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Phase 2a Sam > MICROBIOLOGY > Flashcards

MICROBIOLOGY 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 are virulence factors?

A

factors are microbial factors that cause/modify disease

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6
Q

Define invasiveness

A

the capacity to penetrate mucosal surfaces to reach normally sterile sites

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7
Q

What is asymptomatic carriage?

A

When a pathogen is carried harmlessly

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8
Q

What are round bacteria called?

A

Coccus

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9
Q

What are rod bacteria called?

A

Bacillus

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10
Q

What colour do gram positive bacteria stain?

A

Purple

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11
Q

What colour do gram negative stain?

A

Red/pink

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12
Q

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

A

Mycobacteria e.g., TB.

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13
Q

How would you carry out a gram stain?

A

ComeInAndStain

Apply primary stain - crystal violet (purple) - to heat fixed bacteria
Add iodine which binds to crystal violet and helps fix it to the cell wall
Decolourise with ethanol or acetone
Counterstain with safranin (pink)

  1. CRYSTAL VIOLET
  2. IODINE
  3. ACETONE/ETHANOL
  4. SAFRANIN (COUNTERSTAIN)
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14
Q

What are the differences between gram negative and positive bacteria?

A

Gram positive

  • Thick peptidoglycan layer
  • Single membrane - no outer lipid layer
  • No endotoxin - as no lipopolysaccharide

Gram negative

  • Inner and outer lipid membrane
  • Do have endotoxin, due to large lipopolysaccharide
  • thin peptidoglycan area
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15
Q

Describe the characteristic features of gram positive bacteria?

A
  1. Single membrane.
  2. Large peptidoglycan area.
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16
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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17
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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18
Q

What are the 3 phases of bacterial growth?

A
  1. Lag phase.
  2. Exponential phase.
  3. Stationary phase
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19
Q

Give an example of a slow growing bacteria.

A

TB.

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20
Q

Give an example of a fast growing bacteria.

A

E.coli (Gram positive rod, anaerobic)

S.aureus. (gram positive Clusters Catalase +ve and coagulase +ve)

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21
Q

Give 2 functions of pili

A
  1. Help adhere to cell surfaces.
  2. Plasmid exchange
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22
Q

What is the primary function of flagelli?

A

Locomotion.

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23
Q

What is the primary function of the polysaccharide capsule?

A

Protection; prevents MAC or opsonisation molecules attacking.

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24
Q

What types of bacteria release endotoxin?

A

Gram negative

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25
Q

What types of bacteria release exotoxins?

A

Gram negative and positive

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26
Q

Describe endotoxins.

A

Endotoxin: component of the outer membrane of bacteria e.g. LPS in Gram negative bacteria

Non Specfific, Heat stable

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27
Q

Describe exotoxins.

What bacteria have them

A

Proteins secreted from gram positive and gram negative bacteria.

They are specific, but heat labile.

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28
Q

What are endotoxins made from?

A

Lipopolysaccarides

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29
Q

What are plasmids?

A

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

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30
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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31
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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32
Q

What are obligate intracellular bacteria? Give examples

A

Bacteria that can only grow inside a host cell i.e. we cannot grow them on agar. e.g.

  • Rickettsia
  • Chlamydia
  • Coxiella

RICKETTSIA

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33
Q

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

A

Gram positive and gram negative

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34
Q

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

A

Aerobic vs anaerobic

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35
Q

Give an example of a gram-positive aerobic cocci?

A

Staphylococcus and streptococcus.

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36
Q

What are the 3 types of streptococcus bacteria?

Map their classifications

A
  • Beta-haemolytic
  • Alpha-haemolytic
  • Non-haemolytic

Streptococcus - Gram neg, Aerobic, Catalase negative

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37
Q

What is anaerobic gram-positive bacteria?

A

PEPTOSTREPTOCOCCUS

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38
Q

What are aerobic gram-negative bacilli bacteria?

A

Either lactose fermenting
- E Coli
- Klebsiella

Or non fermenting
- Salmonella
-Shigella
- Pseudomonas

or other
Vibrio
Legionella

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39
Q

How would you describe the arrangement of staphylococci?

A

Clusters of cocci

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40
Q

How would you describe the arrangement of streptococci?

A

Chains of cocci.

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41
Q

What bacteria would be coagulase positive?

A

Staphylococci aureus differentiating S.Aures from other staphs is key, as S aureus is much more virulent, has coagulase/DNAase

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42
Q

What bacteria would be coagulase negative?

A

All others e.g. staphylococci epidermidis.

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43
Q

What is the normal environment of staphylococci?

A

Nose and skin

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44
Q

How is Staphylococci aureus spread?

A

Aerosol and touch
- carriers and shedders

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45
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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46
Q

What drug would be used to treat staphylococci?

A

Flucloxacillin

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47
Q

What type of infection is S. epidermidis

A

opportunistic

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48
Q

What test could be done to distinguish between different streptococci? How does it work?

A

Blood agar haemolysis.

The haemolysis test used hydrogen peroxide to test reaction with haemoglobin

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49
Q

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

Give an example of this

A

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

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50
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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51
Q

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

Give an example of this

A

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

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52
Q

What is are two examples of beta haemolytic strep infections?

A

S.agalactiae and S.pyogenes

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53
Q

Give examples of alpha haemolytic bacteria.

A
  • S.pneumoniae
  • Viridans group streptococci
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54
Q

MISC - Give examples of aerobic gram-positive bacilli. Rods

A
  • Listeria monocytogenes (can cause menigitis)
  • Bacillus anthracis
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55
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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56
Q

Give examples of gram-negative bacilli: 2 lactose fermenting and 2 non lactose fermenting.

A

Are either Lactose Fermenting, eg
- Escherichia (E
Coli)
- Klebsiella

Or non-Lactose fermenting
	- Salmonella 
	- Shigella  Pseudomonas (oxidase +Ve)
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57
Q

What kind of bacteria is MacConkey agar used with?

A

Gram negative bacilli

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58
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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59
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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60
Q

Does e-coli have an H antigen?

A

Yes, as it is motile

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61
Q

Key Gram Negative Bacteria:
For E coli, give
a) Lactose fermenting or not
b) Associated infections
c) Commensal Locations
d) Sensible Antbx

A

Lactose fermenting

UTIs, traveller’s diarrhoea, cholecystitis, cholangitis
GI tract

Co-amoxiclav

Causes majoirty of UTIs

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62
Q

Does shigella have an H antigen?

A

No as it is not motile

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63
Q

Key Gram Negative Bacteria:
For Shigella , give
a) Lactose fermenting or not
b) Associated infections
c) Commensal Locations
d) Sensible Antbx
e)What are the symptoms of shigella infection?

A

It is non lactose fermenting, and oxidase negative
Shigellosis (diarrhoea, fever), frequent pooing

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

No commensal location, it comes from water
Treat with Quinolones, Azithromycin

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64
Q

Does salmonella have an H antigen?

A

Yes as it is motile

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65
Q

Key Gram Negative Bacteria:
For Salmonella , give
a) Lactose fermenting or not
b) Associated infections
c) Commensal Locations
d) Sensible Antbx
e) Symptoms

What infections are caused by salmonella?
It is gram negative and non lactose fermenting and so appears white on Macconkey agar

A

Non lactose fermenting, oxidase negative.
Salmonellosis (diarrhoea)
Intestines (from raw meats, poultry, eggs
Amoxicillin, Quinolones,

  • Gastroenteritis/enterocolitis e.g., food poisoning
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66
Q

What is nisseria? What 2 main disease does it cause, what anbx would you treat it with?

A

Gram negative Cocci

It mainly causes gonorrhoea and meningitis

Some species commensal, some pathogenic only
Anbx treatment Cephalosporins, Ceftriaxone

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67
Q

Why are there pathogenic strains of e.coli?

A

Due to the acquisition of genes from other bacteria

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68
Q

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

A

Enterotoxigenic e.coli (ETEC).

Most common cause of travellers diarrhoea

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69
Q

What are the symptoms of enteropathogenic e.coli infection?

A

Chronic watery diarrhoea

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70
Q

What are the symptoms of enterohaemorrhagic e.coli infection?

A

Bloody diarrhoea.

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71
Q

What are the symptoms of v.cholerae?

A

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

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72
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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73
Q

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

A

It grows at 18 - 42°C.

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74
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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75
Q

What is the pathogenesis of cholera?

A

Cholera toxin - causes Gs subunit to be locked on
uncontrolled cAMP production
increase PKA
Increased activity of CFTR channel
Loss of Cl- and Na+
Water follows and massive H2O loss

aka releases A toxin that deregulates ion transport in epithelial cells

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76
Q

Name the bacteria that can cause legionnaires disease?

A

Legionella.

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77
Q

Who might be susceptible to infection by legionella?

A

Immunocompromised individuals.

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78
Q

What type of bacteria are Neisseria?

A

Gram negative diplococci.

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79
Q

What are the two medically important species of neisseria?

A

N.meningitidis and N.gonorrhoeae.

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80
Q

How is N.meningitidis transmitted?

A

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

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81
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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82
Q

How can you detect chlamydia?

A

Serum antibodies or PCR.

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83
Q

Name the spirochaete that is responsible for causing lyme disease.

A

B.burgdorferi.

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84
Q

Name the spirochaete that is responsible for causing syphilis.

A

T.pallidum.

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85
Q

What is the ziehl-neelsen stain?

What gives what colours?

A
  • Used for mycobacteria which don’t take up gram stain
  • Acid fast bacilli are red
  • Non-acid-fast bacilli are blue
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86
Q

What is the catalase test?

A
  • Add h2o2 to bacteria to see for bubbling reaction
  • Bubbles= positive test
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87
Q

What is the catalase test used to distinguish between?

A

Streptococci and Staphylococci

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88
Q

Are Streptococci catalase negative or positive?

A

Negative

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89
Q

Are Staphylococci catalase negative or positive?

A

Positive

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90
Q

Are most gram-negative bacteria catalase negative or positive?

A
  • Most are positive
  • E-coli and fungi are positive
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91
Q

What is the coagulase test?
What does the coagulase enzyme do?

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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92
Q

Is Staphylococci aureus positive or negative for the coagulase test?

A

Positive (clumping) due to formation of fibrin, making solution cloudy

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93
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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94
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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95
Q

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

What bacteria would you see here

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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96
Q

What is the lancefield test

A
  • Specific antibodies (A B, C) BOUND to set of latex beads
  • Bacteria added and mixed

If bacteria have the antigen that corresponds to the antibody, the latex beads clump together === white dots

If they do not, then the suspension will remain milky white

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97
Q

What is the optochin test? For what bacteria would you use it for

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

For gram postive Streptococcus, that are alpha haemolytic eg Streptococci Pneumoniae Optochin Sensitive or Viridans Strep - optochin Resistant

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98
Q

What bacteria are optochin resistant?

A

Viridans streptococci (infective endocarditis) and other alpha haemolytic streptococci

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99
Q

What bacteria are optochin sensitive?

A

Streptococcus pneumoniae (causes lobar pneumonia and meningitis)

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100
Q

What is the oxidase test? For what bacteria would you use it for

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

Gram negative Bacilli, that are non lactose fermenting (MC agar =white)

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101
Q

What are the colour changes for the oxidase test?

A
  • Oxidase positive: Blue
  • Oxidase negative: No colour change
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102
Q

Name some oxidase positive bacteria?

A
  • Pseudonomas
  • V. cholerae
  • Campylobacter e.g., C. jejuni
  • Helicobacter
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103
Q

Why does MacConkey agar only grow gram negative bacteria?

A

Bile salts inhibit the growth of gram positive bacilli

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104
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
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105
Q

Name some lactose fermenting bacilli?

A
  • E. COLI
  • KLEBSIELLA PNEUMONIAE (typical organism that causes
    biliary infection)
  • ENTEROBACTER SPP.
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106
Q

Name some non-lactose fermenting bacilli?

A
  • Salmonella spp.
  • Shigella spp.

Psuedomonas

They appear white/transparent

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107
Q

What is XLD agar used for?

A

To differentiate between Shigella and Salmonella

Gram -ve bacilli, Non lactose fermenting, oxidase -ve test

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108
Q

What colour does Shigella go on XLD?

A

White spots on dark red

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109
Q

What colour does Salmonella go on XLD?

A

Black spots on bright pink

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110
Q

What shape are most gram-positive bacteria?

A

Round (cocci)

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111
Q

What shape are most gram-negative bacteria?

A

Rod (bacilli)

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112
Q

Which Lancefield groups are associated with tonsilitis and skin infection?

A

A , C and G.

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113
Q

Which Lancefield groups are associated with neonatal sepsis and meningitis?

A

B.

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114
Q

Which Lancefield groups are associated with UTI’s?

A

D. (Enterococci)

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115
Q

Describe CLED agar and explain why it might be used.

What bacteria is it good for diagnosing?

A

Cysteine Lactose electrolyte deficient

Used to differentiate microorganisms in urine

Also allows the classification of lactose fermenting (yellow) and non-lactose fermenting (blue) of gram-negative bacilli

Good for culturing E.coli - LACTOSE FERMENTING yellow and Salmonella and shigella as blue

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116
Q

What agar is used to culutre TB?

A

Lowenstein-Jensen agar

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117
Q

What type of agar is often used to culture Neisseria bacteria?

A

Gonoccoccus agar

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118
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.

(A fastidious organism is any organism that has complex or particular nutritional requirements. In other words, a fastidious organism will only grow when specific nutrients are included in its medium)

eg H.Influenzae

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119
Q

What bacteria would be assciated with theses infections, and have the commensal location of nasal passages and skin?

Impetigo, boils, cellulitis, endocarditis, toxic shock syndrome
Nasal passages + skin

A

Staphyl. Aureus.

Clusters
Coagulase +ve

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120
Q

Key Gram positive bacteria: Outline bacterium Group A Strep (Strep pyogenes) (beta haemoyltic)

a) Associated infections
b) Commensal Location
c) Sensible Antbx

A

Cellulitis, tonsillitis, impetigo, scarlet fever, pharyngitis

Resp tract

Amoxicillin (any penicillins)

Throat + skin infections

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121
Q

Key Gram postive bacteria: What antibiotic would you give to treat MRSA?

A

A big gun, like
Gentamicin, Vancomycin

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122
Q

What is Sabouraud’s agar used for?

A

Used to culture fungi.

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123
Q

Describe mycobacteria.

A
  • Aerobic.
  • Non-motile.
  • Non spore forming.
  • Bacilli.
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124
Q

What are the 3 classes of mycobacteria of medical importance and give an example of each

A
  • MTB (Mycobacterium Tuberculosis) Complex
    • M. tuberculosis (Tuberculosis)
  • Non-Tuberculosis Mycobacterium
    • M. kansasii (chronic lung infection)
  • Non-cultivable
    • M. leprae (leprosy)
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125
Q

What is the cell wall of Mycobacteria like? How is it classified in terms of gram staing?

A

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

Sit within the gram-positive family

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126
Q

What do you use to stain mycobacteria?
b) What can be used to aid the visualisation of mycobacteria?

A
  • Do not stain with normal method therefore known as Ziehl-Neelsen/Acid fast Positive
    • Composition of cell wall makes it impervious to staining
    • High lipid content with mycolic acids in cell wall

b) Fluorochrome stain augmentation

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127
Q

Are mycobacteria
a) Aerboic or anaerobic
b) Spore forming
c) Motile

A

Aerobic
No
No

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128
Q

What is the significance of the waxy cell wall of mycobacteria?

A
  • Difficult to target with antibacterial agents
  • Survive inside macrophages, even in low pH environments
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129
Q

Why is it hard to use therapeutic antibodies against mycobacteria?

A
  • Slow reproduction - one of the targets for antibacterials is their fast reproduction time (Some as short as 20 minutes whereas mycobacteria can reach 20 hours)
  • Slow growth in humans - gradual onset of disease
  • Slow growth in culture - difficult to diagnose
  • Slow response to treatment
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130
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.
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131
Q

Name some sterile sites in the body.

A
  1. Urinary tract.
  2. CSF.
  3. Pleural fluid.
  4. Peritoneal cavity.
  5. Blood.
  6. Lower respiratory tract.
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132
Q

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

A
  1. Mouth.
  2. Skin.
  3. Vagina.
  4. Urethra.
  5. Large intestine.
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133
Q

What is a virus?

A

an infective agent that typically consists of a nucleic acid molecule in a protein coat, and is able to multiply only within the living cells of a host.

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134
Q

Which viruses are Non-enveloped?

A
  • Adenovirus
  • Parvovirus
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135
Q

What viruses are enveloped?

A
  • Influenza
  • HIV
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136
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
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137
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
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138
Q

What diagnostic tests are used for identifying viruses?

A
  • PCR - identifies viral genetic material
  • Serology - identifies if there is immunological memory of a particular virus (e.g. IgG is used to detect long-term memory)
  • Histopathology - identifies features of viral infection
  • Viral cultures, with light microscopy
  • Electron Microscopy
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139
Q

Outline how Serology works

A
  • Serology - identifies if there is immunological memory of a particular virus (e.g. IgG is used to detect long-term memory)
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140
Q

Outline some pros and cons of PCR testing

A

Pros
Very fast
Cheap
Can test for multiple viruses at the same time, by using a mix of primers
Very sensitive - (if you have it, a PCR will almost definitely give a positive result)

Cons
Need to suspect viruses before hand
Risk of giving false positive

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141
Q

What colour swabs do you use for diagnosing viruses and bacteria?

A

Green viral swab

and black charcoal swab for bacteria

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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
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143
Q

What are protozoa?

A

One celled animals”

Single cell with nucleus
(Eukarytoic)

> 30,000 species

144
Q

What are the 5 types of protoza?

A
  1. Flagellates
  2. Microsporidia
  3. Sporozoa
  4. Amoebae
  5. Cilliates
145
Q

What is African Trypanosomiasis? (flagellates) How is it transmitted

A
  • Human African Trypanosomiasis (or sleeping sickness)
  • endemic in Africa.

Spread by the bite of an infected tetse fly

146
Q

How is American Trypanosomiasis transmitted?

A
  • Spread through contact with faeces of triatomine “kissing” bug
    Also through blood, vertically and eating contaminated food
147
Q

What is the main type of Malaria?
What two types can incubate for up to a year?

A
  1. Plasmodium falciparum (most severe disease)
  2. Plasmodium ovale
  3. Plasmodium vivax

Others:
4. Plasmodium malariae
5. Plasmodium knowlesi

148
Q

What two types of malaria can persist in
humans long-term without proper treatment? What do they stay dormant as, and what can you give to prevent this?

A

P. ovale and P. vivax -

These two species can persist in the liver as
hypnozoites.

To prevent relapses, patients with Plasmodium vivax
or Plasmodium ovale infection should be given a 14-
day course of primaquine, which will treat the
hypnozoite forms

149
Q

How is malaria transmitted?

A

By bite of the female anopheles mosquito

150
Q

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

A

fever and recent travel

151
Q

How would you diagnose malaria? What do thick and thin films show

A

A blood flim by using light microscopy

Thick - Sensitive but low resolution - Only does the person have malaria = yes or no

Thin film - helps identify different species

152
Q

What is the main symptom of malaria?

A

Fever

153
Q

What are some other symptoms of malaria?

A

Chills
Headache
Myalgia
Fatigue
Diarrhoea
Vomiting
Abdo pain

154
Q

What are some Haemolysis specific signs of malaria?

A

Anaemia
Jaundice
Hepatosplenomegaly
‘Black Water Fever’- Hb passes into urine

155
Q

Malaria life cycle - Outline first human liver stage

A
  • 1️⃣ Mosquito takes a blood meal, injecting the indiviual with sporozoites (infected for of the Plamsodium)
  • 2️⃣ Sporozoites travel in the blood and infect liver cells (hepatocytes)
  • 3️⃣ Hepatocytes mature and develop into Shizonts
  • 4️⃣ Schizonts eventually bursts and releases Merozoites into the blood
156
Q

Malaria life cycle - Outline second human blood stage

A
  • 5️⃣ Merozoites infect RBCs
  • 6️⃣ Once within the RBC, plasmodium become Trophozoites
  • 7️⃣ 🅰️ Trophozoite develop into Schizonts, which ruptures and reinfects RBC with merizoites - this cycle continues as the disease develops
  • 7️⃣ 🅱️ Some Trophozoites differentiate into sexual stage gametocytes
  • ✳️ At this stage, as RBCs rupture, the individual develops cyclical fever and haemolytic clinical manifestations, such as anaemia, jaundice (bilirubinaemia), haemoglobinuria
157
Q

Malaria life cycle - Outline second human blood stage

A
  • 8️⃣ Another mosquito takes a blood meal from this infected individual will ingest gametocytes
  • 9️⃣ Gametocytes mature into an oocyst
  • 🔟 Oocysts ruptures and release sporozoites
  • 🔟+ 1️⃣ Sporozoites are injected into the blood of a different individual - cycle.
158
Q

Describe the pathogenesis of p.falciparum?

A

Causes complicated malaria happnes in 3 stages

  • 1️⃣ CytoadherenceInfected RBCs present membrane proteins that bind to microvascular endothelial cells in vessels
  • 2️⃣ RosettingInfected RBCs also adhere to non-infected RBCs, causing small vessels to become obstructed by clumbs of RBCs - this causes hypoxia.
  • 3️⃣ SequestrationMicroinfarcts form in major organs (brain, heart, lungs, liver, kidney) where they are able to mature and evade the immune system.
159
Q

Malaria complications - Outline what happens in
a)cerebal malaria
b) Renal failure
c) Acute respiratory distress syndrome ARDS

A

Cytoadherence in the brain; vessel occlusion causes hypoglycaemia or haemorrhage.

Vascular occlusion of the kidneys causes dehydration, hypotension, haemoglobinuria, haemolysis

Vascular occlusion of the lungs causes anaemia, lactic acidosis and increased vascular permeability.

160
Q

What genetic conditions can give immunity to malaria?

A

Someone with sickle cell anaemia or thalassaemias.

161
Q

Can immunity to malaria be acquired?

A

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

162
Q

What is the treatment for malaria?

A

Chloroquine.

163
Q

What is the treatment for severe malaria?

A

IV artesunate

164
Q

What are the symptoms of complicated malaria?

A
  • Cerebral
  • ARDS/Pulmonary oedema
  • Renal failure
  • Sepsis
  • Bleeding/Anaemia
165
Q

What do viruses need to do in order to be successful?

A

Need rapid cell entry

Free viruses in the blood stream are easily neutralised

166
Q

What is in the cell mediated response that viruses elicit?

A

Interferons from Th (CD4+) or Cytotoxic T lymphocytes have
direct antiviral action

CTL can kill infected cells
NK cells and macrophages are involved in antibody-dependent cellular cytotoxicity(ADCC) killing

Interferons induces anti viral proteins for bystander cells

167
Q

Viral evasion: How does influenza virus evade detection?

A

they change the coat antigen, and coat themselves in a lipid bilayer acquired from they infected host cell

Haemagglutinin HA
and Neuraminidase NA

168
Q

What are the two thibngs that changes of coat antigens result in?

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.

      That’s why the flu vaccine changes each year
169
Q

What are the 4 main ways that antibiotics work?

A

Where they work:

Disrupting:

  1. Cell wall synthesis
  2. Nucleic acid synthesis
  3. Protein synthesis
  4. Folate synthesis
170
Q

What is a bacteriostatic antibiotic?

A

Bacteriostatic
Prevent the growth of bacteria; defined as a ratio of Minimum Bactericidal Concentration (MBC) : Minimum Inhibitory Concentration (MIC) of > 4

Includes antibiotics that:

  • Inhibit protein synthesis
  • Inhibit DNA replication
  • Inhibit metabolism

Useful in disease where its the bacteria exotoxin that’s causing the symptoms as they reduce toxin production.

171
Q

What is a bacteriocidal antibiotic?

Give an example How does it work?

A

Will kill the bacteria; kills 99.9% in 18-24 hours

Includes antibiotics that:
- Inhibit cell wall synthesis

Useful in cases of poor drug penetration due to poor blood supply (endocarditis); difficult to treat infections or when we need to eradicate infections quickly (meningitis).

172
Q

What does the MBC:MIB ratio tell us?

test

A

The Minimum Bactericidal Concentration (MBC) is the lowest concentration of an antibacterial agent required to kill a bacterium over a fixed time (18 hours or 24 hours), under a specific set of conditions.

The Minimum Inhibitory Concentration (MIC) is defined as the lowest concentration of an antimicrobial ingredient or agent that is bacteriostatic (prevents the visible growth of bacteria).

Antibacterial agents are usually regarded as bactericidal if the MBC is no more than four times the MIC.

173
Q

Antibiotics that inhibit cell wall: How do B-lactam antibiotics work?

A
  • ○ disrupt peptidoglycan production
    ○ by binding covalently and irreversibly to the Penicillin Binding Proteins
    ○ cell wall is disrupted and lysis occurs
    ○ results in a hypo-osmotic or iso-osmotic environment
    ○ Active only against rapidly multiplying organisms

Baso, cause lysis by messing up peptidoglycan production
- Won’t affect human cells

is bactericidal

174
Q

Name some B-lactam antibiotics categories (3) , with some key examples

A
  • Penicillin (any of the cillins)
    eg Penicillin V
    Penicillin G (Benzyl penicillin)
    Flucloxacillin
    Amoxicillin / Ampicillin
    Pipericillin
  • Cephalosporin
    eg Cefuroxime
    Cefotaxime
    Ceftriaxone
  • Carbapenems
    eg Meropenem
175
Q

Antibiotics that inhibit the cell wall - How do we administer Glycopeptides? When do we use them? Give some examples of them

A

IV only

Only work on Gram positive:

- MRSA
- Penicillin allergy

Examples
Vancomycin - For MRSA
Teicoplanin

176
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

Differences in the spectrum and activity of β-lactam antibiotics are due to their relative affinity for different PBPs.

177
Q

Antibiotics that inhibit DNA synthesis: Name some, and what they target. When would we use quinolines?

A

Rifampicin - Targets RNA polymerase
Metronidazole - KEY ONE
Fluoroquinolones - target both DNA Gyrase and DNA topoisomerase

Quinolines are more effective against GRAM NEGATIVE than positive, use then and in
- Penicillin allergy
- UTIs
- intra-abdominal infections

178
Q

Antibiotics that work by inhibiting protein synthesis - Name the 2 name categories, that work on 30S subunit and with examples

A

Aminoglycosides
eg Gentamicin

Tetracyclines
eg Doxycycline

179
Q

Antibiotics that work by inhibiting protein synthesis - Name the 2 name categories, that work on 50S subunit and with examples

A

Lincosamides
eg Clindamycin

Macrolides
eg Clarithromycin

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, but don’t give to pregnant women!!
181
Q

What are the two major determinants of antibacterial effects?

A
  1. Concentration (number of binding sites taken up)
  2. Time (that the antibiotic remains on the binding sites)
182
Q

What is MIC?

A

MIC - lowest conc THAT IS BACTERIOSTATIC (lowest amount required to prevent visible growth of bacteria)

183
Q

What is time dependant killing?

A

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

184
Q

What antibiotics rely on time dependant killing?

A
  • beta-lactams (penicillins, cephalosporins, carbapenems, monobactams),
  • clindamycin,
  • macrolides
  • oxazolidinones
185
Q

What is concentration dependant killing?

A
  • Key parameter is how high the concentration is above MIC
186
Q

What antibiotics rely on concentration dependant killing?

A
  • aminoglycosides
  • quinolones
187
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

188
Q

What mechanisms can make bacteria resistant to antibiotics

A
  • Change the antibiotic target
  • Destroy antibiotic
  • Prevent antibiotic access
  • Remove antibiotics from bacteria
189
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 – Vancomycin Resistant Enterococci
  • Rifampicin activity is reduced by changes to RNA polymerase in MTB ===> Become multidrug resistant TB (MDR-TB)
190
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
191
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
192
Q

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

A
  • Proteins in bacterial membranes pump the antibiotic out the cell.
  • ## S. aureus or S. pneumoniae resistance to fluoroquinolones
193
Q

What is intrinsic resistance?

A
  • Bacteria that have a natural resistance to an antibiotic
  • All subpopulations will be equally resistance
194
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
  • Penicillin’s struggle more against Gram Negative Bacteria as they have less peptidoglycan to target and have to get through an outer membrane in order to get at it. They are better suited to Gram positive bacteria

-

195
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.
196
Q

What are the two ways that bacteria develop resistance?

A
  • Spontaneous gene mutation
  • Horizontal gene transfer
197
Q

What are the 3 ways in which a horizontal gene transfer can occur, in order for bacteria to Develop resistance?

A

Conjugation
Transduction
Transformation

198
Q

Types of Horizontal Gene transfer - What is conjugation?

A

Sharing the DNA on Plasmids via Pilus, aka “Bacterial Sex”

199
Q

Types of Horizontal Gene transfer - What is transduction?

A

insertion of DNA from one bacterium is transferred to another bacterium via a Bacteriophage (viruses that infect bacteria)

200
Q

Types of Horizontal Gene transfer - What is Transformation?

Where have we seen it?

A

When some bacteria can take up free DNA from the environment and incorporate it into their one chromosome.

Seen how foregin DNA from S. Mitis to S. Pneumoniae , which leads to Penicillin Resistance

201
Q

What are the 4 main ways that antibiotics work?

A

Where they work:

Disrupting:

  1. Cell wall synthesis
  2. Nucleic acid synthesis
  3. Protein synthesis
  4. Folate synthesis
202
Q

What does the MBC:MIC ratio tell us?

A

The Minimum Bactericidal Concentration (MBC) is the lowest concentration of an antibacterial agent required to kill a bacterium over a fixed time (18 hours or 24 hours), under a specific set of conditions.

The Minimum Inhibitory Concentration (MIC) is defined as the lowest concentration of an antimicrobial ingredient or agent that is bacteriostatic (prevents the visible growth of bacteria).

Antibacterial agents are usually regarded as bactericidal if the MBC is no more than four times the MIC. (Because at relatively lower times of dosing (<4 Times) they can still Kill bacteria/be bactericidal

203
Q

Resistant gram-positive bacteria: How has VRE developed resistance?

A

VRE
vancomycin-resistant enterococci
- Plasmid mediated acquisition of gene
That alters the sequence of amino acid on peptide chain

====> This means Vancomycin cant bind to Enterococci

Has been Promoted by cephalosporin use

204
Q

Resistant gram-positive bacteria: How has MRSA become resistant?

A

MRSA
Methicillin-resistant Staphylococcus aureus
Has acquired Staphylococcal cassette chromosome mec (SCCmec)

  • confers resistance to all β-lactam antibiotics in addition to methicillin (= flucloxacillin)
205
Q

Resistant gram negative bacteria: How have ESBL developed resistance?

A

A B-lactamase enzyme , that has gone under Further mutation

Known as extended spectrum beta lactamase (ESBL) enzymes - extended antimicrobial resistance

These hydrolyse oxyimino side chains of cephalosporins cefotaxime,ceftriaxone, andceftazidime and monobactams: aztreonam

206
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
207
Q

What is a mechanism by which Gram negative strains confer resistance?

A

They produce β-lactamase enzymes which hydrolyse penicillins. (they break the beta lactim ring in the penicllin)

208
Q

How can we combat gram negative resistant bacteria that produce beta lactamase?

A

Design drugs that utilise agents that inhibit β-lactamase e.g. Co-Amoxiclav = Amoxicillian + Clavulanate. Clavulanate inhibits the β-lactamase.

209
Q

What is AmpC-β-lactamase? Where would you find it?

A

A cephalosporinase enzyme; encoded on the chromosomes the Enterobacteriaceae;

It is b-lactamase inhibitor resistant!

It mediates resistance to cephalothin, cefazolin, cefoxitin, most penicillins, and beta-lactamase inhibitor-beta-lactam combinations.

210
Q

What Kind of antibiotic should you give if you need to combat bacteria with lots b-lactamases or cephalosporinases?

A

Carbapenems such as Meropenem

===> They are highly resistant to degradation by b-lactamases or cephalosporinases.

treat infections due to ESBL or AmpC -producing organisms of the Enterobacteriacae family.

(Known as the last resort)

211
Q

What bacteria do B-lactam antibiotics work most effectively against

A

Gram-positive bacteria as they have a thick peptidoglycan layer - this is what Penicillin targets.

Gram negative bacteria, therefore, already have some intrinsic resistance to Penicillin as they only have a thin peptidoglycan layer, in-between an inner and outer membrane

212
Q

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

A

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

213
Q

What antibiotic would be used for S. pneumoniae

A

PO amoxicillin
IV benzylpenicillin

214
Q

When would you use a glycopeptide?

A
  • Vancomycin and teicoplanin

only use with gram-positive bacteria
- They target the cell wall, so use with B-lactam bacteria

  • Used when patient has penicillin allergy, and with MRSA
215
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
216
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
217
Q

What group of antibiotics would you use commonly against:
- Use against gram negatives and staphs
- Use for UTIs
- Use for infective endocarditis

A

Aminoglycosides (protein synthesis, 30s unit)
- Gentamicin IV only

218
Q

Use of what antibiotic group has been associated with

  • Use for gram negatives
  • Use for UTIs
  • Use for intra-abdominal infectionshas been

How does it work?

A

QUINOLONES Target Nucleic acid synthesis
- Ciprofloxacin

219
Q

When would co-amoxiclav be used?

A
  • Use for aspiration pneumonia, severe CAP and more resistant UTIs
220
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
221
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.
222
Q

What is lentivirus?

A

Lentivirus represents a genus of slow viruses with long incubation period

223
Q

Fungi are eukarytoic - what does this mean? Whats in their cell wall?
How do they get their nutrients?

A

Eukaryotic means they have a nuclear membrane

They have a chitinous cell wall

They are heterotrophic - they get nutrients from what they are living from.

224
Q

How do fungi move?

A

By means of growth of spore release

225
Q

Outline how
a) Yeasts
b) Moulds
spread

What is dimorphic fungi?

A

Yeasts are small single celled organisms that divide by budding

Moulds form multicellular hyphae and spores

Dimorphic fungi - fungi that can exist as either yeast or moulds - can switch in between

226
Q

Why won’t most fungi harm humans?

A

Fungi have an inability to grow at 37 degrees (body temperature)

  • Fungi also cannot evade the adaptive/innate immune response
227
Q

Key fungal infections - what is Pneumocystis?
When would you get it?

A

A type of pneunomia - often in people with healthy lungs

Source of opportunistic infection, causing infections of people with weak immune systems eg HIV/AIDS (30-40% of PCP) ,

228
Q

Key fungal infections - what is Candidiasis?
When would you get it?

A

Known as thrush - common in children’s mouth (yellow tongue) and vaginal thrush

eg caused by candida albicans

229
Q

What enzyme is used to integrate HIV DNA into the host cell?

A

Reverse transcriptase

230
Q

HIV: (Human Immunodeficiency Virus) What does it lead to?

A

Complications of HIV lead to Aquired Immundeficiency Syndrome AIDS

231
Q

Name some risk factors for getting HIV/AIDS.

What age group makes up for 50% of all new infections worldwide?

A

Men who have sex with men, IVDU, Commercial sex workers

Age group 50% all new infections occur worldwide: 19-24yo

232
Q

Where would you most likely find HIV1?
HIV2?

What were they both derived from?

A

HIV1 - more common, and seen in US and worldwide
Chimpanzee-dreived Simian Immunodeficiency Viruses (SIVcpz) - thought to have been transmitted the 1950s

HIV2 - alot Rarer, seen in Western Africa and Southern Asia
Sooty Mangabey-derived Simian Immunodeficiency Viruses (SIVmp)

233
Q

HIV affects CD4+ cells. (this includes T Helper Cells, Macrophages and Dendritic Cells). CD4 + molecule helps immune cells communicate,

How does HIV get into them?

A

HIV attaches a CD4 cell via BOTH gp120 protein and a co receptor

CXCR4 - In T Cells
CCR5 - In T cells, macrophages, monocytes, dendritic cells

People with mutations to co proteins can be protected from HIV

234
Q

What type of Virus is HIV? What does reverse transcriptase do?

A

A single stranded RNA retrovirus

The Virus injects a single strand of RNA into the cell.
Retrovirus - needs reverse transcriptase enzyme to transcribe a piece of complimentary proviral DNA,

235
Q

When in the cell, what does HIV virus do?

A

Uses reverse transcriptase enzyme to transcribe a piece of complimentary proviral DNA, to make a double strand with the original RNA strand.

This double stranded DNA then pops itself into the DNA of the cell (via integrase enzyme.) , ready to be transcribed into another virus cell, when the old immune cell becomes activated and starts trying to transcribe proteins for the immune response. (sneaky)

236
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
237
Q

How does HIV go from entering the body to infecting loads of cells at the lymph node? What does this lead to?

A
  1. Enters, say, through Genito urinal mucosa
  2. Macrophage recognise virus as forgein and phagocytose it, and then present HIV antigens on its surface
  3. Antigen presenting macrophage present HIV virus to a reservoir of immune cells T cells at lymph node.
  4. HIV virus can infect all these cells, leading to a massive spike of HIV in the blood, leading to flu like symptoms
238
Q

What is viral tropism?

A

The host cell preference that different strains of HIV cells in the body want to target due to mutations.

It is determined by the virus’s ability to interact with the cell’s receptors, which determine the cell type that the virus can infect

239
Q

HIV infection - How long is the acute phase? What happens after this? How long is the chronic phase and what happens here?

A

12 weeks, After this the immune system will launch a counterattack and the number of normal T cells will begin to rise again.

The chronic phase then starts, lasting from 2 - 10 years, as the virus slowly increases and T cell number slowly start to decrease

240
Q

HIV infection: What do patients with 200-500 T cell/mm^3 present with?

A

Swollen lymph nodes
Hairy leukoplakia (white patch tongue)
Oral Candidiasis (Yeast infection in mouth)

241
Q

What do patients with <200 T cell/mm^3 present with?

A

Persistent fever, fatigue, Weight loss and diarrhoea

AIDS defining conditions appear

eg Recurrent bacterial pneumonia
Pneumocystis pneumonia
Fungal infections

242
Q

What are the percentages of the different modes of transmissions of HIV?

A

75% Sexual contact
the rest IV drug abuse
Mother to child (via placenta or breast milk)

Accidental needlestick injury and error in blood transfusion are least likely.

243
Q

What tests can you do for HIV. What is recommend as the first test?

A

Antibody tests (look for antibodies against HIV)
Antibody/Antigen (Look for virus directly and also antibodies
RNA tests - (look for viral RNA)
DNA tests -( look for Copies of the viral RNA)

Antibody/antigen test is recommended first

244
Q

If your first test for HIV is postive (Antibody/antigen test), what tests should you do next?

A

Antibody test, and RNA tests

245
Q

Once it has been diagnosed,how can we go about treating HIV?

A

With HAART drugs (Hight active Anti-retroviral inhibitors)

==> It usually consist of 3+ antiretroviral drugs, that suppress viral replication, eg Nucleoside reveres transcriptase inhibitor

246
Q

what Anbtx should you use to traet MRSA?

A

Vancomycin

247
Q

What are common bacterial causes of meningitis in
a) Neonates
b) In infants

A

a) E coli, Group B strep, Listeria Monocytogenes
b) Neisseria Meningitidis, haemophilus Influenzae, Strep Pneumoniae

248
Q

What are common bacterial cuases of meningitis in
c) Young adults
d) In the elderly

A

c) Neisseria meningitidis, Strep Pneumoniae
d) Neisseria meningitidis, Strep Pneumoniae, Listeria Monocytogenes

249
Q

What are the two most common causes of Meningitis? Are they gram negative or positive?

A

N.meningitidis + S.pneumoniae = diplococci

N. Meningitidis= Negative
S. Pneumoniae = Positive

250
Q

Name some viral causes of Meningitis

A

mumps virus, echo virus, coxsackie virus, herpes simplex virus, poliovirus

251
Q

What antibiotic group to we tend to give instead of penicillins to those with a penicillin allergy?

A

Macrolides, eg Clarithromycin, and Erythromycin (these inhibit protein synthesis)

252
Q

What antbx do we often give to treat Meningitis?

A

Bacterial: start antibiotics before tests come back if suspected
Cephalosporins: IV cefotaxime/ IV ceftriaxone

If over 50/immunocompromised add IV amoxicillin to cover listeria

Meningococcal septicaemia: immediate IM benzylpenicillin in community/ IV cefotaxime in hospital
Viral: supportive treatment, self-limiting in 4-10 days, acyclovir for HSV meningitis

253
Q

What is the main bacterium responsible for most UTIs?
What would be some sensible antbx to use to treat it?

A

Escherichia Coli - Gram Negative Bacilli, non lactose fermenting

Use Co amoxiclav, or Trimethoprim, (that inhibits folate synthesis)

254
Q

What antbx would you use to treat chlamydia?

A

Those that effect PROTEIN SYNTHESIS

Doxyclicne (a tetracycline)
Azithromycin (a Macrolide)

255
Q

What antibiotic would you use to treat Neisseria Gonorrhoea?

Is this bacterium gram positive or negative, rod or bacilli?

A

ceftriaxone = A CEPHLASPORIN

(its a gram negative diplococci)

256
Q

What is the most common form of viral meningitis? What would cause it and how would you treat it?

A

-Enteroviruses (echoviruses, Coxsackieviruses, polioviruses)- most common
-Mumps in countries without routine childhood immunisation

There is no specific antiviral therapy
-Supportive: analgesics, antipyretics, hydration

257
Q

What are the two main drugs given to treat drug-susceptible pulomonary TB?

A

rifampicin, isoniazid - BOTH ACT ON NUCLEIC ACID SYNTHESIS

258
Q

What disease can viridains strep cause? What drug would you give?

A

Endocarditis.

Treat with Penicillin and supplement with Gentamicin if needed

259
Q

What is the empirical treatment for cellultis?

A

Empirical treatment for cellulitis (before the organism is confirmed) would usually be with flucloxacillin to cover S aureus which is also a common cause

Clarithromycin as an oral alternative for those with Beta lactam / penicillin allergy. Vancomycin is an IV alternative for that can also be used if allergic to beta lactam antibiotics.

260
Q

What is the empirical treatment for an UTI, while you await for the results

A

Either Nitrofurantoin or Trimethoprim can be used first line as empirical treatment

  • Note that the local STH guidance is slightly different from national guidance -higher rates of trimethoprim resistance among UTI pathogens in the local community STH serves make this option less appropriate.*
261
Q

Why is urinalysis for protein and blood performed at all antenatal visits?

A

TO screen for Preeclampsia, not for UTIs

262
Q

Why is it important to collect urine from asymptomatic pregnant women?

A

In pregnancy, asymptomatic bacteriuria is present in around 4-7% of women. Left untreated, there is a high risk of ascending infection, with pyelonephritis and subsequent risk of miscarriage. To screen for this, mid stream urine samples are collected in antenatal clinics, irrespective of urinalysis.

263
Q

What are some associated conditions caused by S.pyogenes?

Outline its classification

A

Wound infections - cause cellulitis
Tonsilitis and Pharyngitis
Otitis media
Impetigo
Scarlet Fever
Can lead to Rheumatic Fever

Gram positive, catalase negative, Beta haemolytic on Blood agar, Group A on Lancefield

264
Q

Where is Streptococcus pneumoniae often found as a commensal organism?

map its classification

A

In the oropharynx in roughly 30% of the population

Is a gram positive, Alpha Haemolytic, optochin sensitive

265
Q

What are the associated conditions caused by S.pneumoniae?

A

Pneumonia
Otitis media
Sinusitis
Meningitis

266
Q

What are the associated conditions caused by viridans group strep?

map classification

A

Dental caries and abscesses
Infective endocarditis
Deep organ abscesses

Postive, Coccus, Catalse negative, and Alpha haemolytic, optochin resistant

267
Q

What is the purpose of bacteria possessing the coagulase enzyme?

A

This means that they can clot the blood plasma around the bacteria to attempt to protect themselves from phagocytosis

An enzymes produced by staph aureus turns fibrinogen (soluble) into insolubale fibrin - clot, cloudy, fibrin clumping

268
Q

What are the associated conditions caused by Staphylococcus aureus?

Map classification

A

Wound infections
Abscesses
Impetigo
Septicaemia
Osteomyelitis
Pneumonia
Endocarditis

Toxins could also cause toxic shock syndrome and food poisoning

Staphylococcus aureus - Gram Positive, catalase positive, and coagulase positive - quite virulent

269
Q

Where are the likely sites of infection for S.epidermidis?

Map classification

A

Prostheses
Catheters

Mainly affects immunocompromised individuals

Gram positive, Catalase positive, and coagulase negative

270
Q

What are the associated infections caused by E.coli?

map classification

A
  1. Wound infections (surgical)
  2. UTIs (cystitis; ~80% of female UTIs - faecal source or sexual activity; catheterisation - most common nosocomial infection)
  3. Gastroenteritis
  4. Traveller’s diarrhoea
  5. Bacteriemia
  6. Meningitis (infants) - rare in the UK

Gram negative, bacilli, Lactose fermenting

271
Q

What is special about shigella?

map its classification

A

It is acid tolerant and so it will not be destroyed by gastric acid

Gram negative bacilli, non lactose fermenting, oxidase negative and White spots on dark red XLD agar

272
Q

How is shigella spread?

A

Via person to person contact
Via contaminated food and water

273
Q

What is the pathogenesis of Salmonella infection?

A

Invasion of gut epithelium (SI)

Transcytoses to basolateral membrane

Enters submucosal Macrophages; survive and replicate within the macrophage.

Systemic infection due to dissemination within macrophages: serovar Typhi

Gram negative bacilli, non lactose fermenting, oxidase negative, Black on Pink XLD agar

274
Q

What kind of bacteria is Klebsiella pneumonia?

A

Environmental - not gut
It is an opportunistic pathogen and so will infect immunocompromised subjects

Anaerobic gram negative bacilli, Lactose fermenting (along with E.Coli)

275
Q

What kind of patients get infected with Klebsiella?

A

It is an opportunistic pathogen so will infect immunocompromised patients
Including:
Neonates
Elderly
Immunocompromised

276
Q

What are the associated infections caused by Klebsiella pneumonia?

A

UTIs
Pneumonia
Surgical wound infection
Sepsis

277
Q

What is Haemophilus influenzae?

A

Exclusively human parasite
opportunistic infection
Fastidious - requires chocolate agar to culture
non-motile

278
Q

Where is Haemophilus influenzae often found on the body?

A

Nasopharyngeal carriage in 25-80% of the population

279
Q

What is the major associated condition caused by Bordetella pertussis?

A

Whooping Cough (pertussis)
Caused by the Pertussis toxin

280
Q

Is helicobacter spread?

A

No - it is not spread but exists in the gastric mucus of roughly 50% of the global population
Therefore only a fraction of people develop disease

281
Q

What composes a granuloma?

A

Infected macrophage in the centre
Other recruited Macrophages aggregated together (aggregates of epithelioid histocytes)
Surrounded by Lymphocytes (T and B cells)

282
Q

What is the function of a granuloma?
What is a problem with this?

A

It will wall off the bacteria
However this can create a niche for the bacteria to enter latency and survive

283
Q

What cell type is responsible for walling off the granuloma?

A

Fibroblasts

284
Q

What conditions can make granulomas unstable and at risk of rupture?

A

CD4 depletion caused by HIV

TNFa depletion caused by therapies against RA or organ transplant

285
Q

What are some characteristics of a virus?

A

Grow inside living cells - replicate inside host machinery
Possess only one type of nucleic acid - DNA OR RNA (not both)
No cell wall - Have a protein coat (capsid) or membrane lipid evenlope
Inert outside of host cell
Protein receptors on virus surface to allow for attachment to susceptible host cells

286
Q

How do viruses cause disease?

A

Direct destruction of host cells
Modification of host cells
Over reactivity of the immune system
Damage through cell proliferation
Evasion of Host defenses

287
Q

Give examples of diseases caused by flagellates?

A

Human African Trypanosomiasis (sleeping sickness)
American Trypanosomiasis (Chagas disease)
Leishmaniasis
Trichomoniasis
Giardiasis

288
Q

Why do patients with malaria experience high fever spikes every 48 hours?

A

Due to the replication of the merozoites in the RBCs taking 48 hours at which point the RBC ruptures leading to an inflammatory response

289
Q

What are the scenarios where you would carry out an HIV test?

A
  • Clinician indicate diagnoses - clinical indications of immunosuppressive disease
  • Routine screening in high prevalence locations
  • Antenatal screening
  • Screening in high risk groups
  • Patient initiated request for testing
290
Q

What conditions would indicate that an HIV test may be needed?

A
  • Unexplained lymphadenopathy
  • Unexplained weight loss or diarrhoea, night sweats of PUO
  • Oral or esophageal candidiasis or hairy leukoplakia
  • Flu like illness, rash, meningitis
  • Unexplained blood dyscrasias
291
Q

What are some recognised risk factors for HIV?

A

Heterosexual and homosexual sex (men to women and men to men)
IVDU
Multiple sexual parteners
Rape
Vertical transmission

292
Q

What type of virus is HIV?

A

Retrovirus

293
Q

What are the HIV associated neoplasms?

A
  • Lymphoma
    • Caused by EBV
  • Cervical neoplasia
    • Caused by HPV
  • Kaposi’s sarcoma
    • Caused by human Herpesvirus 8
  • Hepatocellular Carcinoma
    • Caused by Hepatitis B/C
294
Q

What is the marker for AIDS?

A

CD4 count less than 200/ul

295
Q

When are antibacterial agents regarded as bactericidal?

A

Antibacterial agents are usually regarded as bactericidal if the MBC is no more than four times the MIC.

(Because at relatively lower times of dosing (<4 Times) they can still Kill bacteria/be bactericidal

296
Q

Name 2 Gram-Positive resistant strains of clinical importance

A

MRSA - Methicillin (Flucloxacillin) resistant Staphylococcus Aureus
VRE - Vancomycin resistant enterococci

297
Q

How does VRE have antibiotic resistance?

A

Vancomycin resistant enterococci
Have acquired an mutation amino acid change via plasmid acquisition, that prevents vancomycin binding to bacteria - has been promoted by cephalosporin use

298
Q

How can we combat drugs that have beta lactamases?

A

Design drugs that utilise agents that inhibit beta lactamase
Co-amoxiclav - Amoxicillin and Clavulanate
Clavulanate inhibits the beta lactamase

299
Q

What are the 2 main classes of antibiotics that inhibit bacterial cell walls?

A

Beta Lactams
Glycopeptides

300
Q

What compound do beta lactam antibiotics target?

A

Peptidoglycan

301
Q

What is the mechanism of action of beta lactam antibiotics?

A

Disrupt peptidoglycan production by:

  1. Binding covalently and irreversibly to the penicillin-binding proteins (PBPs) particularly transpeptidase
  2. Cell wall synthesis is disrupted and cell lysis occurs as peptidoglycan crosslinking can not occur

→ Active only against rapidly multiplying organisms.

302
Q

What are carbapenems?

A

Antibiotics designed to overcome the actions of beta lactamases and cephalosporinases
Therefore these are the most broad specturm antibiotics and used as a last resort

303
Q

What are CREs?
Give examples of them

A

Carbapenem resistant enterobacteriaceae:
Pseudomonas aeruginosa
Escherichia coli
Klebsiella pneumoniae

304
Q

Give examples of some Glycopeptides

A

Vancomycin
Teicoplanin

305
Q

What is the route of administration for glycopeptides?

A

IV only

306
Q

What types of antibiotics will inhibit protein synthesis?
Give an example for each

A

Aminoglycosides - Gentamicin (30s)
Tetracyclines - Doxycycline (30s)
Lincosamides - Clindamycin (50S)
Macrolides - Clarithromycin/ Erythromycin (50s)
Chloramphenicol

307
Q

What are endogenous infections?

A

Infections caused by the patients own flora

308
Q

What common procedures often cause endogenous infections?

A

Surgery
Catheterisation
Cannulisation

309
Q

When can chickenpox infection be serious?

A
  • Immunocompromised patients
  • Patients who have had transplants
  • Adults
  • Pregnant people
  • Smokers
  • Infants
310
Q

What symptoms would a varciella zoster virus show?

A

SHINGLES, and a red painful rash confined to a single dermatome

311
Q

What is the treatment for VZV infection?

A

Acyclovir

312
Q

What disease is Epstein Barr Virus known to cause? How would you diagnose it?

A

Infectious Mononucleoisis (Glandular fever)

Need to do a blood test, will see atypical lymphocytes

313
Q

What importnat differential for EBV glandular fever do you need to rule out when testing for it?

What would serology show for acute and past infections of EBV?

A

unlike alot of viral illness, EBV can leads to white/yellowish purulent lining over tonsils – So you also need to a black charcoal swab to exclude S. Pyogenes, an imporatnt differential cause

IgM - EBV+ve - Acute
IgG EBV +ve - chronic/past infection

314
Q

Where do Quinolones act?

A

DNA topoisomers

315
Q

Where does Rifampicin act?

A

RNA polymerase

316
Q

Where do Penicillins, Cephalosporins and Carbapenems act?

A

Inhibit peptidoglycan cross linking

317
Q

Where do Glycopeptides (vancomycin) act?

A

Inhibit peptidoglycan Synthesis

318
Q

What are the Gram positive anaerobes and how do you remember them?

A

CLAP:
Clostridium
Lactobacillus
Actinomyces
Propionbacterium

319
Q

How do you remember the atypical penumonia

A

Legions of Psittaci MCQs

Legionella pneumophilia a
Chlamydia psittaci
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Q fever (coxiella)

320
Q

What is the first line option for treating cellulitis?

A

Flucloxacillin

321
Q

What is the first lie option for treating UTIs?

A

Nitrofurantoin
Trimethoprim

322
Q

What is the first line treatment for treating chest infections?

A

Amoxicillin

323
Q

What is the first line treatment for treating tonsilitis?

A

Phenoxymethylpenicillin

324
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.
325
Q

Name 4 diseases that haemophilus influenzae can cause.

A
  1. Meningitis.
  2. Otitis media.
  3. Pharyngitis.
  4. Exacerbations of COPD.
326
Q

Name a bacteria that can cause cholecystitis

What antbx would you use against it?

A

Bacteria that can cause this - EECK

Enterococci +ve Cocci
E Coli - Gram -ve Rod
Clostdrium +ve Rod
Klebsiella -ve Rod

  • Antibiotics IV - Cefuroxime and Metronidazole
327
Q

What is the first line treatment for meningitis?

A

Cephalosporins - IV Cefotaxime, of Ceftriaxone

328
Q

Give examples of macrolide antibiotics?

A

Clarithromycin
Erythromycin

329
Q

Give examples of tetracycline antibiotics

A

Doxycycline

330
Q

Give examples of aminoglycoside antibiotics?

A

Gentamicin
Streptomycin

331
Q

What drugs inhibit folate acid synthesis?

A

Trimethoprim
Sulphonamides
Sulphamethoxazole

Trimethoprim and Suulfamethoxazole = Co Trimoxazole

332
Q

Why should you not give a pregnant women trimethoprim?

A

Because it will inhibit folate acid synthesis which is required for neural tube closure and therefore could cause the child to have spina bifida or anencephaly

333
Q

What is Co-trimoxazole?

A

Combination therapy of:
Trimethoprim + Sulphamethoxazole

334
Q

What antibiotics would be used to treat atypical bacterial pneumonia?

A

Staph Aureus - Flucoxacillin, or cefuroxime
MRSA - vancomycin
Klebsiella Pneumoniae
Co amoxiclav
P.Aerruginosa
Tazocin

335
Q

What is the main source of bacteria to cause a UTI?

A

Normal intestinal bacteria contaminate the urethral opening via faeces
Usually E.coli

336
Q

How may a UTI Present?

A

Dysuria (pain, stinging or burning when passing urine)
Suprapubic pain or discomfort
Frequency
Urgency
Incontinence
Confusion is commonly the only symptom in older more frail patients

337
Q

What are the main causes of UTIs?

A

E.coli (most common)

Klebsiella
Enterococcus
Pseudomonas
S. saprophyticus
Candida albicans

338
Q

What are the antibiotics of choice for UTIs?

A

Trimethoprim

Nitrofurantoin

339
Q

When would Nitrofurantoin be avoided?

A

Third trimester as it is linked with haemolytic anaemia of the newborn

340
Q

When would Trimethoprim be avoided?

A

Generally safe in pregnancy but avoided in the first trimester as it can affect folic acid metabolism and synthesis.

341
Q

What is Cellulitis?

A

An infection of the skin and soft tissues underneath.

342
Q

What are the most common causes of cellulitis?

A

Staphylococcus aureus and Streptococcus pyogenes are the most common causative organisms in cellulitis

Group C strep - S. dysgalactiae

343
Q

What is the antibiotic of choice to treat cellulitis?

What are some alternatives that could be used?

A

Choice treatment: Flucloxacillin.

Clarithromycin
Clindamycin
Co-amoxiclav

344
Q

key bacteria - outline the classification of
Pseudomonas. Aeruginosa, what it can typically cause and anbtx it can be treated with.

A

Gram negative Bacilli,
Postive on the oxidase test

Pneumonia

Tazocin, Gentamicin, Quinolones

345
Q

What type of agar is often used to culture Neisseria bacteria?

A

Gonoccoccus agar

346
Q

Outline some pros and cons of PCR testing

A

Pros
Very fast
Cheap
Can test for multiple viruses at the same time, by using a mix of primers
Very sensitive - (if you have it, a PCR will almost definitely give a positive result)

Cons
Need to suspect viruses before hand
Risk of giving false positive

347
Q

What symptoms would a varciella zoster virus show?

A

SHINGLES, and a red painful rash confined to a single dermatome

348
Q

What disease is Epstein Barr Virus known to cause? How would you diagnose it?

A

Infectious Mononucleoisis (Glandular fever)

Need to do a blood test, will see atypical lymphocytes

349
Q

Recap - what colour does
a) Salmonella
B) shigella

Show up as on XLD agar?

A

Salmonella - BLACK colononies on Pink/red agar

Shigella - WHITE COLONIES on red agar.

350
Q

Side effects of TB medication - Give some side effects of
Rifampicin

A

Haematuria

351
Q

Side effects of TB medication - Give some side effects of Isoniazid

A

Peripheral Neuropahty,

352
Q

Side effects of TB medication - Give some side effects of Pyrazinamide

A

Hepatitis, Also gout

353
Q

Side effects of TB medication - Give some side effects of Ethambutol

A

– Eye problems e.g. uveitis

354
Q

How long should you give each of the TB medications for?

A

Note RI = 2 months, PE = 6 months

355
Q

What prophylactic medication can be given to those at a very high risk of TB? aka family member who has with TB

A

one off dose of ciprofloxacin

356
Q

name some aids defining illness?

A

pneumocystis jirovecii
Cyptomegalovirus infection of any organ other than liver, spleen or glands

Phase 2a Sam (18 decks)

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