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OCR A-Level Biology > Chap 12 - Communicable Diseases > Flashcards

Chap 12 - Communicable Diseases Flashcards

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1
Q

Define communicable diseases

A

a disease that can be passed from one organism to another due to pathogens

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2
Q

Define pathogen

A

microorganism that causes disease

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3
Q

Name 4 different pathogens and their examples

A

Virus - Bacteriophage, HIV, SARS‑CoV‑2
Protoctista - Amoebic dysentery, Giardia, Plasmodim
Bacteria - MRSA, E.coli
Fungi - Tinia pedis

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4
Q

Describe 4 ways in which pathogens can damage host tissue, causing harm.

A
  • viruses take over cell metabolism, using it to make new viruses which burst out of cell, destroying it and spreading to other cells
  • some protoctista take over cell but digest and use cell contents as they reproduce - they dont take over genetic material
  • fungi digest living cells & destroy them
  • most bacteria and some fungi can produce toxins that affect host cells/damage them and cause disease
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5
Q

What type of pathogen causes ring rot?

A

gram-positive bacterium

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6
Q

What type of pathogen causes TMV?

A

virus

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7
Q

What type of pathogen causes potato blight?

A

protoctist

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8
Q

What type of pathogen causes black sigatoka?

A

fungus

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9
Q

Identify host species of ring rot.

A

potatoes, tomatoes and aubergines

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10
Q

Identify host species of TMV.

A

tobacco plant, tomato, peppers, cucumbers, petunias

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11
Q

Identify host species of blight.

A

potatoes, tomatoes

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12
Q

Identify host species of black sigatoka.

A

bananas

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13
Q

What type of pathogen causes tuberculosis?

A

bacterium

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14
Q

What type of pathogen causes bacterial meningitis?

A

bacterium

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15
Q

What type of pathogen causes AIDS?

A

virus

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16
Q

What type of pathogen causes Influenza?

A

virus

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17
Q

What type of pathogen causes malaria?

A

protoctist

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18
Q

What type of pathogen causes ring worm?

A

fungus

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19
Q

What type of pathogen causes athletes foot?

A

fungus

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20
Q

Identify host species of TB.

A

cattle, humans, badgers, deer

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21
Q

Identify host species of bacterial meningitis.

A

humans

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22
Q

Identify host species of AIDS.

A

humans

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23
Q

Identify host species of influenza.

A

mammals and birds

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24
Q

Identify host species of malaria.

A

humans

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25
Q

Identify host species of ring worm.

A

mammals

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26
Q

Identify host species of athletes foot.

A

humans

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27
Q

Define vectors

A

living or non-living factor that transmits a pathogen from one organism to another

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28
Q

Define spores

A

reproductive cell capable of developing into a new individual without fusion with a gamete

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29
Q

Define contagious disease

A

passed on from one person to another through direct contact

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30
Q

Describe what is meant by direct transmission of a pathogen.

A

pathogen transferred directly from one individual to another

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31
Q

Give types and examples of direct transmission.

A
  • direct contact (kissing/body fluid contact, skin-to-skin contact, microorganisms fro faeces transmitted on hands)
  • inoculation (break in the skin, animal bite, puncture wound)
  • ingestion (taking in contaminated food/drink or transferring pathogens to the mouth from hands)
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32
Q

Give types and examples of indirect transmission.

A
  • fomites (inanimate objects such as bedding, socks, cosmetics)
  • droplet infection (droplets of saliva and mucus expelled from mouth)
  • vectors (mosquitoes and malaria, water and diarrhoeal diseases)
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33
Q

How does ring rot spread?

A
  • direct contact between plants
  • soil contamination
  • human vectors
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34
Q

How does TMV spread?

A
  • direct contact
  • soil contamination
  • human vectors
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35
Q

How does potato blight spread?

A
  • soil contamination
  • wind vector
  • water vector
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36
Q

How does black sigatoka spread?

A
  • wind vector
  • direct contact
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37
Q

How does TB spread?

A
  • droplet infection
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38
Q

How does bacterial meningitis spread?

A
  • direct contact from kissing/contact w body fluids
  • droplets from sneezing/coughing
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39
Q

How does AIDS spread?

A

through a break in the skin - inoculation of infected blood in contact with non infected blood, sharing needles

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40
Q

How does influenza spread?

A
  • droplet infection
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41
Q

How does ring worm spread?

A
  • direct contact
  • fomites
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42
Q

How does malaria spread?

A
  • mosquito vector bite
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43
Q

How does athlete’s foot spread?

A
  • direct contact
  • fomites
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44
Q

Describe 7 factors that affect the transmission of communicable diseases in animals.

A
  • overcrowded living and working conditions
  • poor nutrition
  • compromised immune system
  • poor disposal of waste providing breeding site for vectors
  • climate change - introduce new vectors and diseases by increasing temperature
  • culture and infrastructure - traditional medical practises increase transmission
  • socioeconomic factors - lack of trained health workers
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45
Q

Describe and explain 6 factors that affect the transmission of communicable diseases in plants.

A
  • planting varieties of crops susceptible to disease
  • overcrowding increases likelihood of contact
  • poor mineral nutrition reduces resistance of plants
  • damp, warm conditions increase the survival and spread of pathogens and spores
  • climate change - increased rainfall and wind
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45
Q

Describe and explain 6 factors that affect the transmission of communicable diseases in plants.

A
  • planting varieties of crops susceptible to disease
  • overcrowding increases likelihood of contact
  • poor mineral nutrition reduces resistance of plants
  • damp, warm conditions increase the survival and spread of pathogens and spores
  • climate change - increased rainfall and wind
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46
Q

State 3 examples of barriers to pathogens in plants

A
  • waxy cuticle on leaves
  • bark on trees
  • cellulose cell wall
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47
Q

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

A
  • they do not heal diseased tissue, they seal it off and sacrifice it
  • they are continually growing at meristems so they can replace damaged parts unlike animals
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48
Q

Describe 2 ways in which a plant cell can detect the presence of a pathogen.

A
  • receptors respond to mols from pathogens
  • receptors respond to chemicals produced when cell wall is being broken down/attacked
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49
Q

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

A

callose, lignin

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50
Q

Describe the strucutre of callose.

A
  • polysaccharide
    ß-1,3 linkages and ß-1,6 linkages
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51
Q

List 6 different types of plant chemical defences.

A
  • insect repellent
  • insecticide
  • antibacterials
  • antifungals
  • anti-oomycetes
  • toxins
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52
Q

Give example for insect repellents.

A

pine resin

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53
Q

Give example for insecticides.

A

pyrethrins made by chrysanthemums, act as insect neurotoxins

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54
Q

Give example for antibacterials

A

Phenols - antiseptics made in many different plants

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55
Q

Give example for antifungals.

A

chitinases -break down chitin fungal cell wall

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56
Q

Give example for anti-oomycetes.

A

glucanases - made by some plants that break down glucans - polymers found in cell walls of oomycetes

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57
Q

Give example for toxins.

A

chemicals that can be broken down to form cyanide compounds when the plant cell is attacked

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58
Q

Define non-specific defences.

A
  • innate immune system, made up of phagocytes and barriers
  • quicker than specific
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59
Q

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

A
  • skin
  • mucous membranes
  • eyelashes & nose hair
  • tears
60
Q

Explain how the skin acts as an effective barrier to the entry of pathogens.

A
  • acts as a physical barrier
  • skin flora of healthy microorganisms that outcompete pathogens on body surface
  • sebum production to inhibit growth of pathogens
61
Q

Explain how mucous membranes act as an effective barrier to the entry of pathogens.

A
  • secrete sticky mucus that traps microorganisms
  • contains lysozymes to destroy fungal and bacterial cell walls and phagocytes
62
Q

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

A
  • cough & sneeze - eject pathogen-containing mucus from gas exhange system, rapidly and in large quantity
  • vomiting & diarrhoea - expel contents of gut along with infective pathogens also rapid and large quantity
63
Q

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

A
  • when there’s a cut - pathogens can enter body & cause infection, also blood loss
  • serotonin makes smooth muscle in walls of blood vessels contract so they narrow and reduce supply of blood to the area
64
Q

Describe the processes involved in inflammatory response and explain their value for protection against pathogens.

A
  • mast cells activated in damaged tissue and release histamines and cytokines
  • histamines make blood vessels dilate, causing localised heat & redness - raised temp prevents pathogen reproduction
  • histamines make blood vessels more leaky so blood plasma is forced out - swelling
65
Q

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

A
  • when infected, cytokines stimulate hypothalamus to reset thermostat and temperature increases
  • most pathogens reproduce best at or below 37*C - higher temp inhibits reproduction
  • specific immune system works faster at higher temp
66
Q

Define phagocyte

A

specialised white blood cells that engulf and destroy pathogens

67
Q

Name the two types of phagocytes

A

neutrophils
macrophages

68
Q

Describe the stages of phagocytosis

A
  • pathogens produce chemicals that attract phagocytes
  • phagocytes recognise non-self antigens on pathogen - recognising self or non-self
  • phagocyte engulfs pathogen and encloses it in a vacuole - phagosome
  • phagosome combines with lysosome to form phagolysosome
  • enzymes from lysosome digest and destroy pathogen
69
Q

Describe the role of the major histocompatibility complex in the cytoplasm of macrophages at the end of phagocytosis.

A
  • glycoprotein
  • macrophage combines antigens from pathogen surface membrane with MHC
  • MHC moves pathogen antigens to macrophage surface membrane becoming an antigen-presenting cell which stimulates
70
Q

Define antigen-presenting cell.

A

a cell that displays foreign antigens complexed with MHC on their surfaces

71
Q

Describe the role of cytokines in non-specific defences.

A
  • cell signalling molecules informing other phagocytes the body is under attack
  • stimulating phagocytes to move to site of infection/inflammation
  • increase body temp and stimulate specific immune system
72
Q

Describe the role of opsonins in phagocytosis.

A
  • chemicals that bind to pathogens and tag them so they can be more easily recognised by phagocytes
  • antibodies act as opsonins
73
Q

Explain why blood smears need to be stained for viewing under the light microscope and name a stain used for this procedure.

A
  • stains allow for differentiating between white blood cells, red blood cells and platelets
  • stain: methylene blue
74
Q

Name diff types of cell found in blood and outline how to identify them on blood smear slides.

A
  • erythrocytes - red, biconcave shape, majority of cells in blood
  • macrophages - kidney bean-shaped nucleus, non-grainy cytoplasm
  • neutrophils - multi-lobed nucleus and grainy cytoplasm
  • lymphocyte - very large nucleus, takes up almost entire cell
75
Q

Define antigen

A

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

76
Q

Explain the difference between self and non-self antigens.

A
  • self - on surface of your own cells
  • non-self - on surface of cells of pathogens
77
Q

Define antibody

A

y-shaped glycoproteins made by B cells of the immune system in response to the presence of an antigen

78
Q

Define antigen-antibody complex.

A

complex formed by binding of an antibody to an antigen

79
Q

Define lymphocyte

A

WBC that make up the specific immune system

80
Q

Define specific immune response.

A
  • acquired immune response triggered by antigens which is able to distinguish between different pathogens
  • slower than non-specific
81
Q

Describe & explain the structure of antibodies.

A
  • glycoproteins made up of two identical long pp chains - heavy chains and 2 shorter identical chains - light chains
  • chains held together by disulfide bonds
  • hinge region provides flexibility - allowing one antibody to bind to two separate antigens, one at each binding site
82
Q

Describe and explain 4 ways in which antibodies defend the body.

A
  • opsonins - antigen-antibody complex easily engulfed and digested by phagocytes
  • pathogens can no longer effectively invade host cells when they are part of antigen-antibody complex
  • agglutinins - cause pathogens carrying complexes to clump together - prevents them from spreading and easier to engulf multiple at same time
  • anti-toxins - make toxins harmless
83
Q

Explain why B lymphocytes are called B whereas T lymphocytes are called T.

A
  • B lymphocytes mature in Bone marrow
  • T lymphoctes mature in the Thymus gland
84
Q

Name 4 main types of T lymphocytes.

A
  • T helper cell
  • T killer cell
  • T memory cell
  • T regulator cell
85
Q

Describe the role of T helper cells.

A
  • produce interleukins (type of cytokine) that:
  • stimulate activity of B cells - increasing antibody production
  • stimulate production of other T cells
  • attract and stimulate macrophages to ingest pathogens with antigen-antibody complexes
86
Q

Describe the role of T killer cells.

A

produce perforin that kills pathogen carrying the antigen by making holes in the cell membrane

87
Q

Describe the role of T memory cells

A
  • live for long time, part of immunological memory
  • if they meet an antigen a second time they divide rapidly to form many clones of T killer cells to destroy the pathogen quickly
88
Q

Describe the role of T regulator cells.

A
  • suppress the immune system once a pathogen has been eliminated
  • make sure the body recognises self-antigens and does not perform an autoimmune response
89
Q

Name 3 main types of B lymphocytes.

A
  • B plasma cells
  • B effector cells
  • B memory cells
90
Q

Describe the role of B plasma cells.

A

produce antibodies to a particular antigen and release them into circulation

91
Q

Describe the role of B effector cells.

A

Divide to form plasma cell clones

92
Q

Describe the role of B memory cells.

A
  • live for long time, provide immunological memory
  • if they meet a specific antigen a second time they enable the body to make a rapid response
93
Q

Define cell-mediated immunity

A

T lymphocytes respond to cells of an organism that have been changed in some way

94
Q

Suggest what it cell-mediated immunity is particularly effective against.

A
  • effective against virus infection & early cancers
95
Q

Describe the process of cell mediated immunity.

A
  • in non-specific defence macrophages phagocytosed pathogens, process their antigens and form antigen-presenting cells
  • T helper cell with complementary surface receptors to non-self antigens binds to APC
  • T helper cell is stimulated to divide by mitosis to form many clones that differentiate into:
  • T killer cells - destroy pathogen using perforins and toxins that trigger apoptosis
  • T helper cells - secrete interleukins to stimulate phagocytosis and B cell division
  • T memory cells - immunological memory of pathogen
  • T regulator cells - suppress immune respomnse when pathogen removed
96
Q

Define humoral immunity

A

B lymphocytes produce antibodies in response to antigens pathogens outside of cells

97
Q

Suggest what humoral immunity is particularly effective against.

A

effective against bacteria and fungi

98
Q

Describe the process of humoral immunity.

A
  • B cell with complementary surface receptor to pathogen binds to it and engulfs
  • antigens are processed, B cell becomes APC
  • T helper cell with complementary receptor to presented antigen binds to the APC - clonal selection
  • T helper cells induced to secrete interleukins
  • interleukins stimulate B cell to divide by mitosis, produce many clones of that B cell variant - clonal expansion
  • the B cell then differentiates into:
  • plasma cells - secrete antibodies that fit the antigens on pathogens
  • B memory cells - retain immunological memory of that pathogen, stored in lymphatic tissue
  • secretion of many specific antibodies by plasma cells that circulate in blood and act as: opsonins, agglutinins, anti-toxins act against pathogens - defence
99
Q

Define clonal selection

A

theory that exposure to a specific antigen selectively stimulates the proliferation of the cell with the appropriate antibody to form numerous clones of these specific antibody-forming cells

100
Q

Define clonal expansion

A

mass proliferation of antibody-producing cells by clonal selection

101
Q

Summarise the role of antigen presentation in specific immune response.

A

ensures that specific immune response can be initiated through recognition by T cells

102
Q

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

A

cell signalling that occurs - interleukins

103
Q

Define primary immune response.

A

relatively slow production of small number of correct antibodies the first time a pathogen is encountered

104
Q

Define secondary immune response.

A

relatively fast production of very large quantities of the correct antibodies a second time a pathogen is encountered as a result of immunological memory

105
Q

Define active immunity.

A

exposure to antigen, triggering specific immune response, antibodies made by individual

106
Q

Define passive immunity

A

no exposure to antigen, pre-made antibodies received by individual

107
Q

Define artificial passive immunity

A

results from administration of antibodies from another animal against a dangerous pathogen

108
Q

Define artificial active immunity

A

results from exposure to a safe form of a pathogen like in vaccination

109
Q

Define natural active immunity

A

results from response of body to invasion of a pathogen

110
Q

Define natural passive immunity

A

given to an infant mammal by the mother through the placenta/breast milk

111
Q

Define autoimmune disease

A

condition/illness resulting from the immune system acting against its own cells and destroying healthy tissue in the body

112
Q

Name 3 examples of autoimmune diseases.

A
  • type 1 diabetes
  • rheumatoid arthritis
  • lupus
113
Q

Describe type 1 diabetes

A
  • affects insulin-secreting cells of pancreas
  • treated with insulin injections, pancreas transplants and immunosuppressant drugs
114
Q

Describe Rheumatoid arthritis

A
  • affects joints (esp. hands, wrists, ankles, feet)
  • treated with anti-inflammatory drugs, steroids, immunosuppressants, pain relief
115
Q

Describe Lupus

A
  • affects skin and joints causing fatigue
  • treated with anti-inflammatory drugs, steroids, immunosuppressants
116
Q

Suggest how autoimmune diseases may occur.

A

when the immune system recognises ‘self’ antigens as ‘non self’, triggering immune response against its own cells

117
Q

Define vaccine

A

safe form of an antigen which is injected into the bloodstream to provide an artificial active immunity against a pathogen bearing the antigen

118
Q

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

A
  • killed/inactivated bacteria and viruses
  • weakened strains of live bacteria/viruses
  • toxin molecules that have been altered/detoxified
  • isolated antigens extracted from the pathogen
  • genetically engineered antigens
119
Q

Describe how vaccination results in artificial active immunity.

A
  • small amount of safe antigen-containing vaccine is injected into blood
  • primary immune response triggered by foreign antigens and body produces antiodies and memory cells as if infected by live pathogen
  • if in contact with that pathogen, but live, secondary immune response triggered and pathogen destroyed rapidly before suffering symptoms of disease
120
Q

Define epidemic

A

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

121
Q

Define pandemic

A

same disease spreads rapidly across number of countries and continents

122
Q

Define herd immunity

A

large part of population of an area is immune to a disease making the chances of an outbreak very low

123
Q

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

A

if there are enough vaccinated people, herd immunity is reached. less transmission = less likely for disease to reach unvaccinated person - it cannot spread through a population that is already immune

124
Q

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

A
  • people allergic to the vaccine
  • people with weakened immune system that maybe take immunosuppressants
125
Q

Give 3 examples of vaccination programmes that aim to provide herd immunity.

A
  • COVID-19
  • measles
  • polio
126
Q

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

A
  • virus causing flu mutates regularly - its antigens on surface change too
  • vaccines redeveloped as people will no longer be able to form secondary response against the mutated variant
127
Q

Name 6 examples of common medical drugs derived from living organisms.

A
  • penicillin
  • docetaxel/paclitaxel
  • aspirin (acetylsalicylic acid)
  • prialt
  • vancomycin
  • digoxin
128
Q

Describe penicillin

A
  • source: commercial extraction from mould growing on melons
  • action: antibiotic - effective against common bacterial diseases
129
Q

Describe Docetaxel/paclitaxel

A

source: derived from yew trees
action: treatment of breast cancer

130
Q

Describe aspirin

A

source: compounds from sallow (willow) bark
action: painkiller, anti-coagulant, anti-pyretic, anti-inflammatory

131
Q

Describe prialt

A

source: derived from the venom of cone snail
action: pain-killer (1000x more effective than morphine)

132
Q

Describe vancomycin

A

source: soil fungus
action: one of the most powerful antibiotics

133
Q

Describe digoxin

A

source: extracted from foxgloves
action: powerful heart drug - treats atrial fibrillation and heart failure

134
Q

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

A
  • make sure we do not destroy an organism which could be key to a life-saving drug
135
Q

Define personalised medicine.

A

combination of drugs that work with your individual combination of genetics and disease

136
Q

Give an example of how treatment is being personalised.

A
  • 30% of breast cancer patients have mutation on a certain gene
  • activity of that gene can be shut down by a drug to reduce deaths from that type of cancer
137
Q

Suggest the value of personalising medicine to a person’s genetic information.

A
  • we can improve how we treat disease by working out the best approach for a specific person
138
Q

Define synthetic biology.

A

design and construction of new biological parts, devices and systems and re-designing existing natural biological systems for useful purposes

139
Q

Give 3 examples of how synthetic biology may lead to better medical treatments.

A
  • develop bacteria using genetic engineering that can produce drugs that are rare/expensive
  • genetically modify mammals to produce therapeutic proteins in milk
  • nanotechnology to deliver drugs to very specific sites within cells of pathogens or tumors
140
Q

Define antibiotic.

A

chemical that kills or inhibits the growth of bacteria

141
Q

Define selective toxicity.

A

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

142
Q

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

A
  • destroy/affect peptidoglycan production bc humans dont need it - what the bacterial cell wall is made of
  • target their metabolic pathways and not human ones
143
Q

Explain why antibiotics do not work on viral infections.

A
  • antibiotics specifically target machinery in bacteria
  • they have completely diff structure and are non-living
  • do not have a cell wall that can be attacked by antibiotics, instead they have protein coat
144
Q

Outline different ways 4 common antibiotics have their effect.

A
  • penlillin and cephalosporins weaken cell wall - bacterium more easily damaged by immune reaction
  • sulfonamides interfere with metabolic reactions
  • tetracyclines and streptomycin inhibit protein synthesis
  • polymixines make holes in cell surface membrane altering its activity
145
Q

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

A
  • over-prescribing antibiotics
  • giving farm animals antibiotics to prevent them from getting infected and reducing business profits
146
Q

Give two examples of antibiotic resistant bacteria.

A
  • MRSA
  • C. difficile
147
Q

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

A
  • minimise use of antibiotics
  • good hygiene - inpact on spread of all infections including antibiotic-resistant strains

OCR A-Level Biology (16 decks)

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