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communicable diseases, disease prevention and the immune system Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

pathogen definition

A

an infectious micro-organisms that causes disease

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2
Q

4 major types of pathogen that cause disease in animals and plants

A

bacteria (prokaryotic)
viruses (non-living parasites)
protoctists (animal-like or plant-link eukaryotes)
fungi (eukaryotic)

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3
Q

communicable disease definition

A

a disease that can be transmitted from one organism to another

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4
Q

infectious definition

A

infectious diseases are those caused by micro-organisms (mostly bacteria, viruses, fungi, protozoa, parasites) that spread by direct or indirect means form one individual to another

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5
Q

vector-borne disease definition

A

diseases spread by other animals. for diseases of humans and domestic animals, the most important vectors are flies (mosquitoes, midges), fleas, lice and ticks. aphids are important vectors of disease in plants
water is also a vector because it carries parasites

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6
Q

why have infectious diseases e.g. diphtheria, leprosy, scarlet fever largely died out?

A

due to vaccines, antibiotics, improvements to sanitation ad changes in land use

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7
Q

which aspects of modern life have given rise to disease emergence

A

increased tourism to exotic locations
increased trade of animals and animal products
intensification of farming
cutting down of rainforests
climate change causing rise in global temps, so increasing distribution of vectors and their capacity to transmit pathogens. can also turn non-vectors into vectors
climate change may impact agriculture so increase reliance on bush meat

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8
Q

pandemic definition

A

an epidemic of a disease across huge areas of the world

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9
Q

how did the H1N1 influenza virus in 2009 come about?

A

arose from genetic changes in existing influenza viruses

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10
Q

how did the AIDS pandemic come about in the 1980s?

A

it is caused by HIV that is spread through exchange of bodily fluids e.g. via blood transfusion, needle-sharing by drug users, more liberal sexual practices.

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11
Q

examples of diseases?

A

tuberculosis (TB)
bacterial meningitis
ring rot
HIV/AIDS
influenza
TMV
black sigatoka
blight
ringworm
athletes foot
malaria

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12
Q

characteristics/symptoms of tuberculosis (TB)
animal or plant disease?

A

disease that affects many parts of the body, particularly the respiratory system. tubercles form in the lungs
animal

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13
Q

what kind of organism causes tuberculosis?

A

bacteria

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14
Q

tuberculosis method of transmission?

A

respiratory droplets

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15
Q

bacterial meningitis characteristics/symptoms?
animal or plant disease?

A

infection/inflammation of the meninges in the brain. causes major damage to the brain and nerves; lethal if not treated quickly
animal

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16
Q

what kind of organism causes bacterial meningitis?

A

bacteria

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17
Q

bacterial meningitis method of transmission?

A

respiratory droplets

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18
Q

ring rot characteristics/symptoms?
animal or plant disease?

A

ring of decay in vascular tissue of potato tuber or tomato, accompanied by leaf wilting
plant

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19
Q

what kind of organism causes ring rot?

A

bacteria

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20
Q

ring rot method of transmission?

A

infected farming equipment

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21
Q

HIV/AIDS characteristics/symptoms?
animal or plant disease?

A

attacks T helper (CD4+) cells in the immune system and compromises immunity
sufferers often die of opportunistic infections (e.g. pneumonia)

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22
Q

what kind of organism causes HIV/AIDS?

A

virus

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23
Q

HIV/AIDS method of transmission?

A

needle sharing
unprotected sex
blood transfusion

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24
Q

influenza characteristics/symptoms?
animal or plant disease?

A

attacks respiratory system and causes muscle pains and headaches
animal

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25
Q

what kind of organism causes influenza?

A

virus

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26
Q

method of transmission of influenza?

A

respiratory droplets

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27
Q

TMV characteristics/symptoms?
animal or plant disease?

A

causes mottling and discolouration of leaves
plant

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28
Q

disease-causing organism of TMV?

A

virus

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29
Q

method of transmission of TMV?

A

infected farming equipment

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30
Q

black Sigatoka characteristics and symptoms?
plant or animal disease?

A

causes leaf spots on banana plants reducing yield
plant

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31
Q

what kind of organism causes black Sigatoka?

A

fungi

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32
Q

method of transmission of black Sigatoka?

A

spores

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33
Q

blight characteristics/symptoms?
plant or animal disease?

A

affects leaves in potatoes and tomatoes, affects potato tubers
plant

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34
Q

what kind of organism causes blight?

A

protoctist

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35
Q

method of transmission of blight?

A

aphids (VECTOR)

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36
Q

ringworm (cattle) characteristics/symptoms?
plant or animal disease?

A

growth of fungus on skin and spore case erupting through to cause a rash
animal

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37
Q

type of organism that causes ringworm?

A

fungi

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38
Q

method of transmission of ringworm?

A

spore/ direct contact

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39
Q

athletes foot characteristic/symptoms?
plant or animal disease?

A

growth under skin of feet, particularly between toes
animal

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40
Q

type of organism that causes athletes foot?

A

fungi

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41
Q

athletes foot method of transmission?

A

direct contact
fomites

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42
Q

malaria characteristic/symptoms?
plant or animal disease?

A

mosquito acts as vector and injects parasite into bloodstream
causes headaches, fevers and potentially comas and death
animal

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43
Q

what type of organism that causes malaria?

A

protoctist

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44
Q

malaria method of transmission?

A

anophales mosquito (acts as a vector)

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45
Q

what is a fomite?

A

an inanimate object that holds a pathogen

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46
Q

antibiotic definition

A

a drug that slows bacterial growth (bacteriostatic) or kills bacteria (bactericidal)

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47
Q

what was the first antibiotic?
what was it derived from?

A

penicillin
the fungus Penicillium

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48
Q

how does penicillin work?

A

by inhibiting cell wall synthesis

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49
Q

what are the 2 general categories of antibiotics?

A

broad-spectrum (act on a wide range of bacteria)
narrow-spectrum (act on only a few)

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50
Q

examples of antibiotics?

A

pencillins, cephalosporins, vancomycin, cycloserine
rifampicin
chloramphenicol
fluoroquinolones
polymixins
sulfonamides

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51
Q

how do penicillin, cephalosporins, vancomycin (last resort) and cycloserine act?

A

act to inhibit cell wall synthesis

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52
Q

how does rifampicin act?

A

acts to inhibit DNA transcription
therefore stop mRNA synthesis so stop translation

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53
Q

example of fluoroquinolones?

A

ciprofloxacin

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54
Q

how do fluoroquinolone (e.g. ciprofloxacin) act?

A

act to inhibit DNA replication
therefore prevent binary fission

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55
Q

how do polymixins act?

A

act to inhibit plasma membrane synthesis

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56
Q

how do sulfonamides act?

A

act to (competitively) inhibit the enzyme DHPS which promotes DNA replication

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57
Q

how is DNA organised in bacteria?

A

single circular chromosome (genes arranged in clusters (OPERONS))
plasmids (can contain resistance genes)

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58
Q

how has antibiotic resistance come about (brief)

A

there is an evolutionary race between scientists and bacteria
incorrect (prescription when not required) and inappropriate use over many years has led to the development of antibiotic-resistant bacteria

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59
Q

how do bacteria become antibiotic-resistant?

A

if a random mutation during reproduction produces a bacterium that is not affected by the antibiotic, it is best-fitted to survive and reproduce, passing on the antibiotic-resistance mutation to its daughter cells

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60
Q

why does it not take long for an antibiotic-resistance gene to become common in a bacterial population?

A

due to the speed at which bacteria grow and divide

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61
Q

natural selection process in bacteria population

A

resistant bacteria present due to random mutation which creates new alleles
antibiotics (selection pressure) applied
susceptible bacteria are killed and resistant bacteria survive & reproduce & pass on the resistance allele to offspring
over repeated exposure to antibiotics, the resistant population grows and the allele frequency for resistance increases

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62
Q

what are the reasons for the acceleration of development of antibiotic resistance?

A

in some countries (e.g. USA) farmers routinely add antibiotics to feed animals prophylactically (prevents animals losing condition due to infection)
over-prescription of antibiotics
patients not completing their course of antibiotics

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63
Q

do viruses usually act extracellularly or intracellularly?

A

intracellular: act inside cells

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64
Q

examples of viruses
how transmitted

A

coronavirus, influenza, common cold
all easily transmitted through respiratory droplets

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65
Q

step-by-step how is HIV able to self-replicate?

A

virus binds to a receptor on the plasma membrane of host cell
virus injects its DNA/RNA into the cell (integrates DNA/RNA into host nucleus)
host cell synthesises viral proteins
proteins are assembled to form mature viruses
viruses continue to be produced
viruses are burst out of the host cell to infect other host cells.

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66
Q

integrase function in a virus

A

inserts the viral DNA into the host cell DNA

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67
Q

reverse transcriptase function in a virus

A

converts virus RNA into DNA

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68
Q

why does virus have RNA rather than DNA

A

acts as extra line of security
harder for target to recognise

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69
Q

what kind of cells does HIV target?

A

T Helper Cells

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70
Q

difficulties encountered treating diseases like ebola, which is caused by a pathogen that has only recently evolved to infect humans

A

correctly identifying symptoms is difficult
no reliable cures or treatments
vaccine only licensed in 2019
viruses evolve quickly and form new variants

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71
Q

how is C.diff infection transmitted?

A

contracted by ingesting spores: usually picked up from contaminated surfaces esp. in hospitals and nursing homes
spores pass through alimentary tract to the colon where they form colonies

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72
Q

what are broad-spectrum antibiotics?
potential implications of use of broad-spectrum antibiotics?

A

they can treat and kill a wide range of bacteria
potential implications: resistance can form. also these drugs can upset the delicate balance of bacteria in the colon. this means C.difficile can dominate (outcompete) gut bacteria & produce toxins which make a person seriously ill

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73
Q

clostridium enters cells by receptor-mediated endocytosis
what does this mean?

A

it binds to a receptor on the plasma membrane of the cell which causes the cell to ingest the pathogen by endocytosis (PHAGOCYTOSIS)

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74
Q

what 2 antibiotics are used to treat C.diff?
how do they work?

A

metronidazole- bacteria cannot produce nucleic acids so cannot form DNA
vancomycin- prevents cell wall synthesis

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75
Q

how to prevent infection by C.diff?

A

isolate patients with suspected infection
rigorous hand-washing and disinfecting procedures

76
Q

methods of direct transmission in animals

A

contact
entry through the skin
ingestion

77
Q

methods of indirect transmission in animals

A

fomites
inhalation
vectors

78
Q

transmission of communicable pathogens by direct contact in animals:
description
examples

A

bodily fluids, kissing, contact with skin
STIs, diarrhoeal diseases

79
Q

transmission of communicable pathogens by entry through skin in animals:
description
examples

A

wounds, animal bites, needles
HIV, hepatitis, rabies

80
Q

transmission of communicable pathogens by ingestion in animals:
description
examples

A

contaminated food and drink
diarrhoeal diseases

81
Q

transmission of communicable pathogens by fomites in animals:
description
examples

A

(inanimate object that harbours pathogens)
bedding, socks, cosmetics
athletes foot, coldsore viruses

82
Q

transmission of communicable pathogens by inhalation in animals:
description
examples

A

breathing in respiratory droplets
colds, flu, TB

83
Q

transmission of communicable pathogens by vectors in animals:
description
examples

A

pathogens are carried from one host to another e.g. animals, water
malaria, bubonic plague, African sleeping sickness

84
Q

plants mode of direct transmission of disease

A

direct contact

85
Q

plants modes of indirect transmission of disease

A

soil contamination
vectors

86
Q

transmission of communicable pathogens by direct contact in plants:
description
example

A

between healthy plants & diseases plants
incl. infected farming equipment
e.g. TMV

87
Q

transmission of communicable pathogens by soil contamination in plants:
description
examples

A

reproductive spores are left in the soil
black Sigatoka, ring rot

88
Q

transmission of communicable pathogens by vectors in plants:
description
example

A

wind, water, animals
blight

89
Q

factors affecting rate of transmission of communicable pathogens ANIMALS ONLY

A

immunocompromisation
socioeconomic factors
poor waste disposal
culture (lifestyle, food, drink)

90
Q

factors affecting rate of transmission of communicable pathogens PLANTS ONLY

A

susceptible crops

91
Q

factors affecting rate of transmission of communicable pathogens ANIMALS AND PLANTS

A

damp/warm conditions
climate change
overcrowding
poor nutrition (decreases resistance)

92
Q

types of defence mechanisms to prevent infection in plants

A

passive (prevent entry)
active (induced when pathogen detected)

93
Q

the 2 types of passive defence mechanisms to prevent infection in plants

A

physical
chemical

94
Q

the 7 types of physical passive defence mechanisms to prevent infection in plants

A

cellulose cell wall
lignin thickening of cell wall
waxy cuticles
bark
stomatal closure
callose
tylose formation

95
Q

why is cellulose cell wall important for plant defence?

A

acts as a physical barrier
most contain a variety of chemical defences which can be activated when a pathogen is detected

96
Q

why is lignin thickening of cell walls important for plant defence?

A

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

97
Q

why is waxy cuticle important for plant defence?

A

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

98
Q

why is stomatal closure important for plant defence?

A

stomata= entry points for pathogens
stomatal aperture controlled by guard cells; when pathogenic organism detected, guard cells will close stomata in that part of the plant

99
Q

why is bark important for plant defence?

A

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

100
Q

why is callose important for plant defence?

A

callose= large polysaccharide deposited in sieve tubes at end of the growing season
deposited around sieve plates & blocks the flow in sieve tube so can prevent pathogen spreading around the plant

101
Q

why is tylose formation important for plant defence?

A

a tylose= a balloon-like swelling or projection that fills xylem vessel
when a xylose is fully formed, it plugs the vessel so vessel cannot carry water
blocking a xylem vessel prevents spread of pathogens through the heartwood
tylose contains high conc. of chemicals e.g. terpenes, which are toxic to pathogens

102
Q

chemical passive defence mechanisms in plants?

A

plant tissues contain a variety of chemicals which have anti-pathogenic properties e.g. terpenoids, phenols, alkaloids, hydrolytic enzymes
some of these chemicals e.g. terpenes in tyloses & tannins in bark are present before infection. however, bc production of chemicals requires lots of energy many chemicals are not produced until plant detects an infection

103
Q

forms of active defence mechanisms in plants?

A

increase in the production of chemicals
cell walls become thickened and strengthened w/ additional cellulose
deposition of callose between plant cell wall & plasma membrane nr invading pathogen (impedes cellular penetration @ site of infection, strengthens cell wall, blocks plasmodesma)
oxidative bursts that produce highly reactive oxygen molecules capable of damaging the cells of invading organisms
necrosis (deliberate cell death) whereby a few cells are sacrificed to save the whole plant. pathogen access to water and nutrients and its spread around the plant are limited. process facilitated by intracellular enzymes activated by injury.
canker: sunken necrotic lesions in woody tissues. causes of death of cambium tissue in bark

104
Q

there is an increase in production of certain chemicals in active response to an invading pathogen. list 5 of these

A

terpenoids
phenols
alkaloids
defensins
hydrolytic enzymes

105
Q

outline terpenoids’ role in active response in plants

A

range of essential oils, have antibacterial & anti fungal properties. may also create scent e.g. menthols, menthes produced by mint plants

106
Q

outline phenols’ role in active response in plants

A

have antibiotic & anti fungal properties.
tannins in bark inhibit attack by insects. these compounds bind to salivary proteins & digestive enzymes e.g. trypsin, chymotrypsin, deactivating the enzymes. insects that ingest high amounts of tanning don’t grow & will eventually die
helps prevent transmission of pathogens

107
Q

outline alkaloids’ role in active response in plants

A

nitrogen-containing compounds e.g. caffeine, nicotine, cocaine, morphine, solanine
give bitter taste to inhibit herbivores feeding
act on metabolic reactions via inhibiting/ activating enzyme action
some inhibit protein synthesis
if plant can reduce grazing by larger animals, it will suffer less damage that can allow pathogens to enter plant

108
Q

outline defensins’ role in active response in plants

A

cysteine-rich proteins with broad anti-microbial activity
appear to act on molecules in plasma membrane of pathogens, possibly inhibiting action of ion transport channels

109
Q

outline hydrolytic enzymes’ role in active response in plants

A

found in spaces between cells, include chitinases (break down chitin in fungi cell walls), glucanases (hydrolyse glycosidic bonds in glucans) & lysozymes (degrade bacteria cell walls)

110
Q

why are many protective chemicals only manufactures when infection is detected?

A

the production of chemicals requires lots of energy

111
Q

examples of non-specific responses to disease in animals

A

blood clotting
inflammatory response
wound repair

112
Q

examples of non-specific defences against disease in animals

A

mucous membranes
the skin

113
Q

other non-specific primary defences to disease in animals

A

eyes secrete tears which contain LYSOZYME, a hydrolytic enzyme
ear wax acts as a physical barrier

114
Q

outline mucous membranes as a non-specific defence

A

include airways & reproductive systems
secrete mucus via goblet cells which traps pathogens
cilia waft mucus

115
Q

outline the skin as a non-specific defence

A

contains fibrous proteins like keratin and collagen which are insoluble and impermeable so act as physical barrier to pathogens
contains sebaceous glands which secrete oils so is antibacterial

116
Q

outline expulsive reflexes as non-specific responses

A

coughs/sneezes (esp. when pathogens irritate lining of airways)
response is to expel them

117
Q

outline wound repair as a non-specific response

A

new skin cells formed
stem cells leave cell cycle and enter G0
become specialised and integrate themselves into the existing tissues
scabs form while repairs are made

118
Q

outline inflammatory response as a non-specific response

A

mast cells release histamines and cytokines
histamines increase permeability of capillaries, causing blood plasma to leak into tissues, causing pain and swelling
cytokines increase diameter of arterioles, increasing blood flow to wound and attracting phagocytes, causing redness and heat

119
Q

outline blood clotting as a non-specific response

A

enzyme-catalysed cascade
initiated by platelets at site of wound
platelets are activated by damaged tissues to release thromboplastin, which catalyses the conversion of prothrombin to thrombin (with Ca2+ ions and serotonin). thrombin catalyses the conversion of soluble fibrinogen to insoluble fibrin, which forms a mesh of fibres that traps platelets and blood cells to form a clot

120
Q

neutrophils adaptations

A

lobed nucleus enables them to change shapes and squeeze out of capillaries
have lots of mitochondria, RER, Golgi apparatus
vesicles in granular cytoplasm contain hydrolytic enzymes

121
Q

what are macrophages?

A

differentiated monocytes

122
Q

explain how macrophages are adapted for their function compared to monocytes

A

they are larger
they have many pseudopodia to engulf pathogens
they have more RER/Golgi apparatus/mitochondria
they contain phagosomes

123
Q

describe process of phagocytosis

A

pathogen engulfed into phagocyte by PHAGOCYTOSIS (type of endocytosis) into a phagosome (type of vesicle)
lysosomes fuse with the phagosome to form a phagolysosome. this introduces hydrolytic enzymes e.g. lysozyme into the phagosome & digestion occurs
useful products of digestion reabsorbed & waste is excreted (by exocytosis)

124
Q

role of T helper cells in the immune response

A

are clonal selected by an antigen-presenting cell
undergo clonal expansion
some form memory cells
others activate B cells

125
Q

role of T killer cells in the immune response

A

bind directly to infected cells
insert perforins into plasma membrane
flood in hydrolytic enzymes, hydrogen peroxide and nitric acid
cause cell lysis

126
Q

role of T regulatory cells in the immune response

A

dampen down immune response
induce apoptosis of TH, TK and plasma cells
this prevents autoimmunity

127
Q

role of T memory cells in the immune response

A

are clonal selected and expanded much quicker on 2nd infection by the same pathogen

128
Q

role of B lymphocytes in the immune response

A

directly activated by antigen OR clonal selected by a TH cell
clonal expand by mitosis
some form memory cells
others differentiate to become plasma cells

129
Q

where do T cells come from?

A

thymus gland

130
Q

where do B cells come from?

A

bone marrow

131
Q

where do memory cells circulate?

A

in the spleen and lymph nodes to increase the speed of secondary immune response

132
Q

steps of specific immune response

A

antigen presentation
clonal selection of TH cell
clonal expansion of TH cell
clonal selection of B cell
clonal expansion of B cell
plasma cells formed and secrete antibodies

133
Q

describe antigen presentation step in specific immune response

A

(macrophage becomes an antigen-presenting cell)
macrophage engulfs the pathogen (antigen) and breaks it into fragments
recombines antigenic fragments with its own glycoproteins & expresses the antigen on its own plasma membrane

134
Q

how does clonal expansion occur?

A

by mitosis

135
Q

how do TH cells attract B cells?

A

by secreting cytokines

136
Q

what happens after clonal expansion of B cells?

A

B cells differentiate to form plasma cells
plasma cells secrete antibodies

137
Q

describe and explain the differences between B cell and plasma cell

A

plasma cell contains more RER for synthesis of antibodies (proteins)
plasma cell contains more Golgi apparatus for folding 1ary structure of proteins into 4ary structure
plasma cell is larger bc it contains more organelles
plasma cell has more mitochondria to produce ATP for protein synthesis
nucleus takes up more of the B cell’s cytoplasm bc there are less organelles

138
Q

what are antibodies?

A

proteins with quaternary structure

139
Q

what are antibodies’ 4 polypeptide chains

A

2 heavy chains
2 light chains

140
Q

Parts of antigen structure

A

hinge region
heavy chains
light chains
disulphide bonds
variable region
constant region

141
Q

antibody hinge region fucntion

A

allows flexibility for antibody to bind to more than 1 antigen

142
Q

antibody constant region function

A

same in every antibody
non-specific binding say for neutrophils and macrophages

143
Q

antibody variable region function

A

specific shape to antigen
2 per antigen

144
Q

describe opsonins/opsonisation

A

opsonins bind to the antigen using their variable regions (marks out the antigen for destruction)
neutrophil/macrophage binds to the constant region and phagocytoses the pathogen

145
Q

what do agglutinins do?

A

each antibody has 2 variable regions: each variable region can attach to an antigen on a different pathogen (hinge provides flexibility): cross-links pathogens and clumps them together
eases phagocytosis for neutrophils

146
Q

what do antitoxins do?

A

directly binds to toxin molecules secreted by pathogens
toxins neutralised, which prevents damage to cells

147
Q

example of antitoxin treatment

A

tetanus bacteria secrete toxins
antitoxins can be injected as a treatment

148
Q

describe natural active immunity

A

bodys own response ti a new pathogen
memory cells are produced

149
Q

describe natural passive immunity

A

receipt of maternal antibodies through placenta or breastmilk
no memory cells produced

150
Q

describe artificial active immunity

A

injection of an antigen & immune response occurs
memory cells produced

151
Q

describe artificial passive immunity

A

injection of antibodies made by another organism
no memory cells produced

152
Q

describe artificial passive immunity

A

injection of antibodies made by another organism
no memory cells produced

153
Q

describe primary immune response

A

first encounter w/ a particular pathogen
takes a few days to produce any antibodies (clonal selection/expansion of TH/B cells takes time so symptoms are felt)
number of antibodies increases to a low peak and then drops rapidly
PRIMARY RESPONSE has formed T/B memory cells which circulate in case of reinfection

154
Q

describe secondary immune response

A

clonal selection and expansion are much faster
number of antibodies increases at a greater rate and to a much higher concentration
levels of antibodies stay higher for longer
pathogen is removed before any symptoms are felt

155
Q

what kind of immunity is a vaccination?
why?

A

artificial, active immunity
bc injected and prompts an immune response which results in production of memory cells

156
Q

what are the principles of vaccination?

A
  1. preventing severe illness which could result in death
  2. promoting herd immunity
  3. to promote ring immunity
157
Q

what is herd immunity?

A

vaccinating the majority of a population so that disease carriers are less likely to infect a vulnerable individual

158
Q

who cannot have vaccines?

A

immunocompromised people

159
Q

what is ring immunity?

A

vaccinating a smaller proportion than that required for herd immunity, but vaccinating those most likely to be infected

160
Q

what are the types of vaccine?

A

weakened, live pathogen
dead/inactivated pathogen
toxoids
subunits

161
Q

how do weakened, live pathogens work as vaccinations?
examples

A

modified pathogen that is alive but not pathogenic
mumps, polio, TB, measles

162
Q

advantages/disadvantages of using weakened/live pathogen as a vaccine

A

+strongest response
+long-lasting immunity
-organims may revert and become pathogenic

163
Q

how does dead/inactivated pathogen work as a vaccine?
examples

A

pathogen killed but antigens still present
influenza
whooping cough

164
Q

advantages/disadvantages of using dead/inactivated pathogen as vaccine

A

+stable and safer than live vaccines
-response is weaker (boosters required)

165
Q

how do toxoids work as vaccines?
examples

A

modified toxins
tetanus
diphtheria

166
Q

advantages/disadvantages of using toxoids as vaccines

A

+safe
-may not give strong response (boosters required)

167
Q

how do subunits work as vaccines?
examples

A

isolated antigens
haemophilus
influenza B

168
Q

advantage of using subunits as vaccine

A

vaccines for several strains can be produced

169
Q

epidemic definition

A

disease spread across several countries in the same continent

170
Q

pandemic definition

A

global spread of a disease across many continents

171
Q

why does artificial passive immunity not provide long term immunity?

A

(antibodies injected)
no memory cells are produced
if pathogen enters body again, response will not be quick

172
Q

why does herd immunity reduce spread of disease?

A

majority of population vaccinated ( many people in population have immunity so a disease carrier is less likely to come into contact with someone who is NOT immune)

173
Q

why do vaccinations against tetanus require booster injections?

A

toxoid vaccinations may not give strong long-lasting response
boosters maintain high levels of antitoxin antibodies & memory cells because small concentrations of toxins can be v harmful

174
Q

suggest a barrier that makes it difficult for a virus to enter a sweet potato cell
how could the virus enter the cell?

A

cellulose cell wall
through insect transmission (vectors)

175
Q

why are bacteria resistant and not immune?

A

bacteria are unicellular without an immune system
immunity involves phagocytes and lymphocytes

176
Q

why are erythrocytes containimg plasmodium more likely to be destroyed by phagocytosis than healthy erythrocytes?

A

produce different cell signalling molecules which attract phagocytes more strongly

177
Q

most at risk people to disease?

A

elderly
babies
immunocompromised people

178
Q

distinguish between an antigen and an antibody

A

antigen= cell-surface molecules. specific to cell and antibody
antibody=immunoglobulin manufactured by plasma cells. binds specifically to antigen

179
Q

examples of autoimmune diseases?

A

rheumatoid arthritis
lupus
type 1 diabetes

180
Q

RHEUMATOID ARTHRITIS
causes
body parts affected
symptoms
treatments

A

combination of genetic and environmental
mainly joints (knees, fingers, wrists)
stiffened & pain due to inflammation. destruction of cartilage (joints move less smoothly)
steroidal injections, NSAIDS e.g. ibuprofen, biologics

181
Q

LUPUS
causes
symptoms
body parts affected
treatments

A

combination of genetic & environmental
headaches, high temp, sensitivity to UV light, skin rash (butterfly shaped)
skin, joints, kidney
steroidal injections

182
Q

TYPE 1 DIABETES
causes
body parts affected
symptoms
treatments

A

combination of genetic and environmental
beta cells in pancreas destoryed
thirst, weight loss, fatigue
insulin injections, stem cell therapies

183
Q

which types of antibody bind directly to antigens on the surface of pathogens?

A

opsonins
agglutinins

184
Q

which types of antibody increase the phagocytosis of pathogens?

A

opsonins
agglutinins

185
Q

following a blood test, what would indicate that a patient has lupus?

A

the presence of antibodies for the cell surface antigens of connective tissue

186
Q

compare the roles of B and T lymphocytes in the specific immune response

A

BOTH:
clonally selected, clonal expand by mitosis, can become memory cells, are specific to an antigen
B:
mature in bone marrow, differentiate to become plasma cells & secrete antibodies specific to antigens (T don’t)
T:
mature in thymus, have TH/TK/Treg cells (only B), stimulate B cells to activate (B don’t stim. T), secrete cytokines (B don’t)

187
Q

how do betalain pigments interfere with the action of cytokines

A

prevents cytokines form binding to receptors on the membranes of their target cells

biology (27 decks)

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