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Module 4 > Communicable diseases > Flashcards

Communicable diseases Flashcards

1
Q

Pathogen

A

A micro-organism that causes disease

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2
Q

Host

A

Organism in which a pathogen lives

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3
Q

How do pathogens live on a host

A

By taking nutrition from their host, which also causes damage in the process

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4
Q

Bacteria

A

-Prokaryote
-Reproduce rapidly - every 20 mins
-In the host they can multiply rapidly
-Presence causes disease by damaging cells/ releasing toxic waste products

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5
Q

Bacteria in plants

A

-Live in the vascular tissue
-Cause blackening and death

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6
Q

Examples of bacterial diseases in mammals

A

-Turberculosis
-Bacterial meningitus

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7
Q

TB

A

Mycobacterium tuberculosis
A disease that affects many parts of the body, killing the cells and tissues; lungs are most affected

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8
Q

Bacterial meningitis

A

Streptococcus pneumonia
-Infection of the meninges - membranes that surround the brain and spinal cord
-Membranes become swollen and may cause damage to the brain and nerves

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9
Q

Bacterial diseases in plants

A

Ring rot

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10
Q

Ring rot

A

Ring of decay in the vascular tissue of a potato tuber or tomato, accompanied by leaf wilting

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11
Q

How does a fungi infect mammals

A

Fungus lives in the skin of the animal
-Hyphae forms a mycelium under the skins surface
-Fungus can send out specialised reproductive hyphae, which grow to the surface of the skin to release spores
-Causes redness and irritation

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12
Q

How does a fungi infect plants

A

Lives in vascular tissue where it can gain nutrients
-Hyphae release extracellular enzymes i.e. cellulases
- Digest surrounding tissue which causes decay before dying
-Leaves will become mottled in colour, curl up, and shrivel before dying
-Fruit and storage organs (tubers- potatoes) will turn black and decay

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13
Q

Fungal diseases in mammals

A

Ringworm (cattle)
Athletes foot (humans)

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14
Q

Ringworm (cattle)

A

Growth of fungus in skin with spore cases erupting through skin to feel a rash

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15
Q

Athletes foot (humans)

A

Growth under skin of feet- particularly between toes

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16
Q

Viruses

A

Invade cells and take other the genetic machinery and over organelles of the cell
-Cause the cell to manufacture more copies of the virus
-Host cell bursts releasing many new viruses which will infect healthy cells

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17
Q

Viruses in mammals

A

HIV/AIDS
Influenza

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18
Q

HIV/AIDS

A

Human immunodeficiency disease
-Attacks cells in the immune system and compromises the immune response

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19
Q

Influenza

A

‘Flu’ Viruses
-Attacks the respiratory system and causes muscle pains and headaches

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20
Q

Plant viruses

A

Tobacco mosaic virus

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21
Q

Tobacco mosaic virus

A

Causes mottling and discoloration of leaves

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22
Q

Protoctista

A

Animal-like protocists
-Enter host cells and feed on contents as they grow

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23
Q

Malaria

A

Plasmodium falciparum
-Malarial parasite plasmodium has immature forms that feed on the haemoglobin in RBC
-Causes headache and fever and may progress to coma and death

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24
Q

What organism has been difficult to classify

A

Phytophthora (blight) was classified as a fungus but moved to protoctsita as it has many features that does not fit with other fungi

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25
Q

Pathogen life cycle

A

1) Transmission - travels from one host to another
2) entering the host’s tissues
3) Reproducing
4) Leaving the hosts tissues

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26
Q

Transmisson

A

Passing a pathogen from an infected individual to an uninfected individual

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27
Q

Direct Transmission

A

Passing a pathogen from host to new host with no intermediary
-Most common form of transmission

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28
Q

E.g of direct transmission

A

1)Direct physical contact i.e touching a person who is infected/ touching contaminated surfaces (including the soil) that harbor the pathogens.
2)Faecal - oral transmission, usually by eating food/drinking water contaminated by the pathogen
3) Droplet infection - pathogen carried in tiny water droplets in the air
4) Transmission by spores. resistant stage of the pathogen - carried in the air/surfaces/soil

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29
Q

Diseases transmitted through direct physical contact

A

HIV, Bacterial meningitis, ringworm, athlete’s foot

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30
Q

Factors that affect transmission by direct physical contact

A

Hygiene:
washing hands regularly - especially after using the toilet
Keeping surfaces clean - door handles
Cleaning and disinfecting cuts and abrasions
Sterilising surgical instruments
Using condoms during sex

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31
Q

Factors that affect transmission by Faecal -oral transmission

A

Using human sewage to fertilise crops is a common practice in some parts of the world:
-Treatment of waste products and treatment of drinking water are important ways to reduce risk
-Thorough washing of all fresh food (using treated water)
-Careful preparation and thorough cooking of all food

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32
Q

Factors that affect transmission by droplet infection

A

Catch it- Bin it - Kill it
Cover your mouth when coughing/sneezing
Use a tissue and ensure tissue is disposed of correctly

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33
Q

Factors that affect transmission by spores

A

Use of a mask
Washing skin after contact with soil

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34
Q

Social factors that affect transmission

A

-Overcrowding - many people living and sleeping together in a house
-Poorventiliation
-Poor health - particularly if a person has HIV/AIDS as thy ae more likely to contact other diseases
-Poor diet
-Homelessness
-Living/working with people who have migrated from areas where a disease is common

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35
Q

Transmission of TB

A

Not transmitted easily
-Takes close proximity to people with the disease for long periods of time
-BCG vaccination reduced in teenagers through Western Europe
-Increased migration/ economic migrants living in overcrowded poor ventilated areas causes cases in TB to rise

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36
Q

Indirect transmisson

A

Passing a pathogen from host to new host via a vector

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37
Q

Vector

A

An organism that carries a pathogen from one host to another

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38
Q

E.g of a vector

A

Plasmodium parasite that causes malaria enters the human host via a bite from the female Anopheles mosquito

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39
Q

Indirect transmission of Plasmodium

A

1) A person with malaria
2) Gametes of plasmodium in blood
3) Female Anopheles mosquito sucks blood
4) Plasmodium develops and migrates to a mosquito’s salivary glands
5) An uninfected person is bitten
6) Plasmodium migrates to the liver
7) Plasmodium migrates to the blood
8) Person has malaria

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40
Q

Direct transmission of plant pathogens

A

1) Pathogens present in soil will infect plants by entering the roots - especially if damaged as a result of replanting, burrowing animals, movement caused by a storm
2) Airborne transmission - fungi spores (prduced from sexual/asexual repro) carried in the wind

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41
Q

What happens when a pathogen is inside a plant

A

Infect vascular tissue
-Pathogens in leaves are distributed when leaves are shed and carry pathogen back to the soil where it can grow and infect another plant

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42
Q

Pathogens within fruit and seeds

A

Distributed in the seeds - so that offspring are infected

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43
Q

Indirect transmission in plants

A

Occurs as a result of insect attack
-Spores/bacteria become attached to a burrowing insect such as a beetle after it has attacked an infected plant
-When beetle attacks another plant pathogen transmitted
-Beetle -vector

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44
Q

Example of indirect transmission by plants

A

Fungus that causes Dutch elm disease is carried by the beetle Scolytus multistriatus

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45
Q

Disease and climate

A

Grow and reproduce more quickly in warm, moist conditions - more common in warmer climates cold climates - die
-A greater variety of diseases and animals/plants more likely to be infected

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46
Q

How are plants a rich source of nutrients

A

Manufacture sugars in photosynthesis and convert those sugars to a variety of compounds i.e. proteins and oils

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47
Q

Passive defenses

A

Defensespresent before infection and their role is to prevent entry and spread of the pathogen
-Physical barriers/chemicals

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48
Q

Physical defenses

A

-Cellulose cell wall
-Lignin thickening of cell walls
-Waxy cuticles
-Bark
-Stomatal closure
-Callose
-Tylose formation

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49
Q

How is the cellulose cell wall a physical defense

A

Physical barrier and contains variety of chemical defences that can be activated when pathogen is detected

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50
Q

How is the lignin thickening of the cell wall a physical defense

A

Lignin (phenolic compound) is waterproof and indigestible

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51
Q

How are the waxy cuticles a physical defense

A

Prevent water collecting on the cell surfaces
Pathogens collect in water and need water to survive, absence - defense

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52
Q

How is the stomatal closure a physical defense

A

Stomata possible points of pathogen entry
-Stomatal aperture controlled by the guard cells
-When pathogenic organisms are detected, guard cells will close stomata in that part of the plant

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53
Q

How is callose a physical defense

A

Callose is an large polysaccharide that is deposited in the sieve tubes at the end of the growing season
-Deposited around the sieve plates that block the flow in the sieve tube
-Prevents a pathogen from spreading around the plant

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54
Q

How is tylose formation a physical defense

A

A tylose is a baloon-like swelling/projection that fills the xylem vessel
-When tylose is formed plugs the vessel and so vessel can no longer carry water
-Blocking xylem prevents spread of pathogens through heartwood
-Tylose contains a high concentration of chemicals (terpenes) that are toxic to pathogens

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55
Q

Xylem - parenchyma cells

A

As wood ages, parenchyma cells become filled with terpenes
-Eventually will burst into dead cells through a pit connecting the two
-Parenchyma then dies

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56
Q

Chemical defenses

A

Chemicals have antipathogenic properties: terpenoids, phenols, alkaloids, hydrolytic enzymes

Passive: terpenes in tylose , tannins in bark
But because production requires energy many not formed until after infection

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57
Q

Active defenses

A

Pathogens attack specific chemicals in cell walls and can be detected by plant cells
Chemicals include specific proteins and glycolipids
-Plant responds by fortifying the defence already present
-Increasing physical defenses and producing defensive chemicals

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58
Q

Active defenses that increase the physical defense

A

1)Cell walls thickened and strengthened with additional cellulose
2)Deposition of callose between the plant cell wall and plasma membrane near invading pathogen
- Callose impedes cellular penetration at the site of infection
-Strengthens cell wall and blocks plasmodesmata
-Oxidative bursts produce highly reactive Oxygen molecules capable of damaging cells and invading organisms
-Increase in production of chemicals

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59
Q

Chemicals

A

-Terpenoids
-Phenols
-Alkaloids
-defensive proteins (defensins)
-Hydrolytic enzymes

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60
Q

Terpenoids

A

Range of essential oils that have antibacterial properties and antifungal properties
-Also create a scent i.e. menthols/ menthones produced by mint plants

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61
Q

Phenols - helps prevent spread of pathogens

A

Antibiotic/antifungal
Tannins:
-Found in bark inhibit insect attack
-Bind to salivary proteins and digestive enzymes such as trypsin and chymotrypsin, deactivating enzymes
-Insects that ingest high amounts of tannins do not grow and will die

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62
Q

Alkaloids

A

Nitrogen-containing compounds i.e. caffeine, nicotine, cocaine, morphine, solanine
-Bitter to inhibit herbivore feeding
-Act on a variety of metabolic reactions via inhibiting/ activating enzyme action
-Some alkaloids inhibit protein synthesis
-If plants can reduce grazing by large animals then suffer less damage

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63
Q

Defensive proteins (defensins)

A

Small cytsteine rich-proteins that have broad anti-microbial activity
-Appear to act upon molecules in the plasma membrane of pathogens possibly by inhibiting the action of ion transport channels

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64
Q

Hydrolytic enzymes

A

Found in spaces between cells
-Chitinases - break down chitin in fungal cell walls
-Glucanases - hydrolyse the glycosidic bond in glucans
-Lysozymes - degrade bacterial cell walls

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65
Q

Necrosis

A

Deliberate cell suicide
-Kills plant cells in infected areas and limits pathogens’ access to water and nutrients thus stopping it from spreading further around the plant
-Intracellular enzymes activated on injury
-Enzymes destroy damaged cells and produce brown spots on leaves/dieback

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66
Q

Canker

A

Sunken necrotic lesion in woody tissue ie. main stem/branch
-Causes death of the cambium tissue in bark

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67
Q

Primary defenses

A

Non- specific defenses that prevent pathogens entry into the body

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68
Q

What are the primary defenses

A

-Skin
-Blood clotting and skin repair
-Mucous membrane s
-Coughing/sneezing
-inflammation

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69
Q

The skin as a primary defense

A

Outer layer - epidermis and consists of layers of cells - Keratinocytes
-Produced by mitosis at the base of the epidermis
-Migrate out to the surface of the skin
-As migrate they dry out and cytoplasm is replaced with the protein keratin - Keratinisation
-30 days
-When cells reach the surface no longer alive
-Keratinsied layer of dead cells acts as an effective defense against pathogens
-Eventually dead cells slough off

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70
Q

What must happen when the skin is damaged

A

Abrasions/lacerations - the body must prevent excess blood loss by forming a clot, making a temporary seal to prevent infection, and repair the skin

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71
Q

Blood clotting

A

-Involves calcium ions and 12 factors (Clotting factors)
-many of the factors are released from platelets and from the damaged tissue (factors activate the enzyme cascade)

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72
Q

What must be prevented in blood clotting

A

Blood clots forming in the blood vessels

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73
Q

Once the clot has formed

A

Begins to dry out and form a scab
-Scab shrinks as it dries and draws the side of the cut together - temporary seal under which the skin is repaired

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74
Q

Stages of the skin repair

A

1) Deposition of the fibrous collagen under the scab
2) Stems cells in the epidermis divide by mitosis to form new cells
3) New cells migrate to the edges of curt and differentiate to form new skin
4) New blood vessels grow to supply O2 and nutrients to the new tissue
5) Tissues contract to draw edges of the cut together so repair can be completed

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75
Q

Formation of new skin

A

1) Deposition of fibrous collagen under the scab
2) Stem cells in the epidermis then divide by mitosis to form new cells
3) New cells migrate to the edges of the cut and differentiate to form new skin
4) New blood vessels grow to supply O2 to new tissues
5) Tissues contract to help draw edges of the cut together so that the repair can be completed
6) Scab released

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76
Q

Enzyme cascade

A

1) Damage to blood vessels releases clotting factors
2) Platelets bind to collagen to release clotting factors
3) Inactive thrombokinase in blood (factor X) to active thrombokinase (an enzyme)
4)Prothrombin in blood with calcium ions to active thrombin (an enzyme)
5) Solubefibrinoge in plasma to insolube fibrin
6) Fibres attach to platelets in the plug
7) Clot

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77
Q

Other ways in which a clot can be formed

A

1) Platelets bind to collagen and release clotting factors - temporary platelet plug formed - clot
2) RBC and platelets trapped - clot

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78
Q

Mucous membranes

A

Certain substances such as food and O2 enter the blood and may harbor microorganisms
-Exchange surfaces thinner and less protected
-Cilia/ goblet cells / extra mucous secreting gland under the epithelium - move down trachea where it can enter esophagus and killed by acidic conditions of the stomach

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79
Q

Where can mucous membranes be found?

A

Airways
-Gut
-genital areas
-Anus
-Ears
-Nose

80
Q

Coughing/ Sneezing

A

The sudden expulsion of air will carry with it the microorganisms

81
Q

What is inflammation detected by

A

Detected by mast cells which release histamine

82
Q

Histamine effects

A

Vasodilation makes capillary walls more permeable to WBC and some proteins that enter tissue fluid
-Increased production of tissue fluid causes swelling (oedma)
-Excess TF drained into the lymphatic system where lymphocytes stored

83
Q

Other primary defences

A

-Eyes are protected by antibodies and enzymes in the tear fluid
-Ear canal is lined by wax which traps pathogens
-Female reproductive system protected by a mucus plug in the cervix and by maintaining acidic conditions in the vagina

84
Q

Secondary defences

A

Activated when the pathogen has entered the body
-Recognised as foreign by chemical markers on its outer membrane

85
Q

Antigens

A

Membrane-bound chemical markers on the outer membrane used to recognise a pathogen
-proteins/glycoproteins intrinsic to the plasma membrane
-Specific to the organism
-Own cells have antigens but recognised as our own and so do not produce a response

86
Q

What is an Opsonin

A

Protein that bind to the antigen on a pathogen and then allow phagocytes to bind
-type of antibody
-Some unspecific and can attach to a variety of pathogenic cells

87
Q

Role of an opsonin

A

Role is to enhance the ability of phagocytic cells to bind and engulf a pathogen

88
Q

Phagocytes

A

The first line of secondary defense is phagocytosis
-Specialised cells in the blood and tissue fluid engulf and digest the pathogens

89
Q

Neutrophils

A

Most common type of phagocyte
A type of WBC that engulfs foreign matter and traps it in a large vacuole (phagosome) which fuses with lysosomes to digest foreign matter

90
Q

Structure and role of neutrophil

A

-Multi-lobed nucleus
-Manufactured in the bone marrow
- Travel in blood and squeezed out into tissue fluid
-Short-lived but released in large numbers when infected
-Contain large number of lysosomes
-Engulf and digest pathogens and then die shortly after

91
Q

Pus

A

Dead neutrophils that have collected in the area of infection

92
Q

Phagocytosis

A

1) Neutrophil binds to opsonin attached to antigen of pathogen
2) Pathogen is engulfed by endocytosis forming a phagosome
3) Lysosome fuse to the phagosome and release lytic enzymes into it
4) After digestion the harmless products can be absorbed into the cell

93
Q

Fungi plant diseases

A

Black sigatoka (Bananas)
Causes leaf spots which reduces yield

94
Q

What do WBC differentiate into

A

Phagocytes (Neutrophils/macrophages)
Lymphocytes (B cells/ T cells)

95
Q

What cells mature in bone marrow

A

-neutrophils
-B cells

96
Q

Where do you T cells come from

A

Mature in the thymus gland

97
Q

What is important to note about each antigen

A

A different antibody will be made for each

98
Q

What are specialisations of Phagocytes

A

-Receptors on plasma Membrane that can bind to opsonin or a specific antigen
-Lobed nucleus
-well developed cytoskeleton
-Many lysosomes containing lysin
-many mitochondria
- ribosomes to synthesise enzymes involved

99
Q

What does a well developed cytoskeleton for a phagocyte ensure

A

helps the cell to change shit to engulf pathogens and move lysosomes and vacuoles around inside the cell

100
Q

Antigen presenting cell

A

A cell that isolates the antigen from a pathogen and places it on the plasma membrane so that it is recognised by the other cells of the immune system

101
Q

E.g. of antigen-presenting cells

A

-Macrophage
-Infected cell
-Pathogens in bodily fluids

102
Q

Macrophage

A

-Manufactured in the bone marrow and mature in the lymph nodes
-Travel in the blood as monocytes before settling into bodily tissues
-Large kidney shaped nucleus (largest WBC)

103
Q

Dendritic cells

A

Type of macrophage
-Found in the peripheral tissues

104
Q

Role of macrophages

A

When it engulfs a pathogen it does not fully digest
-Antigen is saved and moved to a special protein complex on the surface of the cell
-Antigen presenting

105
Q

What does a lobed nucleus for a phagocyte ensure

A

that allows the cell to squeeze through narrow gaps

106
Q

How is a macrophage an antigen presenting cell

A

It exposes the antigen on its surface so the immune system can recognise the antigen
-Special protein complex ensures antigen-presenting cell is not mistaken for being foreign

107
Q

Outline the process of the specific immune response

A

1) Pathogen enters the cell lined with antigens
2) Antigens on pathogen are then presented on antigen presenting cells
3)Lymphocytes are made in the bone marrow (B cells mature here whilst T cells mature in thymus gland)
4)These then undergo clonal selection with the antigen presenting cell
5) clonal expansion (proliferation) occurs
6) Cells differentiate into specific functions

108
Q

Clonal selection

A

Activation of the immune response
Selection of specific B/T cells that are specific shape so that it is complimentary to the specific shape of the antigen

109
Q

How is clonal selection triggered

A

Contact between the antigen and lymphocytes can be achieved directly when pathogenic cells enter the lymph nodes or by the presentation of antigen-presenting cells

110
Q

What is clonal expansion (proliferation)

A

-Once found the correct cells are many clones are made of the cell that has the specific complimentary receptors to the foreign antigen

111
Q

Differntation

A
112
Q

What are the different types of T cells

A

-T killer cells
-T memory cells
-T helper cells
-T regulator cells

113
Q

T Killer

A

Cells that attack and destroy our own body cells that are infected by the pathogen

114
Q

T memory

A

Remain in blood providing long-term immunity

115
Q

T helper cells

A

Release cytokines that stimulate B cells to develop and stimulate phagocytosis by the phagocytes

116
Q

T regulator cells

A

Shut down immune response after pathogen has successfully been removed
Also involved in preventing autoimmunity

117
Q

What do the B cells differentiate into

A

B memory cells
Plasma cells which makes antibodies

118
Q

B memory cells

A

Stay in the blood and hold the specific shape of the receptor which is complementary to the specific shape of the antigen of the pathogen to trigger when infected with the same pathogen again a faster response

119
Q

Cells under microscope

A

Macrophage - Kidney shaped nucleus
Neutrophils - multi-lobed nucleus
B/T - smaller and nucleus fills cell

120
Q

Cytokines

A

Hormone like molecules used in cell signalling to stimulate the immune response

121
Q

How do cytokines work

A

Specific shape of receptor is complimentary to the specific shape of the cell surface receptor on the target cell

122
Q

Eg of signalling molecules

A

-Macrophages release monokines
-T cells/ Macrophages release interleukins
-Many cells release interferon

123
Q

The release of monokines

A

Some monokines attract neutrophils ( by chemotaxis- The movement of cells towards a particular chemical)
-Others stimulate B cells to differentiate and release antibodies

124
Q

The release of interleukins

A

Stimulate clonal expansion and differentiation of B and T cells

125
Q

The release of interferon

A

Inhibits virus replication and stimulates the activity of t killer cells

126
Q

How does autoimmune disease occur

A

When antibodies attack own antigens as have receptors which have a specific shape complimentary to our own antigens
-Occurs possibly because antigens that are not normally exposed become exposed to attack

127
Q

What usually prevents the probability of an autoimmune disease

A

B/T cells specific to our own antigens are destroyed during early development of the immune system

128
Q

Causes of autoimmune disease

A

Not known
Environmental/genetics

129
Q

e.g of auto immune disease

A

Arthritis / lupus

130
Q

Arthiritis

A

Painful inflammation of a joint course is in certain that starts with antibodies attacking the membranes around the joint

131
Q

Lupus

A

Can affect any part of the body causing swelling and pain
-May be associated with antibodies that attack certain proteins in the nucleus in cells and affected tissues

132
Q

Antibodies

A

Have receptors with a specific shape that is complimentary to the specific shape of the antigen
-attach to pathogenic antigens neutralising them
-Own antigens recognised by the immune system so do not trigger a response

133
Q

What type of protein is an antibody

A

Immunoglobulins (complex proteins produced by plasma cells in the immune system)

134
Q

Antibody structure

A

-Y shape
-Two binding sites and and an end that can stimulate phagocytosis
- Variable /Constant region
-4X polypeptide chains 2x heavy 2x light
-disulphide bridges to hold polypeptides together
-Hinge region

135
Q

Variable region

A

region with specific shape that is complementary to particular antigen

136
Q

Constant region

A

Same in all antibodies may have a sight for easy binding of phagocytic cells

137
Q

Hinge region of an antibody

A

to allow flexibility so molecule can grip more than one antigen

138
Q

What must the immune system do for every antigen detected

A

-It must manufacture one type of antibody for every antigen that is detected
-it will then attach to the antigen and render it harmless

139
Q

Why do B cells all carry a slightly different DNA code

A

So the antibodies it produces are slightly different from other B cells
-Plasma cell cloned from one antibody will all make identical antibodies

140
Q

Role of opsonin as an antibody

A

Group of antibodies that bind to antigens on pathogen so phagocytes can recognise foreign cell
-then act as a binding site for phagocytic cells so these can easily find and destroy the pathogen
- Two types: non-specific/specific

141
Q

Opsonins that are not specific

A

-Some are not very specific and stick to types of molecules that are not found in the host cell
-Peptidoglycan walls on bacteria

142
Q

Opsonins that are specific

A

Produced as part of the specific immune response and bind to very specific antigens
-Neutralisation - Sometimes binds to pathogen before phagocyte comes along so it can’t invade other cells
-Assist in phagocytosis but also prevents pathogen entering a host cell before it can be attacked by phagocytes

143
Q

Agglutinins

A

Each antibody has two identical binding sites so can cross-link pathogens
-binds to antigen on pathogen at one binding site and bind to another antigen on another pathogen at another other
Many antibodies clump (agglutinate) together

144
Q

Advantages of agglutinins

A

agglutinated pathogens physically impeded from carrying out functions such as entering host cells - noninfective
-can be readily engulfed by phagocytes - particularly effective against viruses

145
Q

Anti-toxins

A

-some antibodies bind to molecules that released by pathogenic cells (neutralisation)
- Molecules may be toxic and the action of anti-toxins render them harmless

146
Q

What does the graph of a primary and secondary response look like

A

primary response:
-lower concentration of antibodies produced
-takes a few days before number of antibodies in the blood can rise to a level that can combat infection
Secondary response:
-more rapid
-produces a higher concentration of antibodies

147
Q

Why is the secondary response more rapid

A

B memory cells produced in primary response stay in the blood and have the memory to create the right antibodies with complimentary receptors to the antigens
-this means it is much faster there is a greater production of antibodies

148
Q

What happens in the primary response

A

differentiation occurs
-Takes a few days to happen but create memory cells that stay in the blood

149
Q

Why don’t you have any symptoms from the pathogen in the secondary response

A

B memory cells in the blood recognise the antigens on the pathogen and B memory cells rapidly differentiate into B plasma cells that produces antibodies with the specific receptor complimentary to the specific shape of the pathogens antigen
- antibody is fast and occurs in high concentrations

150
Q

Vaccination

A

A way of stimulating an immune response so immunity is received provides immunity to specific diseases
- created by deliberate exposure to antigenic material that has been rendered harmless
- antigenic material usually injected but some times can be taken orally

151
Q

Why are vaccinations effective

A

immune system treats antigenic material as a real disease
-antibodies and memory cells produced

152
Q

What are the different forms antigenic material can be used in vaccines

A

whole life microorganisms
-harmless or attenuated (weakened) version of pathogenic organism
-Dead pathogen
-preparation of antigens from a pathogen
- toxoid which is harmless version of a toxin

153
Q

Use of whole life organisms for Vaccines

A

not as harmful as ones that cause real disease but must have similar antigens so antibodies produced will be effective against real pathogen
(e.g.smallpox vaccine which uses similar virus that causes cowpox)

154
Q

e.g. of diseases where harmless or attenuated (weakened) version of pathogenic organism is used for vaccination

A

Measles and TB vaccines

155
Q

e.g. of diseases where a dead pathogen is used for vaccination

A

Typhoid and Cholera

156
Q

e.g. of a vaccine where preparation of antigens from a pathogen is used for vaccination

A

Hepatitis B vaccine

157
Q

e.g. of a vaccine where a toxoid which is harmless version of a toxin is used for vaccination

A

tetanus vaccine

158
Q

What is herd vaccination

A

using vaccines to provide immunity to all almost all of the population at risk
Once enough people are immune disease can no longer be spread through the population and you achieve ‘herd immunity’
-In order to be effective it is essential to vaccinate almost all population

159
Q

How many people that need to be vaccinated to prevent the spread of measles

A

95%

160
Q

How many people that need to be vaccinated to prevent the spread of smallpox

A

80-85%

161
Q

What diseases are vaccinated to immunise young children in the UK

A

-Tetanus
-Meningitis
-Whooping cough
-Measles

162
Q

What is ring vaccination

A

-used when a new case of disease is reported
- involves vaccinating all the people in immediate vicinity of new cases
-May mean vaccinating surrounding houses or even whole villages or towns
-Also used in many parts of the world to control the spread of livestock disease

163
Q

What is a genetic mutation

A

Changes antigen so B memory cells may not recognise new antigens
-Pathogen may be transmitted and incidence of the disease increases

164
Q

What is a deadly about genetic mutations

A

Replaces other versions of the virus
-affect important parts of the virus
-Increases viruses ability to infect cells

165
Q

How do variants emerge

A

In patient with weakened immune system
- unable to beat the virus and instead the body becomes a breeding ground for virus to mutate

166
Q

Do you vaccine still work against genetic mutations

A

Most vaccines train immue system to attack several different parts of the virus so eventhough mutated vaccine should still work
-However ‘vaccine escape’ - When virus changes so dodges full affect of vaccine and can continue to infect more people

167
Q

What is some examples of different variants

A

Beta Variant S. Africa
Omnicrom

168
Q

What is an epidemic

A

-Rapid spread of disease through a high proportion of the population
-when certain pathogens (influenza) Are unstable and regularly undergo changes in the antigens

169
Q

Why do threats from epidemics need to be monitored

A

So new strains of the pathogen can be identified
-Enables health authorities to prepare by stockpiling suitable vaccines and vaccinating those who are at particular risk from the disease

170
Q

What is a pandemic

A

Worldwide epidemic

171
Q

Example of a disease that has caused a pandemic

A

Influenza

172
Q

Those at particlular risk of influenza

A

65+
People with respiratory tract conditions

173
Q

How another pandemic of influenza is prevented

A

-All people over 65 and at-risk immunized
-New versions of influenza vaccination administered via a nasal spray
-Worldwide research to determine the strain of flu

174
Q

What is active natural immunity

A

immunity provided by antibodies made in the immune system as a result of infection
-person suffers from disease once and then is immune (chickenpox)

175
Q

What is passive natural immunity

A

antibodies provided by the placenta or breast milk
-makes the baby immune to diseases to which the mother is immune
-useful in the first years of the babies life when it’s immune system is developing

176
Q

What is active artificial immunity

A

-immunity provided by antibodies made in a new system as a result of vaccination
-Person is injected with a weakened dead or similar pathogen with antigens and this activates immune system
(TB and influenza)

-Giving antigenic material so you are making antibodies

177
Q

What is passive artificial immunity

A

-immunity provided by injection of antibodies made by another individual (hepatitis A and B)
-If antibodies are given no memory cells are made = no immunity
-Stimulates a quick fast response

178
Q

What are the reasons why we need to find new sources of medicine

A

-New diseases are emerging
-many diseases where treatment is ineffective
-Some antibiotic treatments are becoming less effective due to the pathogen gaining resistance

179
Q

What do you use antibiotics against

A

The growth of fungi or bacteria

180
Q

What are the two examples of bacteria that have become resistant to antibiotics

A

-C.diff
-MRSA

181
Q

How has accidental discovery lead to new sources of medicine

A

Pencillin
- fungus Pencillium released compounds that kill bacteria
-Observed then scientists purified

182
Q

How has traditional medicines contributed to sources of new medicines

A

many drugs have been used for centuries because people have noted that plants/extracts have a beneficial effect
E.g
-Poppies
-Willow bark

183
Q

Poppies medicinal properties

A
  • morphine and opium for anaesthetic - reduce nervous action in the central nervous system if the nerves cannot carry impulses then no pain is felt
184
Q

Willow bark medicinal properties

A
  • Relieves pain and fever after discovery of his active ingredient to reduce the side-effect of stomach leading by adding an aceytl group - ibuprofen and aspirin
185
Q

How does observations of wildlife lead to a sources of new medicines

A

-Monkeys/bears etc rub citrus oils on the case as insecticides and antiseptics important to prevent insect bites/infection
-Birds line there nests with medicinal leaves in order to protect chicks from mites

186
Q

What do chimpanzees do that humans have observed

A

Swallow leaves folded in a particular way to remove parasites from their digestive trac

187
Q

How has research into disease-causing mechanisms contributed to new medicine

A

-use of receptors on plasma membrane
-Glycoprotein receptor molecules can be isolated in sequence
-once the amino acid sequence is known molecular modelling can be used to determine the shape of the receptor -Next step is to find a drug that mimics the shape of the receptor and can be used to bind to the virus itself which would block the virus from entering the t helper cells
- in a similar way drugs that inhibit the action of certain enzymes can also be developed

188
Q

Plant research for medicinal drugs

A

Research into plants as traditional remedies:
Enables scientists to isolate the active ingredient
molecule can be analyzed and similair molecules can be manufactured

189
Q

Plant research for medicinal drugs on tropical plants

A

Great diversity hopes that may contain molecules that form new medicinal drugs

190
Q

Personalized medicine

A

The development of designer medicines for individuals

191
Q

How his personalised medicine contributed to new medicines being found

A

Sequencing technology and molecular modelling has huge potential for future medicines:
-possible to screen for genomes of plants/microorganisms to identify potential medicine or compounds from DNA sequences
-hoped that this technology can be taken further once technology is fully developed
-may be possible to sequence change from individuals with particular conditions and develop specific drugs for condition

192
Q

Synthetic biology

A

The re-engineering of biology
-Production of new molecules that mimic natural processes
-Use of new biological systems that do not exist in nature

193
Q

How his synthetic biology contributed to new medicine

A

development of new molecules in particular enzymes that mimic biological systems is one form of synthetic biology
-Another way that synthetic biology is used is to design and construct new devices and systems that may be useful in research/healthcare/manufacturing

194
Q

What are most antibiotics today derivatives from

A

Compound made by the genus Streptomyces

195
Q

Leafcutter ants

A

Fam fungi which they feed to growing larvae
-In order to prevent infection in fungal gardens they carry symbiotic bacteria including Streptomyces which produce antibiotics
-Scientists are currently researching

Module 4 (5 decks)

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