 protein
  3. Protein capsid and p24 - protein houses core enzymes
  4. Viral RNa, reverse transcriptase and intgerase
411
Q

Name the 10 main stages of HIV replication

A
  1. Attachment
  2. Cell entry
  3. Uncoating
  4. Reverse transcription
  5. Genome integration
  6. Transcription of viral DNA
  7. Splicing of mRNA
  8. Translation into proteins
  9. Assembly
  10. Budding
412
Q

Briefly describe HIV replication

A
  1. GP160 binds to CD4 receptors and CCR5 co-receptors
  2. Viral caspid, enzymes and nucleic acids are uncoated and released into the cell
  3. RNA is converted into DNA using reverse transcriptase
  4. Viral DNA is integrated into cellular (host) DNA by intergrase
  5. Viral DNA is transcribed into viral proteins
  6. Splicing of viral RNA and proteins occurs to for new virus
  7. New HIV cells ‘bud’ from CD4
413
Q

Which enzyme is responsible for integrating HIV DNA into cellular DNA?

414
Q

Name 4 enzymes involved in HIV replication

A
  1. Reverse transcriptase
  2. Integrase
  3. RNA polymerase
  4. Proteases
415
Q

What enzyme copies HIV RNA into DNA?

A

Reverse transcriptase

416
Q

Which part of HIV enters the host cell following attachment?

A

Viral capsid enzymes and nucleic acids

417
Q

What cells acts as host cells for HIV?

A

CD4+ cells

Macrophages and dendritic cells can also be invaded by HIV

418
Q

Why might macrophages also be infected by HIV?

A

Also have CD4 and CCR5 receptors

419
Q

Why are mutations common in HIV?

A

HIV replicates via reverse transcriptase and this process is prone to errors and mutations

420
Q

Describe what happens when someone is initially infected with HIV

A

HIV enters via mucosa
Macrophages ingest HIV and presents an epitope of HIV to a T cell
HIV then infects the T cell
Infection spills into the blood stream – viraemia (exponential T cell infection rise)

421
Q

What is the Humoral immune response to HIV?

A

Low number of neutralising antibodies due to viral genetic variability

422
Q

What is the Cell mediated immune response to HIV

A

CD8 CTL’s cause early HIV number reduction - incomplete immune response
CD4 lymphocyte number reduced our to HIV infection - no proliferation

423
Q

What is the affect of HIV infection on CD4 count?

A

Leads to uncontrolled CD4 activation and apoptosis so CD4 numbers decrease over time

424
Q

HIV leads to immune dysfunction, how are the immune system cells affected?

A
  1. CD4 cells are excessively and inappropriately activated which then results in a decrease in the number and function of CD4 cells
  2. CD8 CTL’s have increased activations but decreased cytolytic and non-cytolytic function
  3. There is impaired IL-2 production
  4. B cells have increase activation but decrease proliferation so increased non-specific antibody production
  5. Decreased function of NK cells, neutrophils and macrophages
425
Q

Name 4 sanctuary sites of HIV

A
  1. Genital tract
  2. GI tract
  3. CNS
  4. Bone marrow
426
Q

Name 2 cell reservoirs of HIV

A
  1. Macrophages

2. Microglia

427
Q

What are the markers for HIV in the blood?

A

Antigens
Antibodies
HIV RNA concentration (viral load)

428
Q

What are the 4 main phases in the natural history of HIV?

A
  1. Acute primary infection
  2. Asymptomatic phase
  3. Early symptomatic HIV
  4. AIDS
429
Q

What happens in the acute primary infection phase of HIV?

A

Transient fall in CD4+ count followed by a gradual rise

Also an acute rise in viral load

430
Q

What signs and symptoms might you see when someone is in the acute primary infections phase of HIV?

A

Abrupt onset of non-specific symptoms - fever, rash, myalgia, weight loss, lethargy and depression

431
Q

How long after infection do symptoms start occurring?

432
Q

What happens in the asymptomatic phase of HIV?

A

Progressive loss of CD4+ T-cells occurs –> poor immunity

433
Q

What signs and symptoms might you see when someone is in the asymptomatic phase of HIV?

A

Its is the latent phase so you rarely see symptoms

Sometimes enlarged lymph nodes are seen

434
Q

What happens in the early symptomatic phase of HIV?

A

Manifestations of clinical features (HIV) occurs

435
Q

What is the CD4+ count when someone is diagnosed with having AIDS?

A

CD4+ < 200

436
Q

What is clinical latency?

A

Rise in CD4 numbers to begin then slow decline until person is immunocompromised enough to present with symptoms and opportunistic infections

437
Q

What signs and symptoms might you see when someone is the early symptomatic phase of HIV?

A

Occur in association with many conditions – more frequent or severe with HIV:
Oral/vaginal candida: persistent/difficult to manage
Oral Hairy Leukoplakia
Persistent vernalised lymphadenopathy involving ≥ 2 episodes or multiple dermatomes
Cervical dysplasia
Cervical carcinoma-in-situ
Peripheral neuropathy
Bacillary angiomatosis
Immune-mediated Thrombocytopaenic Purpura (ITP)
Pelvic Inflammatory Disease
Listeriosis
Constitutional symptoms (e.g. fever or diarrhoea > 1 month)

438
Q

Name 3 respiratory diseases associated with HIV

A
  1. Bacterial (pneumococcal) pneumonia
  2. TB
  3. Pneumocystis pneumonia (PCP) - most common opportunistic infection
439
Q

What are the characteristic symptoms fo pneumocystis pneumonia?

A

Decrease CD4+ count
Decreased O2 saturation on exertion
Decreased exercise tolerance

440
Q

Name 3 CNS diseases associated with HIV

A
  1. Mass lesions e.g. primary CNS lymphoma, cerebral toxoplasmosis, tuberculoma
  2. Meningitis e.g. pneumococcal, cryptococcal, tuberculous
  3. Opthalmic lesions e.g. Cytomegalovirus (CMV) retinitis, toxoplasmosis, choroidal tuberculosis etc
441
Q

Name 3 neoplasms often associated with HIV

A
  1. Lymphoma - CD4 count <100
  2. Kaposi’s sarcoma
  3. Cervical neoplasia
442
Q

What is Kaposi’s sarcoma?

A

A low grade vascular tumour caused by HHV-8

443
Q

Where in the cell can HIV drugs target and how does this prevent HIV?

A
  1. Reverse transcriptase inhibitors - nucleoside and non-nucleoside
  2. Protease inhibitors - can’t repackage new viruses
  3. Fusion inhibitors - virus can’t get into CD4 cells
444
Q

What does HAART stand for?

A

Highly active anti-retroviral treatment

445
Q

What is HAART?

A

Antiretroviral treatment where 3 drugs are taken together - 2 nucleoside reverse transcriptase inhibitors and 1 non-nucleoside reverse transcriptase inhibitor OR 1 protease inhibitor

446
Q

What is the aim of HAART treatment?

A

To reduce viral load and increase CD4+ count

Good compliance = good prognosis

447
Q

When is HAART started?

A

When CD4 count is 200-350

448
Q

How does HIV develops drug resistance?

A
  1. Non-adherence

2. Drug-drug interactions

449
Q

What is HIV seroconversion?

A

A period of time during which HIV antibodies develop and become detectable
Generally takes place within a few weeks of initial infection

450
Q

Name 3 types of people who are likely to rapidly progress and develop AIDS?

A
  1. Elderly people
  2. Children
  3. People with a high viral load
451
Q

What is the UNAIDS goal by 2020?

A

90/90/90
90% diagnosed
90% on anti-retorviral treatment
90% viral suppression, undetectable viral load

452
Q

What are the 3 HIV transmission routes?

A
  1. Blood
  2. Sexual
  3. Vertical (mother to child)
453
Q

Name ways HIV transmission can be prevented

A
  1. Antiretroviral treatment
  2. Pre/post-exposure prophylaxis
  3. Behavioural
  4. STI control
  5. Vaccines
  6. Microbicides
  7. HIV diagnosis/partner notification
  8. Screen blood products/needle exchange
454
Q

What does U=U mean?

A

Undetectable = Untransmittable

455
Q

What behavioural modifications can be done in order to prevent HIV transmission?

A

Sex education, reduce frequency changing sexual partners, reduce high risk sexual practices and consistent condom use

456
Q

Give 5 benefits to knowing your HIV status

A
  1. Access to appropriate treatment and care
  2. Reduce transmission by sexual and vertical means
  3. Reduction in morbidity and mortality
  4. Public health
  5. Cost effective - social care, working days off, benefits claimed, costs of onward transmission
457
Q

What is targeted testing for HIV?

A

Clinician initiated diagnostic testing triggered by clinical indications

458
Q

When is HIV screened for?

A

Clinician triggered tests
High risk groups
Patient requested

459
Q

What are 4 risk factors for HIV?

A
  1. Sexual contact with high risk groups - MSM, IV drug users
  2. Multiple sexual partners
  3. Rape in high risk area
  4. Vertical transmission
460
Q

Why is it bad to probe too deeply into a patients risk factors for HIV?

A

Patients may be unaware of their risk factors or may not want to admit them - can lead to alienation and decrease uptake of testing

461
Q

How is HIV tested for?

A

Venous blood sampling
Salivary antigen screening tests
Point of care tests (pinprick of blood)
Home testing kits

462
Q

Why is venous blood sampling the best method of testing for HIV?

A

Detectable after 4 weeks of infections

High sensitivity and specificity

463
Q

What are some disadvantages to point of care tests?

A

Not as reliable

Lower sensitivity and specificity

464
Q

What are 6 advantages to point of care testing?

A
  1. Outreach into community settings/ non-specialist clinics
  2. Increase patient choice
  3. Increased access to testing and case detection
  4. Earlier diagnosis in non-healthcare seeking individuals
  5. Reduce risk of complications
  6. Reduce transmission
465
Q

If a HIV test comes back as negative what should the clinician then do?

A

Retest in high suspicion after the 8-week window

466
Q

What is the window period?

A

Time between potential exposure to HIV infection and the point when the test will give you an accurate result - during this time a person can be infected but still test HIV negative

467
Q

If a HIV test comes back positive what should happen?

A

Tell the patient and send another confirmatory blood sample to be tested

468
Q

What are the 4 main problems that surround HIV treatment?

A
  1. Mainly transmitted by sexual intercourse so people don’t like to talk about it
  2. Period of latency means someone may infect others unwittingly
  3. HIV leads to a weakened immune system so there is a increased risk of infection
  4. HIV mutates a lot and so drug treatment is difficult
469
Q

How would you define a ‘late diagnosis’ of HIV?

A

CD4+ count < 350

470
Q

Why is bad to diagnose HIV late?

A

Associated with a 10 fold increase in risk of death in the first year of diagnosis

471
Q

HIV RNA can be detected using RT-PCR. What is this useful for?

A

To quantify the amount of HIV RNA in the blood therefore can indicate disease progression and how well the individual is responding to antiretroviral therapy

472
Q

Why do doctors not test for HIV?

A

They don’t think of HIV
Underestimate the risk of HIV in their patients
Failure to recognise HIV as a modifiable prognostic indicator
Misconception they need pre-test counselling
Misunderstanding of the implications for insurance etc. Fear of offending the patient

473
Q

Name 5 groups fo people who are at high risk fo HIV infection?

A
  1. Homosexual men
  2. Heterosexual women
  3. Injecting drug users
  4. Sex workers
  5. Truck drivers
474
Q

What are the 3 stages of the HIV epidemic?

A
  1. Nascent - <5% prevalence in risk group
  2. Concentrated - >5% prevalence in one or more risk groups
  3. Generalised - >5% prevalence in the general population
475
Q

How can sexual transmission of HIV be reduced?

A

Condom use

Voluntary medical male circumcision

476
Q

Why does voluntary medical male circumcision reduce sexual transmission fo HIV?

A

Male circumcision leads to a change in muscles

HIV is less able to penetrate due to an increase in keratinisation

477
Q

How can HIV among young children be eliminated?

A

Reduce vertical transmission - Prevent breast feeding, giving lifelong antiretroviral treatments to the mother

478
Q

What are the problems with trying to ensure everyone living with HIV has access to antiretroviral treatments?

A
  1. Lack of awareness
  2. Understaffed clinics
  3. Medication needs monitoring
  4. Cost
  5. Adherence
479
Q

What is the percentage risk of MTCT of HIV for the following:

a) In a mother receiving anti-retroviral therapy and not breast feeding
b) In a mother not receiving anti-retroviral therapy and is breast feeding

A

a) <1%

b) 35%

480
Q

CD4+ cells can differentiate into T helper 1 and T helper 2 cells. What is the function of TH1 cells?

A

Produce interleukins that help coordinate the immune response and activate macrophages and CD8+

481
Q

CD4+ cells can differentiate into T helper 1 and T helper 2 cells. What is the function of TH2 cells?

A

Produce interleukins that help B cells produce immunoglobulins

482
Q

What is PCR?

A

PCR amplifies DNA rot generate millions of copies of a particular DNA sequences
Specimen is mixed with nucleotides, primers and DNA polymerase

483
Q

What laboratory method can be used to detect viral pathogens?

484
Q

What can qPCR detect?

A
  1. The presence or absence of DNA/RNA

2. Can quantify the level of virus in a tissue

485
Q

What virus causes chicken pox?

A

Varicella zoster viral infection

486
Q

What virus causes Shingles?

A

Varicella zoster viral infection

487
Q

What are the primary and secondary infections of Varicella zoster viral infection?

A 
Primary = Chickenpox (Varicella)
Secondary = Singles (Herpes Zoster)
488
Q

What is the course of the varicella zoster viral infection?

A
  1. Enters body by mucous membrane
  2. 7-21 day asymptomatic incubation period
  3. High infectivity 2 days before/after rash appears - nasopahryngeal viral replication so pass circus on when cough/sneeze
489
Q

Give the key features of the primary infection of varicella zoster viral infection

A

Common in children
Highly contagious
Usually benign

490
Q

What are the high risk groups fo people for complications with Chicken pox

A
  1. Immunocompromised
  2. Adults
  3. Infants
  4. Pregnancy
  5. Smokers
491
Q

Briefly explain the crust formation of chicken pox

A
  1. Macule (see but can’t feel)
  2. Papule (see and feel)
  3. Vesicle (blister)
  4. Pustule (WBC response)
  5. Crust (dried pustule)
492
Q

What is the rash distribution of chicken pox?

A

Concurrent different stage lesions
Centrally distributed
Likes to multiply and divide in warm areas of the body

493
Q

What is essential to know when diagnosing chicken pox?

A
  1. Age
  2. Onset of rash
  3. Contacts
  4. High risk complication factors - immunosuppressed, pregnant etc.
494
Q

How do you confirm the diagnosis of varicella zoster viral infection?

A

Pop the lesion with a sterile needle
Absorb vesicle contents onto swab
Send swab for VZH?HSV test

495
Q

What are the complications associated with chicken pox?

A 
Dehydration
GHaemorrhagic change if immunocompromised 
Ataxia 
Encephalitis 
Chickenpox pneumonia 
Infections
496
Q

What is foetal varicella syndrome?

A

Where the foetus has been infected with varicella - usually transient and asymptomatic

497
Q

What are the potential severe defects associated with foetal varicella syndrome?

A

Cicatricial skin scarring
Limb hypoplasia
Visceral and ocular lesion
Microcephaly and growth retardation

498
Q

What is the usual outcome if the foetus is infected with varicella?

A

Gets shingles within the first year of life

499
Q

Explain the pathophysiology of shingles

A

Primary infection = widespread chickenpox
VZV moves down sensory neurones
Dormant in dorsal root o =r cerebral ganglion
Reduced immune system
Localised reactivation = shingles
Affects dermatome

500
Q

What are the main features of shingles?

A

Common in the elderly
Thoracic region most commonly involved (50-70%)
Cervical, lumbar and sacral dermatomes less frequently involved
Nose tip lesion (affects ophthalmic division of trigeminal nerve)

501
Q

What are the consequences of influenza A infection?

A

Increased risk of ARDS and secondary bacterial pneumonia

502
Q

Chains of purple cocci are seen on a gram film. They show alpha haemolysis when grown on blood agar. They don’t grow near the optochin disc. These are probably

a. Streptococcus pneumoniae
b. Staphylococcus epidermidis
c. Viridans Streptococci
d. Group A streptococci (S. pyogenes)
e. Neisseria meningitidis

A

Streptococcus pneumoniae

503
Q

Which of these is a gram negative bacillus that ferments lactose?

a. Shigella sonnei
b. Listeria monocytogenes
c. Neisseria meningitidis
d. Eschericia coli
e. Streptococcus pyogenes

A

Eschericia coli

504
Q

Which is incorrect? Haemophilus influenzae is an important cause of

a. Meningitis in pre-school children
b. Otitis media
c. Pharyngitis
d. Gastroenteritis
e. Exacerbations of Chronic Obstructive Pulmonary Disease (COPD)

A

Gastroenteritis

505
Q

Which is a normally sterile site?

a. The pharynx
b. The urethra
c. Cerebrospinal fluid
d. The lung
e. Skin

506
Q

Which of these is NOT a means by which viruses cause disease?

a. Direct destruction of host cells
b. Cell proliferation and cell immortalisation
c. Inducing immune system mediated damage
d. Endotoxin production
e. Modification of host cell structure or function

A

Endotoxin production

507
Q

When diagnosing viral infections which is not true?

a. The sample must come from a sterile site
b. Electron microscopy is rarely used
c. Use a green swab not a black swab
d. PCR results take 1-2 days
e. A detectable IgM in serum may be diagnostic

A

The sample must come from a sterile site

508
Q

Which is most accurate? The HIV virus envelope contains

a. RNA + capsid + DNA polymerase
b. DNA + capsid + Reverse transcriptase
c. DNA + p24 + protease
d. RNA + capsid + reverse transcriptase

A

RNA + capsid + reverse transcriptase

509
Q

Which pair is correct?

a. Pityriasis versicolor = bacterium
b. Ringworm = helminth
c. Aspergillus fumigatus = mycobacterium
d. Falciparum malariae = fungal
e. Giardia lamblia = protozoal

A

Giardia lamblia = protozoal

510
Q

Mycobacteria. Which is not a feature?

a. Resistance to destaining by acid and alcohol
b. Cell wall contains lipoarabinomannan
c. They only divide every 20 hours
d. They cannot withstand phagolysosomal killing
e. May cause meningitis

A

They cannot withstand phagolysosomal killing

511
Q

Regarding antimicrobial resistance, which is true?

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

A

it is spread by plasmid mediate gene transfer

512
Q

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

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

A

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

513
Q

A 34 year old gay man who has had prolonged diarrhoea now presents short of breath with a dry cough and hypoxia. Which is most accurate?

a. This is bacterial pneumonia caused by pneumocysitis jirovecii.
b. It is too early for a 4th generation HIV test to be positive
c. The CD4 T cell count will be between 500 and 750
d. Even if the HIV test is negative this man has AIDS
e. With appropriate therapy he has a good prognosis

A

With appropriate therapy he has a good prognosis

514
Q

Which of these does NOT feature in the definition of Sepsis?

a. Temperature >38.3oC or <36oC
b. Heart rate >90
c. Systolic blood pressure >130
d. White Cell count >12
e. Hypoxia

A

Systolic blood pressure >130

515
Q

Infection control: which is false? The five steps of hand hygiene are to wash hands

a. Before contact with patient
b. Before bodily fluid exposure
c. Before aseptic procedures
d. After contact with patient surroundings
e. After patient contact

A

Before bodily fluid exposure

516
Q

What are the 3 main groups of helminths?

A
  1. Nematodes (roundworms)
  2. Trematodes (flatworms)
  3. Cestodes (tapeworms)
517
Q

What is the pre-patent period for a helminth infection?

A

Interval between infection and the appearance of eggs in the stool

518
Q

What type of blood cell would have a raised count in a helminth infection?

A

Eosinophils - associated wit parasitic infection and helminths are parasitic worms

519
Q

How are intestinal nematodes (roundworms) often diagnosed?

A

Stool microscopy looking for eggs

520
Q

How are intestinal nematodes spread?

A

Transmission from human to human via eggs or larvae

521
Q

What do helminths develop?

A

Have both endo and exo human development stages

Adult worms cannot usually reproduce without a period of development outside of the body

522
Q

What are the signs and symptoms of ascaris lumbricoides infection?

A

Loeffler’s syndrome - larval migration to lungs results in cough, fever and cheese
Often infection can be asymptomatic otherwise mechanical (bile duct obstruction –> malnutrition)

523
Q

Give the key features of a ascaris lumbricoide worm?

A

15-30 cm roundworm found mainly in tropic children
PPP = 60-75 days
Largest and most common

524
Q

Briefly describe the lifecycle of a ascaris lumbricoide

A
  1. Female lays eggs in small intestine – 200,000 a day
  2. Eggs excreted in faeces and ingested –> hatch in small intestine
  3. Immature larvae invade mucosa –> migrate to lungs via venous return
  4. Juveniles break into alveoli + move up trachea-bronchial tree
  5. Larvae swallowed –> return to small intestine 14 days post-infection
525
Q

What are the signs and symptoms of hookworm infection?

A

Local dermatitis at the site of entry

Iron deficiency anaemia

526
Q

What are the signs and symptoms of threadworm infection?

A

Pruritus ani

527
Q

How would you diagnose threadworm infection?

A

Apply sellotape to the perianal area and then look for eggs under a microscope

528
Q

What are the signs and symptoms of strongloides stercoralis?

A

Pruritus
Pulmonary symptoms
Gut symptoms
Larva currens (skin rashes)

529
Q

Why can the symptoms of strongloides stercoralis persist for years?

A

Associated with auto infection and an immunocompromised state

530
Q

What are the signs and symptoms of Tania saginatum infection?

A

Known as the beef tapeworm

Abdominal pain is a likely symptom

531
Q

What are the signs and symptoms of Tania solium infection?

A

Known as the pork tapeworm
Skin, muscle and the brain can be affects
Patient may suffer from fits

532
Q

What is ringworm?

A

A fungal infection that can cause an itchy, red, scaly, circular rash

533
Q

Is ringworm a helminth?

A

No, it is fungal

534
Q

Name 3 techniques used in serology to detect viral and bacterial infections

A
  1. Complement fixation test (CFT)
  2. Haemagglutination/haemagglutination inhibitor (HA/HAI)
  3. Enzymes linked immunosorbent assay (ELIZA)
  4. Radioimmunoassay (RIA)
  5. Immunofluorescence (IF)
535
Q

Name 2 tests that can be done to detect a viral pathogen

A
  1. PCR
  2. Electron microscopy
  3. Cytopathic effect (CPE) on cell culture
536
Q

Give an advantage of EM and Cell cultures for virus detection

A

‘Catch all’ techniques

537
Q

Give 2 disadvantages of EM and cell cultures for virus detection

A
  1. Depends on skill of user of microscope
  2. Time consuming (culture take 2-4 weeks)
  3. Expensive

PHASE 2A (16 decks)

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