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AS Biology > Communicable diseases, disease prevention and the immune system > Flashcards

Communicable diseases, disease prevention and the immune system Flashcards

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1
Q

Name different types of bacterial diseases

A
  • Tuberculosis
  • Bacterial meningitis
  • ring rot (in potatoes and tomatoes )
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2
Q

Name the different types of viral disease

A
  • HIV
  • AIDS
  • Influenza
  • tobacco mosaic virus
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3
Q

Name the different types of protoctista disease

A
  • Malaria
  • potato/tomatoe late blight
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4
Q

Name the different types of fungal disease

A
  • Black sigatoka (bananas)
  • ringworm (cattle)
  • Athletes foot (humans)
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5
Q

What is a disease?

A

an illness or disorder of the body or mind that leads to poor health

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6
Q

What are communicable diseases?

A

Diseases that are caused by pathogens and that can be spread between organisms

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7
Q

What are non-communicable diseases?

A

Long term degenerative diseases that aren’t caused by pathogens.

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8
Q

Which microorganisms are pathogens?

A

Bacteria, viruses, fungi, protoctists

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9
Q

What pathogen causes tuberculosis?

A

A bacteria called M. tuberculosis

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10
Q

What does tuberculosis do?

A

It infects the lungs , causing a chronic cough and bloody mucus

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11
Q

What pathogen causes bacterial meningitis?

A

A bacteria called N. meningitidis

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12
Q

What does bacterial meningitis do?

A

It causes acute inflammation in the tissue that surrounds the brain and spinal cord

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13
Q

What are the symptoms of bacterial meningitis ?

A

Fever, headache, neck stiffness, rash

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14
Q

What pathogen causes ring rot?

A

Bacteria

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15
Q

What is ring rot?

A

A disease in potato plants, where the bacteria infects the vascular tissue and prevents the transport of water, causing the plant to wilt and die

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16
Q

What are the symptoms of ring rot?

A

A characteristic black ring rot

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17
Q

Do viruses have standard organelles?

A

No

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18
Q

Can viruses respire?

A

No

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19
Q

How do viruses spread?

A

They infect host cells and hijack their machinery to replicate their own genetic material and proteins

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20
Q

What was the first virus ever discovered?

A

Tobacco mosaic virus

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21
Q

What are the symptoms of a plant infected by tobacco mosaic virus?

A

Yellowing of the leaves, mosaic pattern

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22
Q

What are the 3 different influenza viruses that can infect humans and cause the flu?

A

Influenza A, Influenza B, Influenza C

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23
Q

What do the Influenza viruses do?

A

They infect the cells that line the airways

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24
Q

What are the symptoms of Influenza?

A

High temperature, body aches, fatigue

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25
Q

What does HIV stand for?

A

human immunodeficiency virus

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26
Q

What does HIV do?

A

HIV infects the cells of the immune system and weakens the body’s immune response , so a person with HIV is more likely to get sick

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27
Q

What are protists/ Protoctista?

A

Unicellular eukaryotes

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28
Q

What protist causes malaria?

A

Plasmodium falciparum

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29
Q

What are the symptoms of malaria?

A

fever, chills and fatigue

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30
Q

What vector spreads plasmodium falciparum?

A

Mosquitoes

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31
Q

What pathogen causes potato blight?

A

Protist P.infestans

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32
Q

What does potato blight do to potato and tomato plants?

A

Destroys them and leaves them inedible

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33
Q

Why is the pathogen of potato blight unusual?

A

Because despite being a protoctist, it has fungal characteristics. E.g. the pathogen is transmitted via spores

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34
Q

What are the symptoms of potato blight?

A

small, dark brown marks on the leaves which quickly increase in size and number

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35
Q

Are fungi eukaryotes or prokaryotic?

A

They’re eukaryotes that have a similar structure to plants

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36
Q

What is cattle ringworm?

A

A fungal disease that exists on the surface of the skin

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37
Q

What is athletes foot?

A

A fungal disease that exists on the surface of the skin

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38
Q

What is black sigatoka?

A

A fungal disease in bananas that spreads through the leaves of the plant, reducing its ability to photosynthesise

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39
Q

What are the symptoms of Black sigatoka?

A

Black streaks on the leaf ( caused by the leaf dying due to lack of photosynthesis )

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40
Q

What is disease transmission?

A

the transfer of pathogens from an infected host to an uninfected host

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41
Q

What are the 2 types of disease transmission?

A

Direct transmission and indirect transmission

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42
Q

What is direct transmission?

A

The transfer of pathogens from host to host

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43
Q

What is indirect transmission?

A

When a vector transfers the pathogen to a new host

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44
Q

Name the forms of direct transmission

A

-Physical contact
- Air droplets
- Fungal spores
- Exchange of bodily fluids
-

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45
Q

Is it true that the form of TB caused byMycobacterium bovisoccurs incattlebut is spread to humans through contaminatedmeat andunpasteurisedmilk?

A

Yes

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46
Q

Name the forms of indirect transmission

A
  • ## Vectors
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47
Q

What is an endemic?

A

A disease that is always present in a population - even if in very low numbers

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48
Q

What is an epidemic?

A

Where there is a large increase in the number of cases in a population (an outbreak)

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49
Q

What is a pandemic?

A

Where an epidemic occurs on a large scale and crosses international boundaries

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50
Q

What are the different defense mechanisms in plants?

A

Active and passive

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51
Q

What are active defense mechanisms in plants?

A

Active defence mechanisms in plants are activated when pathogens invade

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52
Q

What are passive defense mechanisms in plants?

A

Passive defense mechanisms are mechanisms that are always present I.e bark

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53
Q

What do passive defense mechanisms include?

A

Physical barriers and chemicals

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54
Q

What Physical barriers (passive defense mechanisms) does a plant have?

A
  • Waxy cuticle
  • Cellulose cell wall
  • Closed stomata
  • Bark
  • Casparian strip
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55
Q

What do Physical barriers in plants do?

A

They make it harder for pathogens to gain entry into plants

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56
Q

How does the Waxy cuticle defend the plant?

A

Prevents viruses and bacteria from entering the leaf

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57
Q

How does the casparian strip defend the plant?

A

Pathogens can’t penetrate the casparian strip and so can’t enter the plant

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58
Q

What do chemical defences in plants do?

A

They prevent pathogens from growing on the surface of the plant by creating acidic conditions

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59
Q

What are some examples of chemical defences?

A
  • Toxic compounds
  • Sticky resin found in bark, this traps the pathogens so that they can’t spread
  • Compounds that encourage the growth of competing microorganisms
  • Enzyme inhibitors
  • Receptor molecules, which detect the presence of pathogens and trigger other defence mechanisms
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60
Q

Name some active defence mechanisms in plants

A
  • Cell signalling
  • Hypersensitivity
    -Cell walls reinforced with callose and lignin
  • Narrowing of the plasmodemata
  • Ingrowth into the xylem vessels (tylose)
  • Blockage of the phloem
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61
Q

What is hypersensitivity?

A

The rapid death of tissue surrounding the site infected by a pathogen. This deprives the pathogen of nutrients and energy from the host tissues

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62
Q

Where is callose deposited?

A

Between the cell surface membrane and the cell wall

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63
Q

How does the narrowing of the plasmodesmata help defend a plant against pathogens?

A

Callose helps to reduce the size of the channels that connect neighbouring plant cells. This means that pathogens aren’t transmitted to neighbouring plants

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64
Q

What is the blockage of the phloem?

A

Where the sieve pores are filled with callose which prevents phloem sap from being transported

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65
Q

What does cell signalling allow to happen?

A
  • Allows for pathogen metabolism to be disrupted
  • Delays pathogen reproduction
  • Disrupts bacterial cell surface membranes
  • Stimulates the release of chitinases (enzymes that break down the chitin cell walls in fungi)
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66
Q

What does the first line of defence do?

A

It prevents the entry of pathogens into the body

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67
Q

What makes up the fist line of defence in humans?

A
  • Skin
  • Mucous membranes
  • Expulsive reflexes
  • Chemical secretions
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68
Q

What type of barrier is the skin to pathogens?

A

A physical barrier

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69
Q

What does the skin secrete?

A

Sebum, which has antimicrobial properties

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70
Q

How is the skin an inhospitable environment for pathogens?

A

Because when sweat evaporates from the skin, a salty residue is left behind. This lack of moisture combined with a high salt concentration creates an inhospitable environment for pathogens to live

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71
Q

What do mucous membranes line?

A

the gut, airways and reproductive system

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72
Q

What do the mucous membranes consist of ?

A

Epithelial cells and goblet cells

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73
Q

What do goblet cells do?

A

They secrete mucous, which traps pathogens

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74
Q

What do the cillia do?

A

They move mucus and pathogens along the airway and towards the back of the throat, where the mucus is swallowed and digested by the enzymes in the stomach

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75
Q

What happens when a pathogen irritates the lining of an airway

A

It triggers an expulsive reflex; a cough or sneeze. This sudden expulsion in air expels pathogens from the respiratory tact

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76
Q

What are lysosomes?

A

antimicrobial enzymes that breakdown the cell wall of bacteria

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77
Q

When does the second line of defence respond?

A

When a pathogen manages to evade the first line of defence

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78
Q

What does the second line of defence include?

A
  • Blood clotting
  • Inflammation
  • Wound repair
  • Phagocytosis
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79
Q

How does blood clotting defend the body?

A

Because blood clotting prevents the entry of pathogens and provides a scab ( a wound) for wound healing to occur

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80
Q

What is inflammation?

A

When the surrounding area of a wound becomes swollen, warm and painful to touch

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81
Q

What happens underneath a scab?

A

stem cells divide by mitosis to heal the wound

82
Q

What are the stages that wound healing occur in?

A
  • New blood vessels form
  • Collagen is produced
  • Granulation tissue forms to fill the wound
  • Stem cells move over the new tissue and divide to produce epithelial cell
  • Contractile cells cause wound contraction
  • Unwanted cells die
83
Q

Do phagocytes carry out the specific or non-specific immune response?

A

The non-specific immune response

84
Q

What are the 3 types of phagocytes?

A
  • Neutrophils
  • Macrophages/ monocyte
  • Dendritic cells
85
Q

Do neutrophils ‘patrol’ the body tissues?

A

Yes

86
Q

Are neutrophils released in large numbers during an infection?

A

Yes

87
Q

Are neutrophils long-lived or short-lived?

A

They’re short-lived

88
Q

What shape is the nucleus of a neutrohil?

A

Lobed

89
Q

What attracts neutrophils to the site where pathogens are located?

A

Chemicals released by pathogens. (Chemotaxis)

90
Q

As well as the chemicals released by pathogens, what else triggers a neutrophil to attack pathogens?

A

The antibodies that cover the pathogen

91
Q

What is an antigen?

A

A chemical marker on the pathogen’s outer surface

92
Q

Describe the steps a neutrophil takes in engulfing a pathogen

A

1) Detection
Chemotaxis causes the phagocyte to detect the pathogen

2) Ingestion(endocytosis)
The phagocyte ingests the pathogen via endocytosis

3) Phagosome forms
A vesicle forms around the pathogen

4) Fusion with lysosome
The phagosome fuses with a lysosome to form a phagolysosome

5) Digestion
The pathogen is digested by the enzymes in the lysosome

6) Discharge
Waste material leaves the phagocyte via exocytosis

93
Q

Are macrophages larger or smaller than neutrophils?

A

Larger than neutrophils

94
Q

Do macrophages remain in the blood?

A

No, they move into organs including the lungs, liver, spleen, kidney and lymph nodes

95
Q

What happens after macrophages are produced in the bone marrow?

A

They travel in the blood as monocytes, which then develop into macrophages once they leave the blood to settle in the various organs listed above

96
Q

What do macrophages do?

A

They don’t destroy the pathogen completely and display the antigens on the pathogens cell surface membrane. These displayed antigens can then be recognised by lymphocytes

97
Q

What are dendritic cells?

A

large phagocytic cells with lengthy extensions

98
Q

Where can dendritic cells be found?

A

Throughout the body

99
Q

what is a blood smear?

A

when a small amount of blood is spread on a glass microscope slide, stained and covered with a coverslip

100
Q

What will red blood cells look like in a blood smear?

A

no nuclei and a distinct biconcave shape

101
Q

What will white blood cells look like in a blood smear?

A

irregularly shaped

102
Q

What will neutrophils look like in a blood smear?

A

lobed nucleus

103
Q

What will lymphocytes look like in a blood smear?

A

will have a very large nucleus that nearly occupies the whole cell

104
Q

What produces the third line of defence against pathogens?

A

Lymphocytes and antibodies

105
Q

Is the third line of defence specific or non specific ?

A

Specific

106
Q

Are lymphocytes larger or smaller than phagocytes?

A

Smaller

107
Q

Do lymphocytes have a large or small nucleus?

A

They have a large nucleus that almost fills up the entire cell

108
Q

Where are lymphocytes produced?

A

In the bone marrow

109
Q

What are the 2 types of lymphocytes?

A

The T-lymphocytes and the B-lymphocytes

110
Q

Where do T-lymphocytes mature?

A

In the thymus gland

111
Q

Where do B-lymphocytes mature?

A

In the bone marrow

112
Q

Describe the role of the T-lymphocytes in the immune response

A

Antigen Presentation
- Macrophages engulf pathogens and present the pathogen antigens on their own cell surface membrane. They then become antigen-presenting cells

Clonal Selection
- T cells with T cell receptors that are complementary to the specific pathogenic antigen bind to the antigen-presenting cell

Clonal expansion
- T cells divide by mitosis to increase in number

  • There are now many different T cells in the blood that have different roles

-

113
Q

Name all the different T cells in the blood after clonal expansion

A

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

114
Q

Describe the role of the T helper cells

A
  • They don’t directly damage the host cell, but help other cells destroy it by producing cytokines/interleukins.
  • These chemicals attract macrophages and T killer cells
  • Also activate B-lymphocytes to divide by mitosis
115
Q

Describe the role of T killer cells

A
  • They patrol the body in search of antigen-presenting body cells
  • Attach to the foreign antigens on the cell surface membranes of infected cells and secrete toxic substances that kill the infected body cells, along with the pathogen inside
  • Perforins secreted by T killer cells punch a hole in the cell surface membrane of infected cells, allowing toxins to enter1
116
Q

Describe the role of T regulatory cells

A
  • Without checks the immune system can spiral out of control and cause serious damage to the host
  • T regulator cells down-regulate the host immune response by preventing T cells from attacking and killing uninfected host cells and shutting down the immune system once the body is cleared of the pathogen
117
Q

What do T memory cells do?

A

Memory cells remain in the blood, meaning that if the same antigen is encountered again the process of clonal selection will occur much more quickly (immunological memory )

118
Q

Describe the role of B lymphocytes in the immune response

A

Clonal Selection and activation
- B cells with complementary antibody receptors bind to antigens on antigen presenting cells; this is clonal selection. This binding, together with interleukins released by T helper cells activates the B cells

Clonal expansion
- Activated B cells divide by mitosis to produce clones
- Some of these B-lymphocytes differentiate into plasma cells. The others become B memory cells

119
Q

What do plasma cells make a lot of?

A

Antibodies

120
Q

What is another name for clonal expansion?

A

Proliferation

121
Q

What is a memory cell?

A
122
Q

Explain how you would expect the appearance of a plasma cell to differ from that of a memory/B cell when viewed using an electron microscope?

A
123
Q

Outline the process involved when antibodies are produced in plasma cells?

A
124
Q

What are the 2 types of immune response?

A

The primary immune response and the secondary immune response

125
Q

What is the primary immune response?

A

where the immune system responds to a newly encountered antigen

126
Q

What is the secondary immune response?

A

where the immune system responds to a previously encountered antigen

127
Q

what is opsonin?

A

a protein molecule (like an antibody) that enhances phagocytosis by attaching to the antigen and allowing for easier binding by the phagocytic cells

128
Q

Why does the primary immune response have a considerate time delay?

A

Because it takes considerable time and energy for the clonal selection and expansion of specific T cells and B cells, and because it takes considerable time and energy for the synthesis of antibodies

129
Q

What happens during the time delay of the primary immune response?

A

we often experience symptoms of a disease when we are first exposed to a pathogen

130
Q

Is the secondary immune response considerably quicker than the primary immune response?

A

Yes, because B memory cells divide very quickly and differentiate into plasma cells (to produce antibodies) and more memory cells

131
Q

What are antibodies?

A

globular glycoproteins called immunoglobulins

132
Q

Antibodies have a …………….. structure with 2 ……… and 2 ……….. polypeptide chains bonded together by ………………. bonds

A

quaternary
heavy
light
disulfide

133
Q

Each polypeptide chain of an antibody has a …………………… and a ……………………… region

A

variable
constant

134
Q

do antibodies have an antigen binding site?

A

Yes

135
Q

What does the hinge region of an antibody do?

A

gives flexibility to the antibody molecule which allows the antigen-binding site to be placed at different angles when binding to antigens

136
Q

What are antibodies produced by?

A

B lymphocytes

137
Q

What do anti toxins do to pathogens?

A

They bind to the molecules released by pathogens rendering them harmless

138
Q

What is neutralisation?

A

Where antibodies (opsonins) bind to pathogen’s antigens, covering its binding sites so it can’t enter host cells. Phagocytosis is also stimulated

139
Q

What is agglutination?

A

where large antibodies bind to many antigens on different pathogens. This causes the pathogens to clump together so that they become immobile and can’t enter host cells, and are more easily engulfed by phagocytes

140
Q

What is natural active immunity?

A

The immune response initiated after catching a pathogen

141
Q

What is artificial active immunity?

A

Vaccines

142
Q

What is natural passive immunity?

A

When antibodies pass from mother to foetus across the placenta or the colostrom

143
Q

What is artificial passive immunity?

A

Where antibodies that are raised in another animal or in a lab are injected. This gives immediate, but temporary protection.

144
Q

Roughly what percentage of the british population suffer from an autoimmune disease?

A

Roughly 5%

145
Q

What is an autoimmune disease?

A

Where the immune system is unable to recognise the body’s own molecules and treats its own antigens as foreign antigens. This then triggers an immune response, where the immune system starts attacking the body’s cells

146
Q

What is Systemic lupus erythematosus (SLE) ?

A

an autoimmune disease that affects several organs

147
Q

What is rheumatois arthritis?

A

An autoimmune disease that solely affects the joints

148
Q

Where does rheumatois arthritis usually begin?

A

Begins in the fingers and hands, and spreads to the shoulders and elsewhere

149
Q

What are the symptoms of rheumatoid arthritis?

A

Muscle spasms, inflamed tendons, lethargy, constant joint pain

150
Q

What is lupus?

A

An autoimmune disease caused by the immune system attacking cells in the connective tissue. This means that it affects the skin, joints, kidney, heart, lungs, skin (essentially any organ in the body)

151
Q

Who tends to suffer from lupus more- women or men?

A

Women

152
Q

Is there any cure for lupus?

A

No, but anti-inflammatory steroids and anti-depressants can help with the pain

153
Q

What is the most distinctive symptom of lupus?

A

A butterfly rash

154
Q

Vaccination

A
155
Q

What is vaccination?

A

The deliberate exposure to antigenic material, which activates the immune system to make an immune response and provide immunity

156
Q

What are the 2 main types of vaccination?

A

Live attenuated and inactivated

157
Q

What 2 ways can vaccines be administered ?

A

Via injection or orally

158
Q

Why do vaccinations provide long term immunity?

A

Because they cause memory cells to be created. The immune system remembers the antigen when reencountered and produces antibodies to it, in what is a faster, stronger secondary response

159
Q

What are babies vaccinated against in the UK?

A

Polio and measles

160
Q

What is an attenuated pathogen

A

a strain of a pathogen that is not as virulent (TB)

161
Q

What is a harmless pathogen?

A

A strain of a pathogen with no virulence (measles)

162
Q

What is an example of a dead pathogen?

A

Cholera

163
Q

What are the potential problems with vaccines?

A
  • Some people have a poor response to them
  • There is variation in the antigens of pathogens
    -Viruses have the capacity to change their surface antigen
  • Some pathogens hide from the immune system by hiding inside cells
164
Q

What is herd immunity?

A

Where a sufficiently large proportion of the population has been vaccinated (and are therefore immune) which makes it difficult for a pathogen to spread within that population. V

165
Q

What is herd immunity?

A

Where a sufficiently large proportion of the population has been vaccinated (and are therefore immune) which makes it difficult for a pathogen to spread within that population. Those who are not immunised are protected and unlikely to contract it as the levels of the disease are so low

166
Q

What is ring immunity?

A

Where People living or working near a vulnerable (or infected) person are vaccinated in order to prevent them from catching and transmitting the disease. The vaccinated individuals do not spread the pathogen onto others so those vulnerable individuals “within the ring” are protected as the people they interact with will not have the disease

167
Q

Have bacteria and fungi helped to provide many antibiotics?

A
  • Yes
168
Q

What is Artemisinin?

A

a drug found in Sweet wormwood and it treats malaria by killing the pathogen while it is in the red blood cells

169
Q

What is Quinidine?

A

derived from the Quinine tree and it treats a fast heart rate by blocking channel proteins in cardiac muscle to reduce impulse conduction

170
Q

Why is continued access to drugs and the discovery of new drugs a strong argument for maintaining biodiversity at a global level?

A

because microorganism and plant species may go extinct before we have the chance to discover what drugs they can provide

171
Q

What does personalised medicine involve?

A

the development of more targeted and personalised drugs to treat a variety of human diseases as well as the development of synthetic tissues

172
Q

What can be used to develop genomic medicine?

A

Information gathered from genome projects like the Human Genome Project (HGP)

173
Q

What does genomic medicine do?

A

it uses information about an individuals genes to influence their clinical care. Ideally, doctors could prescribe the most effective drugs for an individual based on their genome

174
Q

Why is genetic screening a form of personalised medicine ?

A

Because it allows for individuals with a high chance of developing specific diseases to be identified and for preventative measures or precautions to be taken

175
Q

What is synthetic biology?

A

a recent area of research that aims to create new biological parts, devices, and systems, or to redesign systems that already exist in nature. It involves assembling an entire genome.

176
Q

What is the most well known use of synthetic biology?

A

the commercial production of artemisinin

177
Q

What are antibiotics?

A

chemical substances that inhibit or kill bacterial cells with little or no harm to human tissue

178
Q

What was the first antibiotic to be discovered?

A

Penicillin

179
Q

Who discovered Penicillin and when ?

A

Sir Alexander Fleming and in 1928

180
Q
A
181
Q

What do bacteriostatic antibiotics do?

A

they inhibit growth processes

182
Q

What can antibiotics be derived from?

A

Fungi or synthetic materials

183
Q

What do broad spectrum antibiotics do?

A

They act on a a wide range of bacteria

184
Q

What do narrow-spectrum antibiotics do?

A

They act on a very small number of bacteria

185
Q

What is an example of a broad spectrum antibiotic?

A

Amoxicillin

186
Q

What does penicillin do?

A

It inhibits the synthesis of the bacterial cell wall

187
Q

What does tetracycline do?

A

It inhibits the translation of bacterial DNA

188
Q

What does Quniolones do?

A

It inhibits the synthesis of bacterial DNA

189
Q

What does Rifampicin do?

A

It inhibits the transcription of bacterial DNA

190
Q

What does Polymixin do?

A

It affects cell surface mebrane function

191
Q

How do bacteria become antibiotic resistant?

A

Some bacteria possess alleles that are resistant to the effects of the antibiotic. These alleles are generated through random mutations. Bacteria have a single loop of DNA with only one copy of each gene so when a new allele arises, it it immediately displayed in the phenotype. Individuals with the allele for antibiotic resistance have a massive selective advantage so they are more likely to survive, reproduce and pass genome (including resistance alleles)

192
Q

How have some bacteria become resistant to penicillin?

A

because they have acquired genes that code for the production of the enzyme β-lactamase (also known as penicillinase), which breaks down penicillin

193
Q

Why are antibiotics becoming increasingly less effective?

A

Because of:
- The overuse of antibiotics
- Large scale use of antibiotics in farming to prevent disease when livestock are kept in close quarters, even when animals are not sick
-Patients failing to complete the full course of antibiotics prescribed by doctors

194
Q

What is the most common example of a resistant bacteria?

A

a strain of Staphylococcus aureus that has developed resistance to a powerful antibiotic, methicillin and is now known as MRSA (Methicillin-resistant Staphylococcus aureus)

195
Q

Where does Staphylococcus aureus live?

A

on human skin, without causing disease however when there is an opportunity for the pathogen to enter the body

196
Q

What is Clostridium difficile ?

A

a bacteria present in the human gut

197
Q

Why are the numbers of Clostridium difficile in the gut usually kept low?

A

due to the presence of other gut bacteria, which are ‘friendlier’

198
Q

What can a Clostridium difficile infection cause?

A

diarrhoea and fever as they disrupt the epithelium of the intestine

199
Q

How can the spread of antibiotic resistance be prevented?

A
  • avoiding the overuse of antibiotics
  • Antibiotics not being used in non-serious infections
  • Antibiotics not being used for viral infections
  • The use of ‘wide-spectrum’ antibiotics being reduced and instead those antibiotics that are highly specific to the infection (‘narrow-spectrum’ antibiotics) being used
  • The type of antibiotics prescribed being changed so that the same antibiotic is not always prescribed for the same infections and diseases (this reduces the chance of a resistant strain developing)
  • The use of antibiotics being reduced and more tightly controlled in industries such as agriculture
200
Q

How can the spread of already-resistant strains can be limited?

A
  • Ensuring good hygiene practices such as handwashing and the use of hand sanitisers
  • Isolating infected patients to prevent the spread of resistant strains, in particular in surgical wards where MRSA can infect surgical wounds

AS Biology (15 decks)

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