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N Biology A Level > Topic 6 Microbiology And Pathogens + 2.2 Viruses > Flashcards

Topic 6 Microbiology And Pathogens + 2.2 Viruses Flashcards

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1
Q

What are microbial techniques?

A

Aseptic techniques
- Bunsen burner: create updraft, sterilise air around Bunsen burner
- use disinfectant to clean surfaces
- flame the inoculating loop - sterilise and kills all microorganisms
- autoclave (heat and high pressure to sterilise Petri dish)

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2
Q

Where to culture bacteria and how?

A

Petri dish containing agar (nutrients like glucose, nitrates)
Put Petri dish on heat proof mat next to Bunsen
Flame and cool inoculating loop, and neck of sample bottle
Dip into bacteria
Slightly open lid of Petri and zig-zag streak on agar
Use tape to seal lid (12, 6 o’clock)
Store in incubator

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3
Q

What temperature would the the incubator for bacteria culture be at and why isn’t it higher?

A

25 C , 3-5 days
Prevent overgrowth and mutation that could become harmful

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4
Q

Why do we want to culture bacteria?

A
  • test antibiotic resistance
  • compare growth rate of bacteria
  • identify bacteria then try to invent cure
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5
Q

Agar is a type of…

A

Culture medium that you grow bacteria on

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6
Q

What requirements are needed for microbial growth?

A
  • organic C source
  • N source
  • mineral salts K, Mg, Fe
  • vitamins
  • purine and pyrimidines
    All are needed
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7
Q

What are forms of culture media?

A
  • liquid culture (stir w magnet to evenly distribute mineral ions, circulation of Oxygen as well) (can batch or continuous culture)
  • solid culture (Agar)(no spillage, useful storage)
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8
Q

What are broad and narrow spectrum culture media?

A

Broad: can grow lots of generic/different bacteria containing general nutrients

Narrow: only specific bacteria can grow in it, designed specifically for particular microorganism. Inhibits growth of other microbes

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9
Q

How to make sure only specific bacteria grow on agar?

A

Use antibiotics

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10
Q

What makes antibiotics?

A

Bacteria to kill other species of bacteria to reduce competition

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11
Q

How do you know you’ve grown the specific species of bacteria you want?

A

Look at
- colour of colony
- shape/structure
- height
- texture
- colour
- form

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12
Q

What is a selective media?

A

Isolates bacteria
Can only grow gram positive/negative bacteria

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13
Q

What can grow on MacConkey Agar?

A

Gram -ve bacteria

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14
Q

How to measure population size of bacteria?

A
  1. serial dilution (so sample is less saturated)
  2. Then count (4 ways)
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15
Q

What are 4 ways of counting bacteria population size?

A
  • haemocytometer (direct count)
  • dilution plating (direct count)
  • dry mass
  • colorimeter
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16
Q

Define the total cell count of bacteria

A

Dead and alive bacteria cell population

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17
Q

Define the viable cell count of bacteria

A

Alive number of bacteria only

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18
Q

What can bacteria do?

A
  • agents of infection
  • invade and destroy host tissues
  • produce toxins
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19
Q

What produces exotoxins?

A

Staphylococcus

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20
Q

What produces endotoxins?

A

Salmonella

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21
Q

What invades host tissues?

A

Mycobacterium tuberculosis

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22
Q

What are endotoxins?

A

Released from dead/broken down bacteria
Are lipopolysaccharide in cell wall membrane
Released by gram negative bacteria only

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23
Q

What are exotoxins?

A

Released from living bacteria
Are proteins
Released by both gram positive and negative

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24
Q

Evaluate methods of controlling malaria

A

Ethical- consent and insecticides affect other organisms
Social- social change, vaccines need to become accepted
Economical-treatment, other better uses of money than malaria treatment

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25
Q

What is a pathogen?

A

Infects another organism by invading the host, causing harm to it

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26
Q

What is an example of a bacterial disease caused by host tissue invasion?

A

Tuberculosis
Caused by bacteria Mycobacterium tuberculosis

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27
Q

What do antibiotics target?

A
  • cell wall synthesis
  • nuclei acid synthesis
  • does NOT kill bacteria!!!
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28
Q

What are the 2 types of antibiotic resistance and describe

A

Primary resistance: natural resistance to narrow spectrum antibiotics
Secondary resistance: acquire resistance to antibiotics they are previously susceptible to

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29
Q

What’s the difference between lytic and latency?

A

Latency has incorporation of genetic material but not lytic
Lytic has symptoms, latency doesn’t
Lytic has protein synthesis

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30
Q

Describe the lytic cycle of a virus? (2 marks)

A
  • viral proteins made
  • virus/genetic material multiply and cell lyse
    (- using host cell organelles)
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31
Q

State what it is meant by the term latency. (3 marks)

A
  • virus nucleoid acid incorporated into host cell
  • virus is inactive
  • virus nucleus acid replicates when host cell divides
  • viral proteins made and assembled
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32
Q

What happens in the lytic cycle?

A
  1. Virus receptors attach to host cell antigens
  2. Inject genetic material (DNA or RNA)
  3. Viral proteins synthesised
  4. New viruses assemble
  5. Host cell lyses
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33
Q

What happens in the latency cycle?

A
  1. Virus receptors attach to host cell antigens
  2. Inject genetic material (DNA or RNA)
  3. Viral genome incorporated into host cell genome
  4. Viral genome replicates with Host cell genome
    (5. Join lytic cycle)
    Or remain, no symptoms shown
    - repressor gene stops rest of genome being read
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34
Q

What are the 4 types of capsid shapes?

A
  • helical
  • polyhedral
  • spherical
  • complex
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35
Q

What is a capsid?

A

Surrounds (protects) genetic material of virus

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36
Q

What virus has helical capsid?

A

Tobacco mosaic virus

37
Q

What virus has polyhedral capsid?

A

Adenovirus

38
Q

What virus has spherical capsid?

A

Influenza virus

39
Q

What virus has complex capsid?

A

Bacteriophage

40
Q

What virus is DNA based?

A

Lambda (λ)phage

41
Q

Which 2 viruses are RNA based?

A

Tobacco mosaic (not enveloped) (both helical capsids)
Ebola (*E**nveloped)

42
Q

What’s an RNA retrovirus?

A

HIV

43
Q

What are properties of Lambda (λ)phage virus?

A
  • host: bacteria
  • no lipid envelope
  • has complex protein capsid
  • viral DNA (double stranded)
  • protein synthesis needed to take place
44
Q

What are properties of Tobacco mosaic / all positive-sense RNA virus?

A
  • no envelope
  • helical capsid
  • single stranded genetic material
  • only translation at ribosomes
45
Q

What are properties of all negative ssRNA viruses?

A
  • host: lymphocytes
  • have lipid envelope
  • helical capsid
  • has antisense so transcribe first then translate at ribosomes (?check)
46
Q

What is ssRNA?

A

Single strand RNA

47
Q

What are properties of RNA retrovirus?

A
  • host: T helper lymphocytes
  • cone shaped capsid
  • contain enzyme called reverse transcriptase
  • lipid envelope
  • 2 copies of ssRNA
  • reverse transcription (RNA>DNA>RNA>DNA hence ‘retro’)
48
Q

Why are bacteria described as agents of infection?

A
  • they produce exotoxins
  • trigger immune responses
  • invade and destroy host tissues
49
Q

What are 2 types of antibiotic bacteria?

A
  • bacteriocidal
  • bacteriostatic
50
Q

What causes antibiotic resistance?

A
  • random genetic mutations (usually on plasmid). Since they have selective advantage they reproduce and pass on allele
  • competitive bacteria
51
Q

What causes antigen variability?

A

Random mutations on base of DNA

52
Q

What impact does antigen variability have on the incidence of diseases?

A

Antigens no longer complementary to receptors, so can catch disease more than once.
Vaccinations less likely to work

53
Q

Replicating DNA vs protein synthesis?

A

DNA Rep / PS
make DNA / proteins
2 identical sets of DNA / mRNA strip
DNA polymerase / RNA polymerase

54
Q

Why does it take time for symptoms of virus to show?

A

Take time for
- attaching complementary antigens to receptors
- viral genome forming
- (transcription and) translation
- takes time to lyse and exocytose

55
Q

Compare and contrast the structures between bacteria and virus

A
  • bacteria is living cell / virus is not
  • no antigens / yes
  • double strand bacterial DNA / can be RNA or DNA (single or double)
  • has flagellum / no
  • has plasmid (circular dna) / no, only linear
  • peptidoglycan cell wall / doesn’t, some have lipid envelope
56
Q

Why do antibiotics not work on viruses?

A

They don’t have Peptidoglycan cell wall to break down so cannot destroy virus

57
Q

What do antiviral drugs to?

A
  • cannot cure virus diseases but can delay symptoms
  • by inhibiting the ways how viruses replicate (via receptors, assembly, or stop new viruses budding)
58
Q

Things to do to prevent spread of a virus:

A
  • education (esp burial of corpses)
  • sterilisation of medical facilities
  • clear public spaces
  • clean water and sewage works
  • isolate people who are infected
59
Q

Ethical implications of using untested drugs (pros and cons)

A

Pros
- disease may have high mortality rate
- new drug is unlikely to affect other people
- it can help develop the drug for other patients
Cons
- unknown side effects
- patients may not have informed consent
- if there is limited supply, who decides who gets treated?

60
Q

How to continuously extend the stationary phase of bacterial growth?

A

When death rate = growth rate
- keep adding nutrients SUCH AS sucrose, nitrates, water, oxygen to keep up with growth

61
Q

What are bacteriostatic antibiotics? + example

A
  • prevents reproduction in DNA replication
  • by attaching to ribosomes
  • tetracycline
62
Q

What are bacteriocidal antibiotics? + example

A

Kills bacteria
Penicillin

63
Q

What are broad and narrow spectrum antibiotics? + examples

A

Broad: targets a range of bacteria (tetracycline)
Narrow: target limited range (penicillin)

64
Q

How does retrovirus replicate?

A
  • bind complementary receptors to antigens
  • viral RNA enters host cell (cannot be used as mRNA)
  • viral RNA translate into viral DNA by reverse transcriptase in cytoplasm
  • viral DNA incorporated into host dna
  • new viral particles are assembled
  • leave host cell via exocytosis
  • repeat
65
Q

What are 3 things antibiotics could target?

A

Synthesis of
- cell wall
- nucleic acid
- proteins

66
Q

How does penicillin kill bacteria?

A
  • targets gram+ bacteria
  • act as inhibitor
  • stop cross links between thick Peptidoglycan cell walls synthesis
  • weaken cell wall > bacteria cannot lyse as cannot respire > die
67
Q

How does tetracycline destroy bacteria?

A
  • stop protein synthesis
  • by stopping tRNA from binding on ribosomes
  • stop translation
    Hence inhibit growth
68
Q

How are antibiotics formed?

A
  • random mutation
  • other competitive bacteria
69
Q

What is primary antibiotic resistance?

A

Natural resistance to narrow-spectrum antibiotics

70
Q

What is secondary antibiotics resistance?

A

Bacteria acquire resistance to antibiotics they were previously susceptible to.

71
Q

What are causes of secondary antibiotic resistance?

A
  • decrease in uptake b increase in expulsion
  • production of enzymes to modify antibiotic
  • development of pathway to bypass effects
    DOESNT MAKE SENSE
72
Q

How often and how do bacteria divide?

A

Via binary fission every 20 mins

73
Q

How and how often does secondary antibiotic mutation occur?

A

Single gene mutation
1 in every 10^6 pairs

74
Q

How is antibiotic resistance bacteria controlled?

A
  • sub-clinical concentrations create selection pressures for resistance
  • UK & EU guidelines to use antibiotics
  • measures to reduce HAIs
75
Q

How to prevent the spread of antibiotic resistance?

A
  • guidelines to finish course of treatment
  • educating doctors when to prescribe, keep everything sterilised, don’t use for viral infections
  • keep prescriptions range small so there’d be backup options if it doesn’t work
76
Q

Why shouldn’t we take antibiotics too much?

A
  • only short term fix
  • can kill good bacteria like ones in gut and worsen health!
  • don’t take unless you need to
77
Q

What is another saying for capsid?

A

Protein coat
All viruses have it

78
Q

Explain why there is a delay before number of lysed cells start to increase. (3 marks)

A
  • virus **attaches*b to host cell
  • protein synthesis, synthesis of dna
  • virus start to assemble
79
Q

Give a structural difference between gram +ve and -ve bacteria

A

Gram +ve has thicker Peptidoglycan cell wall and thinner lipid cell wall
(Or reverse)

80
Q

Give 2 differences between endotoxins and exotoxins

A

Endo / exo
Lipid / protein
Released from dead bacteria / living
Released from gram -ve only / both +ve and -ve

81
Q

What are properties of Salmonella?

A

salmoNella
- thiN Peptidoglycan cell wall
- eNdotoxin

82
Q

Why is reducing prescription helpful to reduce antibiotic resistance?

A
  • ensuring prescribed only for illnesses caused by bacteria not viruses
  • as antibiotics act as selection pressure for resistant bacteria
83
Q

How do bacteriocidal antibiotics work?

A
  • inhibits new crosslinks formed in Peptidoglycan cell walls of bacteria
  • causing cell lyse from osmotic pressure
84
Q

Why are antibiotics ineffective against viruses? (2 marks)

A
  • viruses aren’t living
  • no cell wall
85
Q

What is malaria caused by?

A

Plasmodium

86
Q

What is stem rust fungus caused by?

A

Puccinia

87
Q

What shape do antibodies have?

A

Y shape, always

88
Q

Describe the events that take place resulting in T helper cell activation, following the formation of psuedopodia by the macrophages. (3 marks)

A
  1. Bacteria engulfed AND digested
  2. Antigen attaches to MHC antigen
  3. Macrophage becomes an antigen presenting cell
  4. CD4 receptor of T helper cells bind to antigen / macrophage

N Biology A Level (18 decks)

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