Communicable Diseases Flashcards

1
Q

When are antibodies produced?

A

In response to a non-self antigen

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2
Q

What are antibodies produced by?

A

B lymphocytes

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3
Q

What type of molecule(carb, lipid, protein etc) is an antibody?

A

Y shaped glycoproteins called immunoglobulins

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4
Q

What is the role of the hinge region?

A

Allows the ‘arms’ to move, to give flexibility to the molecule

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5
Q

What does the receptor site bind to?

A

A white blood cell

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6
Q

What holds the light and heavy chain together?

A

Disulfide bridges

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7
Q

What is agglutination?

A

The process of antibodies causing pathogens to

clump together, which immobilise them

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8
Q

What is the benefit of agglutination?

A

The clump becomes too big to enter host cells

The clump cannot travel around due to its size (immobilised) so easier to consume via phagocytosis

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9
Q

What are the two ways antibodies neutralise antigens?

A

1) Acting as anti-toxins and binding to the antigens toxins produced by the pathogen
2) Antibodies block receptors on the pathogen to prevent them being able to bind and enter the host cell

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10
Q

How do antibodies act as opsonins?

A

Antibodies bind to antigens on pathogens and ‘tag’ them marking them for destruction by phagocytes

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11
Q

What is the role of the variable region?

A

To give the antibody specificity to different antigens

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12
Q

How many variable regions does an antibody have? Why?

A

2, allows for binding of more than one of the same anitgens

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13
Q

Which lymphocyte does cell mediated immunity use?

A

T lymphocytes

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14
Q

What two types of lymphocyte are there? Where do they mature?

A

T lymphocytes- thymus gland

B lymphocytes- bone marrow

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15
Q

When does cell mediated immunity occur?

A

In response to self cells changing in some way

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16
Q

Give 4 examples of when cell mediated immunity occurs

A

Virus infection
Antigen processing
Mutation
Cells from transplanted tissue

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17
Q

What are the 4 types of T lymphocytes involved in cell-mediated immunity?

A

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

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18
Q

What are interleukins?

A

Type of cytokine
Produced by T helper cells which stimulate the T helper cells to divide via mitosis to produce a clone of T helper cells.
Involved in stimulating phagocytosis

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19
Q

What are the 3 roles of T helper cells?

A

Stimulate activity of B cells - increasing antibody production
Stimulates production of other types of T cells
Attracts and stimulates macrophages to ingest pathogens with APCs

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20
Q

What is the role of a T killer cell? How do they perform this?

A

Destroy pathogen carrying antigen

Produce a chemical called perforin which kills pathogen by making holes in cell membrane so it is easily permeable

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21
Q

What is the role of T memory cells?

A

Part of immunological memory

Come into contact with an antigen for second time, divide rapidly to form T killer cells

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22
Q

What is the role of T regulator cells?

A

Supress immunes system acting to control and regulate it.
Stop immune system once pathogen has been eliminated
Prevents an autoimmune response occuring

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23
Q

Describe the steps of cell-mediated immunity

A

1) Non-specific defence system,macrophages turn into APCs
2) Some T helper cells fit antigens
3) T helper cells become activated and produce interleukins which stimulates more T cells to divide rapidly by mitosis
4) Clones of T cell formed and could do 4 different things
Developed in to T memory cells
Produce interleukins that stimulate phagocytosis
Produce interleukins stimulate B cells to divide
Stimulate development of T killer cells

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24
Q

What does humoral response occur in response to?

A

Body responds to antigens found outside the cells and APCs. The humoral response produces antibodies that are soluble in blood and tissue fluid and are not attached to cells

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25
Q

What are the 3 main types of B lymphocytes?

A

Plasma cells
B effector cells
B memory cells

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26
Q

What is the role of plasma cells?

A

Produce antibodies to a particular antigen and release them into the circulation

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27
Q

What is the role of B effector cells?

A

Divide to form plasma cell clones

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28
Q

What is the role of B memory cells?

A

Immunological memory

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29
Q

What are the 6 stages of humoral immunity?

A
Recognition
B cell activation
Clonal Expansion
Antibody production
Antibody destruction
Long term immunity
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30
Q

What occurs in the ‘recognition’ stage of humoral immunity?

A

B cell has complementary antibodies to antigens on pathogen

B cell engulfs pathogen and processes to become an APC.

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31
Q

What occurs in ‘B cell activation’?

A

Clonal selection- B cells bind to T cells that are specific for same antigen
B cell turns activated

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32
Q

What occurs in ‘clonal expansion’?

A

Selected B cells divide by mitosis to form identical B cells

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33
Q

What occurs in ‘antibody production? How?

A

Plasma cells secrete antibodies that are specific to that of the antigen that has been encountered

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34
Q

What occurs in ‘antibody destruction’?

A

Antibodies bind to antigens
Forms antibody-antigen complex
Results in: agglutination, neutralisation, opsonisation

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35
Q

What is the primary immune response?

A

The immune system is exposed to an antigen for the first time. During this time the body must learn to recognise the antigen, learn how to produce antibodies against it and to produce memory cells.

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36
Q

What is the secondary immune response?

A

Some of the plasma cells developing into B memory cells which divide to form plasma cells on reinfection. Occurs quickly.

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37
Q

What are auto-immune diseases?

A

When the immune system stops recognising self cells and starts to attack and destroy healthy tissue

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38
Q

Give 4 examples of auto-immune diseases

A

Lupus
Type 1 diabetes
Rheumatoid arthritis
MS

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39
Q

What are 3 problems of immunosuppressant drugs?

A

Lowers overall immunity to all infections
Fewer T cells
Fewer memory cells

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40
Q

What does Type 1 diabetes affect and how is it treated?

A

Insulin-secreting cells of pancreas

Treatment= insulin injections, pancreas transplants, immunosuppressant drugs

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41
Q

What does Rheumatoid arthritis affect and what is the treatment?

A

Joints

Treatment= no cure, anti-inflammatory drugs, steroids, pain relief, immunosuppressants

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42
Q

What does Lupus affect and what is its treatment?

A

Skin, joints, and any organ

Treatment= no cure, anti-inflammatory drugs, immunosuppressants, steroids

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43
Q

What is active immunity?

A

An individual comes into direct contact with a pathogen or its antigens
Immune system responds and produce antibodies
Develop an immunological memory

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44
Q

What are the 2 types of active immunity?

A

Natural active immunity

Artificial active immunity

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45
Q

How does natural active immunity occur?

A

Infected by a pathogen
Body produces specific antibodies
Develop long term immunity

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46
Q

How does artificial active immunity occur?

A

Vaccination

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47
Q

What is passive immunity?

A

Antibodies are introduced into the body from another source, not produced by you
Do not come into direct contact with pathogen
Immunity is immediate
Immunity doesn’t last

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48
Q

Give examples of artificial passive immunity

A

Antibodies injected into your blood

Snake venom, rabies antibodies and tetanus antibodies

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49
Q

Give example of natural passive immunity

A

Colostrum in mother’s breast milk

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50
Q

What is a vaccination?

A

Introducing a safe form of an antigen into the body to stimulate your own B lymphocytes to produce specific antibodies which neutralise antigens

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51
Q

What are the 5 types of vaccination?

A

1) Dead or inactivated bacteria or virus
2) Attenuated(weakened) strains of live virus
3) Modified toxin
4) Isolated antigens
5) mRNA

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52
Q

What is herd immunity?

A

A critical proportion of the population being vaccinated against a disease

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53
Q

How does vaccination work?

A

1) A pathogen is made safe so antigens are intact but no risk of infection
2) Small amounts of vaccine injected into blood
3) Primary immune response is triggered by foreign antigen, production of antibodies and memory cells
4) Next in contact, secondary immune response is triggered

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54
Q

What is an epidemic?

A

A communicable disease spreading rapidly to a lot of people at a local or national level

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55
Q

What is a pandemic?

A

A communicable disease spreads rapidly across a number of countries and continents.

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56
Q

Where are most medicines found?

A

Plants and microorganisms

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57
Q

What is the source and use of penicillin?

A

Source: mould growing on melons
Use: antibiotic

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58
Q

What is the source and use of docetaxel?

A

Source: yew trees
Use: breast cancer

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59
Q

What is the source and use of aspirin?

A

Source: willow bark
Use: pain killer, anti-pyretic, anti-inflammatory

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60
Q

What is the source and use of prialt?

A

Source: Venom of a cone snail
Use: Pain killing drug

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61
Q

What is the source and use of vancomycin?

A

Source: Soil fungus
Use: Antibiotic

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62
Q

What is the source and use of digoxin?

A

Source: Foxgloves
Use: heart drug for atrial fibrillation and heart failure

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63
Q

What is pharmacogenetics?

A

Personalised medicine, a combination of drugs that work with your individual combination of genetics and disease

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64
Q

What are the advantages of producing plant chemicals in a lab?

A
Doesn't have seasonal variation
Can give a measured dose
Requires less plant material
Synthetic biology is quicker and cheaper
More pure
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65
Q

What are antibiotics?

A

Substances that can destroy or inhibit the growth of bacteria without impacting our cells

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66
Q

What are the two ways antibiotics work?

A

1) Some inhibit growth of bacterial cells

2) Some directly destroy bacterial cells

67
Q

Why do antibiotics not work on viruses?

A

Antibiotics work by breaking down peptidoglycan cell wall

Viruses have protein coat not peptidoglycan cell wall so cannot be broken down

68
Q

What is conjugation?

A

The process of genetic material being transferred from one molecule to another by direct contact between the cells

69
Q

How does antibiotic resistance come about?

A

A mutation occurs in a bacteria
Selection pressures mean that the bacteria that is resistant is selected
This mutation is passed on through binary fission and conjugation

70
Q

What are 2 high profile cases of antibiotic resistant bacteria?

A

MRSA

C difficile

71
Q

What is MRSA and what can it cause?

A

Bacterium carried on nose and skin (30% pop)

Causes boils, abscesses and septicaemia

72
Q

What is C difficile and what can it cause?

A

Bacterium found in gut of 5% pop

Produces toxins that damage lining of intestine leading to diarrhoea, bleeding and death

73
Q

Give 3 ways to avoid antibiotic resistance

A

Minimise use of antibiotics
Finish course
Prescribe targeted antibodies

74
Q

What are the 4 main types of pathogen?

A

Fungi
Bacteria
Protoctista
Virus

75
Q

What is the role of vectors?

A

Carry pathogen from one organism to another

76
Q

Name 2 common vectors

A

Water and Insects

77
Q

What are the 2 main ways bacteria can be classified?

A

By basic shapes

By cell walls

78
Q

What are the 5 main shapes of bacteria? (Latin & English) I wouldn’t worry too much about learning this

A
Rod shaped- bacilli
Spherical- cocci
Comma Shaped- vibrios
Spiralled- spirilla
Corkscrew- Spriochaetes
79
Q

What are the 2 main types of cell walls? What do they look like under a microscope?

A

Gram positive bacteria- purple-blue under light microscope

Gram negative bacteria- red

80
Q

Why is knowing the type of cell wall useful?

A

Affects how they react to different types of antibiotics

81
Q

Describe the structure of a virus

A

Nucleic Acid strand
Surrounded by a capsid protein coat that encloses genetic material
Surrounded by a phospholipid bilayer called an envelope that is embedded with envelope proteins

82
Q

What is a bacteriophage?

A

A virus that takes over bacteria

Uses bacteria to replicate and then destroys them at the same time

83
Q

Are all protists pathogenic?

A

No, only a small percentage of protists are pathogenic

84
Q

What is the term used to describe pathogenic protists?

A

Parasitic protists

85
Q

What are the 2 main ways protists enter the body? Give examples of diseases transferred by this method

A

Vector- malaria and sleeping sickness

Body through polluted water- amoebic dysentery and Giardia

86
Q

How do most fungi gain food?

A

Saprophytic- feed on dead and decaying matter

Use extracellular enzymes to digest food

87
Q

How do fungi tend to attack plants?

A

Attack leaves of the plants
Stop it photosynthesising
Quickly kills the plants

88
Q

Give 3 ways that pathogens directly damage host tissues, explain each way

A

Viruses take over cell metabolism (the viral DNA enters host cell, and inserted into DNA, virus uses cell to create new viruses and then bursts, infecting other cells)
Protoctista take over the cells and break open as new generation emerge( use cell contents to reproduce)
Fungi digest living cells and destroy them

89
Q

What are 3 things that bacterial toxins do to the cell?

A

Break down cell membrane
Damage or inactivate enzymes
Interfere with host cell DNA so they cannot divide

90
Q

Give 2 pathogens that produce toxins which damage the tissue

A

Bacteria

Fungi

91
Q

What is ring rot caused by and what does it affect?

A

Bacterial disease of potatoes, tomatoes and aubergines

92
Q

What does ring rot damage?

A

Leaves, tubers and fruit. Causing 80% crop to be destroyed.

93
Q

What are the measures put in place to prevent ring rot spreading?

A

Not growing potatoes in a field for 2 years after infection

94
Q

What is TMV (tobacco mosaic virus) caused by and what does it affect?

A

Virus that affects tobacco plants and 150 other species including tomatoes, peppers, cucumbers, petunias and delphiniums

95
Q

What are the effects of TMV?

A

Damages leaves, flowers and fruit
Stunting growth
Reduces yield
Total crop loss

96
Q

What are the measures of prevention/cure for TMV?

A

No cure

Resistant crop strains available

97
Q

What is potato blight caused by?

A

Fungus like protoctist

98
Q

How does potato blight affect plants?

A

Hyphae penetrate host cells

Destroys leaves, tubers and fruit

99
Q

How is potato blight treated?

A

No cure
Resistant strains are available
Careful management and chemical treatments can reduce infection risk

100
Q

What is black sigatoka and what does it affect?

A

Fungal banana disease

101
Q

How does black sigatoka affect plants?

A

Destroys leaves
Hyphae penetrate and digest cells, turning leaves black
Plants infected= 50% reduction in yield

102
Q

What are the treatments/prevention mechanisms for black sigatoka?

A

Resistant strains
Good husbandry
Fungicide treatment

103
Q

What type of pathogen is TB and what organisms does it affect?

A

Bacterial disease of humans, cows, pigs and badgers and deer

104
Q

How does TB affect an organism?

A

Damages and destroys lung tissue and supresses the immune system

105
Q

How is TB treated/prevented?

A

Curable by antibiotics

Preventable by improving living standards and vaccination

106
Q

How does bacterial meningitis affect the body?

A

Meninges of the brain are affected

107
Q

What is the main symptom of meningitis?

A

Blotchy red/purple rash that doesn’t fade when pressed with a glass

108
Q

How is bacterial meningitis treated?

A

Antibiotics cure disease if delivered early

Vaccines can protect against some form of bacterial meningitis

109
Q

How is HIV inserted into a host cell? (cellular level)

A

HIV= retrovirus= RNA as genetic material
Reverse transcriptase transcribes RNA to single strand of DNA
Single strand of DNA interacts with DNA of host cell

110
Q

How is HIV passed on?

A

Bodily fluids
Unprotected sex, shared needles, contaminated blood products, breast feeding, equipment used in FGM( female genital mutilation)

111
Q

What are the treatments/cures of HIV?

A

No cure
No vaccine
Anti-retroviral drugs administered to slow progress of disease

112
Q

What type of pathogen is influenza and what cells does it affect?

A

Virus

Ciliated epithelial cells in gas exchange system

113
Q

What are the 3 main strains of influenza?

A

A, B, C

114
Q

What is the most virulent strain of influenza and what are they further categorised by?

A

A

Proteins on the surface

115
Q

How do you prevent transmission of flu?

A

Flu vaccine- administered annually to protect against surface protein changes

116
Q

What is malaria caused by and spread by?

A

protoctista Plasmodium and spread by Anopholes mosquito

117
Q

Explain the plasmodium life cycle

A

Reproduce inside female mosquito
Female mosquito takes two blood meals
Passed into people during the blood meals
Invades red blood cells, liver and brain

118
Q

What are the preventative measures used in the fight against Malaria?

A
No cure/vaccine
Get rid of standing water
Mosquito nets
Window and door screens
Long sleeved clothing
119
Q

What type of pathogen is ring worm? What organisms does it affect?

A

Fungal disease affecting mammals (cattles,dogs, cats and humans)

120
Q

What are the symptoms of ring worm?

A

Grey-white, crusty, infectious circular area of skin

121
Q

What is the cure for ring worm?

A

Anti-fungal cream

122
Q

What type of pathogen is athletes foot? How does it affect cells?

A

Fungal disease that grows on and digests the warm, moist skin between toes

123
Q

What are symptoms of athletes foot?

A

Sore, itchy skin that is cracked and scaled on the foot

124
Q

What is the cure for athletes foot?

A

Anti-fungal cream

125
Q

What are the 2 main types of transmission?

A

Indirect

Direct

126
Q

What are the 3 ways direct contact passes on a pathogen? Give examples of diseases spread that way

A

Kissing or any contact with bodily fluids eg. bacterial meningitis and STIs
Direct skin to skin contact- athlete’s foot
Microorganisms from faeces transmitted on hands- diarrhoeal diseases

127
Q

What are 3 ways inoculation spreads a pathogen? Give examples of diseases spread that way.

A

Break in the skin eg. sex
Animal bite eg. rabies
Puncture wound through sharing needles eg. septicaemia

128
Q

How does ingestion spread a pathogen?

A

Taking in contaminated food or drink, which contaminates hands with pathogen which then enter the mouth
eg. amoebic dysentery or diarrhoeal diseases

129
Q

What are fomites and how do they spread pathogens?

A

Inanimate objects such as bedding, socks or cosmetics that can transfer pathogens
eg. athlete’s foot, gas gangrene and staphylococcus infections

130
Q

How are droplets passed on?

A

Droplets of saliva and mucus are passed on during coughing, sneezing and talking.

131
Q

How do vectors pass on pathogens?

A

Vectors pass on communicable diseases from one host to another.

132
Q

Give 3 examples of vectors and what pathogens they spread

A

Mosquitos- malaria
Rat fleas- bubonic plague
Bats- rabies

133
Q

What diseases can be passed on from animals to people?

A

Bird flu strain H1N1

Brucellosis- sheep to people

134
Q

How can you minimise spread of disease from animals to people?

A

Minimise close contact

Wash hands thoroughly after coming into contact

135
Q

Give 7 factors which increase the probability of disease spreading

A
Overcrowding living and working conditions
Poor nutrition
Compromised immune system
Poor disposal of waste
Climate change
Culture and infrastructure
Socioeconomic factors
136
Q

How does soil contamination spread pathogens?

A

Infected plants leave pathogens and reproductive pores in the soil which can infect the next crop

137
Q

What are 4 vectors for plant diseases? How?

A

Wind
Water
Animals- aphids can inoculate plants
Humans

138
Q

Give 5 factors that increase the risk of spread of communicable diseases in plants

A

Planting varieties of crops that are susceptible to disease
Overcrowding
Poor mineral nutrition
Damp, warm conditions aiding survival of pathogens
Climate change

139
Q

Explain the process of plants recognising an attack

A

Receptors in the cells respond to molecules from pathogens
Receptors also respond to chemicals produced when the plant cell wall is attacked
Stimulates release of signalling molecules
Turns on genes in nucleus
Triggers cellular responses such as producing defensive chemicals, and physically strengthening cell walls

140
Q

What is callose made of and what bonds are present?

A

Beta glucose

Beta 1,4 and 1,6 glycosidic bonds

141
Q

What are the 4 major roles of callose? Explain them

A

Deposited between the cell wall and cell membrane (acts as a barrier preventing pathogen entry around site of infection)
Callose continually added to cell wall along with lignin (strengthens the mechanical barrier to make thicker and stronger)
Blocks sieve plates in phloem (seals off infected part and prevents spread of pathogens)
Deposited in plasmodesmata of cells ( seals and prevents spread)

142
Q

What are the 6 examples of plant chemical defences? Give an example of each

A
Insect repellents- citronella
Insecticides- pyrethrins
Antibacterial Compounds- phenols 
Antifungal compounds- caffiene and chitinases
Anti-oomycetes- glucanases
General toxins- cyanide
143
Q

What are the 2 lines of defence in animals?

A

Primary non-specific defences

Specific immune response

144
Q

What are the 3 main barriers of entry of pathogens?

A

Skin
Mucous membranes
Lysozymes

145
Q

How does the skin prevent entry of pathogen?

A

Healthy microorganisms outcompete pathogens for space

Produces sebum which is an oily substance that inhibits growth

146
Q

How do mucous membranes prevent entry of pathogen?

A

Secrete sticky mucus
Traps microorganisms
Contains lysozymes which destroy bacterial and fungal cell walls
Contain phagocytes which remove remaining pathogens

147
Q

Where are lysozymes found and what is there role?

A

Tears, urine and stomach acid

Prevent entry by destroying cell walls

148
Q

Give 2 examples of expulsive reflexes

A

Coughs and sneezes-eject pathogen laden mucus from gaseous exchange system
Vomiting and diarrhoea- expel contents of gut along with any infective pathogens

149
Q

Explain process of blood clotting

A

Platelets come into contact with collagen in skin or wall of damaged vessel
Activated and blood clotting begins
Platelets adhere to the blood vessel and each other
Platelets produce serotonin which makes the smooth mussel in the blood vessel area contract limiting blood supply/loss
Produce thromboplastin which causes a cascade of reaction forming blood clot

150
Q

What are the 2 main chemicals produced in blood clotting?

A

Serotonin

Thromboplastin

151
Q

Explain process of wound healing

A

Red blood cells trapped in fibrin mesh forming a clot
This dries out forming a scab
Epidermal cells below scab start to grow, sealing wound permanently
Damaged vessels regrow
Collagen fibres are deposited to give strength
New epidermis reaches full strength

152
Q

What is inflammation characterised by?

A

Pain
Heat
Redness
Swelling

153
Q

What are mast cells?

A

Type of white blood cell found at boundary to tissue and external environment

154
Q

What 2 things do mast cells release?

A

Histamines & Cytokines

155
Q

What 3 things do histamines do?

A

Make blood vessels dilate causing localised heat and redness
Raise temperature to prevent pathogens from reproducing
Make capillary walls more leaky so plasma is forced out forming tissue fluid

156
Q

What are the 4 roles of cytokines?

A

Cell signalling
Attract phagocytes
Increase temperature
Initiate specific immune response

157
Q

How do cytokines increase temperature?

A

Cytokines stimulate hypothalamus to reset the thermostat, causing an increase in temperature

158
Q

Why is it useful for temperature to increase?

A

Pathogens reproduce best at or below 37

Specific immune response works better at higher temperatures

159
Q

What are phagocytes?

A

Specialised white blood cells that engulf and destroy pathogens

160
Q

What are the 2 main types of phagocytes?

A

Neutrophils and macrophages

161
Q

What is pus made of?

A

Dead neutrophils and pathogens

162
Q

Explain 5 key stages of phagocytosis

A

1) Pathogens produce chemicals that attract phagocytes
2) Phagocytes recognise pathogen is non-self
3) Phagocyte engulfs pathogen and encloses it in vacuole called phagosome
4) Phagosome combines with lysosome to form phagolysosome
5) Enzymes from lysosome digest and destroy pathogen

163
Q

How is an antigen presenting cell formed?

A

Macrophage digests pathogen
Antigens from pathogen combine with glycoproteins called major histocompatibility complex
These are moved to the cell surface membrane of macrophage
Forms an antigen presenting cell

164
Q

What are the roles of opsonins?

A

Chemicals that bind to pathogens and ‘tag’ them so they can be more easily targeted by phagocytes
Facilitate phagocytosis by increasing the number of binding sites for phagocyte and pathogen