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Biology > Disease and Immunity > Flashcards

Disease and Immunity Flashcards

1
Q

What are pathogens?

A
  • Microorganisms that cause disease.
  • They can be viruses, bacteria, fungi, or protoctistans.
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2
Q

What are protoctistans?

A

A type of eukaryotic organism, usually single-called.

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3
Q

What are diseases caused by viruses?

A

Plant: Tobacco mosaic disease
Animal: AIDS, Influenza

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4
Q

What are diseases caused by bacteria?

A

Plant: Ring rot
Animal: Tuberculosis, bacterial meningitis

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5
Q

What are diseases caused by fungi?

A

Plant: Black sigatoka
Animal: Ring worm, athlete’s foot

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6
Q

What are diseases caused by protoctistans?

A

Plant: Potato blight
Animal: Malaria

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7
Q

What are fungi?

A
  • Fungi can be single ceded, like Yeast, or multicellular.
  • If they are multicellular, they form strands of cells joined end-on-end called hyphae.
  • Fungi have a cell wall made of chitin.
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8
Q

What are bacteria?

A
  • Prokaryotic cells.
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9
Q

What are viruses?

A
  • Non-cellular, exceptionally simple reproducing organic entities.
  • Have a protein coat called capsid (contains genetic material of virus).
  • Some have enzymes inside/phospholipid bilayer enveloping it which they have taken out of host cell.
  • Nucleic acid in viruses depend on type of virus — some have single stranded RNA/DNA, some have double stranded RNA/DRNA?
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10
Q

Describe the basic process in viral replication.

A
  1. Virus binds to host cell.
  2. Genetic material is injected into host cell.
  3. The machinery and metabolism upfront the host cell is used to produce more copies of the genetic material.
  4. The genetic material uses the host cell’s machinery and metabolism to produce many copies of the protein needed to make the viral capsid.
  5. The protein and genetic material are assembled into new viruses.
  6. When there are lots of viruses inside the cell, the cell bursts and the viruses are released from the cell (to then start the reproductive cycle all over again).
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11
Q

What are communicable diseases?

A

Diseases caused by pathogens which can be transmitted from one organism to another.

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12
Q

How do viruses damage the tissues of the host?

A
  • They take over the host cell’s metabolism preventing it from doing its normal role in the body.
  • Eventually, the cell dies when it bursts.
  • This means there is loss of function of infected tissues.
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13
Q

How do protoctista damage the tissues of the host?

A
  • Some invade cells, digest the cell’s contents to use for their reproduction and then burst the cell as the new generation emerges.
  • Again, this leads to loss of function of infected tissues.
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14
Q

How do fungi damage the tissues of the host?

A
  • Digest the living cells and destroy them, leading to loss of tissue function.
  • Some fungi also produce toxins which affect the host cell.
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15
Q

How do bacteria damage the tissues of the host?

A
  • Most bacteria produce toxins which interfere with cell function.
  • They could break down cell membranes, stop enzymes from working, or interfere with genetic material to stop cell division.
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16
Q

Describe ring rot.

A
  • Bacterium: Clavibacter michiganennsis
  • Host organisms: Potatoes, tomatoes, aubergines
  • Damage caused: Damages leaves, tubers, and fruit.
  • Mode of transmission: Direct contact with infected plants, soil contamination, humans as vectors.
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17
Q

Describe disease caused by tobacco mosaic virus.

A
  • Virus: Tobacco mosaic virus (TMV)
  • Host organisms: Tobacco plants, tomatoes, peppers, cucumbers, petunias, delphiniums.
  • Damage caused: Damages leaves, flowers, and fruit.
  • Mode of transmission: Direct contact with infected plants, soil contamination, humans as vectors.
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18
Q

Describe potato blight.

A
  • Protoctist: Phytophthora infestans
  • Host organisms: Potatoes and tomatoes
  • Damage caused: Cells are digested destroying leaves, tubers, and fruit.
  • Mode of transmission: Direct contact with infected plants, soil contamination, wind and water.
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19
Q

Describe black Sigatoka.

A
  • Fungus: Mycosphaerella fijiensis
  • Host organism: Bananas
  • Damages caused: Cells of leaves are digested and turn black.
  • Mode of transmission: Direct contact with infected plants, soil contamination, wind.
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20
Q

Describe tuberculosis.

A
  • Bacterium: Mycobacterium tuberculosis or M. bovis
  • Host organisms: Humans, cows, pigs, badgers, deer.
  • Damage caused: Destroys lung tissue and suppresses the immune system.
  • Mode of transmission: Droplet infection/airborne.
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21
Q

Describe bacterial meningitis.

A
  • Bacterium: Streptococcus pneumoniae or Neisseria meningitidis
  • Host organism: Humans
  • Damage caused: infects meninges of the brain and can spread to the rest of the body casing septicaemia and death.
  • Mode of transmission: Direct contact with body fluids.
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22
Q

Describe AIDS.

A
  • Virus: Human immunodeficiency virus (HIV)
  • Host organism: Humans
  • Damage caused: Infects T-helper cells gradually destroying the immune system, opportunistic infections can lead to death.
  • Mode of transmission: Inoculation through a break in the skin (e.g. during sex).
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23
Q

Describe influenza.

A
  • Virus: Orthomyxoviridae spp.
  • Mode of transmission:: Humans, pigs, chickens.
  • Damage caused: Infects ciliated epithelial cells in the gas exchange system, killing them. Leaves airways open to secondary infection which can lead to death.
  • Mode of transmission: Droplet infection.
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24
Q

Describe malaria.

A
  • Protoctist: Plasmodium spp.
  • Host organism: Humans (and mosquitoes).
  • Damage caused: Pathogen invades RBCs, liver and brain cells. Can lead to death.
  • Mode of transmission: Vector — mosquitoes.
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25
Q

Describe ring worm.

A
  • Fungus: Trichophyton verrucosum (in cattle)
  • Host organism: Cattle, dogs, cats, humans
  • Damage caused: Grey-white crusty circular areas of skin.
  • Mode of transmission: Skin to skin contact.
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26
Q

Describe athlete’s foot.

A
  • Fungus: Trichophyton mentagrophytes or
    Trichophyton rubrum
  • Host organism: Humans
  • Damage caused: Grows on warm, moist skin between toes. Causes cracking and scaling.
  • Mode of transmission: Skin to skin contact, indirect transmission from inanimate objects.
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27
Q

What two categories can transmission of disease be split into?

A
  1. Direct Transmission
  2. Indirect Transmission
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28
Q

What is direct transmission?

A

Where the pathogen transfers ‘directly’ from one host to another (e.g. transfer by touch or by being bitten by an infected individual).

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29
Q

What is indirect transmission?

A

Where 1) the pathogen transfers from one host to another ‘indirectly’. (e.g. via a vector or on fomites).

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30
Q

What are the six different ways communicable diseases are transmitted in animals?

A
  1. Direct contact
  2. Droplet infection/airborne
  3. Vomited
  4. Ingestion
  5. Inoculation
  6. Vectors
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31
Q

Describe direct contact.

A
  • This is where an individual is infected by touching an already infected individual.
  • This is clearly direct transmission.
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32
Q

Describe droplet infection/airborne.

A
  • Water droplets created when infected individuals cough, sneeze, sing, talk, or just breathe can be breathed in by ither individuals who then become infected.
  • When droplets are over a certain size, they will settle out of the air very quickly but people close to an infected person can become infected by breathing in the droplets.
  • If droplets are very small, they remain airborne permanently and can be breathed in from much further away.
  • This is indirect transmission unless the person is exceptionally close where, at some point, it would be considered direct transmission.
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33
Q

Describe fomites.

A
  • Fomites are inanimate objects such as bedding, socks, or cosmetics. The infected person deposits the pathogen onto the fomite and it is then transferred to another individual.
  • This is indirect transmission.
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34
Q

Describe ingestion (transmission).

A
  • Some pathogens infect a host when the host eats infected food.
  • This could be indirect transmission, for instance if an infected person prepares food for someone else and ends up transferring the pathogen to them.
  • However, it could also be classed as direct if the food itself was the infected individual.
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35
Q

Describe inoculation.

A
  • Some pathogens can only infect a host if there is inoculation into the blood.
  • This could be direct transmission if the infected individual transfers the pathogen to another individual (e.g. a bite from a dog with rabies).
  • It could be indirect transmission if a fomite is used in the transfer (e.g. sharing of needles in intravenous drug abuse).
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36
Q

Describe vectors.

A
  • Vectors are organisms (some would include water), that transmit the disease from an infected individual to another individual.
  • The pathogen can multiply within the vector but doesn’t tend to cause disease within the vector.
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37
Q

What are 7 factors that could increase transmission of pathogens in animals?

A
  1. Overcrowded living/working conditions
  2. Poor nutrition
  3. Compromised immune system
  4. Poor disposal of waste
  5. Climate change
  6. Culture/infrastructure
  7. Socioeconomic factors
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38
Q

Why do overcrowded living/working conditions increase transmission of pathogens?

A
  • More direct contact and much more likely transmission via the airborne, droplet, fomite, and vector routes.
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39
Q

Why does poor nutrition increase transmission of pathogens?

A
  • A good diet is important for a fully functioning immune system. Where diet is poor there will be more susceptible individuals and so more likely successful transmission from host to susceptible individual.
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40
Q

Why do compromised immune systems increase transmission of pathogens?

A
  • Infected individuals with a compromised immune system may harbour larger pathogen populations for longer and so shed more into the environment.
  • There will also be more susceptible individuals and so more likely successful transmission from host to susceptible individual.
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41
Q

Why does poor disposal of waste increase transmission of pathogens?

A
  • Many pathogens are shed from infected individuals in faeces. Poor waste disposal increases the chances of someone coming into contact with infected waste.
  • If the waste refers to rubbish then poor disposal provides a food source (or more reproduction sites) for animals that act as vectors for disease.
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42
Q

Why does climate change increase transmission of pathogens?

A
  • As climate changes the environment, pathogens may be able to survive longer between hosts, new pathogens could arrive in an area they weren’t able to live in before and infect populations that haven’t evolved to defend against them, or new vectors could arrive in an area that was previous uninhabitable for them.
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43
Q

Why does culture/infrastructure increase transmission of pathogens?

A
  • Some cultural practices can increase transmission, especially in relation to practices around mourning the dead.
  • Poor infrastructure can lead to difficulties in reaching outbreak areas and so more transmission.
  • However, very good infrastructure can mean lots of people travelling very widely and that can lead to more transmission.
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44
Q

Why do socioeconomic factors increase transmission of pathogens?

A
  • Countries without sufficient funding for enough trained health workers or for public health campaigns may well have higher rates of transmission.
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45
Q

What are the 5 fives communicable diseases are transmitted in plants?

A
  1. Direct contact
  2. Soil contamination
  3. Fomites
  4. Vectors
  5. Spores
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46
Q

Describe direct contact (plants).

A

As with animals, this is where an infected individual transfers the pathogen by touching another individual – definitely direct transmission.

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47
Q

Describe soil contamination.

A

Sometimes pathogens lie dormant in the soil where they have previously infected a plant. When a new plant grows in this soil the pathogen is already there to infect this new individual. This is an exam of indirect transmission.

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48
Q

Describe fomites (plants).

A

Tools used in horticulture can transmit pathogens from an infected individual to another individual. This is indirect transmission.

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49
Q

Describe vectors (plants).

A

One of the biggest vectors for plant diseases are aphids.

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50
Q

Describe spores.

A

Spores are cells that types of fungi and bacteria (and ferns and mosses) use for reproduction and dispersal. They have thick walls and a very resistant to harsh environmental conditions. Spores can float in the air for large distances and if they settle on a suitable host they can cause disease. [Although not mentioned in the section on animals, spores can be a method of infection in them too]

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51
Q

What are 7 factors which could lead to increased transmission of pathogens in plants?

A
  1. Planting crop varieties that are susceptible to disease
  2. Overcrowded growing
  3. Poor mineral nutrition
  4. Damn, warm conditions
  5. Climate change
  6. Monoculture practices
  7. Plant cloning practices
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52
Q

Why does planting crop varieties that are susceptible to disease lead to increased transmission of pathogens in plants?

A
  • Infected individuals may harbour larger pathogen populations for longer and so shed more into the environment.
  • There will also be more susceptible individuals and so more likely successful transmission from host to susceptible individual.
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53
Q

Why does overcrowded growing lead to increased transmission of pathogens in plants?

A
  • More direct contact and much more likely transmission via the spore and vector routes.
  • It may also produce high levels of humidity due to poor air flow that provide more favourable conditions for fungal growth.
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54
Q

Why does poor mineral nutrition lead to increased transmission of pathogens in plants?

A
  • Healthy plants are much less susceptible to disease than weakened ones.
  • Sufficient mineral ions are important in the plant’s defences.
  • Where mineral nutrition is poor there will be more susceptible individuals and so more likely successful transmission from host to susceptible individual.
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55
Q

Why do damp, warm conditions lead to increased transmission of pathogens in plants?

A
  • These conditions are more favourable for pathogen survival between hosts and well as for fungal growth.
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56
Q

Why does climate change lead to increased transmission of pathogens in plants?

A
  • As climate changes the environment, pathogens may be able to survive longer between hosts, new pathogens could arrive in an area they weren’t able to live in before and infect populations that haven’t evolved to defend against them, or new vectors could arrive in an area that was previous uninhabitable for them.
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57
Q

Why do monoculture practices lead to increased transmission of pathogens in plants?

A
  • Pathogens are often species specific.
  • In monocultures the same species is planted across a whole field (or larger area) without any other species present.
  • When an infected host releases pathogens into the environment they are much more likely to land on a suitable host. And direct contact is more likely as the same species are planted next to each other.
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58
Q

Why do plant cloning practices lead to increased transmission of pathogens in plants?

A
  • Plant cloning produces genetically identical individuals.
  • Clones aren’t inherently more susceptible to diseases but if one individual is susceptible then they all will be.
  • Transmission from one infected clone will be very high as the chances of a pathogen landing on a susceptible individual are very high.
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59
Q

What are passive defence mechanisms in plants?

A
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60
Q

What are active defence mechanisms in plants?

A
  • Hypersensitivity deprives pathogens of resources.
  • The formation of physical barriers by callose plays a major role in limiting the spread of pathogens.
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61
Q

How does cell signalling act as a defence mechanism?

A
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62
Q

3 reasons why we need new drugs.

A
  1. There are emerging infections that were previously unknown or rare (AIDS).
  2. No treatment for disease or conditon exists (cancers, pain control).
  3. Resistance to current treatments us developing so current drugs no longer work.
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63
Q

How does antibiotic resistance arise?

A
  1. Pathogen population has varying ability to resist drugs (some are susceptible, some are resistant).
  2. Drugs kill off the more susceptible pathogens first.
  3. Remaining population is more resistant.
  4. Exposure to sub-lethal dose of medication allows bacteria to develop resistance by chance mutation.
  5. Over time, resistance of population increases.
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64
Q

State 3 examples of barriers to pathogens in plants.

A
  1. Waxy cuticle
  2. Cell wall (cellulose)
  3. Bark
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65
Q

Describe the major difference between plants’ response to pathogens as compared to animals’ response to pathogens and explain why this is a possible successful strategy for plants.

A
  • Non-specific — aims to destroy pathogen or close off infected area to prevent spread.
  • Plants are able to lose parts of themselves and survive.
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66
Q

Describe 3 ways in which a plant cell can detect the presence of a pathogen.

A
  1. Detect chemicals on surface of pathogens.
  2. Detect break down products of cell wall — beta glucose.
  3. Cells have receptors on plasma membranes — once activates, they send chemical signals to nucleus to switch on defence genes. Chemicals are also sent to other cells via plasmodesmata to initiate defence genes in other cell in preparation for incoming attack.
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67
Q

Name two molecules produced by plants to limit the spread of the pathogen.

A
  • Lignin
  • Callose
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68
Q

Describe the structure of callose.

A
  • Polysaccharide of beta glucose but with 1-3 and 1-6 glycosidic bonds so a different shape to cellulose.
69
Q

Describe 4 ways callose is used to limit the spread of a pathogen.

A
  1. Deposited under cell wall between wall and plasma membrane — pathogen’s cellulose-digesting enzymes will not fit so they cannot digest it.
  2. Production continues after end of infection — investing in defence.
  3. Seal off sieve plates in phloem to infected area to stop spread.
  4. Fills plasmodesmata between infected cells and neighbours to stop spread.
70
Q

List 6 different types of plant chemicals. Give an example for each.

A
  1. Insect repellents: Pine resin
  2. Insecticides: caffeine, nicotine
  3. Antibacterial: Phenols
  4. Antifungal: Chitinases
  5. Anti-oomycetes/anti-protoctists: Glucanases
  6. General toxins: Cyanide
71
Q

Define ‘non-specific’

A

Not targeted — work against all pathogens in the same way.

72
Q

State 4 barriers the human body has to minimise the entry of pathogens.

A
  1. Skin
  2. Mucous membranes
  3. Stomach acid
  4. Blood clotting
73
Q

How does the skin act as an effective barrier to the entry of pathogens?

A
  • Sheds-off — loses pathogens as well.
  • Dead cells in surface layer which cannot be hosts for pathogens, especially viruses.
  • Produces sebum which inhibits pathogen growth.
  • Skin flora — bacteria that compete for space and nutrients.
74
Q

How does the mucous membrane acts as an effective barrier to the entry of pathogens?

A
  • Mucous traps pathogens.
  • Cilia moves mucus out.
  • Mucus has lysosome — digestive enzyme that breaks down bacterial and fungal cell walls.
  • Mucus has phagocytes.
75
Q

Name 4 expulsion reflexes and explain their value for protection against pathogens.

A
  1. Coughing
  2. Sneezing
  3. Vomiting
  4. Diarrhoea

It expels mucus and contents of gut including any pathogens.

76
Q

Describe the process of blood clotting.

A
  • Tissue is damaged.
  • Platelets are activates by damaged tissue.
  • Platelets release the enzyme thromboplastin (and also serotonin which makes smooth muscle in walls of blood vessels contract causing them to narrow and reduce blood loss).
  • Thromboplastin catalyse the conversion of prothrombin into thrombin.
  • Thrombin, an enzyme, catalyses the conversion of fibrinogen (a soluble globular protein) into fibrin )an insoluble fibrous protein).
  • Fibrin molecules form a mesh which traps platelets and red blood cells to form a clot.
  • The clot dries to form a hard, tough scab.
  • The clot and scab minimise blood loss and entry of pathogens.
77
Q

Explain the importance of blood clotting and the release of serotonin by platelets.

A
  • The clot and scab minimise blood loss and minimise entry of pathogens directly into tissues or the blood through broken skin.
  • Platelets release serotonin which makes smooth muscle in walls of blood vessels contract causing them to narrow and reduce blood loss.
78
Q

What is inflammation in the context of the innate immune response?

A
  • Inflammation is a non-specific chemical process that occurs in response to a pathogen and helps to remove it from the body.
  • It involves the activation of immune cells, the release of chemical signals, and the increase of blood flow to the infected area.
79
Q

Describe how fever is initiated in response to pathogen invasion and explain its value fro protection against pathogens.

A
  • Cytokines make hypothalamus maintain a high body temperature.
  • Specific immune response work faster at a higher temperature.
  • Pathogens optimum temperature is normal body temperature — fever inhibits reproduction.
80
Q

How does the innate immune response differ from the adaptive immune response?

A
  • The innate immune reponse is a non-specific response that occurs immediately after a pathogen enters the body, while the adaptive immune response is a specific response that takes a few days to develop and is tailored to a specific pathogen.
  • Innate immune response provides a rapid response to pathogens whereas the adaptive immune response provides long-term protection.
81
Q

State the processes involved in the inflammatory response.

A
  1. Vasodilation
  2. Increases vascular permeability
  3. Leukocyte recruitment
  4. Resolution
82
Q

Describe the 1st stage, vasodilation, in the inflammatory response.

A
  • Blood vessels in affected area become wider, allowing more blood to flow to the area.
  • This causes redness and heat in the affected area.
83
Q

Describe the 2nd stage, increases vascular permeability, in the inflammatory response.

A
  • Blood vessels in affected area become more permeable, allowing fluid and immune cells to enter the tissue.
  • This causes swelling and pain in the affected area.
84
Q

Describe the 3d stage, leukocyte recruitment, in the inflammatory response.

A
  • White blood cells (leukocytes) are recruited to the affected area.
  • These cells can help destroy invading pathogens and remove damaged tissue.
85
Q

Describe the 4th stage, resolution, in the inflammatory response.

A
  • Once the inflammatory response has served its purpose, the affected area will begin to heal.
  • Immune cells will remove any debris, and the blood vessels will return to their normal size.
  • This stage can take several days or weeks, depending on the severity of the initial insult.
86
Q

Define ‘phagocyte’

A

Specialised white blood cells that engulf and destroy pathogens.

87
Q

State two examples of phagocytic cells.

A
  1. Neutrophils
  2. Macrophages
88
Q

Describe the stages in phagocytosis.

A
  1. Phagocyte is attracted by pathogens by chemicals the pathogen produces.
  2. Phagocyte recognises the pathogen as ‘non-self’ and binds to it.
  3. Phagocyte engulfs the pathogen (endocytosis) to form a phagosome.
  4. Lysosomes move towards the phagosome and the two combine to form a phagolysosome.
  5. Inside the phagolysosome, hydrolytic enzymes, such as lysosomes, digest the pathogen.
  6. The molecules produced from the digestion of the pathogen are absorbed by the phagocyte.
  7. Antigens from the pathogen combine with the major histocompatibilty complex (MHC) glycoproteins in the cytoplasm.
  8. The MHC/antigen complexes are moved to the phagocyte’s cell surface membrane are displayed.
  9. The phagocyte is now an antigen-presenting cell and can activate the specific immune response.
89
Q

What is endocytosis?

A

When phagocytes engulf the pathogen.

90
Q

What does MHC stand for?

A

Major histocompatibiltiy complex

91
Q

Define ‘antigen-presenting cell’

A

A cell that displays foreign antigens complexed with major histocompatibility complexes (MHCs) on their surfaces.

92
Q

Describe the role of cytokines in the non-specific defences.

A
  • Phagocytes that have digested a pathogen release cytokines which signal to other phagocytes to move to the area.
  • Cytokines also encourage the inflammatory response.
93
Q

Describe the role of opsonins in phagocytosis.

A
  • Opsonins are chemicals that bind to pathogens, tagging them, and are recognised by phagocytes so that they engulf and destroy them.
94
Q

Define ‘antigen’

A

Identifying chemical on the surface of a cell that triggers an immune response.

95
Q

Differentiate between ‘self’ and ‘non-self’ antigens.

A
  • Cells of own body have self antigens which the immune system will not target these.
  • Non-self antigens are recognised and trigger a response.
96
Q

Define ‘antibody’

A

Y shaped glycoproteins made of B cells of the immune system in response to non-self antigens.

97
Q

Define ‘antigen-antibody complex’

A

The complex formed when an antibody binds to an antigen.

98
Q

Define ‘lymphocyte’

A

White blood cells that make up the specific immune system.

99
Q

Define ‘specific immune response’

A

Targets specific pathogen due to specific antigen — create memory cells.

100
Q

State 4 ways in which antibodies defend the body.

A
  1. Opsonins
  2. Neutralise pathogens
  3. Agglutinins
  4. Anti-toxins
101
Q

How do opsonins defend the body?

A

Tap pathogens for effective phagocytosis.

102
Q

How do neutralise pathogens defend the body?

A

The binding of antibodies block the function of molecules on the surface of pathogens e.g. those required for the pathogen to bind to a host cell.

103
Q

How do Agglutinins defend the body?

A

Cause pathogens to clump together which reduces the spread of the pathogen, and phagocytes can engulf many pathogens at the same time.

104
Q

How do anti-toxins defend the body?

A

Antibodies bind to toxins to make them harmless.

105
Q

Explain why B lymphocytes are called ‘B’ whereas T lymphocytes are called ‘T’.

A
  • T mature in the thymus gland.
  • B mature in bone marrow.
106
Q

Name the 4 main types of T lymphocytes.

A
  1. T-helper cells
  2. T killer cells
  3. T memory cells
  4. T regulator cells
107
Q

Describe T helper cells.

A
  • T lymphocyte
  • CD4 receptors on surface bind to antigens on APCS.
  • Produce interleukins that stimulate the activity of B cells.
108
Q

Describe T killer cells.

A
  • T lymphocyte
  • Destroy pathogens with the ‘antigen’.
  • Produce perforin which makes holes in membrane.
109
Q

Describe T memory cells.

A
  • T lymphocyte
  • Live a long time — immunological memory.
  • Divide rapidly to produce T killer cells on contact with antigen.
110
Q

Describe T regulator cells.

A
  • T lymphocyte
  • Suppress the immune system: controls and regulates.
  • Stop response once pathogen is eliminated which prevents autoimmune response.
111
Q

Describe the role of interleukins in the specific immune response.

A

Activate T and B cells to clone by mitosis.

112
Q

Name the 3 main types of B lymphocytes.

A
  1. Plasma cells
  2. B effector cells
  3. B memory cells
113
Q

Describe the role of plasma cells.

A
  • B lymphocyte
  • Produces antibodies to a particular antigen.
114
Q

Describe the role of B effector cells.

A
  • B lymphocyte
  • Divide to form plasma cell clones.
115
Q

Describe the role of B memory cells.

A
  • B lymphocyte
  • Long-lived — ‘remember’ a specific antigen causing rapid response to pathogen.
116
Q

Define ‘cell-mediated immunity) and suggest what it is particularly effective against.

A
  • Immune response that does not involve antibodies, but rather involves the activation of phagocytes, T killer cells, and memory cells.
  • Effective against viruses and early cancers.
117
Q

Describe the process of cell-mediated immunity.

A
  1. APCs formed.
  2. APC comes into contact with many T helper cells — only T helper cells with complementary receptors to the antigens will be activated (clonal selection).
  3. T helper cells produce interleukins which stimulates other types of activated T cell to clone by mitosis (clonal expansion).
  4. T memory cells are produced, T killer cells are produced (destroys infected cells), T helper cells are produced — interleukins produced to stimulate B cells to clone by mitosis, interleukins produced to stimulate phagocytosis.
118
Q

State 4 main products of cell-mediated immunity and what they then do as part of the immune response.

A
  1. T memory cells produced — immunological memory
  2. T killer cells produced — destroy infected cells.
  3. T helper cells — interleukins produced to stimulate B cells to clone by mitosis.
  4. Interleukins produced to stimulate phagocytosis.
119
Q

Define ‘humoral immunity’ and suggest what it is particularly effective against.

A
  • Immunity involving chemicals in the ‘humours’ of the body rather than cells — produces antibodies.
  • It is particularly effective against Extracellular pathogens e.g. bacteria, virus.
120
Q

Desire the process of humoral immunity.

A
  1. Pathogen enters body and comes into contact with many different B cells — only B cells with complementary antibodies/receptors on their plasma membrane will bid to the pathogen and engulf it.
  2. B cells processes antigen and becomes an APC.
  3. Activated T helper cells bind to B cell APCs as they have complementary receptors to the antigens as well.
  4. T helper cell produces interleukins to activate the B cells which then clone by mitosis.
  5. B effector cells are produced.
  6. Memory cells and plasma cells are produced from B effector cells.
  7. Plasma cells produce and secrete antibodies that have the same shaped antigen binding site as those antibodies/receptors on the plasma membrane on the initial B cells that were selected
  8. Antibodies help to destroy/neutralise pathogens.
121
Q

Define ‘clonal selection’

A

Selection of cells with complementary shaped receptors for the antigens.

122
Q

Define ‘clonal expansion’

A

Cytokines/interleukins make the activated cells clone by mitosis.

123
Q

State the 2 main products of humoral immunity and what they do as part of the immune response.

A
  1. Antibodies: Destroy/neutralise/mark pathogen for phagocytosis.
  2. B memory cells: Quicker response upon second exposure.
124
Q

Summarise the role of antigen presentation in the specific immune response.

A

Allow cells with complementary receptors and ability to produce correct antibodies to be selected.

125
Q

Describe the role of cell signalling in the specific immune response.

A

Interleukins released by T helper cells stimulate the cloning by mitosis required by all cells to produce effective immunity.

126
Q

Define ‘primary immune response’

A

The relatively slow production of a small umber of correct antibodies for the first time a pathogen is encountered.

127
Q

Define ‘secondary immune response’

A

The relatively fast production of a large number of correct antibodies the second time a pathogen is encounters as a result of immunological memory — the second stage of specific immunity.

128
Q

Define ‘active immunity’

A

The immunity which results from the production of antibodies by the immune system in response to the presence of an antigen.

129
Q

Define ‘passive immunity’

A

The short-term immunity which results from the introduction of antibodies from another person or animal.

130
Q

Define ‘Artifical immunity’

A

Immunity which results from exposure to a safe form of a pathogen e.g. by vaccination or immunity from the administration of antibodies from t other animal against a dangerous pathogen.

131
Q

Define ‘natural immunity’

A

Immunity which results from the response of the body to the invasion of a pathogen or immunity given to an infant mammal by the mother through the placenta and the colostrum.

132
Q

Describe examples for natural active immunity.

A
  1. Exposure to pathogen — response of the body.
133
Q

Describe two examples for Artifical active immunity.

A

Vaccination

134
Q

Describe two examples for natural passive immunity.

A

Antibodies from mother to baby via placenta/colostrum.

135
Q

Describe two examples for Artifical passive immunity.

A

Injection of antibodies.

136
Q

Give 2 similarities between active and passive immunity.

A
  • Both provide protection against pathogens.
  • Both involve the presence of antibodies in the body.
137
Q

Give 4 differences between active and passive immunity.

A

Occurs when…
- A: Occurs when the body’s immune system is activated by exposure to an antigen, either through natural infection or vaccination.
- P: Occurs when pre-formed antibodies are introduced into the body, either naturally through breast milk or artificially through injection of antibodies from another person or animal.

Time for protection to take place…
- A: Takes time to develop, usually a few weeks, before the body produces enough antibodies to provide protection.
- P: Provides immediate protection, as the antibodies are already present in the body.

Length of protection
- A: Provides long-term protection, as the body retains memory cells that can quickly produce antibodies upon subsequent exposure to the same antigen.
- P: Provides temporary protection, as the pre-formed antibodies are gradually broken down and eliminated from the body.

Antibodies
- A: Involves the production of antibodies by the individual’s own immune system.
- P: Involves the transfer of antibodies from an external source, rather than the produ

138
Q

Define ‘autoimmune disease’

A

A condition/illness resulting from an autoimmune response — a response where the immune system acts against its own cells and destroys healthy tissue in the body.

139
Q

Give 4 examples of autoimmune diseases.

A
  1. Type 1 diabetes
  2. Rheumatoid arthritis
  3. Celiac disease
  4. Lupus erythematous
140
Q

Suggest how autoimmune diseases may occur (5).

A
  1. Bacteria/virus: If receptors are modified to improve response during clonal expansion they can become neared to ‘self’ shape.
  2. Drugs
  3. Chemical irritants
  4. Environmental irritants.
  5. More susceptible due to genetics.
141
Q

Define ‘vaccine’

A

A safe from of an antigen which is injected into the bloodstream to provide Artifical active immunity against a pathogen bearing the antigen.

142
Q

Define ‘vaccination’

A

Injection of the vaccine, process of become vaccinated. The deliver of a vaccine to an organism.

143
Q

Describe 5 ways in which antigens can be obtained for use in vaccines.

A
  1. Killed/inactivated bacteria and viruses (not by boiling as this would denature proteins and change antigen shape).
  2. Attenuated (weakened) strains of live bacteria/viruses.
  3. Toxin molecules that have been altered and detoxified.
  4. Isolated antigens extracted from the pathogen.
  5. Genetically engineered antigens.
144
Q

Desire how vaccination results in Artifical active immunity.

A
  1. Small amounts of safe antigen injected.
  2. Primary immune response triggered by foreign antigens and body produced antigens and memory cells.
  3. Subsequent exposure to live pathogen triggers secondary immune response — faster, no symptoms.
145
Q

Suggest why a vaccine may not provide immunity in some people.

A
  • If immune system is weak as it relies on primary response to vaccine creating the memory cells for an effected secondary response to the real pathogen.
146
Q

Define ‘epidemic’

A

When a communicable disease spreads rapidly to a lot of people at a local/national level.

147
Q

Define ‘pandemic’

A

When a communicable disease spreads rapidly to a lot of people across a number or countries.

148
Q

Define ‘herd immunity’

A

The resistance to the spread of a contagious disease within a population that results if a sufficiently high proportion are immune (especially through vaccination).

149
Q

Explain how vaccination of a significant number of people in a population can provide protection for unvaccinated people.

A

Difficult for disease to spread as so few people susceptible people to infect.

150
Q

Suggest members of a population who are likely to need protection through herd immunity.

A
  • Those who cannot be vaccinated
  • Very young/old
  • Weakened immune systems e.g. AIDS, cancer, drugs, immuno-suppressants.
151
Q

Give two examples of vaccination programmes that aim to provide herd immunity.

A
  1. MMR
  2. 5 in 1 - diphtheria, tatanus, whooping cough, polio, and haemophilias influenza type B.
152
Q

Suggest why the influenza vaccine needs to be redeveloped and people need to be revaccinated each year.

A
  • Virus mutates quickly therefore gene for antigen mutates causing antigens to change shape.
  • Different antigens need different antibodies so there will be no memory cells present for the new, mutated virus.
153
Q

Describe 6 examples of common medicinal drugs derived from living organisms.

A
  1. Penicillin
  2. Doxetaxel/Paclitaxel (breast cancer drugs derived from Yew trees)
  3. Aspirin (from willow bark)
  4. Prialt (painkiller from cone snail venom)
  5. Vancomycin (soil fungus — most powerful antibiotic)
  6. Digoxin (foxgloves, heart drug)
154
Q

Explain the need to maintain biodiversity in relation to the discovery of new medicines.

A
  • Many medicines are inspired by/extracted from other living organisms.
  • Maintaining biodiversity allows scientists to study more organisms which have potentially helpful chemicals in them.
155
Q

Define ‘personalised medicine’, give an example of how treatment is being personalised, and suggest the value of personalising mediocre to a person’s genetic information.

A
  • A type of medical care in which treatment is customised for an indivual patient.
  • Genome can be analysed relatively quickly/cheaply.
  • Greater understand of genetic basis of diseases.
  • Target cancer types (genetic tissue type).
  • Avoid potential side effects.
  • Most effective treatments for specific genome.
156
Q

Define ‘synthetic biology’

A

The design and construction of novel biological pathways, organisms or devices, or the redesign of existing natural biological systems.

157
Q

Give 4 examples of how synthetic biology may lead to better medical treatments.

A
  1. Genetically modifying mammals to produce therapeutic proteins in their milk.
  2. Nanotechnology — tiny, non-natural particles used e.g. to deliver drugs to specific sites within cells of pathogens/tumours.
  3. Computer modelling to develop or modified drugs.
  4. Developing populations of bacteria as biological factories to produce drugs.
158
Q

Define ‘antibiotic’

A
  • A chemical or compound that inhibits reproduction or growth/kills bacteria.
  • Effective in low concentrations.
  • Obtained or derived from molecules produced by other organisms.
159
Q

Define ‘selective toxicity’

A

The ability to interfere with the metabolism of a pathogen without affecting the cells of the host.

160
Q

Suggest 5 ways in which antibiotic may act selectively on bacterial cells but not human cells.

A
  1. Inhibition of cell wall synthesis (peptidoglycan).
  2. Inhibition of protein synthesis (70s ribosomes).
  3. Alteration of cell membranes (different type of phospholipids).
  4. Inhibition of nucleic acid synthesis (circular DNA has different process).
  5. Antimetabolite activity (target specific enzymes).
161
Q

Explain why antibiotics do not work on viral infections.

A
  • They target living chemical processes and structures which viruses do not have.
  • Viruses use host cell’s equipment to reproduce — harder to target without also harming the host.
162
Q

Explain why antibiotics are useful.

A

They kill bacteria, curing infections and preventing deaths of humans.

163
Q

Explain how a population of bacteria may develop resistance to an antibiotic.

A
  • If a mutation occurs during bacterial reproduction which produces an indidivual unaffected by a drug, it is the ‘fittest’ to survive and pass on resistance to daughter cells.
  • Use of antibiotics is a selection pressure causing the ‘strongest’ individuals to survive, reproduce, and pass on these advantageous alleles to the next generation of bacteria who are now more resistant to the drug than the generation before.
164
Q

Suggest 2 ways in which the use of antibiotics may be increasing the likelihood of resistance evolving.

A
  • Adding antibiotics to animal feed/overprescribing/ use of broad spectrum antibiotics/not completing a course.
  • Exposure of bacteria to antibiotics is a selection pressure causing resistance to develop so any situation in which bacteria are exposed and some survive is another step towards resistance.
165
Q

Give 2 examples of antibiotic resistant bacteria.

A
  1. MRSA
  2. C. Difficile
166
Q

Suggest methods used to reduce the likelihood of resistance developing in bacteria.

A
  1. Minimising use of antibiotics
  2. Ensuring courses are finished
  3. Narrow spectrum where possible
  4. Minimise spread of bacteria
167
Q

Explain why not completing a course of antibiotics may lead to antibiotic resistance developing.

A

The more resistant individuals survive and reproduce to develop populations of resistant strains.

168
Q

Suggest methods used to reduce the spread of bacterial infections.

A
  1. Good hygiene e.g. hand washing
  2. Isolation
  3. Minimise public entering hospitals

Biology (25 decks)

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