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Biology - Module 4 > Chapter 12 - Communicable Diseases > Flashcards

Chapter 12 - Communicable Diseases Flashcards

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1
Q

Define disease

A

an illness or disorder of the body or mind that leads to poor health

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2
Q

What are communicable diseases caused by

A

Pathogens

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3
Q

4 types of pathogens

A

Bacteria
Virus
Fungus
Protoctists

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4
Q

What type of cells are bacteria

A

Unicellular prokaryotic

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5
Q

What are bacterial cell walls made of

A

Peptidoglycan

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6
Q

Size of bacteria

A

0.2 – 2 micrometres

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7
Q

How do bacteria move

A

Flagella

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8
Q

How do bacteria reproduce

A

Asexually = binary fission

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9
Q

Can bacteria exchange DNA

A

Yes

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10
Q

How can bacteria exchange DNA

A

through conjunction = two cells temporarily fuse + transfer DNA (beneficial traits)

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11
Q

How do bacteria cause disease

A

produce toxins ( metabolic waste products) + cause symptoms by cell damage

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12
Q

What type of cell damage do bacteria do

A
  • damage cell membranes / enzymes / genetic material
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13
Q

Do bacteria always cause disease

A

No - can remain within body cavities or spaces

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14
Q

Draw a diagram of a bacteria

A
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15
Q

Structure of a virus

A
  • No cellular structure
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16
Q

What makes viruses controversial

A

Are they living or not = No cellular structure + can’t produce ATP without living cells

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17
Q

How do viruses infect a host

A
  • Attach to receptors on surface of host cell + penetrate its genetic material via endocytosis
  • Virus uses host cells machinery to replicate DNA
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18
Q

Two ways virus cause disease / replicate

A
  • Lytic / lysogenic cycle
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19
Q

Why are viruses likely to mutate

A
  • RNA = more likely to mutate = as only one strand
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20
Q

Structure of a virus

A
  • Nucleic aid core + capsid = DNA/RNA enclosed in protein coat
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21
Q

Draw the structure of a virus

A
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22
Q

How do viruses replicate their DNA / RNA

A

reverse transcription

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23
Q

What is reverse transcription

A
  • single stranded RNA instead of DNA = reverse transcriptase enzymes use RNA as a template to make single stranded DNA
  • DNA polymerase enzymes makes double stranded DNA
  • Attached to the host DNA
  • Host cell now able to make new viruses which travel to the host membrane to be released
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24
Q

What is a bacteriophage

A

virus that attacks bacteria

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25
Q

What is the lytic cycle

A

involves the reproduction of viruses using a host cell to manufacture more viruses = then burst out of the cell.

  • With lytic phages, bacterial cells are broken open (lysed) and destroyed after immediate replication of the virion. As soon as the cell is destroyed, the virus can find new hosts to infect
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26
Q

What is the lysogenic cycle

A
  • viral genome will integrate with host DNA and replicate along with it fairly harmlessly = may even become established as a plasmid.
  • virus remains dormant until host conditions deteriorate = e.g depletion of nutrients = at some point switches from lysogenic to lytic
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27
Q

Is the lysogenic cycle itself dangerous

A

No - dormant

Only dangerous when switches to lytic cycle + bursts

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28
Q

What type of cells are fungus

A
  • Multicellular or unicellular saprophytes

EUKARYOTIC

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29
Q

Cell walls of fungus

A

Chitnin

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30
Q

Structure of fungus

A
  • Filamentous body = mycelium / hyphae
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31
Q

How do fungus reproduce

A

sexually + asexually = gametes + spores

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32
Q

Draw structure of a fungus

A
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33
Q

What type of cells are protoctists

A
  • Eukaryotic – unicellular or multicellular
  • Heterotrophic / autotrophic
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34
Q

How do protoctists reproduce

A
  • Asexual or sexual reproduction
  • Sexual = budding in yeast
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35
Q

Draw structure of protoctists

A
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36
Q

How to calculate number of cells after dividing for a set amount of time

A

Number of original X 2^number of cycles

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37
Q

What is TB caused by

A

Bacteria

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38
Q

Organisms affected by TB

A

Humans / cows / pigs / badgers / deer

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39
Q

Transmission of TB

A

Direct – airborne droplets

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40
Q

How does TB manifest

A

Damages + destroys lung tissue

Supresses immune system

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41
Q

How is TB treated

A

Antibiotics

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42
Q

What causes bacterial meningitis

A

Bacteria

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43
Q

Who is effected by bacterial meningitis

A

Humans

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44
Q

Transmission of bacterial meningitis

A

Direct – airborne droplets

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45
Q

What is bacterial meningitis

A

Infection of the meninges of the brain

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46
Q

What is the meninges

A

protective membrane on brains surface

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47
Q

How does bacterial meningitis cause death

A

nfection can spread to rest of body = causing septicaemia = blood poisoning = leads rapid death

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48
Q

What causes ring rot

A

Bacteria

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49
Q

Organisms effected by ring rot

A

Potato

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50
Q

Transmission of ring rot

A

Direct – contact with other infected tubers

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51
Q

Effects of ring rot

A

Damages leaves / tubers / fruit

Prevent soil use for at least 2 years

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52
Q

What is AIDS / HIV caused by

A

Virus

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53
Q

Organisms effected by AIDS / HIV

A

Humans + non-human primates

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54
Q

Transmission of HIV

A

Direct – transfer via bodily fluids
Sharing needles / sex / mothers to babies in pregnancy / breastfeeding

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55
Q

How does HIV work

A

Targets T helper cells in the immune system = gradually destroys the immune system = more vulnerable to other infections = TB + flu

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56
Q

What type of virus is HIV

A

retrovirus with RNA as genetic material

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57
Q

How is HIV treated

A

Anti-retroviral drugs

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58
Q

What causes influenza

A

Virus

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59
Q

Organisms effected by influenza

A

Mammals

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60
Q

Transmission of influenza

A

Direct – airborne droplets

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61
Q

How does influenza work

A

Viral infection of the ciliated epithelial cells in gas exchange system = kills cells = leaving airways open to secondary infections

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62
Q

What causes tobacco mosaic virus

A

Virus

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63
Q

Organisms effected by TMV

A

Tobacco + 150 other species

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64
Q

Transmission of TMV

A

Direct – contact with leaves of infected plants
Indirect – vectors - aphids

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65
Q

Effects of TMV

A

Damages leaves / flowers / frui
Stunts growth
Reduces yield

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66
Q

What causes malaria

A

Protoctist

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67
Q

Organisms effected by malaria

A

Humans

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68
Q

Transmission of malaria

A

Indirect – female mosquito

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69
Q

How does malaria spread

A

Parasite = has 2 hosts = mosquitos + humans = reproduce inside female mosquitos
Female needs to take 2 blood meals before lays eggs = where transmission occurs
Invades red blood cells / liver / brain

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70
Q

What causes Potato / tomato blight

A

Protoctist

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71
Q

Organisms effected by Potato / tomato blight

A

Potato / tomato

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72
Q

Transmission of Potato / tomato blight

A

Direct – spread via spores = wind

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73
Q

Effected of Potato / tomato blight

A

Destroys leaves / tubes / fruits
Penetrate host cell

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74
Q

What causes black Sigatoka

A

Fungus

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75
Q

Organisms effected by black Sigatoka

A

Bananas

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76
Q

Transmission of black Sigatoka

A

Direct – dispersion of spores

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77
Q

How does black Sigatoka work

A

Attacks + destroys leaves
Hyphae penetrate + digest cell = turning leaves black

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78
Q

What causes ring worm

A

Fungus

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79
Q

Organisms effected by ring worm

A

Mammals

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80
Q

Transmission of ring worm

A

Direct – contact with infected organisms

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81
Q

What causes athletes foot

A

Fungus

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82
Q

Organisms effected by athletes foot

A

Humans

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83
Q

Transmission of athletes foot

A

Direct – contact with items touched by infected individuals = warm / moist environments

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84
Q

What must be true in order for pathogens to survive

A

must successfully transfer from host to host

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85
Q

Define disease transmission

A

defined as the transfer of pathogens from an infected host to an uninfected host

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86
Q

Direct transmission

A

from one host to another host

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87
Q

Indirect transmission

A

second organism (vector) that is unaffected by the pathogen transfers it to a new host

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88
Q

Examples of direct transmission

A

• Physical contact
• Inoculation
• Ingestion
• Close proximity
• Spores

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89
Q

Ingestion

A

contaminated food + drink / pathogens from hand to mouth

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90
Q

Inoculation

A

break in skin/animal bite/puncture wound

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91
Q

What are spores

A

small reproductive structures

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92
Q

How do sores spread

A

via wind or water

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93
Q

How are spores produces

A

• Depending on the organism, spores can be produced via mitosis or meiosis so they can be haploid or diploid

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94
Q

What type of virus is HIV

A

Retrovirus

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95
Q

What are retroviruses

A

a group of viruses that has the ability to make DNA from RNA because they have the enzyme reverse transcriptase

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96
Q

How is HIV transmitted

A

Exchange of bodily fluids

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97
Q

When does TB spread more quickly

A

Overcrowded conditions

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98
Q

How can TB be Transmitter other than airborne droplets

A

form of TB = occurs in cattle but is spread to humans through contaminated meat + unpasteurised milk

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99
Q

Examples of indirect transmission

A

Fomites

Droplet infections

Vectors

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100
Q

What are fomites

A

inanimate objects = bedding / socks / cosmetics

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101
Q

Why are insects ideal vectors

A

reproduce in large numbers which increases the likelihood of pathogen transmission

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102
Q

Example of a disease transmitted via a vector

A

Malaria

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103
Q

How is malaria Transmitted to humans

A

o Female Anopheles mosquitoes feed on human blood to obtain the protein they need to develop their eggs

o If the person they bite is infected with Plasmodium, the mosquito will take up some of the pathogen with the blood meal

o When feeding on the next human, Plasmodium pass from the mosquito to the new human’s blood

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104
Q

Factors that effect disease transmission = overall

A

presence of the pathogens
= If the pathogen is not present in the population then it cannot spread

o The presence of susceptible individuals
= A high number of immune or resistant individuals in a population will reduce the likelihood of transmission

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105
Q

Factors that effect direct disease transmission

A

• Overcrowding
• Lack of ventilation

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106
Q

Factors that effect indirect disease transmission

A

• Population of vectors = influenced by weather + climate

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107
Q

Explain the distribution of malaria

A

• Caused by insect vector (female Anopheles mosquitoes)
• mosquitoes favour habitats that have high rainfall, high temperatures and high humidity
• Therefore = tropics + sub tropics = AFRICA
• Social factor = migration due to war
• migration happens due to war the parasite can be transferred from areas that have the infection to new region

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108
Q

What is an endemic

A

a disease that is always present in a population (even if very low numbers)

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109
Q

What is an epidemic

A

a large increase in the number of cases in a population (an outbreak)

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110
Q

What is a pandemic

A

an epidemic occurs on a large scale and crosses international boundaries.

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111
Q

Symptoms of TMV

A

discolouration in leaves

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112
Q

How does TMV cause stunted growth

A

• Less chlorophyll = less photosynthesis = less growth

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113
Q

How to stop spread of TMV

A

Burn plant

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114
Q

What type of pathogen causes barley powdery mildew

A

Fungus

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115
Q

What causes crown gall disease

A

Bacteria

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116
Q

What are passive defence mechanisms

A

mechanisms are always present

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117
Q

What’s re active defence mechanisms

A

activated when pathogens invade

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118
Q

Plant physical passive defences (6)

A

• cellulose cell walls

• lignin thickening of cell walls – lignin is water proof + indigestible

• waxy cuticle – prevent water collecting on cell surface = absence of water is passice defence

• stomatal closure – guard cells close when pathogens detected

• bark

• casparian strip = some fungi can invade all the way to endodermis but through this strip

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119
Q

Physical active plant defences

A

Reinforced cell walls

Necrosis

Cal lose deposited

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120
Q

How does depositing callose act as a physical active plant defence

A

strengthens cell wall + blocks plasmodesmata + blocks sieve plates = limiting spread

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121
Q

How does reinforcing cell walls act as a physical active plant defence

A

invasion of pathogens stimulates the release of compounds callose and lignin = molecules are deposited between the cell surface membrane and the cell wall

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122
Q

What is necrosis and how is it an active physical plant defence

A

deliberate cell suicide = few cells sacrificed = limits the pathogens access to water + nutrients

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123
Q

Chemical passive defences in ola ts

A

• Toxic compounds

• Sticky resin found in the bark

• Compounds that encourage the growth of competing microorganisms

• Enzyme inhibitors

• Receptor molecules

124
Q

Example of toxic compounds = chemical passive plant defences

A

Catechol

125
Q

How does sticky resin act as a chemical passive plant defence

A

traps the pathogens so they can’t spread

126
Q

Example of enzyme inhibitors in plants

A

Tannins

127
Q

Chemical active plant defences

A

• Antibiotic / antifungals = tannins in back inhibit attack by insects = bind to salivary proteins + digestive enzymes to deactivate them = insects to ingest large amount of tannins = no growth / die

128
Q

Cell signalling in plants

A

• Pathogens possess cellulase enzymes that digest the cellulose in plant cell walls

• The molecules produced from this breakdown of cellulose act as signals to cell surface receptors

• By stimulating these receptors they cause the release of defence chemicals

  • phytoalexins / Salicylic acid / ethylene
129
Q

What do Phytoalexins do

A

o Disrupting pathogen metabolism
o Delaying pathogen reproduction
o Disrupting bacterial cell surface membranes
o Stimulating the release of chitinases (enzymes that break down the chitin cell walls in fungi)

130
Q

What does salicylic acid do

A

migrates through the plant to uninfected areas. Once there it activates defence mechanisms that protect the plant against pathogens for a period of time

o This long-term protection is called systemic acquired resistance

131
Q

What does ethylene do

A

ethylene vaporises, stimulating other leaves on the same plant to react (as well as other plants)

132
Q

Four types of non specific immune responses

A

Physical

Cellular

Chemical

Commensal

133
Q

physical non specific immune responses

A

body tissues act as barriers, preventing the entry of pathogens
o E.g. skin, mucous membrane of the alimentary canal

134
Q

Cellular non specific immune responses

A

cells detect and signal the presence of pathogens.

135
Q

Chemical non specific immune responses

A

secreted substances generate an inhospitable environment for the growth of pathogens. trap pathogens, cause them to burst / prevent them from entering cells and reproducing

136
Q

Commensal organisms non specific immune responses

A

harmless bacteria and fungi present on and in the body compete with pathogens for nutrients

137
Q

How does the skin act as first line of defence

A

Physical barrier

Skin flora

Secretes antiseptics

Colleges

Sweatv

138
Q

How does skin act as a physical barrier

A

outermost layer = stratum corneum = made of dead skin cells tightly packed together = protective barrier

139
Q

How does skin flora act as defence

A

harmless bacteria prevent harmful bacteria colonising

140
Q

What antiseptics does the skin secrete

A

sebum (produced by sebaceous glands / contains fatty acids that have antimicrobial properties)

141
Q

How is sweat a first line of defence

A

dermcidin = antimicrobial properties that help prevent growth of bacteria

142
Q

Where is sebum secreted from

A

sebaceous glands

143
Q

Human first life of defence

A

Skin

Mucous membranes

Expulsion reflexes

Stomach

Eyes

144
Q

What are mucous membranes

A

• Moist tissue that line the respiratory + digestive tract = bronchi / nose / trachea
• Ciliated epithelial + goblet cells

145
Q

How are mucous membranes a first line of defence

A

• Mucus = secretes thick / sticky fluid = contains antibodies = trap + destroy pathogens

• Helps lubricate + protect tissue from damage

• Cilia = beat in coordinated manner – waft away mucus + pathogens

146
Q

Why is mucous sticky

A

made up of glycoproteins with long carbohydrate chains

147
Q

Examples of expulsive reflexes

A

• Coughing / sneezing/ vomiting

148
Q

How are expulsive reflexes first line of defence

A

• Involuntary responses designed to expel foreign substances / pathogens from body

149
Q

How is stomach a first line of defence

A

• HCL = acidic = kills pathogens

• Lining = produces mucus

• Peristalsis = muscles of stomach + intestines contract / relax to move food + waste materials through digestive system

150
Q

How is the gut a first line of defence

A

• Gut microbiota = beneficial / harmless microorganisms prevent growth of harmful pathogens by competing with them for resources = inhibiting their growth

151
Q

Parts of the eyes that are part of the first line of defence

A

Tears

Eyelashes

Conjunctiva

Cornea

152
Q

How are tears first line of defence

A

lysozymes = break down cell wall of bacteria

153
Q

How are eyelashes first line of defence

A

traps larger particles = dust / dirt

154
Q

How are conjunctiva first line of defence

A

thin layer of tissue that covers front of eye + inside eyelid = produces mucus

155
Q

How are cornea first line of defence

A

covered by layer of epithelial cells = physical barrier

156
Q

Second line of defence

A

o Blood clotting
o Inflammation
o Wound repair
o Phagocytosis

157
Q

Describe the clotting cascade

A

• Damage to skin = exposes collagen = platelets stick = thromboplastin (+ serotonin) released

• Thromboplastin combines with Ca 2+ = calcium deficiency = clotting cascade slows down

• This triggers conversion of prothrombin into thrombin

• Triggers fibrinogen into fibrin

  • fibrin forms a network of fibres that traps platelets + blood cells
158
Q

Ion needed in blood clotting

A

Calcium 2+ ion

159
Q

What is released / happens when skin is damages + there is exposed collagen

A
  • thromboplastin
  • seratonin
  • activates mast cells
160
Q

What does serotonin do

A

• causes smooth muscle walls to contract = vasoconstriction = restricts blood flow

161
Q

When do activated mast cells carry out their effects

A

• Later than serotonin effects

162
Q

What do mast cells release

A

Histamine + cytokines

163
Q

What does Histamine do

A

o Vasodilation increases blood flow through capillaries

o “Leaky” capillaries allow fluid to enter the tissues and creating swelling

o A portion of the plasma proteins leave the blood

o Phagocytes leave the blood and enter the tissue to engulf foreign particles

164
Q

What do cytokines do

A

Attract phagocytes

165
Q

Put all the second line of defence in one diagram

A
166
Q

What is formed as a result of blood clotting

A

A scab

167
Q

What happens underneath this scab

A

stem cells that divide by mitosis to heal the wound

168
Q

Describe how would healing / repair happens

A

o Blood clots = to make barrier to keep pathogens out

o Epidermal cells grow beneath cut = seal barrier more effectively

o New blood vessels form

o Collagen is produced / collagen fibres are deposited

o Granulation tissue forms to fill the wound

o Stem cells move over the new tissue and divide to produce epithelial cells

o Contractile cells cause wound contraction

o Unwanted cells die

169
Q

Three types of phagocytes

A

• Neutrophils = Macrophages = Dendritic cells

170
Q

Features of neutrophils

A

• Released in large numbers
• Short-lived cells
• Lobed nucleus

171
Q

Purpose of lobed nucleus in neutrophil

A

Allow for increased flexibility = get through capillaries

172
Q

How to identify neutrophils in blood smears

A

Lobed nucleus

173
Q

Features or macrophages

A

• Larger than neutrophils

• Long-lived

• rather than remaining in the blood, they move into organs including the lungs, liver, spleen, kidney and lymph nodes

174
Q

Where are macrophages produced

A

Bone marrow

175
Q

How do macrophages travel in the blood

A

As monocytes

176
Q

Describe phagocytosis = neutrophils

A

• mast cells secret cytokines
• attract phagocyte + then detects pathogen
• pathogen = antigens = normally glycolipids on surface
• phagocyte grows cytoplasmic extensions + changes shape
• phagocyte engulfs pathogen = via endocytosis
• pathogen = may be coated in opsonin
• phagosome formed
• phagosome fuses with lysosome = phagolysosome
• upon fusion = releases lysozymes = break down pathogen
• absorbs digestive products e.g proteins

177
Q

What happens after neutrophils absorb digestive products

A

GO AND DIGEST SOMETHING ELSE = SHORT-LIVED DUE TO TOXIC WASTE

178
Q

What happens in terms of phagocytosis if a macrophage

A

After absorb digestive products…
• Combines antigen with glycoproteins

• display the antigens of the pathogens on their surface = through a structure called the major histocompatibility complex

• displayed antigens (the cell is now called an antigen-presenting cell) can then be recognised by lymphocytes = T-cells

179
Q

What are dendritic cels

A

• large phagocytic cells with lengthy extensions

180
Q

Features of dendritic cells

A

large surface area to interact with pathogens + lymphocytes

181
Q

What do dendritic cells do

A

• Once they have ingested foreign material they transport it to the lymph nodes

182
Q

What is the role of antigen presenting cells

A

• T-lymphocytes produce an immune response when they are exposed to a specific antigen

• T cells will only bind to an antigen if it is present on the surface of an antigen-presenting cell

• Once the surface receptor of the T cell binds to the specific complementary antigen it becomes sensitised and starts dividing to produce a clone of cells

183
Q

Where are T lymphocytes made

A

Bone marrow

184
Q

Where do T lymphocytes mature

A

Thymus gland

185
Q

What type of immunity is carried out by T lymphocytes

A

Cell - mediated immunity

186
Q

What does T lymphocytes respond to (foreign material)

A

Foreign material INSIDE body cells

187
Q

What do T lymphocytes respond to (type of cell)

A

Own cells = altered by virus / cancer / transplanted tissue

188
Q

Where are B lymphocytes made

A

Bone marrow

189
Q

Where do B lymphocytes mature

A

Bone marrow

190
Q

Type of immunity carried out by B lymphocytes

A

humoral immunity

191
Q

What do B lymphocytes respond to (foreign material)

A

Foreign material OUTSIDE cell

192
Q

What do B lymphocytes respond to (type of cell)

A

Bacteria / virus

193
Q

Which type of cell makes antibodies

A

B lymphocytes

194
Q

What are T and B lymphocytes part of

A

Third line of defence

195
Q

Features of the third line of defence

A
  • Specific + adaptive + slower
196
Q

What are lymphocytes

A

type of white blood cell

197
Q

How to distinguish between lymphocytes and phagocytes

A

• Smaller than phagocytes

• have a large nucleus that fills most of the cell

198
Q

Process of maturation = T

A

o T gain specific cell surface receptors = T cell receptors (TCRs)

o A small number of T cells have the same TCRs = a clone

o T cells within each clone differentiate into different types of T cell: T helper cells, T killer cells and T regulator cells after binding to antigen

199
Q

Shape of T cell receptors

A

similar structure to antibodies and are each specific to one antigen

200
Q

How do T cells differentiate into helper / killer / suppressor / memory cells

A

T cell binds to antigen

201
Q

How are T helper cells activated

A
  • T cell binds to antigen on antigen presenting cell e.g cancerous cells
  • clonal selections
  • clonal expansion
202
Q

How does clonal selection work in T helper cells

A

o T helper cells with receptors complementary to the specific pathogenic antigen bind to the APC

o The APC secretes molecules of the cytokine interleukin 1 (IL-1)

IL-1 stimulates the activation of selected T helper cells

203
Q

How does clonal expansion work in T helper cells

A

o Selected T helper cells divide by mitosis to produce larger clones = all clones have complementary antigen

204
Q

What do T helper cells secrete

A

Interleukin 2

205
Q

What does interleukin 2 do

A
  • B cells to divide and produce plasma cells
  • The T helper cells to become more active and release more cytokines, including interferon (IFN) that stimulates macrophage activity
  • The activation of T killer cells
206
Q

B cells divide + produce plasma cells. What do these plasma cells do

A

secrete antibodies specific to the antigen (that belongs to the pathogen)

207
Q

How are T killer cells activated

A

Colonial selection + clonal expansion

208
Q

Clonal selection - T killer cells

A

• When a T killer cell encounters an infected cell that is displaying a foreign antigen complementary to its TCR it becomes activated = clonal selection

209
Q

What do T killer cells do after binding to antigen / clonal selection

A

• attaches to the foreign antigens + secretes toxic substances that kill the body cells + pathogen = e.g = perforins

210
Q

What do perforins do

A

secreted by T killer cells punch a hole in the cell surface membrane of infected cells, allowing toxins to enter

211
Q

Clonal expansion - t killer cells

A

• The IL-2 released by specific T helper cells helps to stimulate the expansion of specific T killer cells = clonal expansion

212
Q

Function of T suppressor cells

A

o Preventing T cells from attacking and killing uninfected host cells

o Shutting down the immune system once the body is cleared of the pathogen

213
Q

OVERALL - T CELL MODE OF ACTION

A
  • Antigen presenting cells = ACTIVATES T cells
  • T helper = release interleukins = activate T killer cells + B lymphocytes
  • T – killer = kills pathogens
  • T regulator
  • Each T cell = different protein receptors = complimentary to antigen
214
Q

Overall how does clonal selection + clonal expansion work in T cells

A

T helper cells bind to the antigen (clonal selection ) + differentiation + divide (clonal expansion)

215
Q

What does humoral mean

A

Body fluids

216
Q

What do B cells produce when they are mature

A

can make one type of antibody molecule

217
Q

How are B cells activated

A

Clonal selection + clonal expansion

218
Q

Clonal selection - B cels

A

o B cells with B cell receptors complementary to the specific pathogenic antigen bind to it
o clones that have been selected for replication

219
Q

Clonal expansion - B cells

A

elected B cells divide by mitosis to produce larger clones
o T large numbers of identical B-lymphocytes being produced over a few weeks

220
Q

What do some B cells differentiate into

A

Plasma cells or memory cells

221
Q

Why do they divide into plasma cells

A

 T helper cells release interleukin 2 (IL-2) which stimulates B cells to divide and produce plasma cells

222
Q

Overall - draw out all differentiation of T and B cells

A
223
Q

Which one produces memory cells - T or B

A

Both

224
Q

Two types of immune response

A

Primary + secondary

225
Q

What is primary immune response

A

responding to a newly encountered antigen

226
Q

What is secondary immune response

A

responding to a previously encountered antigen

227
Q

Features of the primary immune response

A
  • considerate time delay
228
Q

Why is there a considerate time delay in the primary immune system

A

 The clonal selection and expansion of specific T cells and B cells
 The synthesis of antibodies

229
Q

What does that time delay mean for us

A

why we get symptoms of a disease when we are first exposed to a pathogen

230
Q

Features of plasma cells

A

Short lived

231
Q

What do memory cells do

A

remain circulating in the blood for a long time and allow for a rapid secondary immune response

232
Q

B memory cells and the secondary immune response

A

• If t same foreign antigen is found in the body a second time = B memory cells recognise the antigen

• B memory cells divide very quickly + differentiate into plasma cells (to produce antibodies) + more memory cells

• very quick = destroyed before the pathogen population increases + symptoms develop

233
Q

Why is the secondary immune response quicker

A

more memory cells present to be selected than there were cells within the original clone(that existed prior to the first infection)

o More memory cells can be selected and so more antibodies are produced within a short time period

234
Q

Describe / draw the secondary immune response

A
235
Q

Name the four types of T cells

A

Killer

Helper

Suppressor

Memory

236
Q

Name the three types of B cells

A

Memory

Effector

Plasma

237
Q

How long do neutrophils last

A

5 days

238
Q

What are antigens

A

Functional proteins / glycosidic proteins intrinsic to the plasma membrane

239
Q

What are T killer cells stimulated by

A

Interferons

240
Q

What cells are most important in cell mediated immunity

A

T killer cells

241
Q

Draw a graph of antibody concentration against time / days - primary + secondary

A
242
Q

How to identify lymphocytes

A

very large nuclei that nearly occupy the entire cell.

243
Q

How to identify red blood cells

A

Round shape

244
Q

How to identify platelets

A

Small size

245
Q

How to identify neutrophils

A

Lobed nucleus

246
Q

What are immunoglobulins

A

• Globular glycoproteins produced by plasma cells

247
Q

Structure of antibodies

A

• Quaternary structure = 2 heavy + 2 light polypeptide chains

• Bonded by disulphide bridges

  • constant region
  • variable region
  • antigen binding site
  • hinge region
248
Q

What is the constant region

A

does not vary within class / isotype but do vary between classes = determines the mechanism used to destroy pathogen

249
Q

What’s the variable region

A

different for each antibody = where antibody attaches to antigen = antigen – antibody complex

250
Q

What’s at the end of the variable region

A

antigen-binding site

251
Q

What is special about the antigen binding site

A

specific for each antigen = different antibodies need to be produced

252
Q

Why is it significant that there are 2 antigen binding sites

A

aids in agglutination = stops pathogen causing damage

253
Q

What’s the hinge region

A

where disulphide bonds join heavy chains = give flexibility = allows ABS to be placed at diff angles

254
Q

Draw an antibody

A
255
Q

Function of antibodies

A

• bind to specific antigens = trigger the specific immune response.

• Every antigen has one antibody

256
Q

What did antibodies act as

A

anti-toxins, opsonins and agglutinins

257
Q

What region of the antibody does the phagocyte bind to

A

Constant

258
Q

Why are the ops owning in the specific immune response more effective than those in the moon immune response

A

They don’t bind tightly to specific antigens

259
Q

Primary function of opsonins

A

Promoting phagocytosis by acting as a marker

260
Q

What can’t pathogens do when attached to antibodies

A

Enter host cells

261
Q

How can antibodies act as agglutinins

A

Each antibody - two binding sites = bind to several pathogens + cross link them =become agglutinated

262
Q

How does agglutination help

A

reduces the chance that the pathogens will spread through the body + makes it possible for phagocytes to engulf a number of pathogens at one time

263
Q

How do antibodies act as antitoxins

A

by binding to toxins produced by pathogens (e.g. the bacteria that cause diphtheria and tetanus) which neutralises them making them harmless

264
Q

What else can antibodies do

A

• can create holes in the cell walls of pathogens causing them to burst (lysis) when water is absorbed by osmosis

265
Q

How many polypeptide chains does an antibody contain an

A

4

266
Q

What allows for sulfide bonding

A

Amino acid - cysteine

267
Q

What is formed when an antibody binds to an antigen

A

Antigen-antibody complex

268
Q

How do antibodies defend body

A
  • act as opsonins
  • acts as antitoxins
  • cause agglutination
269
Q

When do auto immune diseases occur

A

When the immune system recognised a ‘self’ antigen as a foreign antigen + attacks healthy body tissue

270
Q

Immunity

A

Being able to kill pathogens if infected before getting symptoms

271
Q

Active immunity

A

Achieved when the immune system is activated + makes its own antibodies

272
Q

Passive immunity

A

Achieved when antibodies are supplied from another source

273
Q

Natural immunity

A

Achieved through normal life processes

274
Q

Artificial immunity

A

Achieved through medical intervention

275
Q

Natural active immunity

A

Achieved as a result of infection - individual gets disease + immune system makes memory cells

276
Q

Artificial active immunity

A

= injects inactive pathogen to activate an immune response

277
Q

Natural passive immunity

A

Antibodies provided via the placenta or via breast milk

278
Q

Artificial passive immunity

A

Injection / infection of antibodies from another animal / individual

279
Q

Examples of artificial passage immunity

A

o tetanus = antitoxin = antibodies were collected from people whose immune system had been triggered by a vaccination to produce tetanus antibodies

280
Q

Are there memory cells in active immunity

A

Yes

281
Q

Are there memory cells in passive immunity

A

No

282
Q

What is a vaccine

A

a suspension of antigens that are intentionally put into the body to induce artificial active immunity.

283
Q

What can vaccines be

A

Whole live organisms

Dead microorganisms

Attenuated microorganisms

Toxoids

mRNA

284
Q

Features of whole live organism vaccines

A

multiply slowly = allowing body to recognise antigens = stronger + longer-lasting immunity

285
Q

Dead microorganisms vaccine

A

do not trigger a strong or long-lasting immune response like live attenuated vaccines = repeated doses and/or booster doses are often required = Polio vaccine

286
Q

Attenuated vaccine

A

multiply slowly = allowing body to recognise antigens = MMR = stronger + longer lasting immunity

287
Q

Toxoid

A

harmless form of toxin = Diptheria

288
Q

Benefits of vaccines

A

• Highly effective with one vaccination giving a lifetime’s protection(although less effective ones will require booster / subsequent injections)

• Generally harmless as they do not cause the disease they protect against because the pathogen is killed by the primary immune response

289
Q

Attenuated

A

Weakened

290
Q

Problems with vaccines

A

Allergic reactions

Poor response

Antigenic variation

Virus have capacity to change their surface antigens

291
Q

What are people allergic to in vaccines

A

allergic reactions / local reactions (eg. sore arm) to inactivated vaccines as adjuvants (eg. aluminium salts) may be conjugated (joined) to the subunit of the pathogen to strengthen and lengthen the immune response

292
Q

Why may people have a poor response to a vaccine

A

malnourished and cannot produce the antibodies – proteins or their immune system may be defective

293
Q

Antigenic variation

A

variation in antigens of pathogens = vaccines don’t trigger an immune response

294
Q

Types of changing surface antigens

A

Antigenic drift

Antigenic shift

Antigenic concealment

Cross breeding

295
Q

Antigenic drift

A

over time there are small changes in the structure and shape of antigens = same strain

296
Q

Antigenic shift

A

there are major changes in antigens (within the same strain of virus)

297
Q

Antigenic concealment

A

the pathogen ‘hides’ from the immune system by:

 Living inside cells

 Coating their bodies in host proteins

 Parasitising immune cells such as macrophages and T cells (eg. HIV)

 Remaining in parts of the body that are difficult for vaccines to reach (eg. Vibrio cholerae – cholera, remains in the small intestine)

298
Q

Herd immunity

A

• sufficiently large proportion of the population has been vaccinated (and are therefore immune) which makes it difficult for a pathogen to spread within that population

299
Q

Benefits of here immunity

A

• allows for the individuals who are unable to be vaccinated (e.g. children and those with weak immune systems) to be protected from the disease

300
Q

Ring immunity

A

• People near a vulnerable / infected person are vaccinated in order to prevent them from catching and transmitting the disease

301
Q

Benefits of ring immunity

A

vaccinated individuals do not spread the pathogen onto others so those vulnerable individuals “within the ring” are protected as the people they interact with will not have the disease

302
Q

for a disease to be eradicated by a vaccine it should not:

A

• Mutate
• Have a life cycle that includes other organisms
• Have symptoms that make it hard to diagnose or trace

303
Q

Challenges of eradicating a disease

A

• some pathogens = complicated a+ present with disease processes that are not straightforward and so a successful vaccine has not been developed

• diseases where a vaccine does exist = not eliminated because too few in the community have been vaccinated = ANDREW WAKEFIELD

• Unstable political situations in areas such as Africa, Latin America and parts of Asia, perhaps resulting in civil unrest or wars

• Lack of public health facilities (poor infrastructure, few trained personnel, limited financial resources)

304
Q

Causes of rheumatoid arthritis - read

A

In RA, the immune system becomes overactive and produces antibodies = rheumatoid factors + anti-cyclic citrullinated peptide (anti-CCP) antibodies, which attack the synovial membrane (lining) of the joints. This causes the synovial membrane to become inflamed and thickened, leading to the formation of a pannus (abnormal tissue growth) and eventually erosion of the cartilage and bone in the joint.

The immune system in RA can also attack other parts of the body such as the eyes, lungs, and heart = can lead to complications such as inflammation of the lung lining, and damage to the heart muscle and blood vessels.

305
Q

Why is RNA virus more dangerous

A
  • more easily mutated as only has 1 strand
  • keeps mutating - vaccines must keep being updated

Biology - Module 4 (3 decks)

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