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Big Yerp > Unit 4 - Communicable disease, disease prevention and the immune system > Flashcards

Unit 4 - Communicable disease, disease prevention and the immune system Flashcards

1
Q

Pathogen

A

Microorganism that causes disease

Lives in hosts

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2
Q

Communicable diseases

A

Any disease transmitted from one person or animal; contagious

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3
Q

4 groups of microorganisms

A

Bacteria
Fungi
Viruses
Protoctista

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4
Q

Diseases caused by bacteria

A

Tuberculosis
Bacterial meningitis
Ring rot in plants

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5
Q

Diseases caused by viruses

A

HIV/ AIDS
Influenza
Tobacco mosaic virus

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6
Q

Diseases caused by fungi

A

Black sigatoka
Ringworm
Athletes foot

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7
Q

Diseases caused by protoctista

A

Malaria

Potato/ tomato blight

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8
Q

Prokaryotic pathogens

A

Bacteria

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9
Q

Eukaryotic pathogens

A

Fungi

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10
Q

How do bacteria damage hosts

A

Multiply rapidly

Damage cells by releasing waste products and/or toxins

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11
Q

How do fungi damage hosts

A

Hyphae release extracellular enzymes e.g. celluloses to digest plant tissue
Causes decay and leaf death —> no photosynthesis
May produce toxins

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12
Q

Are viruses eukaryotic or prokaryotic

A

Neither; they’re dead

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13
Q

How do viruses damage hosts

A

Invade living cells where genetic material in virus takes over the biochemistry of the host cells
Makes more copies
Host cell bursts, releasing viruses

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14
Q

Bacteriophages

A

Viruses that can attack bacteria

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15
Q

How do protoctista damage hosts

A

Enter host cells and feed on contents before breaking over cells

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16
Q

How may protoctista enter through the body directly

A

Polluted water

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17
Q

Transmission

A

Passing a pathogen from an infected individual to an uninflected individual

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18
Q

Direct transmission

A

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

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19
Q

Types of direct transmission

A

Physical contact
Faecal - oral transmission
Droplet infection
Transmission by spores

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20
Q

Physical contact

A

Touching an infected person
Touching contaminated surfaces
Exchanging bodily fluids

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21
Q

Faecal - oral transmission

A

Eating food or drinking water contaminated by pathogen

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22
Q

Droplet infection

A

Pathogens are carried in tiny water droplets in the air

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23
Q

Transmission by spores

A

Spores are the resistant stage of some pathogens

Can be carried in the air or reside on surfaces or in the soil

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24
Q

Indirect transmission

A

Pathogens are transmitted indirectly via a vector

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25
Q

Vector

A

Another organism that may be used by the pathogen to gain entry to the primary host

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26
Q

Cause of malaria

A

Plasmodium parasite

It enters the human host via a bite from a female Anopheles mosquito

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27
Q

Social factors affect direct transmission

A 
Overcrowding 
Poor ventilation 
Poor sanitation 
Poor health - likely to contract other diseases 
Poor diet (malnutrition) 
Lack of education
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28
Q

Why is there a greater variety of diseases to be found in warmer climates

A

Many protoctists, bacteria and fungi can grow and reproduce more rapidly in warm and moist conditions

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29
Q

Why are plants targets for microorganisms

A

Manufacture sugars in photosynthesis and convert this into wide variety of compounds such as proteins and oils - rich source of nutrients for microorganisms

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30
Q

Passive defences

A

Prevent entry

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31
Q

Active defences

A

Induced when pathogen is detected

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32
Q

Plant passive defences

A 
Cell wall
Waxy cuticle
Bark 
Stomatal closure 
Chemicals with anti pathogenic properties
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33
Q

Plant active defences

A 
Production of callose
Strengthen cell walls with additional cellulose and lignin 
Tylose formation 
Wide range of chemicals produced 
Necrosis
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34
Q

Callose as an active defence

A

Blocks plasmodesmata and sieve plates in the phloem, sealing off the infected part

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35
Q

Tylose

A

Ballon like swelling that fills the xylem vessel. When a tylose is fully formed it blocks the vessel

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36
Q

Necrosis as an active defence

A

Deliberate cell suicide

By killing cells surrounding the infections, pathogens access to water and nutrients is limited

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37
Q

Chemicals produced as a part of plants active defences

A 
Terpenoids 
Phenols 
Alkaloids 
Defensins 
Hydrolysis enzymes
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38
Q

Terpenoids

A

Essential oils with anti-fungal and antibacterial properties

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39
Q

Phenols

A

Have antibiotic and anti-fungal properties

Tannins bind to salivary proteins and digestive enzymes, deactivating them

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40
Q

Alkaloids

A

Nitrogen-containing compounds that have a bitter taste to inhibit herbivores feeding
Inhibit protein synthesis
Also inhibit or activate enzyme action

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41
Q

Defensins

A

Small cysteine-rich proteins with anti-microbial properties
Act upon molecules in plasma membrane of pathogens

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42
Q

Hydrolytic enzymes

A

Found in spaces between cells

Include chitinases, glucanases and lysozymes

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43
Q

Glucanases

A

Hydrolyse glycosidic bonds in glucans

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44
Q

Primary Defences

A

Defences that prevent pathogens from entering the body

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45
Q

Non-specific defences

A

Prevent the entry of all pathogens

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46
Q

Primary non-specific responses

A 
Blood clotting; vessels/skin receptor 
Expulsive reflexes 
Stomach acid 
Tears (enzymes break down e.g. bacterial cell wall)
Wax in ears 
Mucous membranes
Skin 
Inflammatory response
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47
Q

Main primary response

A

Skin

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48
Q

Cells in epidermis

A

Keratinocytes

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49
Q

How are keratinocytes produced

A

Cells produced at base by mitosis

Cells migrate to the top and keratinisation takes place

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50
Q

Keratinisation

A

Cytoplasm dries out and is replaced by keratin

Keratinised layer forms an effective barrier to pathogens

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51
Q

Where are mucous membranes found

A

In many of the body tracts that are at risk of infection as they are in contact with the external environment

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52
Q

What happens when mucus wafts to the top of the trachea

A

It enters the oesophagus and is swallowed. Most pathogens are killed by the acidity of the stomach

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53
Q

Examples of expulsive reflexes

A

Coughing
Sneezing
Vomiting

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54
Q

What are expulsive reflexes a result of

A

Irritation by micro-organisms or toxins in areas that are sensitive. The aim is to expel the microorganism

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55
Q

What happens when platelets come into contact with collagen in the skin or walls of damaged blood vessels

A

They adhere and begin secreting several substances including clotting factors and serotonin

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56
Q

Clotting factors

A

Thromboplastin

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57
Q

What does thromboplastin trigger

A

An enzyme cascade of reactions resulting in the formation of a blood clot. The final step is soluble fibrinogen being converted into insoluble fibrin fibres which forms a barrier

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58
Q

What does serotonin do

A

Makes the smooth muscle in the walls of the blood vessels contract, reducing supply of blood to the area

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59
Q

Inflammatory response

A

This is a localised response to pathogens resulting in inflammation at the site of a wound
Causes pain, heat, redness and tissue swelling

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60
Q

When mast cells are activated in damaged tissues, what chemicals are released from the cell

A

Histamines

Cytokines

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61
Q

Histamines

A

Makes arterioles dilate to increase blood flow (cause redness) and makes the capillary walls more leaky so more plasma is forced out. The extra tissue fluid causes oedema and pain

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62
Q

Oedema

A

Swelling

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63
Q

What do macrophages measure

A

Amount of bacteria entering the body

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64
Q

Roles of macrophages

A

Swallow pathogens and trap them in membranes
Breaks down pathogens by enzymes and kills them
Cause inflammation by ordering blood vessels to release water
Release interleukins

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65
Q

How long do neutrophils last

A

Only 5 days

66
Q

Parasite

A

A microorganism that lives on a host and feeds on it

Causes harm to host

67
Q

secondary defences

A

Defences that combat pathogens once they have entered the body

68
Q

How is it that we identify pathogens as foreign

A

All cells have antigens. Antigens not specific to the organism (self) are recognised as foreign

69
Q

Antigens

A

Functional proteins/glycosidic proteins intrinsic to the plasma membrane

70
Q

Opsonins

A

Opsonins are protein molecules (antibodies) that attach to the antigens on the surface of a pathogen and assist binding to phagocyte
Can be vey specific or not depending if they’re part of the non-specific response or specific response

71
Q

Role of opsonins

A

Enhances the ability of phagocytic cells to bind and engulf the pathogen by acting as a marker

72
Q

Phagocytes

A

Specialised cells in the blood and tissue fluid that engulf and digest pathogens (phagocytosis)

73
Q

Examples of phagocytes

A

Neutrophils
Macrophages
Dendrites

74
Q

Dendritic cells

A

Specialised forms of macrophages

75
Q

Process of phagocytosis

A

Neutrophils bind to opsonins attached to antigen on pathogen
Pathogen engulfed (endocytosis) –> phagosomes
Lysosomes fuses with phagosome, releases hydrolytic enzymes (digestion)
After digestion harmless products are absorbed by the cell

76
Q

When are neutrophils released in large numbers

A

During infection

77
Q

When is pus formed

A

When neutrophils have collected in an area of infection

78
Q

Antigen Presenting Cells (APCs)

A

Macrophages

Dendritic cells

79
Q

How do cells become APCs

A

Larger cells manufactured in the bone marrow
Travel in the blood as monocytes before maturing into macrophages and dendritic cells
When pathogen is engulfed, it is not fully digested but instead saved and moved onto MHC proteins on the surface of the cell

80
Q

MHC proteins

A

Special protein complex

81
Q

What do MHC proteins ensure

A

That the APCs aren’t mistaken for a foreign cell and attacked by other pathogens

82
Q

What happens when APCs move to the lymph node

A

The APC binds to the T cell with the correct receptors and activates to so it can start clonal selection

83
Q

Where are dendritic cells found

A

In peripheral tissues

84
Q

What are neutrophils attracted to

A

Monokines - type of cytokines (chemotaxis)

85
Q

What do T helper cells release

A

Cytokines

These stimulate phagocytosis and B cells to develop

86
Q

What do all T cells release

A

Interleukins (type of cytokines)

87
Q

T killer cells

A

Attack and kill host-body cells that display the foreign antigen

88
Q

What are T killer cells stimulated by

A

interferon

89
Q

What do T memory cells provide

A

Long term immunity

90
Q

Plasma cells

A

Develop from B cells
Circulate in the blood manufacturing & releasing antibodies
Produce antibodies that attach to antigens on pathogens and disable them

91
Q

B memory cells

A

Develop from B cells
Remain in the body for a number of years & act as the neurological memory
If infected by the same pathogen again divide rapidly to form plasma cell clones

92
Q

What does the specific immune response produce

A

Antibodies

93
Q

Clonal expansion

A

Once activated the T-lymphocyte divides rapidly by mitosis

94
Q

What do T-lymphocytes differentiate into

A 
Mature T cells:
T helper cells 
T killer cells 
T memory cells 
T regulator cells
95
Q

T regulator cells

A

Shut down the immune response after the pathogen is removed. Involved in preventing autoimmunity

96
Q

B cell activation

A

Activated T helper cells bind to B cells with matching BCR
Interleukins promote activation (clonal selection)
Activated B cells divides by mitosis (clonal expansion)

97
Q

Cell mediated immunity

A

Refers to attacking infected host cells

98
Q

What cells are most important in cell mediated immunity

A

T killer cells

99
Q

Humoral immunity

A

important in attacking antigens outside of host cells e.g. bacteria and fungi

100
Q

Humoral response

A

Produces plasma cells that produce antibodies

101
Q

Cytokines

A

Chemicals that allow communication of cells in the immune system

102
Q

What does interferon inhibit

A

Virus replication

103
Q

Immunoglobulins

A

Complex proteins produced by plasma cells e.g. antibodies

104
Q

Distinct regions of antibodies

A

Variable

Constant - same in all antibodies

105
Q

Structure of antibodies

A

4 polypeptide chains (2 light and 2 heavy help together by disulphide bonds)

106
Q

Which region of the antibody does the antigen bind to

A

Variable

107
Q

Which region of the antibody does the phagocyte bind to

A

Constant

108
Q

Main groups of antibodies

A

Opsonins
Agglutinins
Anti-toxins

109
Q

Why are the opsonins in the specific response more effective than those in the non-specific response

A

They don’t bind tightly to specific antigens

110
Q

Primary function of opsonins in the primary response

A

Promoting phagocytosis by acting as a marker

111
Q

How do opsonins neutralise pathogens

A

If the antigen on the pathogen has a function (e.g. attachment to the host cell), the pathogen can no longer carry out this function

112
Q

What can’t pathogens do when attached to antibodies

A

Enter host cells

113
Q

Agglutinins

A

Because each antibody has two identical binding sites they can bind to several pathogens and crosslink them
When many antibodies perform this cross linking, pathogens become agglutinated

114
Q

Agglutinated pathogens are …

A

Physically impeded from carrying out functions (neutralised)
Readily engulfed by phagocytes
Non-infective

115
Q

Toxin

A

Protein that harms us

116
Q

Antitoxins

A

Bind to toxins released by pathogenic cells. The actions of antitoxins renders them harmless

117
Q

Primary immune response

A

Immune response when a pathogen is encountered for the first time

118
Q

How long does it take for the no. of antibodies in the blood to rise

A

5 days for everything to occur (e.g. phagocytosis, APCs, migration to lymph, T &B clonal selection and expansion)
In the meantime, pathogens multiply and we experience symptoms

119
Q

Secondary immune response

A

T and B memory cells circulating in blood are rapidly activated if the pathogens infect again
V. quick production of antibodies for higher conc. and sustained for longer
Pathogen is killed before we notice symptoms

120
Q

When do autoimmune diseases occur

A

When the immune system recognises a ‘self’ antigen as a foreign antigen & attacks healthy body tissue

121
Q

Immunity

A

Being able to kill pathogens if infected before getting symptoms

122
Q

-ve of immunosuppressants

A

May deprive the body of its natural defence against pathogens

123
Q

Active immunity

A

Achieved when immune system is activated and manufactures its own antibodies

124
Q

Passive immunity

A

Achieved when antibodies are supplied from another source

125
Q

Natural immunity

A

Achieved through normal life processes

126
Q

Artificial immunity

A

Achieved through medical intervention

127
Q

Natural active immunity

A

Achieved as a result of infection

128
Q

Active artificial immunity

A

Achieved as a result of vaccination

129
Q

Passive natural immunity

A

Antibodies provided via the placenta or via breast milk

130
Q

Passive artificial immunity

A

Provided by infection of antibodies made by another individual

131
Q

what are vaccinations

A

Deliberately exposing the body to pathogenic material to trigger long-term immunity (through activation of the specific immune response leading to memory cells)

132
Q

Types of antigenic material

A

Whole live organisms that aren’t as harmful as ones causing the disease but have same antigens - cowpox for smallpox virus
Harmless or attenuated - Measles
Dead pathogen - cholera
Antigens from the pathogen - Hepatitis B
Toxoid - Tetanus

133
Q

Toxoid

A

Harmless version of a toxin

134
Q

Attenuated

A

Weakened

135
Q

Herd vaccinations

A

Using a vaccine that provides immunity to all/nearly all at risk. To achieve this 80-95% of the population has to be vaccinated

136
Q

Ring vaccination

A

Used when new case of disease is reported

Only those in immediate vicinity are vaccinated

137
Q

When do epidemics rise

A

When some pathogens undergo genetic mutations which change their antigens so the memory cells may not remember them

138
Q

Pandemics

A

Worldwide epidemics

139
Q

How are pandemics avoided

A

Epidemics are closely monitored on a global level so that new strains can be identified and controlled

140
Q

Source of penicillin

A

Penicillium

141
Q

Source of morphine

A

Unripe poppy seeds

142
Q

Source of aspirin

A

Willow-bark extract

143
Q

Why do we still need new drugs

A

New diseases emerging
Many diseases w/ no effective treatments
Some antibiotic treatments are becoming ineffective

144
Q

Why is it important to maintain biodiversity in terms of medicines

A

To make sure we don’t destroy a plant, animal or microorganisms which could give us a life-saving drug

145
Q

Personalised medicines

A

Once gene sequencing technology is fully developed it will be possible to sequence the genes from individuals with particular conditions and develop specific drugs fro their condition

146
Q

Pharmacogenomics

A

The science of interweaving knowledge of drug actions with personal genetic material

147
Q

Synthetic biology

A

We can genetically modify microorganisms or plants to contain a gene that produces a beneficial protein e.g. bacteria are modified to produce human insulin

148
Q

Antibiotics

A

Drugs that interfere with the metabolism of bacteria without the metabolism of human cells - selective toxicity

149
Q

Polymixines

A

Makes holes in bacterium cell membrane –> altering permeability

150
Q

Penicillin and cephalosporins

A

Weaken the peptidoglycan cell wall so bacterium can be more easily damaged by immune system

151
Q

Why is antibiotic resistance growing

A

Overusing antibiotics in both the health sector (prescribing when unnecessary) in meat industry

152
Q

How does antibiotic resistance develop

A 
Random mutation
Selection pressure (adding antibiotics)
Those with mutations that allow resistance survive & reproduce, others die
Next generation has more individuals with the characteristic (resistance)
153
Q

Examples of resistance

A

MRSA (Methicillin-resistant Staphylococcus aureus)

Clostridium difficile

154
Q

What can we do about antibiotic resistance

A

Promote good hygiene in hospitals, care homes and in general prevent spread of resistant strains
Use new, innovative ways of developing antibiotics (computer modelling and/or looking for new sources of medicine in unusual places)
Educate public and healthcare professionals to minimise use of antibiotics and ensure all courses of antibiotics are completed

155
Q

Lymphocyte involved in cell mediated response

A

T cells

156
Q

Lymphocytes involves in humoral response

A

B cells

157
Q

What are interleukins used for

A

Cell signalling in the specific immune response

158
Q

Blood smear analysis

A

Most cells are RBC as they have no nucleus

Darker cells are neutrophils

159
Q

Types of cytokines

A

Monokines - attract neutrophils

Interleukins - released by t helper cells and activate B cells

160
Q

Why may some people experience discomfort in their armpits after an infection

A

Excess tissue fluid drained to lymph nodes

Pathogens in tissue fluid enter lymph

161
Q

B effector cells

A

B lymphocytes that divide to form plasma cell clones

Big Yerp (42 decks)

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