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Phase 2a Medicine EK Mine > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Define pathogen.

A

An organism capable of causing disease.

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2
Q

Define commensal.

A

An organism that colonises the host but causes no disease.

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3
Q

Define opportunist pathogen.

A

An organism that only causes disease if host defences are compromised.

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4
Q

Define virulence.

A

The degree to which a given organism is pathogenic.

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5
Q

What would gram positive bacteria look like down the microscope?

A

Red/pink.

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6
Q

What type of organism would you stain with Ziehl Neelsen?

A

Mycobacteria e.g. TB.

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7
Q

How do you apply the gram stain?

A

Apply crystal violet to heat fixed bacteria. Treat with iodine. Decolourise the sample and then counterstain.

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8
Q

Describe the characteristic features of gram positive bacteria?

A
  1. Single membrane.
  2. Large peptidoglycan area.
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9
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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10
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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11
Q

What are the 3 phases of bacterial growth?

A
  1. Lag phase.
  2. Exponential phase.
  3. Stationary phase.
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12
Q

Give an example of a slow growing bacteria.

A

TB.

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13
Q

Give an example of a fast-growing bacteria.

A

E.coli and S.aureus.

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14
Q

Give 2 functions of pili.

A
  1. Help adhere to cell surfaces.
  2. Plasmid exchange.
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15
Q

What is the primary function of flagelli?

A

Locomotion.

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16
Q

What is the primary function of the polysaccharide capsule?

A

Protection; prevents MAC or opsonisation molecules attacking.

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17
Q

What types of bacteria release endotoxin?

A

Gram negative.

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18
Q

What types of bacteria release exotoxin?

A

Gram positive and gram negative.

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19
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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20
Q

Describe exotoxins.

A

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

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21
Q

What are endotoxins made from?

A

Lipopolysaccharides (LPS).

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22
Q

What are exotoxins made from?

A

Proteins.

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23
Q

What are plasmids?

A

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

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24
Q

Give an example of a gram negative diplococci?

A

Neisseria e.g. N.meningitidis and N.gonorrhoeae.

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25
Q

Give an example of a gram positive cocci?

A

Staphylococcus and streptococcus.

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26
Q

What test can be done to distinguish between staphylococcus and streptococcus?

A

The catalase test; detects the presence of catalase enzyme using hydrogen peroxide. Staph = catalase + ve.
Strep = catalase - ve.

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27
Q

How would you describe the arrangement of staphylococci?

A

Clusters of cocci.

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28
Q

How would you describe the arrangement of streptococci?

A

Chains of cocci.

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29
Q

What test could be done to further distinguish between staphylococci bacteria.

A

Coagulase test: looks at whether a fibrin clot is produced.

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30
Q

What bacteria would be coagulase positive?

A

Staphylococci aureus.

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31
Q

What bacteria would be coagulase negative?

A

All others e.g. staphylococci epidermidis.

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32
Q

What test could be done to distinguish between different streptococci?

A

Blood agar haemolysis.

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33
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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34
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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35
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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36
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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37
Q

Give examples of gram negative bacilli.

A

Shigella, salmonella, E.coli etc.

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38
Q

Give examples of gram positive bacilli.

A
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39
Q

What kind of bacteria is MacConkey agar used with?

A

Gram negative bacilli.

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40
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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41
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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42
Q

Where in the body might you find staphylococci?

A

Nose and skin.

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43
Q

How is staphylococcus aureus spread?

A

Aerosol and touch.

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44
Q

Give 4 virulence factors of staphylococci?

A
  1. Toxins.
  2. Proteases.
  3. Toxic shock syndrome toxin.
  4. Protein A.
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45
Q

How is c.diptheriae spread?

A

Droplet spread.

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46
Q

Does shigella have a H antigen?

A

Shigella is non motile and doesn’t have flagellum. It therefore doesn’t have a H antigen.

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47
Q

What category of bacteria does shigella fall under?

A

Gram negative bacilli.

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48
Q

Does shigella give a positive result with MacConkey agar?

A

No. Shigella does not ferment lactose and so gives a negative result.

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49
Q

Does salmonella have a H antigen?

A

Salmonella is motile and has a flagellum; it therefore does have a H antigen.

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50
Q

Does salmonella give a positive result with MacConkey agar?

A

No. Salmonella does not ferment lactose and so gives a negative result.

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51
Q

Does e.coli have a H antigen?

A

E.coli is motile and has a flagellum; it therefore does have a H antigen.

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52
Q

Does e.coli give a positive result with MacConkey agar?

A

Yes. E.coli does ferment lactose and so you would see a red/pink colour indicating a positive result.

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53
Q

How can you distinguish between gram negative bacilli (salmonella, shigella and e.coli)?

A

Use MacConkey agar and use serology to detect the presence of the H antigen.

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54
Q

Why are there pathogenic strains of e.coli?

A

Due to the acquisition of genes from other bacteria.

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55
Q

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

A

Enterotoxigenic e.coli (ETEC).

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56
Q

Describe the process by which enterotoxigenic e.coli (ETEC) causes traveller’s diarrhoea?

A

Heat labile ETEC toxin modifies Gs protein, it is in a ‘locked on’ state. Adenylate cyclase is activated and there is increased production of cAMP. This leads to increased secretion of Cl- into the intestinal lumen, H2O follows this down an osmotic gradient and this subsequently results in traveller’s diarrhoea.

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57
Q

What effect do enteropathogenic and enterohaemorrhagic e.coli (EPEC and EHEC) have on the mucosa?

A

They adhere to microvilli, rearrange actin, and lead to pedestal formation.

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58
Q

What are the symptoms of enteropathogenic e.coli infection?

A

Chronic watery diarrhoea.

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59
Q

What are the symptoms of enterohaemorrhagic e.coli infection?

A

Bloody diarrhoea.

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60
Q

What are the symptoms of shigella infection?

A

Severe bloody diarrhoea and frequent passage.

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61
Q

How is shigella passed on?

A

Via contaminated food/water or from person to person.

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62
Q

Shigella is acid tolerant. Why is this advantageous for shigella?

A

It means shigella can pass through the stomach without being destroyed by the low gastric pH. It can then move onto the intestine.

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63
Q

What is the action of shigella in the intestine?
A

A

In the intestine it induces self uptake and leads to macrophage apoptosis. Cytokines are released and neutrophils are attracted = inflammation. Shigella spread to adjacent cells.

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64
Q

What bacteria is responsible for salmonellosis?

A

S.enterica.

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65
Q

Name the 3 forms of salmonellosis.

A
  1. Gastroenteritis.
  2. Enteric fever.
  3. Bacteraemia.
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66
Q

What is gastroenteritis?

A

Frequent cause of food poisoning, 24 hour incubation period. Highly infective dose.

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67
Q

What is enteric fever?

A

Enteric fever: typhoid fever. Systemic disease.

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68
Q

What are the symptoms of v.cholerae?

A

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

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69
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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70
Q

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

A

It grows at 18 - 42°C.

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71
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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72
Q

How would you grow haemophilus influenzae?

A

On chocolate agar as it requires haem and NAD.

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73
Q

What diseases can haemophilus influenzae cause?

A

Meningitis and pneumonia.

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74
Q

Describe the pathogenesis of gastro-enteritis.

A
  1. Endocytosis.
  2. Chemokine release.
  3. Neutrophil recruitment and migration.
  4. Neutrophil induced tissue injury.
  5. Fluid and electrolyte loss -> diarrhoea.
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75
Q

Describe the pathogenesis of enteric fever.

A
  1. Endocytosis.
  2. Migration to the basolateral membrane.
  3. Survival in macrophage -> systemic spread.
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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

What are the virulence determinants of N.meningitidis?

A
  1. Capsule; anti-phagocytic.
  2. Pili; adherence to host cell.
  3. LPS.
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83
Q

What are the consequences of N.gonorrhoeae infection?

A

STI - rectal, vaginal or oral inflammation.

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84
Q

Can you grow chlamydia on agar?

A

No, chlamydia is an obligate intracellular parasite.

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85
Q

How can you detect chlamydia?

A

Serum antibodies or PCR.

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86
Q

What are the 2 developmental stages of chlamydia’s unique growth cycle?

A
  1. Elementary bodies (infective).
  2. Reticulate bodies (intracellular multiplication).- Reticulate bodies are converted back into elementary bodies and are released. The cycle continues.
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87
Q

What can c.trachomatis cause?

A

Chlamydia; the most common STI.

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88
Q

Name 2 bacteria in the chlamydophila genre.

A
  1. C.pneumoniae - respiratory tract infection.
  2. C.psittaci - associated with birds.
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89
Q

Describe the flagellum of a spirochaete.

A

Spirochaete’s have an endoflagellum, it lies between the inner and outer membrane.

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90
Q

Name the spirochaete that is responsible for causing lyme disease.

A

B.burgdorferi.

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91
Q

Name the spirochaete that is responsible for causing syphilis.

A

T.pallidum.

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92
Q

Describe the three stages of syphilis.

A
  1. Primary stage: localised infection.
  2. Secondary stage: systemic - skin, lymph nodes etc.
  3. Tertiary stage: CV syphilis and neuro syphilis.
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93
Q

Describe yeast.

A

Single celled organism. Asexual reproduction.

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94
Q

Describe mould.

A

Multicellular organism. Reproduce by spore formation.

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95
Q

What are dimorphic fungi?

A

Fungi that can exist as both yeast and mould; they are yeast in tissues but mould in vitro.

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96
Q

Give an example of a dimorphic fungi.

A

Coccidioides immitis.

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97
Q

Why are severe fungal infections rare?

A

Fungi are unable to grow at 37°C and are often killed by the innate and adaptive immune response.

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98
Q

Name 3 common fungal infections.

A
  1. Nappy rash.
  2. Tinea pedis.
  3. Onychomycosis (fungal nail infection).
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99
Q

Name a drug that is good for treating onychomycosis.

A

Terbinafine - it reaches poorly perfused sites e.g. nails.

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100
Q

What is the fundamental principle behind antifungal treatments?

A

Selective toxicity!

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101
Q

What can antifungal treatments target?

A
  1. Fungal cells walls; they contain polysaccharides and chitin.
  2. Ergosterol containing plasma membrane.
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102
Q

Antifungal treatments: how does amphotericin work?

A

It targets ergosterol in the plasma membrane and causes pore formation, this leads to cell death.

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103
Q

Antifungal treatments: how do azoles work?

A

They affect the ergosterol synthetic pathway.

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104
Q

Give 4 disadvantages of azoles.

A
  1. High first pass metabolism, bioavailability = 45%.
  2. ADR’s, can cause hepatitis.
  3. Drug interactions due to CYP450.
  4. Resistance can develop e.g. in candida.
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105
Q

What is candida?

A

A yeast. It grows in warm, moist areas and has high levels of β-D-Glucan.

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106
Q

What test can be done to identify fungal antigens?

A

β-D-Glucan test.

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107
Q

What fungal infection can often be a presenting factor for HIV?

A

Pneumocystis pneumonia; opportunistic infection, can cause lung infection in immunocompromised people.

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108
Q

Why is pneumocystis pneumonia not commonly found in the lungs of healthy people?

A

It is opportunistic and so can cause disease in immunocompromised individuals.

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109
Q

Give an example of a mould.

A

Aspergillus fumigatus.
Aspergillus niger.

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110
Q

What are moulds composed of?

A

Branched filamentous filaments called hyphae.

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111
Q

Describe mycobacteria.

A
  • Aerobic.
  • Non-motile.
  • Non spore forming.
  • Bacilli.
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112
Q

Give an example of mycobacteria.

A

M.tuberculosis (TB).
M.leprae (leprosy).

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113
Q

Why is it hard to use the gram stain on mycobacteria?

A

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

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114
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).

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115
Q

How would you stain mycobacteria?

A

Using Ziehl-Neelsen stain for acid fast bacili.

116
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.
117
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.
118
Q

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

A
  1. Mouth.
  2. Skin.
  3. Vagina.
  4. Urethra.
  5. Large intestine.
119
Q

Give an advantage and a disadvantage of the slide coagulase test as opposed to the tube test.

A

Advantage: quicker and easier.
Disadvantage: less sensitive as it only detects bound coagulase and not free coagulase too.

120
Q

What colour do staphylococcus aureus colonies appear on blood agar?

A

Creamy/yellow.

121
Q

Which Lancefield groups are associated with tonsilitis and skin infection?

A

A , C and G.

122
Q

Which Lancefield groups are associated with neonatal sepsis and meningitis?

A

B.

123
Q

Which Lancefield groups are associated with UTI’s?

A

D.

124
Q

What is the oxidase test?

A

Detects the presence of cytochrome oxidase in bacteria. A positive test is indicated by the disk turning blue.

125
Q

Which group of streptococci can cause infective endocarditis?

A

Alpha haemolytic streptococci.

126
Q

How can you differentiate streptococci pneumoniae from other streptococci?

A

The optochin test can differentiate streptococci pneumoniae from other streptococci. Pneumococci are sensitive and so a clear area would be seen.

127
Q

Describe chocolate agar and explain why it might be used.

A
128
Q

What is the function of bile salts in MacConkey agar?

A

They inhibit gram positive bacteria growth.

129
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.

130
Q

What is Gonococcus agar used for?

A

It contains growth factors to promote the growth of Neisseria. It also contains antibiotics and antifungal agents to inhibit growth of other organisms.

131
Q

What is XLD agar used for?

A

It is a very selective growth medium used to isolate salmonella and shigella. Salmonella shows black dots.

132
Q

What is Sabouraud’s agar used for?

A

Used to culture fungi.

133
Q

Why do bacteria produce coagulase?

A

They use it as a defence mechanism by clotting the areas of plasma around them, thereby resisting phagocytosis.

134
Q

What are protozoa?

A

Single celled eukaryotic organisms.

135
Q

What genus of parasitic protozoa is responsible for causing malaria?

A

Plasmodia spp.

136
Q

How is malaria transmitted?

A

Via the bite of female mosquitos from dusk till dawn.

137
Q

Why are there different clinical manifestations of malaria?

A

The difference in clinical manifestation can be due to variation in the plasmodia life cycle. The plasmodia life cycle has stages in the human and the mosquito.

138
Q

What are the stages of the plasmodia life cycle in the human called?

A

Exo-erythrocytic and endo-erythrocytic stages.

139
Q

What happens in the stages of the plasmodia life cycle that occur inside the human?

A

Exo-erythrocytic: Hepatcoytes become infected by sporozoites, the cells mature and develop and are released as tropozites.
Endo-erythrocytic: tropozites invade RBC’s. Parasite numbers expand rapidly with a sustained cycling of the parasite population.

140
Q

What 2 species of the plasmodia genus lie dormant and cause late relapse of malaria?

A

P.ovale and p.vivax.

141
Q

What signs and symptoms might you see in someone who has been infected with malaria?

A

Fever, haemolysis, chills, sweats, headaches etc.

142
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!

143
Q

What are the clinical features of haemolysis?

A

Anaemia, jaundice (dark urine due to increased Hb).

144
Q

Malaria diagnosis: what can thick and thin films tell you?

A
  • Thick films: sensitive but low resolution, tell you if you have malaria.
  • Thin films: tell you species and parasite count.
145
Q

What genetic conditions can give immunity to malaria?

A

Someone with sickle cell anaemia or thalassaemias.

146
Q

Can immunity to malaria be acquired?

A

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

147
Q

Do viruses have a cell wall?

A

NO! Viruses have an outer protein coat that is sometimes surrounded by a lipid envelope but they do not have a cell wall.

148
Q

How do viruses attach to a host cell?

A

Viruses have proteins on their surface that interact with receptors on host cell membranes.

149
Q

What are the 6 stages of viral replication?

A
  1. Attachment.
  2. Cell entry.
  3. Interaction with host cell.
  4. Replication.
  5. Assembly.
  6. Release.
150
Q

What part of the virus will enter the host cell?

A

Only the viral core carrying the nucleic acids will enter the host cell cytoplasm. Sometimes proteins that act as enzymes may enter too.

151
Q

How do viruses interact with host cells?

A

Viruses use cell materials e.g. enzymes, amino acids and nucleotides, for their replication and they evade host defence mechanisms.

152
Q

Where in a cell does viral replication occur?

A

In the nucleus, cytoplasm or both.

153
Q

How can viruses be released from a cell?

A
  1. Bursting open; lysis of cell.
  2. ‘Leaking’ from the cell over a preiod of time; exocytosis
154
Q

What are the 5 ways by which viruses can cause disease?

A
  1. Damage by direct destruction: cell lysis.
  2. Damage by modification of cell structure.
  3. ‘Over-reactivity’ of the host as a response to infection: immuno-pathological damage.
  4. Damage via cell proliferation and immortalisation.
  5. Evasion of host defences.
155
Q

Give an example of a virus that causes damage by direct destruction of host cells.

A

Poliovirus or HIV.

156
Q

Give an example of a virus that causes damage by modification of cell structure.

A
  1. Physical modification: Rotaviruses, HIV.
  2. Functional modification: Rotaviruses, HIV.
157
Q

Give an example of a virus that causes damage by triggering host cell ‘over-reactivity’ as a response to infection.

A

Hepatitis B and C viruses, HIV.

158
Q

Give an example of a virus that causes damage via cell proliferation and immortalisation.

A

HPV’s.

159
Q

Give an example of a virus that everts host defences via virus persistence.

A

Herpesviruses, hep B and C viruses, measles virus.

160
Q

Give an example of a virus that everts host defences via virus variability.

A

Influenza type A, HIV, hep B and C viruses, rhinoviruses.

161
Q

Give an example of a virus that everts host defences via viral modulation of host defences.

A

Most viruses.

162
Q

What are the 5 ways in which viruses can evert host defences.

A
  1. Virus persistence or latency.
  2. Down regulation of interferons.
  3. Virus variability due to gene reassortment or mutation.
  4. Prevention of host cell apoptosis.
  5. Viral modulation of host defences.
163
Q

Pathogenesis of hepatitis B infection: how does hepatitis B cause damage by triggering host cell ‘over-reactivity’?

A

Hep B infection leads to an antibody and T cell response that destroys infected hepatocytes; this causes extensive liver damage.

164
Q

Pathogenesis of cervical carcinoma: how does HPV cause damage via cell proliferation and immortalisation?

A

HPV types 16 and 18 infect the genital tract; there is viral replication. HPV genome integrates into host cell chromosome. p53 and Rb are inhibited and there is excessive cell growth and proliferation leading to cervical carcinoma.

165
Q

Which HPV viral gene product controls viral gene expression?

A

E2.

166
Q

Which HPV viral gene products inhibit p53 and Rb?

A

E6 and E7.

167
Q

Give an example of a virus that prevents host cell apoptosis.

A

Herpesvirus, HIV.

168
Q

What are the 3 main groups of helminths?

A
  1. Nematodes (roundworms).
  2. Trematodes (flatworms).
  3. Cestodes (tapeworms).
169
Q

Helminth infection: What is the pre-patent period?

A

The interval between infection and the appearance of eggs in the stool.

170
Q

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

A

Eosinophils. Eosinophils are associated with parasitic infection and helminth’s are parasitic worms.

171
Q

How are intestinal nematodes (roundworms) often diagnosed?

A

Stool microscopy looking for eggs.

172
Q

How are intestinal nematodes spread?

A

Transmission is from human to human via eggs or larvae.

173
Q

Intestinal nematodes: what are the signs and symptoms of ascaris lumbricoides infection?

A
  • Loeffler’s syndrome: larval migration to lungs results in cough, fever and wheeze.
  • Often infection can be asymptomatic.
174
Q

Intestinal nematodes: what are the signs and symptoms of hook worm infection?

A

Local dermatitis at the site of entry. Iron deficiency anaemia.

175
Q

Intestinal nematodes: what are the signs and symptoms of threadworm infection?

A

Pruritus ani.

176
Q

Intestinal nematodes: how would you diagnose threadworm infection?

A

Apply sellotape to the perianal area.

177
Q

Intestinal nematodes: what are the signs and symptoms of strongyloides stercoralis infection?

A

Pruritus, pulmonary and gut symptoms, larva currens (skin rashes).

178
Q

Intestinal nematodes: why can the symptoms of strongyloides stercoralis persist for years?

A

Strongyloides stercoralis is associated with auto-infection and an immunocompromised state.

179
Q

Intestinal nematodes: what are the signs and symptoms of taenia saginatum infection?

A

Taenia saginatum is also known as beef tapeworm. Abdominal pain is a likely symptom.

180
Q

Intestinal nematodes: what are the signs and symptoms of taenia solium infection?

A

Taenia solium is also known as pork tapeworm. Skin, muscle and the brain can be affected, the patient may suffer from fits.

181
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.
182
Q

What enzyme copies HIV RNA into DNA?

A

Reverse transcriptase.

183
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.

184
Q

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

A

HIV belongs to the lentivirus genus. These viruses are characterised by having a long incubation period.

185
Q

What did HIV arise from?

A

SIV - originally from chimpanzees.

186
Q

What cells act as ‘host cells’ for HIV?

A

CD4+ cells. Macrophages and dendritic cells can also be invaded by HIV.

187
Q

What is the affect of HIV infection on CD4 count?

A

HIV leads to uncontrolled CD4 activation and apoptosis. CD4 numbers decrease over time.

188
Q

Which glycoproteins are on the surface of HIV?

A

GP41 and GP120.

189
Q

How does HIV attach onto a host cell?

A

GP160 binds to CD4 receptors and also CCR5 co-receptors.

190
Q

What part of HIV enters the host cell following attachment?

A

The viral caspid, enzymes and nucleic acids.

191
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.
192
Q

Name 4 enzymes involved in HIV replication.

A
  1. Reverse transcriptase.
  2. Integrase.
  3. RNA polymerase.
  4. Proteases.
193
Q

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

A

Integrase.

194
Q

What are the 10 main stages of HIV replication?

A
  1. Attachment.
  2. Cell entry.
  3. Uncoating.
  4. Reverse transcription.
  5. Genome integration.
  6. Transcription of viral DNA.
  7. Splicing of mRNA.
  8. Translation into proteins.
  9. Assembly.
  10. Budding.
195
Q

How many genes are encoded in the HIV genome?

A

9

196
Q

What does Pol encode?

A

Enzymes e.g. reverse transcriptase, integrase etc.

197
Q

Which gene encodes reverse transcriptase?

A

Pol.

198
Q

Why might macrophages also be infected by HIV?

A

Macrophages also have CD4 and CCR5 receptors.

199
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.

200
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.
201
Q

Name 4 ‘sanctuary sites’ for HIV.

A
  1. Genital tract.
  2. GI tract.
  3. CNS.
  4. Bone marrow.
202
Q

Define antibiotics.

A

Agents produced by micro-organisms that kill or inhibit the growth of other micro-organisms.

203
Q

Where on the bacteria would penicillin bind?

A

Bacterial cell wall.

204
Q

Define bacteriostatic.

A

Antibiotics that prevent bacterial growth by inhibiting DNA synthesis.

205
Q

Define bactericidal.

A

Antibiotics that kill bacteria by inhibiting cell wall synthesis.

206
Q

What is MIC?

A
207
Q

Does the lowest MIC mean the best antibiotic?

A

No. There are many other important factors that need to be considered e.g. the number of binding sites occupied and how long they’re being occupied for.

208
Q

What does a drug need to do to ensure it inhibits metabolic processes?

A
  1. Occupy an adequate number of binding sites.
    2.Occupy these binding sites for a sufficient period of time.
209
Q

What is concentration dependent killing?

A

Antibiotics that eradicate pathogenic bacteria by achieving high concentrations at the site of binding: Peak conc/MIC ratio.

210
Q

What is time dependent killing?

A

The time that serum concentrations remain above the MIC: t > MIC.

211
Q

Give an example of a class of antibiotics that uses concentration dependent killing mechanisms?

A

Aminoglycosides e.g. gentamicin.

212
Q

Give an example of a class of antibiotics that uses time dependent killing mechanisms?

A

Beta lactams e.g. penicillin.

213
Q

What are 4 mechanisms of antibiotic resistance?

A
  1. Change antibiotic target.
  2. Destroy antibiotic.
  3. Prevent antibiotic access.
  4. Remove antibiotic from bacteria.
214
Q

How can an antibiotic target change result in resistance?

A

Target site mutation can mean that the antibiotic can no longer attach to the bacteria. e.g. in MRSA.

215
Q

Give an example of how an antibiotic is destroyed.

A

The beta lactam ring of penicillin can be hydrolysed. The ring is essential for the antibiotic and without it it is destroyed.

216
Q

How can access to antibiotics be prevented?

A

Modification of membrane porin channel size, number and selectivity.

217
Q

How can antibiotics be removed from bacteria?

A

Antibiotics can be removed via efflux pumps.

218
Q

How does resistance develop?

A
  1. Intrinsic: natural resistance.
  2. Acquired:
    - Spontaneous mutation.
    - Horizontal gene transfer.
219
Q

How can spontaneous mutation lead to antibiotic resistance?

A
  • Change in AA sequence.
  • Change to cell structure.
  • Decrease affinity/activity of antibiotic.
  • New nucleotide base pair.
220
Q

Give 3 methods of horizontal gene transfer.

A
  1. Conjugation.
  2. Transduction.
  3. Transformation.
221
Q

What is a clinically important gram positive resistant bacteria?

A

MRSA - plasmid transfer resistance.

222
Q

What is a clinically important gram negative resistant bacteria?

A

ESBL (extended spectrum b lactamase) - mutation at active site.

223
Q

What are antibiotics used for?

A
  • Treatment.
  • Prophylaxis.
  • Prevention of post-surgical infection.
224
Q

What antibiotic might be used for the treatment of s.pneumoniae?

A

Amoxicillin.

225
Q

When might you use penicillin?

A

For treatment of skin and soft tissue infections, endocarditis.

226
Q

Give an advantage of penicillin.

A

It has a narrow spectrum and so there is a reduced chance of resistance.

227
Q

What antibiotic might be used for the treatment of bacterial pharyngitis: ‘strep throat’?

A

Phenoxymethylpenicillin.

228
Q

How can amoxicillin be given?

A

Orally or intra-venously.

229
Q

Amoxicillin can be given to people infected with which bacteria?

A

H.influenzae, enterococci, e.coli, shigella, streptococci etc.

230
Q

What antibiotic would you give to someone infected with staph. aureus (MSSA)?

A

Flucloxacillin.

231
Q

A person presents with cellulitis. What antibiotic might you give them?

A

Flucloxacillin - s.pyogenes and staph.aureus are often a cause of cellulitis.

232
Q

What types of bacteria do monobactams work against?

A

Gram negative bacilli.

233
Q

Why would you give someone monobactams?

A

If they have a penicillin allergy.

234
Q

What types of bacteria does vancomyocin work against?

A

Gram positive only!
Good for MRSA treatment.

235
Q

A person presents with a UTI. What antibiotic might you give them?

A

Trimethoprin.

236
Q

What are Carbapenemase producing enterobacteriaceae (CPEs)?

A

Gram negative bacteria that are resistant to broad spectrum antibiotics (carbapenems).

237
Q

What is carbapenemase?

A

An enzyme that hydrolyses carbapenems and confers antibiotic resistance.

238
Q

What virus can cause shingles?

A

Varicella Zoster Virus.

239
Q

Where might you see a shingles rash?

A

Shingles rash can appear on various dermatomes but it is usually seen at areas associated with tight clothing.

240
Q

What laboratory method can be used to detect viral pathogens?

A

PCR.

241
Q

What is PCR?

A

PCR amplifies DNA to generate millions of copies of a particular DNA sequence. The specimen is mixed with nucleotides, primers and DNA polymerase.

242
Q

Give some signs and symptoms of infective mononucleosis (glandular fever).

A
  1. Reddening, swelling and white patches on the tonsils. 2. Swollen lymph nodes.
  2. Spleen enlargement.
  3. Chills, fever.
  4. Cough.
  5. Sore throat.
  6. Fatigue, malaise, loss of appetite, headache.
243
Q

What is the management/treatment of glandular fever?

A

Supportive therapy and advise the patient to avoid contact sport for 6 weeks in order to avoid splenic rupture.

244
Q

What can qPCR detect?

A
  1. The presence or absence of DNA/RNA.
  2. It can quantify the level of virus in a tissue.
245
Q

What are the consequences of influenza A infection?

A

Increased risk of ARDS and secondary bacterial pneumonia. The patient is also highly infective to others.

246
Q

What are the markers for HIV in the blood?

A

Antigens, antibodies, HIV RNA.

247
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.

248
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.

249
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.

250
Q

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

A

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.

251
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.
252
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.
253
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.
254
Q

How can sexual transmission of HIV be reduced?

A

Condom use!
Voluntary medical male circumcision.

255
Q

Briefly explain why voluntary medical male circumcision can reduce sexual transmission of HIV.

A

Male circumcision leads to a change in mucosa. HIV is less able to penetrate due to an increase in keratinisation.

256
Q

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

A

Harm reduction measures e.g. needle exchange.

257
Q

How can HIV among young children be eliminated?

A

To reduce MTCT; prevent breast feeding where possible; give lifelong antiretroviral treatments to the mother.

258
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.
259
Q

How can awareness of HIV be increased?

A

TESTING! Ensure it is accurate, high quality and provides care, support and ultimately treatment.

260
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.
261
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.

262
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.

263
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.

264
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.

265
Q

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

A

CD4+ <200.

266
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.
267
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.
268
Q

What is HIV seroconversion?

A

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

269
Q

Name 3 respiratory diseases associated with HIV.

A
  1. Bacterial (pneumococcal) pneumonia.
  2. TB.
  3. Pneumocystis pneumonia (PCP).
270
Q

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

A

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

271
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.
272
Q

What does HAART stand for?

A

Highly active anti-retroviral treatment.

273
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.

274
Q

Where in the cell can HIV drugs target?

A
  1. Reverse transcriptase inhibitors.
  2. Protease inhibitors.
  3. Fusion inhibitors.
275
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.

276
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!

277
Q

Why is knowing your HIV status so important?

A

Knowing you HIV status will help to reduce MTCT and sexual transmission. It is good for public health and is cost effective.

278
Q

What is targeted testing for HIV?

A

Clinician initiated diagnostic testing triggered by clinical indications e.g. immunosuppression.

279
Q

What is targeted testing for HIV?

A

Clinician initiated diagnostic testing triggered by clinical indications e.g. immunosuppression.

280
Q

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

A

Patients may be unaware of their risk factors or may not want to admit to them. Asking about risk factors can lead to alienation and a decreased uptake of testing.

281
Q

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

A

CD4+ count < 350.

282
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.

283
Q

Chains of purple cocci are seen on a gram film. They show alpha haemolysis when grown on blood agar. They don’t grow near the optochin disc. What bacteria is likely to have caused this?

A

Streptococcus pneumonia.

284
Q

Name a gram negative bacillus that is a lactose fermenter.

A

E.coli.

285
Q

Name 4 diseases that haemophilus influenzae can cause.

A
  1. Meningitis.
  2. Otitis media.
  3. Pharyngitis.
  4. Exacerbations of COPD.
286
Q

What does the HIV envelop contain?

A

RNA, caspid, reverse transcriptase.

Phase 2a Medicine EK Mine (2 decks)

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