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OCR AS/A Level Biology Context > module 4.1: communicable disease > Flashcards

module 4.1: communicable disease Flashcards

1
Q

what is a pathogen

A

a microorganism that causes a disease

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2
Q

what is a host

A

the organism in which the pathogen lives in

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3
Q

how do pathogens live

A

by taking nutrition from their host, but also cause damage in the process

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4
Q

what is the kingdom that bacteria belongs to

A

prokaryotae

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5
Q

can bacteria reproduce rapidly or slowly

A

slowly

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6
Q

what is the cause of reproduced-rapidly bacteria

A

causes disease by damaging cells or releasing waste products and/or toxins that are toxic to the host

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7
Q

what is the effect of bacteria in plants and what does it live

A

the bacteria can often live in the vascular tissues
causes blackening and death of these tissues

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8
Q

where does fungi normally live

A

lives under the skin where it is hyphae, which forms a mycelium which grow under the skin surface

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9
Q

what does fungus sending out specialised reproductive hyphae do

A

grow to the surface of the skin to release spores which causes redness and irritation

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10
Q

in plants, where does the fungus live

A

in the vascular tissue, where it gains nutrients

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11
Q

what does the hyphae do in plants

A

it releases extracellular enzymes eg. cellulases, to digest the surrounding tissue, which causes decay

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12
Q

what will fungus do to plants overall

A

leaves will often become mottled in colour , curl up and shrivel, before dying. fruit and storage organs, such as tubers (potatoes), will turn black and decay

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13
Q

what do viruses do

A
  • invade cells
  • take over the genetic machinery and other organelles of the cell
  • they then can cause the cell to manufacture more copies of the virus
  • these will eventually burst, releasing many new viruses which will infect healthy cells
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14
Q

how do protoctista harm organisms

A
  • enter host cell
  • feed on the content as they grow
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15
Q

what are the examples of pathogens (bacteria)

A

tuberculosis
bacterial meningitis
ring rot in plants

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16
Q

what are the examples of pathogens (virus)

A

HIV/AIDS
influenza
tobacco mosaic virus

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17
Q

what are the examples of pathogens (fungus)

A

black sigatoka in banana plants
ringworm in cattle
athlete’s foot

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18
Q

what are the examples of pathogens (protoctista)

A

malaria
blight

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19
Q

what causes tuberculosis

A

Mycobacterium tuberculosis and M.bovis

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20
Q

what does tuberculosis affect

A

affects many parts of the body, killing the cells and tissues. the lungs are often the most affected

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21
Q

what is bacterial meningitis caused by

A

the bacteria Neisseria meningitidis or Streptococcus pneumonia

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22
Q

what does Bacterial Meningitis affect

A

it is an infection of the meninges, that is, the membranes that surrounds the brain and spinal cord
- the membranes become swollen, which may cause damage to the brain and nerves

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23
Q

what is ring rot in plants caused by

A

bacterium Clavibacter michiganensis susp. Sepedonicus

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24
Q

what does ring rot in plants affect

A

ring rot is a disease causing a ring of decay in the vascular tissue of the potato tuber, accompanied by leaf wilting

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25
Q

what is HIV/AIDS caused by

A

human immunodeficiency virus

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26
Q

what does HIV/AIDS affect

A

it attacks cells in the immune system and compromises the immune response

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27
Q

what is influenza affected by

A

viruses from the Orthomyxoviridae family

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28
Q

what does influenza affect

A

it attacks the respiratory system and causes muscle pains and headaches

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29
Q

what is tobacco mosaic virus caused by

A

a virus of the same name

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30
Q

what does tobacco mosaic virus affect

A

it causes mottling and discolouration of leaves

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31
Q

what is black sigatoka in banana plants caused by

A

the fungus Mycosphaerella fijiensis

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32
Q

what does black sigatoka affect

A

causes leaf spots on banana plants and reduces yield

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33
Q

what is blight caused by

A

the protoctistan Phytophthora infestans

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34
Q

what does blight affect

A

affects tomatoes and potatoes, particularly the leaves and (in potatoes) the tubers

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35
Q

what is ringworm in cattle caused by

A

the fungus Trichophyton verrucosum

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36
Q

what does ringworm in cattle affect

A

growth of the fungus in the skin causes spores to erupt through the skin, causing a rash

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37
Q

what is athletes foot caused by

A

the fungus trichophyton rubrum

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38
Q

what does athletes foot affect

A

grows under the skin on the feet, particularly between the toes

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39
Q

what is malaria caused by

A

the protoctistan Plasmodium falciparum, P. vivax, P. ovale, or P. malariae

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40
Q

what does malaria affect

A

it is a parasite in the blood that causes headache and fever and may progress to coma and death

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41
Q

what is direct transmission

A

passing a pathogen from host to new host, with no intermediary

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42
Q

what is indirect transmission

A

passing a pathogen from host to new host, via a vector

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43
Q

what is transmission

A

passing a pathogen from an infected individual to an uninfected individual

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44
Q

what is a vector

A

an organism that carries a pathogen from one host to another

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45
Q

in short, what is the life cycle of a pathogen in their host

A
  • travel from one host to another (transmission)
  • entering the host’s tissues
  • reproducing
  • leaving the host’s tissues
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46
Q

what are the different types of direct transmission

A
  • direct physical contact
  • faecal-oral transmission
  • droplet infection
  • transmission by spores
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47
Q

describe how pathogens are transmitted by physical contact

A

touching a person who is infected or touching contaminated surfaces (including soil) that harbour the pathogens

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48
Q

how can pathogen transmitted by direct contact be prevented

A

better hygiene (i.e: washing hands regularly — especially after using the toilet, keeping surfaces clean — especially door handles, cleaning and disinfecting cuts and abrasions, sterilising surgical instruments, and using condoms during sexual intercourse

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49
Q

describe how pathogens transmitted by faecal - oral

A

usually by eating food or drinking water contaminated with the pathogen. For example food poisoning and cholera

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50
Q

how can faecal-oral transmission be prevented

A

by not using human sewage as crop fertiliser, and by treating wastewater and drinking water, as well as by thoroughly washing fresh food (using treated water), and via careful preparation (i.e: thoroughly cooking all food)

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51
Q

describe how pathogens are transmitted by droplets

A

the pathogen is carried in tiny water droplets in the air

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52
Q

how do we reduce the risk of droplet infection

A

by covering your mouth when coughing or sneezing. use a tissue and ensure the tissue is disposed of correctly

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53
Q

describe transmission by spores

A

these can be carried in the air or reside on surfaces or in the soil

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54
Q

how do you reduce transmission by spores

A

by wearing a face mask and washing skin after contact with soil

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55
Q

what are some social factors that affect transmission

A

. overcrowding — many people living and sleeping together in one house
. poor ventilation
* poor health — particularly if a person has HIV/AIDS, as they are more likely to contract other diseases
* poor diet
* homelessness
* living or working with people who have migrated from areas where a disease is more common

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56
Q

why is tuberculosis not transmitted easily but still could be spread

A

it often takes living in close proximity to people with the disease for a long time before it is transmitted. the BCG vaccination given to teenagers successfully reduced the prevalence of tuberculosis in Western Europe
- however, with increased migration and many economic migrants living in overcrowded, poorly ventilated conditions, the incidence of tuberculosis is rising in many Western cities

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57
Q

what is the life cycle of Plasmodium

A
  • a female anopheles mosquito sucks blood from a person infected with malaria
  • the plasmodium develops from the gametes in the infected blood and migrates to the salivary glands of the mosquito
  • the mosquito bites an uninfected person
  • the plasmodium from the mosquito migrate into the person’s liver
  • the plasmodium then migrate into their blood
  • the person now has malaria
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58
Q

describe the transmission in plants

A

plant pathogens can also be spread by direct and indirect means
- many pathogens are present in the soil and will infect plants by entering the roots — especially if these have been damaged as a result of replanting, burrowing animals or movement caused by a storm
- any fungi produce spores as a means of sexual or asexual reproduction. these spores may be carried in the wind — airborne transmission
- once a pathogen is inside the plant, it may infect all the vascular tissue. pathogens in the leaves are distributed when the leaves are shed and carry the pathogen back to the soil where it can grow and infect another plant
- pathogens can also enter the fruit and seeds, and will then be distributed with the seeds — so that many or all of the offspring are infected
- indirect transmission of a pathogen often occurs as a result of insect attack. spores or bacteria become attached to a burrowing insect, such as a beetle, which attacks an infected plant – when that beetle attacks another plant, the pathogen is transmitted to the uninfected plant. The beetle is acting as a vector

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59
Q

how does disease and climate affect the transmission of plant pathogens

A
  • many protoctists, bacteria and fungi can grow and reproduce more rapidly in warm and moist conditions
  • as global warming alters our climate tropical pathogens will be able to survive more easily in Europe
  • tropical diseases may become more common in Europe as a result
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60
Q

plants don’t have an immune system comparable, what do they have instead

A

they have developed a wide range of structural, chemical and protein-based defences which can detect invading organisms and prevent them from causing extensive damage. this includes both passive defences to prevent entry and active defences which are induced when the pathogen is detected

61
Q

what are passive defences and what do they include

A

these are defences present before infection, and their role is to prevent entry and spread of the pathogen. passive defences include physical barriers and chemicals

62
Q

what are examples of physical defences

A

cellulose cell wall
lignin thickened of cell walls
waxy cuticles
bark
stomach closure
callose
tylose formation

63
Q

describe how cellulose cell wall acts as a physical defense

A

most plant cell walls contain a variety of chemical defences that can be activated when a pathogen is detected

64
Q

describe how lignin thickening of cell walls acts as a physical defence

A

lignin (a phenolic compound) is waterproof and almost completely indigestible

64
Q
A
65
Q

describe how waxy cuticles acts as a physical defence

A

these prevent water collecting on the cell surfaces. since pathogens collect in water and need water to survive, the absence of water is a passive defence

66
Q

describe how bark acts as a physical defence

A

most bark contains a variety of chemical defences that work against pathogenic organisms

67
Q

describe how stomatal closure acts as a physical defence

A

stomata are possible points of entry for pathogens
stomatal aperture is controlled by the guard cells
when pathogenic organisms are detected, the guard cells will close the stomata in that part of the plant

68
Q

describe how callose acts as a physical defence

A

callose is a large polysaccharide that is deposited in the sieve tubes at the end of a growing season
it is deposited around the sieve plates and blocks the flow in the sieve tube
this can prevent a pathogen spreading around the plant

69
Q

describe how tylose formation acts as a physical defence

A

a tylose is a balloon-like swelling or projection that fills the xylem vessel
- when a tylose is full formed, it plugs the vessel and the vessel can no longer carry water. blocking the xylem vessels prevents spread of pathogens through the heartwood
- the tylose contains a high concentration of chemicals such as terpenes that are toxic to pathogens. in active xylem, the vessels are surrounded by living parenchyma cells
- as the wood ages, the parenchyma cells become filled with terpenes
- eventually, the contents of the parenchyma cell burst into the dead vessel through a pit connecting the two. the parenchyma cell dies as its contents enter the empty space of the xylem vessel

70
Q

describe how chemical defences work

A
  • plant tissues contain a variety of chemicals that have anti-pathogenic properties. these include terpenoids, phenols, alkaloids and hydrolytic enzymes
  • some of these chemicals, such as the terpenes in tyloses and tannins in bark, are present before infection
  • however, because the production of chemicals requires a lot of energy, many chemicals are not produced until the plant detects an infection
71
Q

how does active defences work

A

when pathogens attack, specific chemicals in their cell walls can be detected by the plant cells
- these chemicals include specific proteins and glycolipids. the plant responds by fortifying the defences already present
- this includes increasing the physical defences and producing defensive chemicals

72
Q

what does active defences include

A
  • cell walls become thickened and strengthened with additional cellulose
  • deposition of callose between the plant cell wall and cell membrane near the invading pathogen. callose deposits are polysaccharide polymers that impede cellular penetration at the site of infection. it strengthens the cell wall and blocks plasmodesmata
  • oxidative bursts that produce highly reactive oxygen molecules capable of damaging the cells of invading organisms
  • an increase in production of chemicals
73
Q

what are the different types of chemicals used in defence

A

terpenoids
phenols
defensive proteins
hydrolytic enzymes
tannins
alkaloids
necrosis
canker

74
Q

how does terpenoids act as a chemical defence

A

a range of essential oils that have antibacterial and antifungal properties. they may also create scent, for example, the menthols and menthones produced by mint plants

75
Q

how does phenols acts as a chemical defence

A

these have antibiotic and antifungal properties

76
Q

how does defensive proteins (defensins) acts as a chemical defence

A

these are small cysteine-rich proteins that have broad antimicrobial activity. they appear to act upon molecules in the plasma membrane of pathogens, possibly inhibiting the action of ion transport channels

77
Q

how does hydrolytic enzymes acts as a chemical defence

A

these are found in the spaces between cells. they include chitinases (which break down the chitin found in fungal cell walls), glucanases (which hydrolyse the glycosidic bonds in glucans) and lysozymes (which are capable of degrading bacterial cell walls)

78
Q

how does tannins acts as a chemical defense

A
  • found in bark inhibit attack by insects
  • these compounds bind to salivary proteins and digestive enzymes such as trypsin and chymotrypsin, deactivating the enzymes
  • insects that ingest high amounts of tannins do not grow and will eventually die. this helps to prevent the transmission of pathogens
79
Q

how does alkaloids act as a chemical defence

A

nitrogen-containing compounds such as caffeine, nicotine, cocaine, morphine, solanine
- these give a bitter taste to inhibit herbivores feeding. they also act on a variety of metabolic reactions via inhibiting or activating enzyme action
- some alkaloids inhibit protein synthesis. if the plant can reduce grazing by larger animals, then it will suffer less damage that can allow pathogens to enter the plant

80
Q

how does necrosis acts as a chemical defence

A
  • deliberate cell suicide
  • a few cells are sacrificed rest of the plant. by killing cells surrounding the infection, the plant can limit the pathogen’s access to water and nutrients and can therefore stop it spreading further around the plant
  • necrosis is brought about by intracellular enzymes that are activated by injury. these enzymes destroy damaged cells and produce brown spots on leaves or dieback
81
Q

how does canker acts as a chemical defence

A

a sunken necrotic lesion in the woody tissue such as the main stem or branch. it causes death of the cambium tissue in the bark

82
Q

what is inflammation

A

swelling and redness of tissue caused by infection

83
Q

what is the mucous membrane

A

specialised epithelial tissue that is covered by mucus

84
Q

what are primary defences

A

those that prevent pathogens entering the body

85
Q

are primary defences non specific or specific and explain why

A

non-specific
- they will prevent the entry of any pathogen

86
Q

what is the outer layer of the skin called

A

epidermis and it consists of layers of cells

87
Q

how does skin act as a primary defence

A

only effective if it is complete and lacerations can open the body up for infection. when this happens, the body prevents excess blood loss by making a clot and repairing the skin

88
Q

how does blood clotting act as a primary defence

A
  • must not occur when they are not needed and therefore it involves at leas t12 clotting factors
    • the factors are released from platelets and damaged tissue and they activate an enzyme cascade
    • once the clot is formed, it dries and forms a scab which shrinks and pulls the sides of the cut together. this creates a temporary seal under which the skin is repaired
    • fibrous collagen is deposited under the scab and stem cells in the epidermis divide to form new cells
    • new blood vessels grow, and the tissues contract to draw the edges of a cut together
89
Q

what is the process that happens when there is damage to a blood vessel

A
  1. when there is damage to a blood vessel, collagen is exposed to the blood and clotting factors are released
  2. the platelets bind to the collagen and release more clotting factors
  3. these platelets form a temporary plug whilst the clotting factors activate the inactive thrombokinase in the blood
  4. active thrombokinase is an enzyme which turns the prothrombin in the blood into active thrombin with the help of Ca2+ ions
  5. active thrombin is also an enzyme which turns the soluble fibrinogen in the blood into insoluble fibrin
  6. the insoluble fibrin fibres attach to the platelets in the plug and a clot is formed
90
Q

how does mucous membrane act as a primary defence

A

substances such as oxygen and nutrients are absorbed directly into our blood and the exchange surfaces where this occurs are thinner are more vulnerable
- the air and food that enter our system may have microorganisms and therefore the lungs, airways and digestive system are at risk from infection
these areas are protected by mucous membranes. the epithelial tissue contains goblet cells which secrete mucus
- in the airways, mucus lines the airways and traps airborne pathogens. the cilia then waft the mucus up to the top of the trachea and it enters the oesophagus which denatures the pathogen’s enzymes in the acidic stomach

91
Q

how does coughing and sneezing act as a primary defence

A

reflexes such as coughing, sneezing and vomiting are responses to irritation by the presence of microorganisms or the toxins they release
in a cough or sneeze, a sudden expulsion of air will carry the microorganisms causing the irritation

92
Q

how

A
93
Q

how does inflammation act as a primary defence

A

a sign that a tissue is infected
symptoms are swelling, redness, heat and pain

94
Q

what do mast cells

A

detect the presence of pathogens in the tissue and they release histamine as a signal

95
Q

what is the main effect of mast cells

A

vasodilation which makes the capillary walls more permeable to leukocytes makes more tissue fluid and causes swelling
——> excess tissue fluid is drained into the lymphatic system where pathogens will come into contact with lymphocytes to initiate the specific immune response

96
Q

what are secondary defences and what do they do

A

combat pathogens once they are in the body
- the pathogen in the body is recognised by its antigens. the antigens are intrinsic proteins and are specific to the organism

97
Q

what are opsonins and what do they do

A

are proteins that attach to antigens
they are a form of antibody and some are non-specific. they enhance the ability of phagocytic cells to find and engulf the pathogen

98
Q

what is phagocytosis

A

the phagocytes engulf and digest the pathogens
- the first event in the secondary defence

99
Q

what are neutrophils and explain their structure and adaptation

A

the most abundant phagocytes and are recognised by their multi-lobed nucleus
- made in bone marrow and travel in the blood, often going into tissue fluid
- release in large numbers when there is an infection
- contain many lysosomes and engulf and digest pathogens
- they usually die after consuming a few pathogen and once dead they form pus

100
Q

what happens in phagocytosis

A
  • the neutrophil binds to the opsonin attached to the antigen of the pathogen
  • the pathogen is then engulfed by endocytosis, forming a phagosome
  • the lysosomes in the neutrophil then fuse to the phagosome and release lytic enzymes into it
  • after digestion the harmless products can be absorbed into the cell
101
Q

what is a macrophage and describe the structure

A

larger cells made in the bone marrow
- they travel in the blood as monocytes and then settle into body tissues. can be found in the lymph nodes where they mature into macrophages
- play a part in initiating the specific responses. when a macrophage engulfs a pathogen, it does not fully digest it
- takes the pathogen’s antigen and presents it on its surface. the antigen is exposed such that the other immune system cells can recognise the antigen
- the special protein complex ensures that the macrophage is not mistaken for a foreign cell and attacked by other phagocytes

102
Q

what is the specific immune response

A

coordinates B and T lymphocytes which are types of leukocytes with large nuclei and special membrane receptors
- the immune response creates antibodies that neutralise foreign antigens and provides long term immunity from the disease

103
Q

what are the 4 cells T lymphocytes can differentiate into

A

T helper cells
T killer cells
T memory cells
T regulatory cells

104
Q

what do T helper cells do

A

release cytokines that stimulate B cells to develop and stimulate phagocytosis

105
Q

what do T killer cells do

A

attack and kill host body cells that are infected and that display the foreign antigen

106
Q

what do T memory cells do

A

provide long term immunity as they circulate in the body for many years

107
Q

what do T regulator cells do

A

shut down the immune response after the pathogen has been removed to prevent autoimmunity

108
Q

what are the 2 types of cells B lymphocytes differentiate into

A

plasma cells
B memory cells

109
Q

what do plasma cells do

A

they travel in the blood whilst making and releasing antibodies

110
Q

what do B memory cells do

A

provide long term immunity as they circulate in the body for many years

111
Q

for the immune response to be coordinated, the cells have to communicate with each other. how is this achieved

A

achieved through the release of hormone like chemicals called cytokines

112
Q

what are cytokines and what do they do

A

are a group of many chemicals each with a different role and in order to detect a signal, the target cell has to have a receptor on the plasma membrane that has a complementary shape to the cytokine molecule

113
Q

what chemicals do macrophages release

A

monokines
- attract neutrophils and can stimulate B cells to differentiate and release antibodies

114
Q

what chemical do T cells and macrophages release

A

interleukins
- stimulate clonal expansion and the differentiation of B and T lymphocytes

115
Q

what is an autoimmune disease

A

when the immune system attacks a part of the body. usually B or T cells that are specific to our own antigens are destroyed early when developed

116
Q

what happens during the specific response

A
  1. a pathogen enters the host and its antigens are detected by the lymphocytes
  2. the pathogens infect host cells and travel in the body fluids. furthermore, macrophages engulf them and present their antigens
  3. increases the number of foreign antigens present throughout the body. clonal selection is when the right lymphocyte is found to the specific antigen
  4. eventually, there is contact between the foreign antigen and the receptor on the lymphocyte which have complementary shapes
  5. then clonal expansion must occur where the correct lymphocytes have been selected and activated by cytokines. they undergo mitotic division to increase in number
  6. after, they differentiate into the different types of B and T lymphocytes and carry out their specific functions
117
Q

what are antigens

A

molecules that stimulate an immune response and any molecule can act as an antigen however, they are usually proteins or glycoproteins in the membrane of the pathogen
- specific to these antigens and as the antigen is specific to the pathogen, the antibody is also specific to the pathogen.
- antibodies are immunoglobulins which are complex proteins made by plasma cells. they have a region with a specific shape that is complementary to the antigen
- immune system makes antibodies for every antigen that Is detected. attach to antigens and render them harmless

118
Q

describe the structure of antibodies

A

Y shaped molecules that have 2 distinct regions and 4 polypeptide chains
- there is a light and heavy polypeptide chain
- there is a constant and variable region
- the constant region is the same in all antibodies and has a site for the easy binding of phagocytes
- the variable region has shape specific to the antigen
- there is a hinge region to allow the antibody to attach to more than one antigen
- disulphide bridges hold the polypeptide

119
Q

what are 3 main ways that an antibody works

A

opsonins
agglutinins
anti toxins

120
Q

what happens with opsonins

A

they bind to antigens on a pathogen and act as binding sites to phagocytes, so they can carry out phagocytosis
- some opsonins are not specific and stick to molecules such as peptidoglycan which are not found in the host
- other opsonins are produced in the specific immune response and bind to very specific antigens. if this antigen is used as a binding site to host cells then by attaching an antibody to it, the pathogen is rendered useless - neutralisation
- the opsonin assists with phagocytosis but prevents it from entering a host cell

121
Q

how does agglutinins work

A

As each antibody has 2 binding sites, it is able to bind to 2 antigens at once
- when they crosslink pathogens, they clump them together and this is called agglutination
- by doing this, the pathogen cannot infect host cells and phagocytes can engulf more than 1 pathogen at once

122
Q

how do anti toxins work

A

some antibodies bind to toxins released by pathogens and render them harmless

123
Q

what happens in primary responses and in turn secondary reponses

A

during the primary response, the production of antibodies is slow, and it takes a few days to produce sufficient antibodies to combat the infection
- after the pathogen is removes, the number of antibodies in the blood drops rapidly and do not stay in the blood
- if the pathogen returns, antibodies must be remade however, as a result of the memory cells, the antigens are quickly recognised, and the production of antibodies is more rapid and amplified
- this is the secondary immune response and is often quick enough to not even show symptom

124
Q

what is an epidemic

A

a rapid spread of disease through a high proportion of the population

125
Q

what is a vaccination

A

a way of stimulating an immune response so that immunity is achieved

126
Q

what are examples of auto immune diseases

A
  • arthritis is a painful inflammation of a joint. the cause is uncertain, but it starts with antibodies attacking the membranes around the joint
  • lupus can affect any part of the body, causing swelling and pain. It may be associated with antibodies that attack certain proteins in the nucleus in cells and affected tissues
127
Q

what chemical do many cells release and what does it do

A

interferon, which inhibits virus replication and stimulates the activity of T killer cells

128
Q

what happens during the immune response

A

activation -> clonal selection: an invading pathogen has specific antigens. in order to trigger the immune response , these must be detected by T and B lymphocytes that carry the specific receptor molecules on their plasma membranes. the receptor molecules are proteins that have a shape that is complementary to the shape of the antigen. contact between the antigen and lymphocytes can be achieved directly when pathogenic cells enter the lymph nodes or via the action of antigen-presenting cells
- clonal expansion: once the correct lymphocytes have been activated they must increase in numbers to become effective - achieved by mitotic cell division.
- differentiation- the B and T lymphocytes do not manufacture antibodies directly. once selected, clones of the lymphocytes develop into a range of useful cells

129
Q

what are the forms in which the antigenic material used in vaccines take

A

Whole, live microorganisms — usually ones that are not as harmful as those that cause the real disease. But they must have very similar antigens, so that the antibodies produced will be effective against the real pathogen (e.g. the smallpox vaccine, which uses a similar virus that causes cowpox).
* A harmless or attenuated (weakened) version of the pathogenic organism (e.g. measles and TB vaccines).
* A dead pathogen (e.g. typhoid and cholera vaccines).
* A preparation of the antigens from a pathogen (e.g. the hepatitis B vaccine).
* A toxoid, which is a harmless version of a toxin (e.g. the tetanus vaccine)

130
Q

what is herd immunity

A

using a vaccine to provide immunity to all or almost all of the population at risk. once enough people are immune, the disease can no longer be spread through the population and you achieve ‘herd immunity

131
Q

what is ring vaccination

A

when a new case of a disease is reported. ring vaccination involves vaccinating all the people in the immediate vicinity of the new case(s). this may mean vaccinating the people in the surrounding houses, or even in the whole village or town. ring vaccination is also used in many places in the world to control the spread of livestock disease

132
Q

how are epidemics controlled

A
  • once a disease has been eradicated, or reduced to such a low incidence that it is unlikely to spread, the routine vaccination programme can be relaxed - occurred with smallpox
    • TB vaccinations have also been stopped for most children in the UK. however, some pathogens can undergo genetic mutations which change their antigens
    • the memory cells produced by vaccination may not recognise the new antigens. when this occurs, the pathogen may be transmitted, and the incidence of the disease increases
133
Q

how is natural immunity achieved

A

through normal life processes

134
Q

how is artificial immunity achieved

A

through medical intervention

135
Q

what is natural active immunity

A

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

136
Q

what is natural passive immunity

A

when the antibodies are provided via the placenta or via breast milk
- makes the baby immune to diseases to which the mother is immune. it is very useful in the first year of the baby’s life, when its immune system is developing

137
Q

what is artificial active immunity

A

provided by antibodies made in the immune system as a result of vaccination. a person is injected with a weakened, dead or similar pathogen, or with antigens, and this activates his/her immune system
- e.g. immunity to TB and influenza

138
Q

what is artificial passive immunity

A

provided by injection of antibodies made by another individual (e.g. hepatitis A and B). tetanus can also be treated this way when vaccination using a toxoid has not worked well

139
Q

what is an antibiotic

A

a chemical which prevents the growth of microorganisms. antibiotics can be antibacterial or antifungal

140
Q

what is personalised medicine

A

the development of designer medicines for individuals

141
Q

what is synthetic biology

A

the re-engineering of biology
- could be the production of new molecules that mimic natural processes, or the use of natural molecules to produce new biological systems that do not exist in nature

142
Q

what are the reason why new drugs are needed

A
  • new diseases are emerging
  • there are still many diseases for which there are no effective treatments
  • some antibiotic treatments are becoming less effective
143
Q

how are new medicines found

A

Accidental discovery- The accidental discovery of the antibiotic penicillin by Alexander Fleming is well documented. The fungus Penicillium releases compounds that kill bacteria. This is a classic example of how science works — a scientist makes an observation and sets out to explain what he or she has seen. In this case, it was the work of Florey and Chain, who purified penicillin, that really demonstrated the potential value of antibiotics. This shows how important it is for scientists to work together.
Traditional remedies- Many drugs have been used for centuries. They are used because people have noted that certain plants or extracts have a beneficial effect. The World Health Organization calculates that 80% of the world’s population relies on traditional medicines. In India, some 7000 different plants are used for their medicinal properties, and in China they use about 5000 different plants. In Europe, many of our modern drugs have their origins in traditional medicine. * Morphine has its origins in the use of sap from unripe poppy seed-heads as long ago as Neolithic times. In the 12th century, opium from poppies was used as an anaesthetic and, by the 19th century, morphine and opium were being used. These opiate drugs reduce nervous action in the central nervous system. If the nerves cannot carry impulses, then no pain is felt. * Medicinal use of willow-bark extract to relieve pain and fever has a long history. After discovery of its active ingredient, a way was later found in 1897 to reduce the side effect of stomach bleeding, by adding an acetyl group. This led to the development of the drugs aspirin and ibuprofen.
Observation of wildlife- Many animals make use of plants with medicinal properties. For example: * monkeys, bears and other animals rub citrus oils on their coats as insecticides and antiseptics in order to prevent insect bites and infection * birds line their nests with medicinal leaves in order to protect chicks from blood-sucking mites. Chimpanzees swallow leaves folded in a particular way, in order to remove parasites from their digestive tract.

144
Q

describe antibiotic use and abuse

A

Antibiotics are compounds that prevent the growth of fungi or bacteria. However, over-use and misuse of antibiotics have enabled microorganisms to develop resistance, and many of the current antibiotics have limited effectiveness as a result. Some bacteria have become infamous for their multiple resistance to a range of antibiotics. These include Clostridium difficile (C. diff) and methicillin-resistant Staphylococcus aureus (MRSA).
Leaf-cutter ants farm fungi, which they feed to their growing larvae. In order to prevent infection of their fungal gardens, they carry symbiotic bacteria, including Streptomyces, which produce antibiotics. Scientists are studying the bacteria carried by the leaf-cutter ants to see if they have potential to produce new drugs to treat human bacterial infections.

145
Q

describe synthetic biology

A

The 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 or in manufacturing. For example, there is the development of tomatoes which contain the pigment anthocyanin. This pigment is found in fruit such as blueberries, and has specific health benefits. Anthocyanins are antioxidants and help protect against coronary heart disease

146
Q

describe personalised medicine

A

Sequencing technology and molecular modelling have huge potential for future medicines. It is possible to screen the genomes of plants or microorganisms to identify potential medicinal compounds from the DNA sequences. It is hoped that this technology can even be taken a step further. Once the technology is fully developed, it may be possible to sequence the genes from individuals with a particular condition and develop specific drugs for the condition

147
Q

describe research into disease causing mechanisms

A

Pharmaceutical companies have been conducting research into the way that microorganisms cause disease. Many make use of receptors on plasma membranes (cell surface membranes). For example, the HIV virus binds to the CD4 and CCR5 receptors on the surface of T helper cells. If the binding between the pathogen and the receptor site can be blocked, then the disease-causing pathogen cannot gain access to the cell. The glycoprotein receptor molecules can be isolated and sequenced. Once the amino acid sequence is known, molecular modelling can be used to determine the shape of the receptor. The next step is to find a drug that mimics the shape of the receptor and could be used to bind to the virus itself, which would block the virus from entering the T helper cell. In a similar way, drugs that inhibit the action of certain enzymes can also be developed

148
Q

describe further plant research in medicine

A

Scientists have used traditional plant medicines and animal behaviour as a starting point in their search for new drugs. As you will have seen in the case of aspirin, research into the plants used for traditional remedies enables scientists to isolate the active ingredient. This molecule can be analysed, and similar molecules can be manufactured. in recent decades, discovery of natural drugs has concentrated on tropical plants

OCR AS/A Level Biology Context (24 decks)

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