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Biology Module 4 > 1. Communicable Diseases > Flashcards

1. Communicable Diseases Flashcards

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1
Q

Reasons for rapid spread of fungus between trees

A

Mobile vector Moving from tree to tree
Overcrowding of trees
Fungal spores carried by wind

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2
Q

Ways to minimise outbreak of bacteria

A

Increase ventilation
Measures to kill rats
Immediate quarantine for persons w symptoms

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3
Q

How to clone vegetables

A

Tissue culture

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4
Q

Why is asepsis important

A

Reduces contamination

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5
Q

Variables that would be controlled by planting clones in adjacent fields

A

Temperature, wind speed, rainfall, light intensity, soil pH, humidity

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6
Q

Factors that affect spread of communicable diseases

A
  • lack of trained health professionals so lack of vaccinations
  • poor sanitation so easy to pick up pathogen from lack of hand washing
  • overcrowded living conditions = pathogens spread more easily by coughing
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7
Q

How does a virus enter a plant cell

A

Wound, carried by vector

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8
Q

How to observe callose production

A
  • use a microscope
  • take tissue samples from diff sites
  • use a stain
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9
Q

Why does cells recognising and destroying incorrectly formed mRNA counteract infection.

A

Virus RNA recognised + destroyed and virus replication stopped

Benefit: faulty mRNA destroyed

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10
Q

How do malarial parasites bypass the body’s primary defences

A

Mosquito mouthparts pierce skin
Pathogen injected into blood

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11
Q

Role of opsonin

A

Binds to antigen on pathogen and assists binding to pathogycte (increase recognition by phagocytes)

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12
Q

Neutrophil adaptations

A

Many lysosomes
Many mitochondria
Multi Lobed nucleus
Well developed cytoskeleton

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13
Q

Role of cytokines

A

Attract phagocytes

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14
Q

Process that leads to production of antibodies against an unfamiliar bacterium

A
  • b lymphocytes have antigen receptor on surface complementary to only one antigen
  • activated b cell proliferates and differentiates into plasma cells which secrete antibodies complementary to antigen
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15
Q

How do t helper cells speed up production of antibodies

A

Stimulated by antigen presenting cells
Release interleukins that stimulate b cell proliferation

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16
Q

Why are diff strains immunologically distinct

A
  • toxins produced by each strain will be different
  • each toxin will have diff 3d shape
  • toxin acts as antigen
  • immune response determined by shape of antigen
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17
Q

Why is immune response faster when you get a disease for the second time

A
  • first time = slower response because of clonal selection
  • 2nd time = quicker response = more antibodies produced because of memory cells
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18
Q

Bond found between light and heavy region on antibody

A

Disulfide = to hold polypeptides together

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19
Q

What is Autoimmune disease

A

Abnormal immune response against tissues normally in the body (own tissue)

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20
Q

Why are antibodies specific to nuclear proteins not normally made

A

Nuclear proteins normally not exposed to tissue fluids

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21
Q

Agglutination

A

Clump pathogens and stop pathogens reproducing.
Help phagocytes engulf pathogens

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22
Q

Affect of overuse of antibiotics

A
  • antibiotic is selective pressure
  • bacterial gene pool has variation l- only some bacteria have resistance
  • when exposed most resistant survive
  • surviving bacteria continue to reproduce tp make a resistant population p- antibiotic becomes ineffective
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23
Q

Pathogens

A

organisms that can cause disease = bacteria, fungi, viruses, proctoctista

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24
Q

Bacteria

A
  • can cause diseases by damaging your cell or releasing toxins
  • Prokaryotic
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25
Q

Fungi cell wall

A

Chitin

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26
Q

Fungi

A
  • Cause diseases that you can find on the surface of a plant
  • Form spores = dormant stage of their life cycle
  • Divide by budding?
  • Release hyphaes = structure that releases the spores. From the hyphae they can release spores and form mycelium = ‘root’ keeps spores grounded (bundles of hyphaes make a mycelium
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27
Q

Viruses

A
  • not living
  • Hijack a cell and make use of the cell’s organelles to create more viral particles
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28
Q

Protoctist

A
  • Parasites that enter the host and feed off them
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29
Q

Example of protoctista

A

Malaria is caused by a parasite called plasmodium

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30
Q

Diseases caused by bacteria

A

Tuberculosis, bacterial meningitis, ring Rot

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31
Q

Diseases caused by virus

A

HIV/AIDS, influenza, tobacco mosaic virus

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32
Q

Diseases caused by fungus

A

Black Sigatoka, ringworm, athletes foot

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33
Q

Diseases caused by protoctists

A

Blight, malaria

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34
Q

2 forms of transmission

A

Direct and indirect

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35
Q

Direct transmission

A

From one host to the next w nothing in between can pass on disease by physical touch, fecalo-oral, droplet infection, through spores

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36
Q

How to prevent disease transmission by physical touch

A

can be prevented by washing hands + cleaning surfaces + using protection for sexual intercourse

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37
Q

What is fecalo oral transmission caused by

A

Contaminated food e.g. cholera + food poisoning

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38
Q

What can fecalo oral transmission be prevented by

A

treating water + washing all fresh food = careful preparation of food

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39
Q

Droplet infection

A

pathogen is found inside water droplets

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40
Q

What can droplet infection be prevented by

A

covering mouth and nose when sneezing, using tissues and disposing of the properly

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41
Q

Spores

A

can be carried in the air or found in soil

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42
Q

What can spores be prevented by

A

wearing masks and washing skin after contact with soil

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43
Q

Other factors that affect transmission

A

Climate factors, social factors

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44
Q

Climate factors affecting transmission

A

increase in global warming = increasing temperatures so certain diseases can grow in different parts of the world

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45
Q

Social factors affecting transmission

A

overcrowding, poor education, poor ventilation, homelessness

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46
Q

Indirect transmission

A

when a pathogen is transmitted by a vector

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47
Q

Is malaria direct or indirect transmission

A

Indirect

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48
Q

What is malaria transmitted by

A

female mosquitos known as anopheles mosquito and the parasite being transmitted is plasmodium

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49
Q

Transmission of malaria

A

Plasmodium travels in the blood to the liver where it then further replicates and migrates to the blood again. Person = infected w/ malaria and if another female mosquito feeds from that blood the plasmodium replicates in her saliva and the second she bites someone else it spreads.

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50
Q

Direct transmission in plants

A

pathogens found in the soil can enter from the roots. Fungi produces spores = airborne + can affect plants directly, if spores are attached to an insect then it becomes

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51
Q

Indirect transmission of plants

A

pathogen transferred through insects

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52
Q

2 maintain types of responses against pathogens in plants

A

Chemical and non chemical

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53
Q

Physical defences in plants (passive)

A

Cell wall
Lignin
Waxy cuticles
Bark
Stomatal closure
Callose
Tylose formation

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54
Q

Cell wall

A

Acts as a physical barrier

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55
Q

Lignin

A

waterproof + can’t be digested = no pathogens can grow on it

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56
Q

Waxy cuticles

A

waterproof + prevents pathogens from growing on it

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57
Q

Bark

A

contains chemical defences and act as a physical barrier

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58
Q

Stomatal closure

A

if pathogens detected the guard cells will tell the stomata to close

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59
Q

Callose

A

sugar (polysaccharide) that is deposited around the sieve plates which blocks the flow in the sieve tube so the pathogens cannot spread around the plant

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60
Q

Tylose formation

A

swelling in xylem by forming a plug which prevents the spread of pathogens

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61
Q

Active defences in plants

A
  • cell wall becomes thicker
  • Callose deposition increases
  • Oxidative bursts = reactive oxygen species that can damage cells
  • An increase in production of chemicals
62
Q

Chemicals used in plant defences

A

Terpenoids, phenols, alkaloids, hydrolytic enzymes

63
Q

Terpenoids

A

oils that create a scent to prevent insects from biting + can have antibacterial and anti fungal properties

64
Q

Phenols

A

e.g. tannins = found in bark + inhibit attack by insects by deactivating the salivary enzymes if the insects, causing them to die

65
Q

Alkaloids

A

can activate or inhibit enzymes of the attacking animal or insect = can kill the attacking animal or insect by inhibiting processes such as protein synthesis which are vital for the animal/insect

66
Q

Hydrolysis enzymes

A

enzymes produced by the plant that can affect the structure of the pathogen

67
Q

Necrosis

A

deliberate cell suicide = to prevent pathogen from affecting neighbouring cells

68
Q

Primary defences against disease

A

defences that prevented entry of the pathogen = non-specific

69
Q

Primary defences in animals

A

Skin, blood clotting, mucous membranes, coughing and sneezing and vomiting, inflammation

70
Q

The skin

A

acts as a physical barrier = made up of dead cells on the surface and prevents the entry of pathogens

71
Q

Blood clotting

A

prevents entry of pathogens = needs calcium ions and 12 clotting factors + cell needed for clotting = platelets. First step = clot then after you form a scab = a seal which underneath the cells are working to regenerate that skin (skin repair = mitosis occurs + new cells are made)

72
Q

Mucous membranes

A

made by goblet cells which trap the pathogens which is moved by cilia to the trachea. Mucus can either be spat out or swallowed where it will then be destroyed by the hydrochloric acid in the stomach. Mucus membranes are found in any openings of the body.

73
Q

Coughing and sneezing and vomiting

A

aim is to get rid of the pathogen

74
Q

Histamine

A

type of signalling molecule that has many effects e.g. vasodilation

75
Q

Vasodilation

A

when the arterials dilate = allows more blood to reach the site of damage = causes redness and heat , can make the walls of the capillaries more permeable = more white blood cells can reach the site of damage which means that we get more tissue fluid = causes swelling (oedema)

76
Q

Inflammation

A

performed by immune cells - in inflammation master cells (type of immune cell) are the first cell to detect the pathogen in the blood and they release histamine = causes all the symptoms of inflammation e.g. heat, swelling, pain, redness and loss of function.

77
Q

Excess tissue fluid

A

drained into lymphatic system which has lymphocytes (type of white blood cells) therefore allowing more white blood cells to come into contact w/ the pathogen

78
Q

Other primary defences in animals

A
  • eyes protected by enzymes and antibodies in tear fluid
  • Ear Canal is lined by wax which traps pathogens
  • Acidity in stomach and vagina
79
Q

Secondary defences

A

Non specific = used to combat pathogens that have entered the body.

80
Q

What can phagocytosis be performed by

A

Neutrophils and macrophages

81
Q

What reaches site of infection first

A

Neutrophils

82
Q

Phagocytosis w neutrophils

A

detect the antigens on the pathogen and the pathogen is then engulfed, forming a phagosome. The phagosome then fuses with a lysosome allowing the pathogen to be digested and the harmless products can be absorbed into the cell of the neutrophil however the neutrophil dies soon after.

83
Q

Phagocytosis w macrophages

A

carry out phagocytosis however at the end they can prevent the antigens on their surface and become antigen presenting cells (antigen presentation).

84
Q

Neutrophils need for lots of mitochondria’s

A

Need for Endocytosis

85
Q

Neutrophils need for ribosomes

A

Needed to produce lysosomes

86
Q

Macrophages

A

type of white blood cell which travel in the blood as monocytes and when they reach the tissue they become known as macrophages. The best way to identify them is that they’re big and a big portion of the cell is made up of the nucleus. Dendritic cells = another type of macrophage

87
Q

Secondary specific defence

A

specific immune system = every antigen is treated differently

88
Q

2 types of lymphocytes

A

T and b lymphocytes

89
Q

Where are t lymphocytes made

A

in the bone marrow and mature in the thymus gland

90
Q

Where are b lymphocytes made

A

made in the bone marrow and mature in the bone marrow

91
Q

Stages of specific immune response

A

Clonal selection, clonal expansion, differentiation

92
Q

Clonal selection

A

Upon antigen presentation by the macrophage the t-lymphocytes with the complementary receptor to the antigen binds to it

93
Q

Clonal expansion

A

Upon clonal selection the t-cells under mitosis/proliferation, where multiple copies of the t-cells are made.

94
Q

What can T cells differentiate into

A

Killer, memory, helper, regulatory

95
Q

T killer cells

A

attack the pathogen with the complementary antigen

96
Q

T memory cells

A

remain in the blood until the same pathogen enters again + remember the antigen

97
Q

T helper cells

A

release interleukins (type of cytokine) (to activate the B cells

98
Q

T regulatory cells

A

stop the immune system when it’s no longer needed, preventing auto immune diseases from happening

99
Q

What happens once b cells are activated

A

T helper cells prevents the antigens to the B cells and the B cells with the complementary antibodies to the antigen are activated, this is known as clonal selection. The B cells proliferate/expand through mitosis, this is known as clonal expansion. B cells have an antigen receptor that can detach which results in antibodies floating around in your blood.

100
Q

What can b cells differentiate into

A

Plasma cells and memory cells

101
Q

B plasma cells

A

release antibodies that are complementary to the antigen)

102
Q

B memory cells

A

remain in the blood until the same pathogen enters + remember the antibody

103
Q

Autoimmune diseases examples

A

Arthritis and lupus

104
Q

Shape of antibodies

A

Y shaped

105
Q

What are antibodies made up of

A
  • Made up of 4 polypeptide chains, 2 heavy on the bottom and 2 light on the top
  • Polypeptide chains are held by disulphide bonds
106
Q

What is between light and heavy chains of antibodies

A

hinge regions which allows for flexibility (antibody can bend around antigen)

107
Q

Variable region

A

At top of each peak of the y = actual receptor that binds to antigen

108
Q

Wats antibodies can act

A

Opsonin
Agglutination
Anti toxin

109
Q

Anti toxin

A

Neutralises toxins released by bacteria

110
Q

Primary response

A

first time your body sees a pathogen

111
Q

Secondary response

A

Second time your body sees a pathogen

112
Q

Vaccination

A

dead pathogen or harmless pathogen or antigen only vaccine or harmless version of toxins to trigger the body’s primary immune system to create b and t memory cells against the antigen.
Can be live organisms

113
Q

Vaccination programmes

A

Herd vaccination, ring vaccination

114
Q

Herd vaccination

A

aim is to vaccinate all of the people at risk so that the disease can’t spread between people

115
Q

Ring vaccination

A

vaccinating everyone in immediate proximity of the case.

116
Q

Epidemic

A

rapid spread of disease through a population

117
Q

Pandemic

A

rapid spread of disease globally

118
Q

Routine vaccination

A

Viruses such as influenza require a new vaccination every year because they mutate a lot so every year their antigens change so the previous memory cells are no longer effective.

119
Q

Global issues of vaccines

A

Not everyone can have access to vaccines
Vaccines can be really expensive

120
Q

4 types of immunity

A

Active, artificial, natural, passive

121
Q

Active immunity

A
  • when your body produces its own antibodies
122
Q

Artificial immunity

A
  • when the body doesn’t see the pathogen itself, but develops immunity. E.g. vaccines
123
Q

Natural immunity

A
  • No medical intervention = happens over the course of someone’s life
124
Q

Passive immunity

A

When the antibodies are given to the body (patient isn’t producing antibodies

125
Q

Natural active

A
  • immunity provided by antibodies made in immune system as result of infection
126
Q

Example of natural active

A

Immunity to chickenpox (person suffers from disease once and is then immune)

127
Q

Natural passive

A

when the antibodies are given through breast milk or placenta to the baby. Short lived = no antigens/no immune response,cannot make new antibodies

128
Q

Artificial active

A

Antibodies given through vaccination = injected w dead or similar pathogen or antigen = activates immune system

129
Q

Example of artificial active

A

Immunity to TB and influenza

130
Q

Artificial passive

A

antigodies injected in the person made by another individual

131
Q

Artificial passive immunity example

A

Dog bite - tetanus

132
Q

Sources of new medicine needed bc

A
  • new diseases are emerging
  • antibiotic resistance is increasing
133
Q

What are antibiotics used to treat

A

Bacteria and fungi but not viruses

134
Q

Selection pressure

A

forces evolution + survival of the fittest. Factor that promotors survival of the fittest in bacteria.

135
Q

Main reasons for antibiotic resistance

A
  • misuse of antibiotics
  • Course of taking the antibiotics stops earlier than you should have stopped it = causes the alive bacteria to survive and reproduce
136
Q

Implications of antibiotic resistance

A

more people are going to suffer from complications after surgery, more people are going to suffer from infections that can’t be treated.

137
Q

MRSA

A

methicillin-resistant staphylococcus aureus
^found in hospitals

138
Q

Clostridium difficile (C. Diff)

A

When someone has these diseases it is harder for them to be treated = high antibiotic resistance

139
Q

How are medicines discovered

A

Accidental discovery
Tradition remedies
Observation of wildlife

140
Q

Accidental discovery

A
  • antibiotics can be produced by bacterias themselves to try and kill the bacteria next to it
  • E.g. penicillin is an antibiotic which comes from the fungus penicillium
141
Q

Traditional remedies

A
  • e.g. ibuprofen and aspirin come from willow bark trees
  • Morphine comes from poppy seeds
  • Traditional medicine has now been manufactured into
142
Q

Observation of wildlife

A

E.g. monkeys rub citrus oil on their coats

143
Q

Ways to personalise medicine

A

Synthetic biology

144
Q

Synthetic biology

A

making a drug from scratch.

145
Q

Personalised medicine

A

making a drug that treats a specific persons disease and how it affects their body.

146
Q

Why are vaccinations an example of active immunity

A

Antibodies produced by person being vaccinated.
Memory cells remain in person

147
Q

Why can’t one vaccine protect against more than one pathogen

A

different pathogens have different aftigens (1)
antigens have specific shape (1)
shape of antibody must be complementary to (specific) antigen (1)
any of the above linked to different antibody needed for each pathogen (1)

148
Q

2 groups vulnerable to infection

A

Babies and elderly

149
Q

ii.
Name the process that increases the proportion of penicillin-resistant bacteria in the population.

A

Natural selection

150
Q

Macrophages engulfing bacteria

A
  • antigens on the bacteria are detected by receptors on phagocytes
  • Phagocytosis - phagocyte engulfs the bacteria which forms a phagosome
  • Phagosome fuses w lysosome
  • Lysosome contains hydrolytic enzymes which digest the pathogen
  • Useful products are recycled and the antigens are presented on the surface of the macrophage and the macrophage becomes an antigen presenting cell
151
Q

Monocytes vs macrophage

A

Monocytes = when macrophage is in blood
Macrophages: when in tissue

152
Q

Does phagocytosis require energy

A

Yup

Biology Module 4 (3 decks)

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