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Phase 2A Tom > Mircobiology > Flashcards

Mircobiology Flashcards

1
Q

What is a pathogen?

A

An organism capable of causing disease

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2
Q

What is a commensal?

A

Organism which colonises a host but causes no disease

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3
Q

What is an opportunist pathogen?

A

Microbe that causes disease if host defences are compromised

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4
Q

What is virulence?

A

The degree to which a given organism is pathogenic

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5
Q

What is asymptomatic carriage?

A

When a pathogen is carried harmlessly

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6
Q

What are round bacteria called?

A

Coccus

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7
Q

What are rod bacteria called?

A

Bacillus

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8
Q

What colour do gram positive bacteria stain?

A

Purple

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9
Q

What colour do gram negative stain?

A

Red/pink

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10
Q

What type of organism would you stain with Ziehl-Neelsen?

A

Mycobacteria e.g., TB.

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11
Q

What are the differences between gram negative and positive bacteria?

A
  • Gram negatives have endotoxin (lipopolysaccharide layer) can cause endotoxic shock
  • Gram negatives have an outer membrane
  • Gram negatives have a lipoprotein layer
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12
Q

Describe the characteristic features of gram positive bacteria?

A
  1. Single membrane.
  2. Large peptidoglycan area.
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13
Q

Describe the characteristic features of gram negative bacteria?

A
  1. Double membrane.
  2. Small peptidoglycan area. (
  3. LPS (endotoxin area).
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14
Q

Between what temperatures and what pH range can bacteria grow?

A

Between -80 to +80°C. And from a pH of 4 to 9.

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15
Q

What are the 3 phases of bacterial growth?

A
  1. Lag phase.
  2. Exponential phase.
  3. Stationary phase
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16
Q

Give an example of a slow growing bacteria.

A

TB.

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17
Q

Give an example of a fast growing bacteria.

A

E.coli and S.aureus.

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18
Q

Give 2 functions of pili

A
  1. Help adhere to cell surfaces.
  2. Plasmid exchange
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19
Q

What is the primary function of flagelli?

A

Locomotion.

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20
Q

What is the primary function of the polysaccharide capsule?

A

Protection; prevents MAC or opsonisation molecules attacking.

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21
Q

What types of bacteria release endotoxin?

A

Gram negative

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22
Q

What types of bacteria release exotoxins?

A

Gram negative and positive

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23
Q

Describe endotoxins.

A

Endotoxin (LPS) is an outer membrane component released when bacteria are damaged. They are less specific and are toxic to the host. They are heat stable

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24
Q

Describe exotoxins.

A

Proteins secreted from gram positive and gram negative bacteria. They are specific and heat labile.

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25
Q

What are endotoxins made from?

A

Lipopolysaccarides

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26
Q

What are exotoxins made from?

A

Proteins

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27
Q

What are plasmids?

A

Circular pieces of DNA that often carry genes for antibiotic resistance.

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28
Q

How does genetic variation arise in bacteria?

A

Mutation
-Base substitution
-Deletion
-Insertion
Gene transfer
- Transformation e.g., via plasmid
- Transduction e.g., via phage
- Conjugation e.g., via sex pilus

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29
Q

What are the two first classifications of bacteria?

A
  • Obligate intracellular bacteria (bacteria not grown in a lab)
  • Bacteria that may be cultured on Artificial media
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30
Q

What are some types of obligate intracellular bacteria?

A
  • Rickettsia
  • Chlamydia
  • Coxiella
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31
Q

What is the first way to distinguish between Bacteria that may be cultured on Artificial media?

A

Whether they have a cell wall or not

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32
Q

How do you distinguish between cells with cell walls?

A
  • Whether they grow as single cells or as filaments
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33
Q

What are the three different types of cells growing as single cells?

A
  • Rods
  • Cocci
  • Spirochates
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34
Q

How do you differentiate between different types of Rod/cocci bacteria?

A

Gram positive and gram negative

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35
Q

What is the way to differentiate between gram negative/positive bacteria?

A

Aerobic vs anaerobic

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36
Q

Give an example of a gram-positive aerobic cocci?

A

Staphylococcus and streptococcus.

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37
Q

What are the 3 types of streptococcus bacteria?

A
  • Beta-haemolytic
  • Alpha-haemolytic
  • Non-haemolytic
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38
Q

What is anaerobic gram-positive bacteria?

A

PEPTOSTREP-
TOCOCCUS

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39
Q

What are aerobic gram-negative cocci bacteria?

A
  • Coliforms’
  • VIBRIO
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40
Q

How would you describe the arrangement of staphylococci?

A

Clusters of cocci

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41
Q

How would you describe the arrangement of streptococci?

A

Chains of cocci.

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42
Q

What bacteria would be coagulase positive?

A

Staphylococci aureus

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43
Q

What bacteria would be coagulase negative?

A

All others e.g. staphylococci epidermidis.

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44
Q

What is the normal environment of staphylococci?

A

Nose and skin

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45
Q

How is Staphylococci aureus spread?

A

Aerosol and touch
- carriers and shedders

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46
Q

What are virulence factors for Staphylococci aureus?

A
  • Pore-forming toxins e.g., haemolysin
  • Proteases e.g., exofoaltin
  • Toxic shock syndrome toxin
  • Protein A (surface protein which binds to antibodies in wrong orientation)
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47
Q

What drug would be used to treat staphylococci?

A

Flucloxacillin

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48
Q

What type of infection is S. epidermidis

A

opportunistic

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49
Q

What is the main virulence factor of s.epiermidis

A

Can form biofilms

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50
Q

What test could be done to distinguish between different streptococci?

A

Blood agar haemolysis.

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51
Q

What further test can be done for those streptococci in the β haemolysis group?

A

Serogrouping; detecting surface antigens. e.g., lancefield grouping.

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52
Q

What would you see on the agar plate in α haemolysis and give an example of a bacteria in this group.

A

α haemolysis is partial erythrocyte lysis; you see a green colour. Streptococcus pneumoniae falls in this group

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53
Q

What would you see on the agar plate in β haemolysis and give an example of a bacteria in this group?

A

β haemolysis is complete erythrocyte lysis; you see a clear area. Streptococcus pyogenes and streptococcus agalactiae fall in this group.

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54
Q

What would you see on the agar plate in γ haemolysis and give an example of a bacteria in this group.

A

γ haemolysis is when there is no haemolysis. Streptococcus bovis falls in this group.

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55
Q

What is are two examples of beta haemolytic strep infections?

A

S.agalactiae and S.pyogenes

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56
Q

What are the virulence factors of S.pyogenes?

A

Exported factors
- Streptokinase (breaks down clots)
Toxins
- Streptolysins
- Erythrogenic toxin
Surface factors
- capsule
- M protien

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57
Q

What infections do s-agalactiae usually cause?

A

Neonatal

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58
Q

Name some infections caused by S.pyogenes?

A

Respiratory
- Tonsillitis & pharyngitis
- Otitis media
Skin and Soft tissue
- Wound infections
- Impetigo
- cellulitis
- puerperal fever
Scarlet fever
- SPeA and M type
Complications
- rheumatic fever
- glomerulonephritis

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59
Q

Give examples of alpha haemolytic bacteria.

A
  • S.pneumoniae
  • Viridans group streptococci
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60
Q

Give examples of aerobic gram-positive bacilli.

A
  • Listeria monocytogenes
  • Bacillus anthracis
  • Corynebacterium diphtheriae
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61
Q

Give examples of anaerobic gram-positive bacilli

A
  • C. tetani
    Tetanus
  • C. botulinum
    Botulism
  • C. difficile
    antibiotic-associated diarrhea
    pseudomembranous colitis
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62
Q

Give examples of gram-negative bacilli.

A

Shigella, salmonella, E.coli etc.

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63
Q

What kind of bacteria is MacConkey agar used with?

A

Gram negative bacilli

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64
Q

What is MacConkey agar?

A

MacConkey agar contains bile salts, lactose and pH indicator. If an organism ferments lactose, lactic acid will be produced, and the agar will appear a red/pink colour.

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65
Q

Name 2 gram-negative bacilli that will give a positive result with MacConkey agar.

A
  1. E.Coli.
  2. Klebsiella pneumoniae
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66
Q

What antigen do the flagella contain?

A

H

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67
Q

What antigen does the LPS contain?

A

O (somatic)

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68
Q

Does e-coli have an H antigen?

A

Yes, as it is motile

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69
Q

What infections are caused by e-coli?

A

i) Wound infections (surgical)

(ii) UTIs (cystitis; 75-80% of ♀ UTIs - faecal source or sexual activity;
catheterisation - the most common type of nosocomial infection)

(iii) Gastroenteritis

(iv) Travellers’ diarrhoea

(v) Bacteraemia (sometimes leading to sepsis syndrome)

(vi) Meningitis (infants) - rare in UK

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70
Q

Does shigella have an H antigen?

A

No as it is not motile

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71
Q

What are the symptoms of shigella infection?

A

Frequent passage of stools (>30/day)

Small volume, pus and blood, prostrating cramps, pain in straining, fever.

Self-limiting (in adults)

Pathology like EIEC but with the addition of Shiga toxin

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72
Q

Does salmonella have an H antigen?

A

Yes as it is motile

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73
Q

What infections are caused by salmonella?

A
  • Gastroenteritis/enterocolitis e.g., food poisoning
  • Enteric fever - typhoid/paratyphoid fever from drinking poor water quality
  • Bacteraemia (uncommon)
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74
Q

Why are there pathogenic strains of e.coli?

A

Due to the acquisition of genes from other bacteria

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75
Q

Which type of e.coli would you associate with causing travellers diarrhoea?

A

Enterotoxigenic e.coli (ETEC).

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76
Q

What are the symptoms of enteropathogenic e.coli infection?

A

Chronic watery diarrhoea

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77
Q

What are the symptoms of enterohaemorrhagic e.coli infection?

A

Bloody diarrhoea.

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78
Q

What are the symptoms of v.cholerae?

A

Huge volumes of watery stools (no blood or pus).

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79
Q

Why is v.cholerae so dangerous?

A

You’re losing huge amounts of water which can result in hypovolemic shock and severe dehydration, this can lead to death.

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80
Q

Why is v.cholerae not killed if you have a fever?

A

It grows at 18 - 42°C.

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81
Q

Why would you need to be infected with a large amount of v.cholerae to show symptoms of the disease?

A

The optimum pH for v.cholerae growth is 8; alkaline. It is therefore very sensitive to the pH of the stomach.

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82
Q

Name the bacteria that can cause legionnaires disease?

A

Legionella.

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83
Q

Who might be susceptible to infection by legionella?

A

Immunocompromised individuals.

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84
Q

What type of bacteria are Neisseria?

A

Gram negative diplococci.

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85
Q

What are the two medically important species of neisseria?

A

N.meningitidis and N.gonorrhoeae.

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86
Q

How is N.meningitidis transmitted?

A

Aerosol transmission. High risk in colonised people e.g. university, Haj.

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87
Q

Describe the pathogenesis of N.meningitidis.

A

Crosses nasopharyngeal epithelium and enters blood stream. Can cause asymptomatic bacteraemia or septicaemia. If the bacteria crosses the BBB it can cause meningitis.

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88
Q

What are the virulence determinants of N.meningitidis?

A

STI - rectal, vaginal or oral inflammation.

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89
Q

Describe bacteroides.

A

Opportunistic, obligate anaerobes.

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90
Q

Can you grow chlamydia on agar?

A

No, chlamydia is an obligate intracellular parasite

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91
Q

How can you detect chlamydia?

A

Serum antibodies or PCR.

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92
Q

Name the spirochaete that is responsible for causing lyme disease.

A

B.burgdorferi.

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93
Q

Name the spirochaete that is responsible for causing syphilis.

A

T.pallidum.

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94
Q

What is the ziehl-neelsen stain?

A
  • Used for mycobacteria which don’t take up gram stain
  • Acid fast bacilli are blue
  • Non-acid-fast bacilli are red
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95
Q

What is the catalase test?

A
  • Add h2o2 to bacteria to see for bubbling reaction
  • Bubbles= positive test
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96
Q

What is the catalase test used to distinguish between?

A

Streptococci and Staphylococci

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97
Q

Are Streptococci catalase negative or positive?

A

Negative

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98
Q

Are Staphylococci catalase negative or positive?

A

Positive

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99
Q

Are most gram-negative bacteria catalase negative or positive?

A
  • Most are positive
  • E-coli and fungi are positive
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100
Q

What is the coagulase test?

A
  • An enzyme produced by s.aureus turns fibrinogen (soluble) into fibrin (insoluble)
  • Used to distinguish between s.aureus and other types of staphylococci
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101
Q

Is Staphylococci aureus positive or negative for the coagulative test?

A

Positive (clumping) due to formation of fibrin

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102
Q

What would you see on the agar plate in α haemolysis and give an example of a bacteria in this group.

A
  • α haemolysis is partial erythrocyte lysis; you see a green colour.
  • Streptococcus pneumoniae falls in this group
  • Viridians group streptococci
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103
Q

What is the Haemolysis test?

A
  • The ability of bacteria to break down red blood cells
    -It requires the expression of haemolysin
  • Very useful for deciding between streptococci
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104
Q

What would you see on the agar plate in β haemolysis and give an example of a bacteria in this group?

A
  • β haemolysis is complete erythrocyte lysis; you see a clear area.
  • Streptococcus pyogenes and streptococcus agalactiae fall in this group.
  • Staphylococcus aureus and listeria monocytogenes also beta-haemolytic
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105
Q

What further test can be done for those streptococci in the β haemolysis group?

A

Serogrouping; detecting surface antigens. e.g., lancefield grouping.

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106
Q

What is the optochin test?

A
  • Place an optochin-soaked disc and place on agar plate of bacteria
  • If there is growth around the disc then the bacteria are resistant and no growth around disc means bacteria are sensitive
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107
Q

What bacteria are optochin resistant?

A

Viridans streptococci (infective endocarditis) and other alpha haemolytic streptococci

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108
Q

What bacteria are optochin sensitive?

A

Streptococcus pneumoniae (causes lobar pneumonia and meningitis)

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109
Q

What is the oxidase test?

A
  • Test to see if microorganism contains a cytochrome oxidase
  • All bacteria that are oxidase positive are aerobic
  • Bacteria that are oxidase negative may be aerobic or anaerobic
110
Q

What are the colour changes for the oxidase test?

A
  • Oxidase positive: Blue
  • Oxidase negative: No colour change
111
Q

Name some oxidase positive bacteria?

A
  • P. aeruginosa
  • V. cholerae
  • Campylobacter e.g., C. jejuni
  • Helicobacter
112
Q

What is MacConkey agar?

A
  • Only grows gram negative bacilli
  • Good at determining between lactose-fermenting and not
113
Q

Why does MacConkey agar only grow gram negative bacteria?

A

Bile salts inhibit the growth of gram positive bacilli

114
Q

What will happen to the MacConkey agar if lactose fermenting bacilli are present?

A
  • Lactose fermenting produce acid
  • This will turn indicator on agar red
115
Q

Name some lactose fermenting bacilli?

A
  • E. COLI
  • KLEBSIELLA PNEUMONIAE (typical organism that causes
    biliary infection)
  • ENTEROBACTER SPP.
116
Q

Name some non-lactose fermenting bacilli?

A
  • Salmonella spp.
  • Shigella spp.
    They appear white/transparent
117
Q

What is XLD agar used for?

A

To differentiate between Shigella and Salmonella

118
Q

What colour does Shigella go on XLD?

A

White spots on dark red

119
Q

What colour does Salmonella go on XLD?

A

Black spots on bright pink

120
Q

What shape are most gram-positive bacteria?

A

Round (cocci)

121
Q

What shape are most gram-negative bacteria?

A

Rod (bacilli)

122
Q

Which Lancefield groups are associated with tonsilitis and skin infection?

A

A , C and G.

123
Q

Which Lancefield groups are associated with neonatal sepsis and meningitis?

124
Q

Which Lancefield groups are associated with UTI’s?

125
Q

Describe chocolate agar and explain why it might be used.

A

Chocolate agar is blood agar that has been heated so as to release nutrients. Chocolate agar is often used for growing fastidious bacteria.

126
Q

What is CLED agar used for?

A

It is used to differentiate micro-organisms in urine and can classify lactose fermenters and non-lactose fermenters.

127
Q

What is Sabouraud’s agar used for?

A

Used to culture fungi.

128
Q

Describe mycobacteria.

A
  • Aerobic.
  • Non-motile.
  • Non spore forming.
  • Bacilli.
129
Q

Give an example of mycobacteria.

A

Give an example of mycobacteria.

130
Q

Give an example of mycobacteria.

A

The cell wall is very thick and has a high lipid content.

131
Q

Why is it hard to use therapeutic antibodies against mycobacteria?

A

Mycobacteria grow very slowly and so treatment with antibodies is difficult. (This also makes them hard to culture).

132
Q

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

A
  1. Tuberculin skin test (mantoux).
  2. Interferon gamma release assays.
133
Q

Name 6 sterile sites in the body.

A
  1. Urinary tract.
  2. CSF.
  3. Pleural fluid.
  4. Peritoneal cavity.
  5. Blood.
  6. Lower respiratory tract.
134
Q

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

A
  1. Mouth.
  2. Skin.
  3. Vagina.
  4. Urethra.
  5. Large intestine.
135
Q

What is a virus?

A

An infectious, obligate intracellular parasite comprising genetic material surrounded by a protein coat

136
Q

What are the different shapes of viruses?

A
  • Helical
  • Icosahedral
  • Complex
137
Q

Which viruses are Non-enveloped?

A
  • Adenovirus
  • Parvovirus
138
Q

What viruses are enveloped?

A
  • Influenza
  • HIV
139
Q

Describe the process of viral replication?

A
  1. Attachment to receptor on host cell
  2. Cell entry- uncoating of virion within the cell
  3. Host cell interaction and replication- migration of genome to cell nucleus, transcription to mRNA using host material
  4. Assembly of new virion
  5. Release of new virus partciles
140
Q

Describe the process of viral replication?

A
  1. Attachment to receptor on host cell
  2. Cell entry- uncoating of virion within the cell
  3. Host cell interaction and replication- migration of genome to cell nucleus, transcription to mRNA using host material
  4. REPLICATION – may localise in nucleus, cytoplasm or both, production of progeny viral nucleic acid and proteins.
  5. Assembly of new virion
  6. Release of new virus particles
141
Q

How are new virus particles released?

A
  1. Burts out resulting in cell death e.g., rhinovirus
  2. Budding/exocytosis e.g., HIV and influenza
142
Q

How do viruses cause disease?

A
  1. Direct destruction of host cells e.g., poliovirus lysis of neurons
  2. Modification of host cell e.g., rotavirus atrophies villi and flattens epithelial cells
  3. “Over reactivity” of immune system e.g., hepatitis B
  4. Damage through cell proliferation e.g., HPV which causes cervical cancer
  5. Evasion of host defences e.g., Herpesviridae, Measels, HIV
143
Q

Name some Sporozoa

A
  • Cryptosporidiosis
  • Toxoplasmosis
144
Q

What are protozoa?

A

One celled animals”

Single cell with nucleus
(Eukarytoic)

> 30,000 species

145
Q

What is Leishmaniasis?

A
  • Leishmaniasis is a disease that causes a range of clinical pictures, as there are many species that affect humans.
146
Q

What are the 5 types of protoza?

A
  1. Flagellates
  2. Microsporidia
  3. Sporozoa
  4. Amoebae
  5. Cilliates
147
Q

What is African Trypanosomiasis? (flagellates)

A
  • Human African Trypanosomiasis (or sleeping sickness) is a disease that unsurprisingly is endemic in Africa.
  • specices Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense. T.B.gambiense is endemic in West Africa (as is Gambia), and T.B.rhodesiense South East
148
Q

How is African Trypanosomiasis transmitted?

A
  • The trypanosomes are transmitted via the bite of an infected Tsetse fly and can cause a chancre (large red sore) at the site of the bite.
149
Q

How is American Trypanosomiasis transmitted?

A
  • Spread through contact with faeces of triatomine “kissing” bug
    Also through blood, vertically and eating contaminated food
150
Q

What are the symptoms of American trypanosomiasis?

A
  • Two phases, both can be asymptomatic or life-threatening
  • Acutely patients can get flu-like symptoms, lymphadenopathy and a Romaña sign (swollen eyelid where triatomine faeces rubbed into the eye!
151
Q

How is leishmaniasis transmitted? (flagellates)

A
  • It is acquired through the bite of an infected sandfly.
152
Q

What is amoebiasis?

A
  • Microsporidia
  • Poor sanitary conditions/tropical countries
    MSM (men who have sex with men) at risk
  • Entaemoeba histolytica can live in the colon asymptomatically, but also can invade the colon and consume red blood cells
153
Q

How do viruses evade the immune system?

A

Antigenic Drift - spontaneous mutations, occur gradually giving minor changes in HA (haemagglutinin) and NA (neuraminidase). Epidemics.

Antigenic Shift - sudden emergence of new subtype different to that of preceding virus. Pandemics

154
Q

What are the 5 types of malaria?

A
  1. Plasmodium falciparum (most severe disease)
  2. Plasmodium ovale
  3. Plasmodium vivax
  4. Plasmodium malariae
  5. Plasmodium knowlesi
155
Q

How is malaria transmitted?

A

By bite of the female anopheles mosquito

156
Q

When should you think of malaria as a cause of disease?

A

fever and recent travel

157
Q

How would you diagnose malaria?

A

A blood flim by using light microscopy

158
Q

What is the main symptom of malaria?

159
Q

What are some other symptoms of malaria?

A

Chills
Headache
Myalgia
Fatigue
Diarrhoea
Vomiting
Abdo pain

160
Q

What are some signs of malaria?

A

Anaemia
Jaundice
Hepatosplenomegaly
‘Black Water Fever’

161
Q

Describe the pathogenesis of p.falciparum?

A

Unique cerebral malaria, fatal infection. Parasites mature in RBC’s, RBC’s collect in small vessels and cause blockage of cerebro-microvasculature = hypoxia

162
Q

What genetic conditions can give immunity to malaria?

A

Someone with sickle cell anaemia or thalassaemias.

163
Q

Can immunity to malaria be acquired?

A

Recurrent infection can lead to someone being ‘semi-immune’. Antibodies could be transferred by maternal transmission.

164
Q

What is the treatment for malaria?

A

Chloroquine.

165
Q

What is the treatment of complicated malaria

166
Q

What are the symptoms of complicated malaria?

A
  • Cerebral
  • ARDS/Pulmonary oedema
  • Renal failure
  • Sepsis
  • Bleeding/Anaemia
167
Q

What are the 4 stages of pathogenesis?

A
  1. exposure (contact),
  2. adhesion (colonization),
  3. invasion,
  4. infection
168
Q

What is an antibiotic?

A
  • A molecule that works by binding to a target site on a bacteria
  • Points of biochemical reaction crucial to the survival of the bacterium
  • The crucial binding site will vary with different antibiotic classes
169
Q

What are the two modes of action of an antibiotic?

A
  • Slow the growth of bacteria (bacteriostatic) kills 90% in 18-24 hours: antibiotics that inhibit protein synthesis
  • Destroy bacteria (bactericidal) kills 99.9% in 18-24hrs: antibiotics that inhibit cell wall synthesis
170
Q

How do polymyxins and polyenes work?

A
  • Binds to cell membrane and alters its structure
  • Makes the cell membrane more permeable
  • Water will move into the cell via osmosis

Note polyenes can be used for fungal infections

171
Q

How do B-lactam and glycopeptides antibiotics work?

A
  • They are bactericidal
  • They inhibit cell wall synthesis by binding to proteins which inhibit synthesis of peptidoglycan
  • Active only against rapidly dividing organisms
  • Won’t affect human cells
172
Q

Name some B-lactam antibiotics

A
  • Penicillin
  • Cephalosporin
  • Carbapenems
  • Monobactams
173
Q

Name a glycopeptide

A

Bacitracin
Vancomycin

174
Q

What type of bacteria are B-lactams more effective at treating?

A
  • Gram positive as they only have one cell layer. Whereas gram-negative bacteria have an additional LPS layer which reduces the penetration
  • Penicillin poorly penetrate mammalian cells so ineffective at treating intracellular pathogens
175
Q

How do quinolines and nalidixic acid antibiotics work?

A
  • They inhibit RNA/DNA synthesis
  • They are bacteriostatic
176
Q

Name a quinoline

A

Rifamiacin

177
Q

Name a Quinoline/nalidixic acid

A

Rifamycin (inhibits RNA polymerase)

178
Q

How do Erythromycin and Chloramphenicol work?

A
  • They inhibit protein synthesis
  • They do this by targeting the 50s subunit of ribosome
179
Q

How do Tetracyclines and aminoglycosides work

A
  • They inhibit protein synthesis
  • They do this by targeting the 30s subunit of ribosome
  • Protein can still be alive but they can’t do anything (bacteriostatic)
180
Q

How do sulphonamides and trimethoprim work?

A
  • Inhibit folic acid metabolism
  • Bacteria turn PABA to folate
  • Inhibit PABA turning into folate
  • Folate is needed for synthesis Adenine and thymine in DNA
  • Humans don’t synthesise folic acid so safe to use
181
Q

How much antibiotic do you need?

A
  • The drug not only needs to attach to its binding site but must also occupy an adequate number of sites (concentration)
  • To work effectively the antibiotic should remain at the binding site for a sufficient period of time in order for the metabolic process to be inhibited (time)
182
Q

What are the two major determinants of antibacterial effects?

A
  1. Concentration
  2. Time (that the antibiotic remains on the binding sites)
183
Q

What is MIC?

A

Minimum inhibitory concentration (the minimum amount of an antibiotic needed to have the desired effect

184
Q

What is time dependant killing?

A

Key parameter is the time that the serum concentration remains above MIC during the dosing interval

185
Q

What antibiotics rely on time dependant killing?

A
  • beta-lactams (penicillins, cephalosporins, carbapenems, monobactams),
  • clindamycin,
  • macrolides
  • oxazolidinones
186
Q

What is concentration dependant killing?

A
  • Key parameter is how high the concentration is above MIC
187
Q

What antibiotics rely on concentration dependant killing?

A
  • aminoglycosides
  • quinolones
188
Q

What are things to consider when deciding on what antibiotics should be given and how they should be administered?

A

Pharmakinetics
- Absorbtion (how should I give it orally/IV)
- Distribution: which antibiotics will penetrate the site, what is the PH of the site, is the antibiotic lipid soluble
- Metabolism/elimination: what is the half-life, what dosage interval and duration

189
Q

What mechanisms can make bacteria resistant to antibiotics

A
  • Change the antibiotic target
  • Destroy antibiotic
  • Prevent antibiotic access
  • Remove antibiotics from bacteria
190
Q

Define what changing the antibiotic target means and name some bacteria that have done this

A

Bacteria change the molecular configuration of the antibiotic binding site or masks it
- Flucloxacillin (or methicillin) is no longer able to bind PBP of Staphylococci – MRSA*
- Wall components change in enterococci and reduce vancomycin binding – VRE
- Rifampicin activity is reduced by changes to RNA polymerase in MTB – MDR-TB

191
Q

Define what destroying antibiotic means and name some bacteria that have done this

A
  • The antibiotic is destroyed or inactivated e.g.
  • Beta-lactam ring of Penicillins and cephalosporins hydrolysed by bacterial enzyme ‘Beta lactamase’ now unable to bind PBP
  • Staphylococci produce ‘penicillinase’ so penicillin but not flucloxacillin inactivated
  • Gram-negative bacteria phosphorylate and acetylate aminoglycosides (gentamicin)
192
Q

Define what preventing antibiotic access means and name some bacteria that have done this

A
  • modify the bacterial membrane porin channel size, numbers and selectivity e.g.
  • Pseudomonas aeruginosa against imipenem,
  • Gram-negative bacteria against aminoglycosides
193
Q

Define what removing antibiotics from bacteria means and name some bacteria that have done this

A
  • Proteins in bacterial membranes act as export or efflux pumps - so the level of antibiotics is reduced
  • S. aureus or S. pneumoniae resistance to fluoroquinolones
  • Enterobacteriacae resistance to tetracyclines
194
Q

What is intrinsic resistance?

A
  • Bacteria that have a natural resistance to an antibiotic
  • All subpopulations will be equally resistance
195
Q

Give some examples of bacteria that have intrinsic resistance.

A
  • Aerobic bacteria are unable to reduce metronidazole to its active form
  • Vancomycin cannot penetrate the outer membrane of gram-negative bacteria
196
Q

What has acquired resistance?

A
  • A bacterium which was previously susceptible obtains the ability to resist the activity of a particular antibiotic
  • Only certain strains or subpopulations of a species will be resistant.
197
Q

What are the two ways that bacteria develop resistance?

A
  • Spontaneous gene mutation
  • Horizontal gene transfer
198
Q

Name some resistant gram-positive bacteria.

A

MRSA
Methicillin-resistant Staphylococcus aureus
-Bacteriophage mediated acquisition of Staphylococcal cassette chromosome mec (SCCmec)
- confers resistance to all β-lactam antibiotics in addition to methicillin (= flucloxacillin)
VRE
vancomycin-resistant enterococci
- Plasmid mediated acquisition of gene encoding altered amino acid on peptide chain preventing vancomycin binding
Promoted by cephalosporin use

199
Q

What bacteria do B-lactam antibiotics work most effectively against

A

Gram-positive bacteria as they have a thick cell wall

200
Q

When are cephalosporins good to use?

A
  • Good for people with penicillin allergy
  • Work against some resistant bacteria
  • Get into different parts of the body e.g., meningitis
201
Q

What antibiotic would be used for S.aureus and A, C, G strep?

A

Flucloxacillin
A, C, G strep you can also use PO penicillin or IV Benzylpenicillin

202
Q

What antibiotic would be used for S. pneumoniae

A

PO amoxicillin
IV benzylpenicillin

203
Q

When would you use a glycopeptide?

A
  • Vancomycin and teicoplanin only used with gram-positive bacteria
  • Used with B-lactam bacteria
  • Used when patient has penicillin allergy
204
Q

When would you use clarithromycin and erythromycin (macrolides which inhibit protein synthesis)

A
  • Gram positives S.aureus and beta haemolytic strep and atypical pneumonia
  • Use with penicillin allergy
  • Use with severe pneumonia
205
Q

When would you use lincosamides- protein synthesis

A
  • Clindamycin
  • Use in cellulitis
  • Use in necrotising fasciitis
    Turns off nasty toxins made by gram-positive bacteria
206
Q

When would you use aminoglycosides (protein synthesis)?

A
  • Gentamicin IV only
  • Use against gram negatives and staphs
  • Use for UTIs
  • Use for infective endocarditis
207
Q

When would you use quinolones?

A
  • Ciprofloxacin
  • Use for gram negatives
  • Use for UTIs
  • Use for intra-abdominal infections
208
Q

When would co-amoxiclav be used?

A
  • Use for aspiration pneumonia, severe CAP and more resistant UTIs
209
Q

When would meropenem be used?

A
  • They are broad and active against resistant strains
  • Use for sickest patients, resistant gram negatives e.g. MRSA and for immunocompromised
210
Q

What are retroviruses?

A
  • Retroviruses are enveloped viruses.
  • Viral genetic material is RNA which is copied into DNA by reverse transcription and incorporated into the host cell to allow gene transcription.
211
Q

What is lentivirus?

A

Lentivirus represents a genus of slow viruses with long incubation period

212
Q

Where did HIV come from?

A
  • HIV-1 arose from transmission of SIV cpz from chimpanzees to humans sometime pre-1950.
  • HIV 2 (SIV sm) from the sooty mangabey
213
Q

What are the 3 types of HIV?

A

M (main) O (outlying) N (new)

214
Q

How is the M (main) group of HIVS separated

A

Into clades A-D, F-H, J-K.

215
Q

What clade of HIV is most common in Europe and USA?

216
Q

What clade of HIV is most common in West and Central Africa?

217
Q

What clade of HIV is most common in West and Southern Africa?

218
Q

What cells are affected in HIV?

A
  • HIV results in the death of CD4+ T lymphocytes
219
Q

What are the two main ways CD4 cells are affected in HIV?

A
  • Replicating within CD4 T cells leads to their death. However, only a tiny minority <1% of CD4 T cells are ever infected.
  • Uncontrolled activation of CD4 T cells. Activated CD4 T cells are by design, destined to undergo activation induced cell death.
220
Q

What are some other ways cells are affected in HIV?

A

Other processes contribute including bystander cell death (e.g., infected macrophage causes death of infected CD4 T cells), Thymus atrophy (preventing thymic maturation of T cells), loss of bone marrow progenitors and fibrosis of lymph node

221
Q

How does HIV lead to AIDS?

A

Given their central role in coordinating adaptive immune responses, it follows that their depletion by HIV infection leads to an Acquired Immune deficiency.

222
Q

What are the 9 stages of HIV replication?

A
  1. Attachment
  2. Entry
  3. Uncoating
  4. Reverse transcription (error prone so genomic variability)
  5. Genome integration
  6. Transcription of viral RNA
  7. Splicing of mRNA and translation into proteins
  8. Assembly of new virions
  9. Budding
223
Q

How does HIV attach and enter a cell?

A
  • GP120 on HIV virus binds to CD4
  • This induces a conformational change in GP120
  • This enables co-receptor binding
  • This results in membrane fusion between virus and CD4 cells
  • Once it’s attached uses chemokine receptors CCR5 and CXCR4
224
Q

What are 4 main problems that surround HIV treatment?

A
  1. Mainly transmitted by sexual intercourse and so people don’t like to talk about it - taboo.
  2. Period of latency means someone may infect others unwittingly.
  3. HIV leads to a weakened immune system and so there is increased risk of infection.
  4. HIV mutates a lot and so drug treatment is difficult.
225
Q

What enzyme copies HIV RNA into DNA?

A

Reverse transcriptase.

226
Q

Why are mutations common in HIV?

A

HIV is a retrovirus and replicates via reverse transcription. This process is prone to errors and mutations.

227
Q

What part of HIV enters the host cell following attachment?

A

The viral caspid, enzymes and nucleic acids.

228
Q

Briefly describe the mechanism of HIV replication.

A
  1. GP160 binds to CD4 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 DNA by intergrase.
  5. Viral DNA is transcribed into viral proteins.
  6. Splicing.
  7. New HIV cells ‘bud’ from CD4.
229
Q

Name 4 enzymes involved in HIV replication.

A
  1. Reverse transcriptase.
  2. Integrase.
  3. RNA polymerase.
  4. Proteases
230
Q

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

A

Integrase.

231
Q

Why might macrophages also be infected by HIV?

A

Macrophages also have CD4 and CCR5 receptors.

232
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

233
Q

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

A
  1. CD4 cells are excessively and inappropriately activated.
  2. There is impaired IL-2 production.
  3. There is a decrease in the number and function of CD4 cells.
  4. B cells produce fewer specific Ab’s.
  5. There are fewer NK cells, neutrophils and macrophages.
234
Q

If a HIV test comes back as negative in a high risk individual why should a second HIV test be done?

A

A second test should be done after the window period: the window period is the time between exposure to HIV infection and the point when the test will give an accurate result. During this time a person can be infected with HIV and be very infectious but still test HIV negative.

235
Q

HIV: what is the ‘window period’?

A

The time between potential exposure to HIV infection and the point when the test will give an accurate result. During this time a person can be infected with HIV and be very infectious but still test HIV negative.

236
Q

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

A

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

237
Q

Name 5 groups of people who are at high risk of HIV infection.

A
  1. Homosexual men.
  2. Heterosexual women.
  3. Sex workers.
  4. IV drug users.
  5. Truck drivers.
238
Q

What are the 3 stages of the HIV epidemic?

A
  1. Nascent; <5% prevalence in risk groups.
  2. Concentrated; >5% prevalence in one or more risk groups.
  3. Generalised; >5% prevalence in the general population.
239
Q

How can the impact of HIV be reduced?

A
  1. Behaviour change; education, condom use, needle exchange.
  2. Know your status; testing.
  3. Specific interventions; PMTCT, PEP, VMCC, PrEP etc.
240
Q

How can sexual transmission of HIV be reduced?

A

Condom use!
Voluntary medical male circumcision.

241
Q

How can transmission of HIV among IV drug users be reduced?

A

Harm reduction measures e.g. needle exchange.

242
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.
243
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.
244
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.
245
Q

What happens in the acute primary infection phase of HIV?

A

There is a transient fall in CD4+ count followed by a gradual rise. There is also an acute rise in viral load

246
Q

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

A

Abrupt onset of non-specific symptoms e.g. fever, rash. Weight loss, lethargy and depression can also occur.

247
Q

What happens in the asymptomatic phase of HIV?

A

There is a progressive loss of CD4+ cells. This is the latent phase and can last for years.

248
Q

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

A

This phase is the latent phase and so you will rarely see symptoms. However, you might sometimes see enlarged lymph nodes.

249
Q

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

250
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.
251
Q

Name 2 markers that are used for monitoring HIV.

A
  1. CD4+ count.
  2. HIV RNA copies (viral load).
    - These markers are important in determining prognosis.
252
Q

Name 3 respiratory diseases associated with HIV.

A
  1. Bacterial (pneumococcal) pneumonia.
  2. TB.
  3. Pneumocystis pneumonia (PCP).
253
Q

What are the characteristic signs of pneumocystis pneumonia (PCP)?

A

Decreased CD4+ count.
Decreased O2 sats on exertion.
Decreased exercise tolerance.

254
Q

Name 3 CNS diseases associated with HIV.

A
  1. Mass lesions e.g. primary CNS lymphoma, cerebral toxoplasmosis.
  2. Meningitis e.g. pneumococcal, cryptococcal.
  3. Opthalmic lesions e.g. CMV, toxoplasmosis, choroidal tuberculosis etc.
255
Q

What does HAART stand for?

A

Highly active anti-retroviral treatment.

256
Q

What is HAART? What does it aim to do?

A

Anti-retroviral treatment where 3 drugs are taken together.
The aim is to reduce viral load and increase CD4+ count. Good compliance = good prognosis.

257
Q

Where in the cell can HIV drugs target?

A
  1. Reverse transcriptase inhibitors.
  2. Protease inhibitors.
  3. Fusion inhibitors.
258
Q

What is the UNAIDS goal by 2020?

A

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

259
Q

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

A

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

260
Q

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

A

CD4+ count < 350.

261
Q

Why is it bad to diagnose HIV late?

A

A late diagnosis is associated with a 10 fold increase in risk of death in the first year after diagnosis.

262
Q

Name 5 AIDS defining conditions.

A
  1. Oesophageal candidiasis.
  2. TB.
  3. PCP (pneumocystis jirovecii pneumonia).
  4. Recurrent bacterial pneumonia.
  5. Kaposi’s carcinoma.
  6. Hodgkins and Non-Hodgkin’s lymphoma.
  7. HIV dementia.
263
Q

What are routes of HIV transmission?

A
  • Unprotected sexual contact
  • IV drug use
  • Transfusion of untested blood
  • Mother to child transmission (breastmilk and in utero)
  • Contaminated surgical equipment
264
Q

Why does the immune response fail to get rid of HIV?

A
  • Neutralising antibodies take months to be made and are behind the mutations of HIV
  • CD4+ cells are targeted first so it’s harder for immune system to produce antibodies
  • CD8+ cells are effective at first but stop working due to immune exhaustion
265
Q

why does the body take so long to produce an antibody response?

A
  • HIV only contains a few cell membrane spikes to target
  • The spikes are glycosylated which makes it difficult for antibodies to bind
  • Key parts of viral envelope are hidden until binding
  • The virus can evolve quickly
266
Q

Why can excessive immune response be bad for the progression of HIV?

A
  • It can favour viral replication
267
Q

What are two markers used to monitor HIV infection?

A
  1. CD4 count
  2. HIV viral load
268
Q

If a patient has a fever, rash and non-specific symptoms what should you ask?

A
  • Ask about their sexual history
  • Think of HIV seroconversion
269
Q

When should you consider performing a HIV test on a patient?

A

When faced with a common problem in:

  • In an unexpected patient
  • That is recuring
  • That has no clear underlying cause
270
Q

What is the most common type of opportunist infection?

271
Q

What is the most common treatment for Pneumocystis pneumonia (pcp)?

A

Co-trimoxazole

Phase 2A Tom (15 decks)

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