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a-level biology > 4.1.1 Communicable Diseases, Disease Prevention and the Immune System > Flashcards

4.1.1 Communicable Diseases, Disease Prevention and the Immune System Flashcards

1
Q

four main types of pathogens that can cause disease in animals and plants

A

bacteria - prokaryotes
viruses - non-living parasites
protoctists - animal like or plant like; eukaryotes
fungi - eukaryotes

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2
Q

pathogen

A

an infectious micro-organism that causes disease

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3
Q

infectious

A

direct or indirect transmission caused by micro-organisms

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4
Q

communicable disease

A

diseases that can be transmitted from one organism to another

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5
Q

organism that causes tuberculosis

A

bacteria

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6
Q

organism that causes
bacterial meningitis

A

bacteria

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7
Q

organism that causes ring rot

A

bacteria

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8
Q

organism that causes HIV/AIDS

A

virus

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9
Q

organism that causes influenza

A

virus

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10
Q

organism that causes tobacco mosaic virus

A

virus

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11
Q

organism that causes black sigatoka

A

fungus

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12
Q

organism that causes blight

A

protoctist

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13
Q

organism that causes ringworm

A

fungus

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14
Q

organism that causes athlete’s foot

A

fungus

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15
Q

organism that causes malaria

A

protoctist

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16
Q

what is a protoctist

A

an animal like or plant like pathogen

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17
Q

how is tuberculosis transmitted

A

respiratory droplets

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18
Q

how is bacterial meningitis transmitted

A

respiratory droplets

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19
Q

how is ring rot transmitted

A

infected farming equipment

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20
Q

how is HIV/AIDS transmitted

A

needle sharing, unprotected sex, blood transfusion

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21
Q

how is influenza transmitted

A

respiratory droplets

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22
Q

how is tobacco mosaic virus transmitted

A

infected farming equipment

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23
Q

how is black sigatoka transmitted

A

spores

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24
Q

how is blight transmitted

A

aphids - VECTOR

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25
Q

how is ringworm transmitted

A

direct contact
spores

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26
Q

how is athlete’s foot transmitted

A

direct contact
fomite

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27
Q

what’s a fomite

A

an inanimate object that holds pathogens

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28
Q

how is malaria transmitted

A

anopheles
mosquito - VECTOR

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29
Q

antibiotic

A

a drug that slows bacterial growth or kills bacteria

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30
Q

bacteriostatic antibiotic

A

slows bacterial growth

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31
Q

bacteriacidal antibiotic

A

kills bacteria

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32
Q

reasons for the development of antibiotic resistance

A

over prescription of antibiotics
patients not finishing the course of antibiotics
routinely using antibiotics in farming

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33
Q

receptor mediated endocytosis

A

the toxin binds to a receptor site on the cell surface. the two are ‘swallowed’ into the inside of the cell

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34
Q

modes of transmission of communicable pathogens - animals

A

direct: contact, entry through skin, ingestion
indirect: fomites, inhalation, vectors

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35
Q

transmission of communicable pathogens in animals - direct: contact

A

contact with skin, bodily fluids, kissing
e.g STIs, diarrhoeal diseases

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36
Q

transmission of communicable pathogens in animals - direct: entry through the skin

A

wounds, animals bites, needles
e.g HIV, hepatitis, rabies

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37
Q

transmission of communicable pathogens in animals - direct: ingestion

A

contaminated food and drink
e.g diarrhoeal diseases

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38
Q

transmission of communicable pathogens in animals - indirect: fomites

A

bedding, socks, cosmetics
e.g athlete’s foot, cold sore viruses

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39
Q

transmission of communicable pathogens in animals - indirect: inhalation

A

breathing in respiratory droplets
e.g cold, flu, TB

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40
Q

transmission of communicable pathogens in animals - indirect: vectors

A

pathogens are carried from one host to another

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41
Q

modes of transmission of communicable pathogens - plants

A

direct: contact
indirect: soil contamination, vectors

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42
Q

transmission of communicable pathogens in plants - direct: contact

A

between healthy plants + diseased plants
infected farming equipment
e.g. tobacco mosaic virus

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43
Q

transmission of communicable pathogens in plants - indirect: soil contamination

A

reproductive spores are left in the soil
e.g. black sigatoka, ring rot

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44
Q

transmission of communicable pathogens in plants - indirect: vectors

A

wind, water, animals
e.g. blight

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45
Q

factors that affect the rate of transmission of communicable diseases (9)

A
46
Q

how does penicillin work

A

inhibits cell wall synthesis

47
Q

describe natural selection - bacteria resistance

A

•antibiotics are applied (selection pressure) - forcing bacteria to be selected
•susceptible bacteria killed, resistant bacteria survive, reproduce and pass on the resistance allele to offspring
•over repeated exposure to antibiotics, the resistant population grows + the allele frequency for resistance increases

48
Q

where does the resistance allele come from

A

a mutation

49
Q

how do viruses spread

A

virus binds to a receptor on plasma membrane of host cell, injects DNA into the nucleus of host cell.
host cell synthesises viral proteins that are assembled to form mature viruses.
viruses continue to be produced then burst out of host cell to infect others

50
Q

how is HIV able to replicate

A

reverse transcriptase converts virus RNA into viral DNA
integrase inserts viral DNA into host cell DNA

51
Q

active and passive defence in plants

A

passive - prevents entry of pathogens
active - induced when a pathogen is detected

52
Q

two categories of passive defence mechanisms

A

physical, chemical

53
Q

physical passive defence mechanisms in plants

A
  • cellulose cell wall acts as a physical barrier
  • lignin thickening of cell wall is indigestible + waterproof
    *waxy cuticles prevent water from collecting on cell surface ( pathogens need water for survival)
  • callose prevents a pathogen spreading around the plant
  • tyloses are balloon-like outgrowths of parenchyma cells to block xylem vessels
54
Q

chemical passive defence mechanisms in plants

A
  • usually produced when an infection is detected
  • chemicals that have anti-pathogenic properties
    *tylose contains a high concentration of chemicals
55
Q

forms of active defence in plants

A
  1. production of chemicals
  2. additional cellulose
  3. deposition of callose
  4. oxidative bursts
  5. necrosis - cell suicide
  6. canker
56
Q

active defence in plants: additional cellulose

A

cell walls become thicker and stronger = stronger barrier

57
Q

active defence in plants: deposition of callose

A

deposition of callose between plant cell wall and cell membrane of invading pathogen - prevents cellular penetration at site of infection. strengthens cell wall, blocks plasmodesmata

58
Q

active defence in plants: oxidative bursts

A

produce highly reactive oxygen molecules which are capable of damaging cells of invading organims

59
Q

active defence in plants: necrosis

A

cells deliberately kill themselves to save the rest of the plant
killing cells that surround the infection can limit the pathogen’s access to water and nutrients = stopping further spreading.

60
Q

chemicals in active response to an invading pathogen

A

terpenoids
phenols
alkaoloids
defensins
hydrolytic enzymes

61
Q

non-specific response: expulsive reflexes

A

coughing + sneezing
expels pathogens that irritate lining of airways

62
Q

non-specific defence: the skin

A

contains fibrous proteins: keratin, collagen - insoluble + impermeable
contains sebaceous glands: secrete antibacterial oils

63
Q

non-specific response: inflammatory response

A

mast cells release histamines + cytokines
histamines increase permeability of capillaries = blood plasma to leak into tissues - pain, swelling
cytokines: increase diameter of arterioles, increases blood flow to wound + attracting phagocytes

64
Q

non-specific response: wound repair

A

new skin cells formed: stem cells leave cell cycle, enter G0, become specialised + integrate themselves into existing tissues
scab formed while repairs are made

65
Q

non-specific defence: mucous membrabes

A

airways and reproductive systems
goblet cells secrete mucus which traps pathogens
cilia wafts mucus along airway

66
Q

non-specific response: blood clotting

A

enzyme catalysed cascade initiated by platelets at site of wound

67
Q

process of blood clotting

A

tissue damages
platelets activated by tissue
platelets release thromboplastin
thromboplastin catalyses prothrombin into thrombin. calcium ions = cofactor
thrombin catalyses fibrinogen into fibers
fibers clot into thrombus

68
Q

non-specific: other primary defences

A

eyes secrete tears - contain lysozyme
ear wax - physical barrier

69
Q

phagocytosis

A

pathogen engulfed into phagocyte by phagocytosis into a phagosome
lysosomes fuse with phagosomes to form phagolysosomes - introduces hydrolytic enzymes e.g. lysozyme into phagosome + digestion occurs
useful digested products = reabsorbed
waste = excreted

70
Q

where are t cells released from

A

thymus gland

71
Q

where are b cells released from

A

bone marrow

72
Q

t helper cells

A

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

73
Q

t killer cells

A

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

74
Q

t regulatory cells

A

dampen down immune response
induce apoptosis of t helper, t killer and plasma cells - prevents autoimmunity

75
Q

t memory cells

A

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

76
Q

b lymphocytes

A

directly activated by antigen
clonally selected by t helper cell
clonally expanded by mitosis
some form memory cells
others differentiate to become plasma cells

77
Q

what happens when an antigen is recognised

A

either:
macrophage engulfs + expresses antigen (APC)
antigen directly activates cell

78
Q

antibody structure: variable region

A

specific shape to antigen
2 per antibody

79
Q

antibody structure: hinge region

A

allows flexibility for antibody to bind to more than 1 antigen

80
Q

antibody structure: constant region

A

non-specific binding site for neutrophils + macrophages
same in every antibody

81
Q

opsonins

A

bind to antigen using its variable regions
marks out the antigen for destruction
neutrophil/macrophage binds to constant region + phagocytoses pathogen
bind to patogens, foreign cells
eases phagocytosis

82
Q

agglutinins

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 + clumps them together
eases phagocytosis for neutrophil

83
Q

antitoxins

A

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

84
Q

primary immune response

A

first encounter with a particular pathogen
takes a few days to produce antibodies - clonal selection/expansion of t/b cells takes time
number of antibodies increase to low peak then drops rapidly
primary response has formed t/b memory cells - circulate in case of reinfection

85
Q

secondary immune response

A

clonal selection + expansion must faster
number of antibodies increase at greater rate/ to a much higher conc.
levels of antibodies stay higher for longer
pathogens removed before symptoms are felt

86
Q

natural active immunity

A

body’s own response to a new pathogen
memory cells produced

87
Q

natural passive immunity

A

receipt of maternal antibodies through placenta or breast milk
no memory cells produced

88
Q

artificial active immunity

A

injection of an antigen + immune response occurs
memory cells produced

89
Q

artificial passive immunity

A

injection of antibodies made by another organism
no memory cells produced

90
Q

type of immunity: vaccination

A

active: prompts immune response - results in memory cells
artificial: injected

91
Q

principles of vaccinations

A

preventing severe illness which could result in death
promote herd immunity
promote ring immunity

92
Q

herd immunity

A

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

93
Q

ring immunity

A

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

94
Q

types of vaccine

A

weakened, live pathogen
dead, inactivated pathogen
toxoids
subunits

95
Q

how does a weakened, live pathogen work?

A

modified pathogen that is active but not pathogenic

96
Q

how does a dead, inactivated pathogen work?

A

pathogen killed but antigens are still present

97
Q

how does a toxoid work?

A

modified toxins

98
Q

how do subunits work?

A

isolated antigens

99
Q

advantages of weakened, live pathogen vaccine

A

strongest response
long-lasting immunity

100
Q

disadvantages of weakened, live pathogen vaccine

A

organism may revert + become pathogenic

101
Q

advantages of dead, inactivated pathogen vaccine

A

stable
safer than live vaccines

102
Q

disadvantages of dead, inactivated pathogen vaccine

A

response is weaker
boosters required

103
Q

advantages of toxoids vaccine

A

safe

104
Q

disadvantages of toxoids vaccine

A

may not give strong response
boosters required

105
Q

advantages of subunits vaccine

A

vaccines for several strains can be produced

106
Q

epidemic

A

disease spread across several countries in the same continent

107
Q

pandemic

A

global spread of a disease across many continents

108
Q

autoimmune disease

A

the immune system fails to recognise body cells as ‘self’
attacks itself and own cells, mistaking them for pathogens
destruction of self tissue

109
Q

examples of autoimmune diseases

A

rheumatoid arthritis
lupus
type 1 diabetes

110
Q

cytokines

A

attract phagocytes

a-level biology (26 decks)

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