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EDEXCEL BIOLOGY > TOPIC 6: Infection > Flashcards

TOPIC 6: Infection Flashcards

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1
Q

What is a bacterial cell wall made of?

A
  • peptidoglycan

- polysaccharides held together by oligopeptides

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2
Q

What happens to Gram-positive bacteria under crystal violet?

A

turns blue

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3
Q

What happens to Gram-negative bacteria under crystal violet?

A

nothing, but absorbs pink from counter stain safranin

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4
Q

Describe the cell wall of Gram-positive bacteria

A
  • thick layer of peptidoglycan

- one cell membrane

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5
Q

Describe the cell wall of Gram-negative bacteria

A
  • thin layer of peptidoglycan

- cell membrane and outer cell membrane

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6
Q

How does Gram-staining work?

A
  • CV+ ions enter cell walls and Gram-negative outer membrane
  • I- ions bind to and fix CV+ ions
  • decolouriser disrupts Gram-negative outer membrane so CV+I- lost
  • counter stain adds pink colour to visualise cells
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7
Q

How can bacteria obtain foreign DNA? (3)

A
  • transformation: DNA taken up from environment
  • transduction: bacterial DNA transferred by phages
  • conjugation: DNA passed through cytoplasm in pills to another cell
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8
Q

How can bacteria cause illness?

A
  • produce endotoxins

- release exotoxins which inhibit neurotransmitters

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9
Q

Why are viruses not living?

A
  • non cellular

- can only reproduce using a host cell

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10
Q

Describe the structure of a virus

A
  • protein coat (capsid) made of repeating protein units

- RNA or DNA

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11
Q

Describe the bacteriophage life cycle

A
  • attach to host bacterium
  • phage DNA enters and destroys host DNA
  • viral genome synthesised
  • new phages assembled
  • phages released as cell lyses
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12
Q

What is the different between the lytic and lysogenic cycle?

A

lytic phages lyse immediately whereas lysogenic ones integrate their DNA and replicate with it until host conditions deteriorate

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13
Q

Describe the influenza virus life cycle

A
  • docking to host receptor
  • entry into host cytoplasm
  • synthesis of viral components
  • assembly of new viruses
  • budding from host cell
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14
Q

How does the retrovirus life cycle differ to the influenza life cycle?

A
  • RNA is transcribed into DNA

- RNA directly uses in protein synthesis

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15
Q

How do viruses cause illness? (3)

A
  • destruction of cell during lysis
  • hijack host cell’s protein synthesis to slow down metabolism
  • toxins
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16
Q

Differences between non specific and specific immune system

A
  • NS is non-antigen specific, specific is
  • NS has immediate maximum response, S has a time lag between exposure and response
  • NS makes no memory cells, S does
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17
Q

Examples of chemical barriers in the body (4)

A
  • saliva, tears, mucus, lysozyme
  • earwax
  • stomach acid
  • sebum on skin
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18
Q

Examples of physical barriers in the body (2)

A
  • ciliated cells

- keratin

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19
Q

Examples of biological barriers in the body

A
  • gut microbiome

- skin microbiome

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20
Q

What gives keratin its properties?

A
  • disulphide bridges: insolubility and strength

- fibrous protein

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21
Q

What is cornification?

A

skin surface cells stop metabolic reactions and fill with keratin so nucleus and organelles disappear

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22
Q

Where is lysozyme found?

A

tears, saliva, mucus, human milk

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23
Q

How does lysozyme protect against pathogens?

A

hydrolyses glycosidic bonds in peptidoglycan which causes lysis of bacterial cells due to osmotic shock

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24
Q

Where are complement proteins?

A

circulate in blood as inactive precursors and activated when needed

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25
Q

What is chemotaxis?

A

attraction of phagocytes to sites on infection

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26
Q

How do cytokines work?

A

initiates intracellular changes in gene expression and transcription factors

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27
Q

How does interferon work?

A

produced by virus infected cells which induces resistance in unaffected cells by turning on genes for antiviral protection

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28
Q

How does inflammation happen?

A
  • mast cells release histamines
  • vasodilation in arterioles increases blood supply
  • increased vascular permeability so plasma proteins reach site and cause swelling
  • more WBC’s arrive to clear bacteria
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29
Q

What are the two types of phagocytes?

A

neutrophils, monocytes + macrophages

30
Q

Describe neutrophils

A
  • multi lobed nucleus

- produce free radicals to break down bacterial DNA

31
Q

Describe macrophages + monocytes

A
  • bean shaped nucleus

- circulate in blood as monocytes and mature into macrophages when move into tissues

32
Q

Describe the stages of phagocytosis

A
  1. Chemotaxis
  2. Binds to bacterium & engulfs
  3. Phagosome and lysosome fuse to form phagolysosome
  4. Digestion of bacterium by lysosome
  5. Egestion of debris
  6. Antigen presentation on MHC
33
Q

Where are B cells found?

A

FOUND: blood, lymph nodes
MATURE: bone marrow

34
Q

What is the difference between BCR and antibodies?

A

antibodies are soluble version of BCR that are specific for the same antigens

35
Q

Describe the structure of an antibody

A
  • Y shaped
  • 2 light pp chains and 2 heavy pp chains held by disulphide bridges
  • variable + constant regions
  • specific binding site
36
Q

What is the role of an antibody?

A
  • opsonisation
  • agglutination
  • neutralisation
37
Q

What is a BCR?

A
  • membrane bound version of antibody
  • signal transduction functional area
  • recognises antigen and initiates response in B cell
38
Q

How are antigens presented?

A

MHC on cell membrane

39
Q

How are B cells activated?

A
  • antigen binding to B cell leads to antigen presentation
  • T helper binds to antigen on B cell and becomes activated
  • activated T cell releases cytokines
  • cytokines stimulate B cell to develop plasma and memory cells
40
Q

What happens in clonal expansion?

A

selection, activation, expansion by mitosis & maturation to plasma + memory cells

41
Q

What is the difference between primary and secondary immune response?

A
  • 1 has a time lag, 2 is immediate
  • 1 is long lasting, 2 short lasting
  • 1 produces fewer antibodies, 2 produces more
42
Q

Where are T cells found?

A

FOUND in blood and lymph nodes

MATURE in thymus gland

43
Q

How are T cells activated?

A
  • TCR recognises processed antigen bound to MHC

- antigen binding to TCR triggers activation of T cell

44
Q

What is the role of T helper cells?

A
  • B + T killer cell activation

- phagocyte enhancement by opsonisation of microbes

45
Q

How do T killer cells work?

A
  • T killer cell activated by helper
  • T killer binds to presented antigens on infected cell
  • T killer releases perforin
  • pores form in infected cells and water enters so cell lyses
46
Q

Explain how macrophages present antigens to T helper cells

A
  • macrophage binds to T helper
  • MHC presents antigen
  • antigen binds to CD4 receptor which is complementary
47
Q

How could mutations affect antigen presentation on T helper cells?

A
  • changes in antigen of bacteria
  • memory T cells can’t recognise new antigen so new primary response needed to activate T cells
  • no antigen presentation
48
Q

How does the skin flora protect humans from pathogenic bacteria?

A
  • outcompete pathogens for nutrients & space
  • secretion of chemicals with antimicrobial properties
  • affects pH
  • stimulation of skin immune system
49
Q

What does the TCR do?

A
  • recognises processed antigen bound to MHC

- antigen binding to TCR triggers activation of T cell

50
Q

Describe the first phase of TB (5)

A
  1. M. Tuberculosis reach alveoli and cause inflammatory response
  2. Macrophages recruited to infected area & ingest bacteria and contain infection by forming a granuloma
  3. Granuloma becomes encapsulated by collagen, forming a tubercle
  4. Inside is starved of O2, killing bacteria and macrophages
  5. Infection fought off and tissue heals
51
Q

How do Mycobacterium tuberculosis evade the immune system?

A
  • M tuberculosis taken up by phagocytosis cannot be destroyed due to their thick waxy cell wall
  • survive inside macrophages and lie dormant until reactivation
52
Q

When does TB become active?

A
  • first phase cannot be contained because of too many bacteria
  • reactivation with latent bacteria if immune system weakened
53
Q

When might the immune system be weakened? (3)

A
  • the old and young
  • malnourishment
  • HIV/AIDS
54
Q

What does active TB do to the lungs?

A

rapid multiplication of bacteria, destroying lung tissues (appearance of holes)

55
Q

How does fever happen? (4)

A
  1. Neutrophils and macrophages release interleukin 1 (IL-1)
  2. IL-1 causes hypothalamus to release prostaglandin
  3. Prostaglandin resets hypothalamic thermostat to higher body temp set point
  4. Nerve impulses activate body effectors leading to increase of body temperature
56
Q

What are the body effectors activated in fever? (4)

A
  • shivering
  • higher metabolic rate
  • inhibition of sweating
  • inhibition of vasodilation
57
Q

How can fever aid immune response? (3)

A
  • increasing phagocytosis
  • increasing number of T cells
  • decreasing reproduction rate of pathogens (TB can’t reproduce at 42C)
58
Q

How can a skin test diagnose TB?

A
  • injection of antigen (tuberculin)

- if antibodies are present, inflammation happens

59
Q

How might the skin tests provide false results?

A
  • positive if person had been vaccinated

- negative if disease is latent

60
Q

How can a blood test diagnose TB?

A

test for presence of TB antigen specific T cells

61
Q

How can analysis of bacteria diagnose TB?

A
  • sputum coughed up is tested for bacteria species
  • cell wall stain
  • DNA analysis
62
Q

What is the treatment for TB?

A

antibiotics for 6 months

63
Q

How can TB be controlled? (3)

A
  • improved living standards
  • screening by X-ray
  • BCG vaccine
64
Q

How is HIV transmitted? (4)

A
  • unprotected sex
  • sharing needles
  • mother to foetus
  • blood transfusions
65
Q

Describe the structure of the HIV virus (4)

A
  • retrovirus
  • 2 copies of ssRNA with 9 genes
  • lipid membrane envelope
  • viral enzymes: protease, integrase, reverse transcriptase
66
Q

Describe the HIV life cycle

A
  1. HIV gp120 binds to CD4 on Th cell
  2. HIV fuses with cell membrane and releases ssRNA into host
  3. Reverse transcriptase copies viral ssRNA to make dsDNA
  4. Integrase inserts viral DNA into host DNA in nucleus
  5. Transcription and translation of viral envelope gp 160
    - transcription of viral DNA to RNA for new virus
    - translation of RNA to make polyprotein
  6. gp160 passes through secretory pathway and cleaved to form gp120 and 41
  7. Viral envelope proteins incorporated into host cell membrane
  8. New immature HIV vision forms by budding
  9. Virus matures as HIV protease cleaves HIV proteins and enzymes from polyprotein
67
Q

What happens in the acute phase of HIV?

A
  • 2-6 weeks: loss of T helper cells, rapid replication of virus
  • 3-12 weeks: antibodies appear in blood
  • 8-12 weeks: infected Th cells recognised and destroyed by T killer cells
68
Q

What happens in the latent phase of the HIV?

A
  • provirus dormant in Th cell genome
  • virus reproduces slowly and immune system control infection
  • possible reactivation
69
Q

What happens if drugs aren’t given to HIV patients?

A

develops into AIDS

70
Q

What happens in the disease phase of HIV?

A
  • rapid decline of Th cells
  • increase in viral load
  • weight loss, fatigue
  • risk of opportunistic infections such as TB
71
Q

How are T helper cells killed in HIV?

A
  • non permissive infected Th killed as incomplete reverse transcripts trigger immune response
  • permissive infected Th killed by virus production
72
Q

What are the types of HIV drugs?

A
  • fusion inhibitors
  • gp120-CD4 inhibitors
  • protease inhibitors
  • reverse transcriptase inhibitors
  • integrase inhibitors

EDEXCEL BIOLOGY (14 decks)

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