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Diseases Flashcards

1
Q

What are the three forms of direct transmission?

A
  1. Direct contact
  2. Inoculation
  3. Ingestion
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2
Q

What are the three forms of indirect transmission?

A
  1. Formites
  2. Droplets
  3. Vectors
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3
Q

What are the factors affecting transmission of disease in animals?

A
  1. Overcrowding
  2. Poor nutrition
  3. Compromised immune system (AIDS)
  4. Disposal of waste
  5. Climate change
  6. Culture
  7. Socioeconomic factors
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4
Q

What are bacteria and how many can cause infection?

A

Prokaryotic organisms and a small proportion of bacteria are pathogens, causing communicable diseases.

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5
Q

What are the two main types bacteria can be classifed?

A
  • By basic shape

- By cell wall type

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6
Q

How are bacteria classed by shape?

A
  • Bacilli (rod)
  • Cocci (spherical)
  • Vibrios (comma)
  • Spirilla (spiralled)
  • Spirochaete (corkscrew)

Chain- Strepto
Cluster- Staphylo

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7
Q

How are bacteria classed by cell wall?

A
  • Main two types
  • Different structures
  • React differently when stained
  • Gram +ve (purple-blue)
  • Gram -ve (red)
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8
Q

What are the some examples of bacterial infections?

A
  • Tuberculosis
  • Bacterial meningitis
  • Ring rot
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9
Q

Which animals does tuberculosis affect?

A

Humans, cows, badgers and more

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10
Q

What does tuberculosis damage?

A

Damages and destroys lung tissue (alveoli) and then spreads throughout the body. This is why breathlessness and coughing are the common symptoms

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11
Q

What are the symptoms, cure and prevention for tuberculosis?

A

Symptoms: Vigorous cough, chest pain, breathlessness, fever, sweating
Cure: Antibiotics
Prevention: Vaccination

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12
Q

What is the incubation period for tuberculosis?

A

Several weeks

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13
Q

When are people vaccinated against TB?

A

In school as teenagers

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14
Q

Where is TB a large problem and why is this?

A

In inner cities of developing countries due to overcrowding and poor diet

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15
Q

What is meningitis caused by?

A

Bacterial infection of the meninges (protective membranes of the brain)

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16
Q

Why is meningitis so fatal?

A

It can easily spread to the rest of the body in the blood, causing septicaemia, which can lead to rapid death. Also, survivors are often left with severe brain damage.

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17
Q

What are the symptoms of meningitis?

A
  • Purple/red rash that doesn’t disappear when a glass is pressed on it
  • High temp
  • Cold hand and feet
  • Vomiting
  • Muscle/joint pain
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18
Q

What is the treatment and prevention for meningitis?

A
  • Antibiotics can cure it if delivered early
  • Patients are often isolated and given painkillers
  • Children in UK receive vaccine an regular boosters
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19
Q

How is meningitis spread?

A

Spread by respiratory secretions (saliva) so coughing/kissing/sharing untensils etc.

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20
Q

How is tuberculosis spread?

A

Spread through airborne droplets

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21
Q

What does ring rot damage?

A

Damages leaves, tubers and fruit

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22
Q

What are the symptoms of ring rot?

A
  • Brown discolouration
  • Wilt of lower leaves
  • Leaf rolling
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23
Q

Why is ring rot such an issue?

A
  • Can destroy up to 80% of crop
  • Once it infects a field it cannot be used to grow crops for at least two years
  • Lowers crop yield so farmers make less money
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24
Q

How is ring rot spread?

A

Planting infected seed potatoes and use of contaminated containers, equipment and premises

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25
Q

Where is ring rot and major threat to potatoes?

A

Norther Ireland and Western Europe. There is national legislation in some places to prevent its entry

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26
Q

What is a virus?

A
  • Non living infectious agents
  • Basic structure is some genetic material (DNA or RNA)surrounded by protein
  • 0.02 to 0.3nm in diameter
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27
Q

What do viruses do in the body?

A
  • Invade living cells and take over biochemistry of host cell to replicate
  • Reproduce rapidly
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28
Q

Do viruses only affect humans and plants?

A

No, some viruses are able to infect bacteria, known as BACTERIOPHAGES

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29
Q

What are some examples of viral infections?

A
  • HIV/AIDS
  • Influenza
  • Tobacco Mosaic Virus
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30
Q

Why is HIV damaging to the body?

A
  • Virus attacks T helper cells
  • So, a lower number of T cells means less protection against pathogens (less B cells divided and less antibodies produced)
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31
Q

What type of virus is HIV?

A

A retrovirus

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32
Q

What is a retrovirus?

A

-Virus that contains RNA and reverse transcriptase, which it uses produces its own DNA from the RNA

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33
Q

How is HIV spread?

A

Exchange of bodily fluids, such as semen, vaginal fluids, infected blood or across placenta/breast milk from mother to baby

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34
Q

When was HIV first identified?

A

In the 1980s

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35
Q

Which group of people did HIV affect worse and why was this?

A

Homosexual men as there was limited education about STD’s so partners often had sexual intercourse without condoms, as they didn’t need to worry about getting pregnant

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36
Q

What species did HIV jump from to humans?

A

Apes

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37
Q

How long does it take for HIV to develop into AIDS?

A

Around 10 years

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38
Q

What does AIDS stand for?

A

Acquired Immune Deficiency Syndrome

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39
Q

What are the symptoms of HIV?

A
  • Flu like

- Prolonged symptoms of TB, pneumonia, cancers when AIDS develops

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40
Q

How is HIV treated?

A

-Antiretroviral drugs can be taken, which can allows a person with AIDS to live to the normal life expectancy.

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41
Q

How do antiretroviral drugs work on HIV?

A

Drugs bind to reverse transcriptase and stops replication

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42
Q

Where is HIV still a large issue?

A

In African countries where FGM is still practised due to the sharing of equipment or unprotected intercourse

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43
Q

How does the influenza virus damage the body?

A

Infects the ciliated epithelial cells in gas exchange systems, damaging them and leaving airways open to secondary infections

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44
Q

What are three main strains of influenza?

A

A, B and C

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45
Q

Which of the three strains is more virulent (damaging)?

A

A strain

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46
Q

What is the issue of influenza strands from birds or other animals to humans?

A

These strains can be particularly serious as few people have natural immunity to them

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47
Q

What is the prevention of HIV?

A
  • Currently no vaccine

- Wearing condoms during sexual intercourse and informing partners of infection is the best prevention

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48
Q

Which groups are especially vulnerable to flu?

A

Children, elderly and those with chronic illness/compromises immune systems

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49
Q

What is the main cause of death from influenza?

A

Secondary infections, such as pneumonia

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50
Q

What are the symptoms of influenza?

A
  • Cough
  • Sore throat
  • Fever
  • Runny/stuffy nose
  • Headaches
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51
Q

How is influenza treated?

A
  • Painkillers, fluids and rest to reduce symptoms

- No cure

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52
Q

How is influenza spread?

A

Airborne droplets

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53
Q

How is influenza prevented?

A

Vulnerable groups are given seasonal flu vaccines, based on the strain that scientists think will be most prevalent that year

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54
Q

How does Tobacco Mosaic Virus affect plants?

A

Infects chloroplasts and reduces the chlorophyll content, affecting the plant’s ability to photosynthesise properly so crop yields are reduced

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55
Q

How is Tobacco Mosaic Virus spread?

A

Transmitted through contact between plants either naturally or through hands/equipment of farmers

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56
Q

How is Tobacco Mosaic Virus cured?

A

There is no cure however there are resistant crop strains

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57
Q

What are the symptoms of Tobacco Mosaic Virus?

A
  • Mosaic discolouration of leaves
  • Stunted growth
  • Yellow or white leaves
  • Leaves can crinkle/curl up
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58
Q

How to prevent plants diseases?

A

-Sanitise equipment and hands regularly when tending to plants, especially if used on a potentially infected plant

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59
Q

What are protoctista?

A
  • Group of eukaryotic organisms with a variety of feeding methods
  • A small percentage act as pathogens, causing mostly devastating communicable disease in both animals and plants
  • Protists that causes disease are PARASTITIC
  • May need a vector to transfer them to their host
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60
Q

What are the examples of protist infections?

A
  • Malaria

- Potato/tomato late blight

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61
Q

What vector carries malaria?

A

Female Anopheles mosquito

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62
Q

What protist do mosquitos carry?

A

Plasmodium

63
Q

How does the female anopheles mosquito infect a person with malaria?

A
  • Mosquito will feed on the blood of an infected person, and the plasmodium gametes will fuse in its stomach
  • This will produced thousands of immature Plasmodium
  • Plasmodium migrate to mosquitos salivary glands
  • Infected mosquito feeds on non-infected person
  • Mosquito punctures skin and injects saliva containing an anti-coagulant, an anaesthetic and the Plasmodium
  • Plasmodium enters blood stream and migrates to liver
  • Plasmodium then exits liver cells and hides in the red blood cells
64
Q

What tissues does Malaria affect?

A

Liver, red blood cells and then eventually the brain

65
Q

How is Malaria prevented?

A
  • Nets
  • Vector control
  • Removal of stagnant water
  • Prophylactic drugs
66
Q

What are the symptoms of Malaria?

A
  • Flu like fever
  • Shivering
  • Sweating
  • Anaemia
  • Headache
  • Bleeding
67
Q

Which group of people are immune to Malaria?

A

People with sickle cell disease

68
Q

How many deaths a year does Malaria cause?

A

Well over 1million

69
Q

In which countries in Malaria an endemic?

A

DRC, Angola and many other Sub-Saharan African countries

70
Q

Why is malaria so difficult to vaccinate against?

A

-Plasmodium hides in erythrocytes which have self antigens so leucocytes don’t recognise the foreign antigens in case of an infection

71
Q

What causes potato/tomato late blight?

A

Caused by a fungus-like protoctist

72
Q

What parts of the plants are affected by potato/tomato late blight?

A

Leaves, tubers and fruit

73
Q

How to prevent potato/tomato late blight?

A

Resistant strains, careful management and chemical treatment

74
Q

What are the symptoms of potato/tomato late blight?

A
  • Watery rot of leaves
  • Leaves shrivel and turn brown
  • Brown lesions on stem
  • White fungal growth on underside of leaf
75
Q

What is the issue with the protist that causes potato/tomato late blight?

A

Stays in the soil so you have to kill them in order to reuse the soil again

76
Q

What is fungi?

A
  • Can be multicellular or unicellular
  • Most of sarophytes (feed on dead/decaying matter)
  • Some are parisitic
  • Can spread huge distances (produce millions of spores)
  • Chitin makes up the cell wall
77
Q

What are the examples of fungal infections?

A
  • Black sigatoka
  • Ring worm
  • Athlete’s foot
78
Q

Which crop does Black Sigatoka affect?

79
Q

How is Black Sigatoka spread?

80
Q

How can the spread of Black Sigatoka be controlled?

A
  • Resistant strains

- Fungicide treatment

81
Q

What part of the plant does Black Sigatoka affect?

82
Q

What are the symptoms of Black Sigatoka?

A

Brown, paint-like specks on the leaves and spots on the underside

83
Q

What does ring worm cause?

A

Itchy grey-white, crusty circular areas of skin

84
Q

How to stop the spread of ring work?

A
  • Not touching infected area

- Washing things on high temperature

85
Q

What is an antigen?

A

Molecular tracers on the plasma membrane of a cell or virus used for cell signalling and can illicit an immune response

86
Q

How to cure ring worm?

A

Antifungal creams

87
Q

What does athlete’s foot cause?

A

Causes cracking and scaling which can be extremely sore

88
Q

Where does the fungi grow in athlete’s foot?

A

Grows on and digests warm, moist skin between toes

89
Q

How is athlete’s foot treated?

A

Antifungal creams

90
Q

How to prevent athlete’s foot?

A
  • Regularly washing feet

- Rotating shoes/socks

91
Q

What are the main symptoms of plant diseases?

A

Viruses-
discolouration/distortion/crop yield reduction
Bacteria-
rot/crop yield reduction
Fungi-
mildew/rust/scabs/leaf spots/blight/crop yield reduction

92
Q

What is Ash dieback disease? (Plant)

A
  • caused by fungi
  • found across Europe
  • being treated as a quarantine pest under national emergency measures
  • causes leaf loss and crown dieback, may cause death
93
Q

What is Xylella fastidiosa? (Plant)

A
  • caused by aerobic gram negative bacteria
  • affects the xylem
  • transmitted exclusively by xylem fluid feeding sap insects (insects act as a vector)
  • grapevine, citrus and olive plants at risk
94
Q

What is Dutch Elm Disease?

A
  • fungal infection

- majority of native UK elms have died due to this disease

95
Q

How did Dutch Elm Disease get brought to the UK?

A
  • UK imported some Elm timber from America which has foreign fungus and beetles
  • Beetles from American elms flew the UK trees and infected the new trees
  • Fungal infection completely blocked the xylem so the elms died
  • Beetles moved northwards of UK, infecting trees which caused most of them to die
  • There may be some left alive on the Isle of Wight/Scotland
  • Now we have to import all of our Elms from America
96
Q

How do pathogens enter plants?

A
  • Wounds
  • Cuts
  • Where insects have penetrated bark/waxy cuticle
  • Where animals have latent part of a plant
  • Direct contact with an infected plant
  • Soil contamination
97
Q

How are plant pathogens transmitted?

A
  • Wind
  • Water
  • Animals
  • Humans
  • Non-indigenous species
  • Direct contact
98
Q

What are the factors that increase plant susceptibility to disease?

A

1) Selective breeding- genotype variety, lack disease resistance
2) Overcrowding (monoculture)
3) Lack of minerals (NPK)
4) Damp and warm weather
5) Increase rainfall/wind

99
Q

What are the plants barriers against disease?

A
  • Waxy cuticle
  • Bark
  • Cellulose cell wall
100
Q

What is callose?

A
  • Polysaccharide of beta glucose
  • beta 1,3 linkages with some beta 1,6 branches
  • exists in a variety of cell walls
101
Q

What are human defences against plant diseases?

A
  • Fungicides
  • Genetic engineering
  • Selective breeding
  • Seed treatment prior to sowing
  • Crop drying/storage
  • Crop rotation
  • Correct harvest time
  • Biological control (using a predator to kill off vector insects)
102
Q

What happens to the callose level when plants detect pathogens?

A

Plant rapidly produces high levels of callose

103
Q

What is the role of callose in plant defences?

A

1) Callose is deposited between cell walls and cell membranes next to the infected cells- this barrier prevents further spread
2) Lignin is added to the callose to strengthen the barrier
3) Callose also blocks the sieve cells of the phloem preventing spread this way
4) Callose is also deposited in the plasmodesmata of connecting cells

104
Q

What is the non-specific response?

A

First lines of defence against a pathogen, barriers that consist of surfaces exposed to the external environment

105
Q

What is the first line of defence in animals?

A
  • Eyes (tears contain enzyme lysozyme)
  • Trachea (mucus, cillia, cilliated epithelial/goblet cells)
  • Bladder (periodic flow of urine ,acidic pH)
  • Vagina (acidic pH, mucus flow)
  • Anus (mucus)
  • Stomach (acidic pH)
  • Skin
  • Nasal passage (mucus)
106
Q

How is skin a barrier in animals?

A
  • Physcial barrier
  • Sebaceous oil glands (contain fatty acids, inhibit growth of certain bacteria and fungi by lowering pH)
  • Sweat glands (lysozyme)
  • Commensal bacteria (friendly)
107
Q

What is cystic fibrosis?

A
  • Mucus produced is too sticky so it can’t be wafted

- Vulnerable to secondary infections

108
Q

What does smoking do to cillia?

A

Paralyses them

109
Q

What is the second line of non specific response?

A
  • Inflammatory response
  • Phagocytosis
  • Blood clotting (of a wound)
110
Q

What is the inflammatory response?

A
  • localised response to pathogens, resulting in the inflammation at the site of a wound
  • inflammation is characterised by pain, heat, redness and swelling of tissue
111
Q

How does the inflammatory response occur?

A

1) Mast cells are activated in damaged tissues and release chemicals called histamine and cytokines
2) Histamines make the blood vessels dilate, causing localised heat and redness. The raised blood pressure prevents pathogens reproducing
3) Histamines make blood vessels more leaky, so blood plasma is forced out of the blood, which causes swelling and pain
4) Cytokines attract phagocytes to the site

112
Q

What is the process for blood clotting?

A

1) Platelets activated by damaged tissues and migrate to the site and release two substances- Thromboplastin and Serotonin
2) Serotonin causes muscles around the wound to contract, reducing the gap
3) Thromboplastin is an enzyme that catalyses the formation of thrombin from prothrombin
4) Thrombin then catalyses the formation of fibrin from fibrinogen
5) Fibrin goes on to forms a clot, which then dries out forming a hard scab, keeping pathogens from entering
6) Epidemical cells grow beneath the scab, collagen fibres reinforced the skin cells

113
Q

What is the basic structure of an antibody?

A

1) Constant regions - same in every antibody
2) Variable region - different on different antibodies
3) Light chain
4) Heavy chain
5) Receptor binding site
6) Two antigen binding sites

114
Q

What are the functions of the different parts of an antibody?

A

1) Binding site - Binds to the antigen
2) Disulphide bridge - Holds the shape of the antibody
3) Constant region - Allows antibody to bind to phagocytes
4) Hinge region - Allows molecules to flex when it binds to antigen

115
Q

Why is the part of the antibody incorporating the binding site called the variable region?

A

Because different antibodies have different shapes so the variable region allows it to fit to different antigens

116
Q

What is the process of phagocytosis?

A

1) Phagocyte attracted by cytokines
2) Phagocyte and pathogen make contact and phagocyte recognises pathogen as non-self and binds to it
3) Phagocyte engulfs pathogen via endocytosis to form a phagosome
4) Lysosome moves towards the phagosome and combines with it, forming phagolysosome
5) In phagolysosome enzyme breaks down pathogen
6) Digested pathogen absorbed by phagocyte and useful products absorbed in the cytoplasm and un-useful products are released by exocytosis

117
Q

How do macrophages become APC’s?

A

When macrophage has digested the pathogen, it combines its antigens with MHC (glycoproteins) , which moves the antigens to the plasma membrane of the macrophage. Then, it becomes a APC

118
Q

What is cell mediated immunity?

A

1) In non-specific defence system, the macrophages become APCs
2) Receptors on some of the Th cells fit the antigens
3) Th cells become activated and produce interleukins, stimulating more T cells to divide by mitosis
4) Clone of Th cells that all carry right receptor to bind to right antigen
5) The cloned T cells may:
- become Tm cells or Tk cells
- stimulate activity (division) of B cells
- attract more macrophages

119
Q

What do macrophages cause?

A

The clonal selection of virgin B and T cells, which then lead to clonal expansion

120
Q

What is antibody mediated immunity?

A

1) Activated Th cells bind to B cell APC
2) Clonal selection occurs where B cell with correct antibody is selected for cloning
3) Interleukins produced by Th cells activated B cells
4) B cells divide by mitosis and differentiate into either plasma cells, releasing antibodies or memory cells

121
Q

What do plasma cells do?

A

Release antibodies and bind to antigens and disable the pathogen (part of the primary response)

122
Q

What do memory cells do?

A

Circulate blood and tissue fluid in readiness to respond to future infection (ready to divide into plasma cells and produce antibodies to the specific antigens)

123
Q

How do antibodies defend the body?

A

Acts as an OPSONIN-
chemical that binds to the pathogen to make them more recognisable
Acts as an AGGLUTININS-
causes pathogens carrying antigen-antibody complexes to clump together, making it easier for phagocytes to engulf them
Acts as ANTITOXINS
binds to toxins and neutralises them to make them harmless

124
Q

How do antibodies defend the body?

A
  • Immobilise bacteria by attaching to flagella
  • Together with complement proteins, make membrane channels allowing water to enter the bacterial cells causing them to burst
125
Q

What do Tk cells do?

A

Produce perforin which kills the pathogen by making holes in its plasma membrane

126
Q

What do Tm cells do?

A

If they meet an antigen for the 2nd time, they will divide rapidly and form many clones of Tk cells

127
Q

What do Tr cells do?

A

Suppress the immune system, acting to control and regulate it. They stop the immune response once a pathogen has been eliminated and makes sure the body recognises self antigens and does not set up an autoimmune response

128
Q

What is an autoimmune disease?

A

A disease where the immune systems can sometimes stop recognising ‘self’ antigens and attack healthy body tissues

129
Q

How many autoimmune diseases are there?

A

Around 80 (some causing chronic inflammation to complete breakdown of some tissues)

130
Q

How are autoimmune diseases treated and what is the issue with this method?

A
  • Immunosuppressant drugs

- The issue is that the drugs weaken the immune systems, which leaves the person vulnerable to secondary infections

131
Q

What is an example of an autoimmune disease and which tissues are affected?

A

Type 1 diabetes where the immune systems starts attacking the insulin-secreting cells of the pancreas

132
Q

How is type 1 diabetes managed?

A
  • Insulin injections
  • Pancreas transplants
  • Immunosuppressant drugs
133
Q

What are the main types of vaccines?

A
  • Killed pathogens
  • Isolated antigens
  • Attenuated strains
  • Toxoids
  • Genetically engineered antigens
134
Q

Killed pathogen vaccines:

A
  • e.g. Whooping cough
  • Effective for many years
  • Vaccine injected into muscle
  • Dead cells cannot cause disease because they cannot replicated
  • Body reacts to antigens and primary response is induced
135
Q

Isolated antigens vaccine:

A
  • e.g. some Influenza vaccines
  • Isolate antigens from microorganisms to produce vaccine
  • Vaccine injected into muscles
  • 1 to 3 years effectiveness
136
Q

Attenuated strain vaccine:

A
  • e.g. Rubella vaccine
  • A less virulent strain of the pathogen used
  • Mutated form of pathogen doesn’t cause disease
  • Vaccine injected subcutaneously (under skin)
  • Permanent effectiveness
137
Q

Toxoid vaccines:

A
  • e.g. Diptheria vaccine
  • Altered or modified toxin used to make vaccine
  • Toxin is usually the antigen that induces the immune response
  • Vaccine injected into muscle
138
Q

Genetically engineered antigens vaccine:

A
  • Genetically engineered yeast and bacteria used to produce vaccine
  • e.g. Hepatitis B
  • Gene coding for viral antigen is cloned then inserted into bacterial cells
  • Large scale production of antigenic protein
  • Purification
  • Vaccine injected into muscle
  • Long lasting immunity generated
139
Q

What is active natural immunity?

A
  • T and B memory cells
  • Foreign Ag. exposure
  • Long term
140
Q

What is active artificial immunity?

A
  • Vaccination
  • Attenuated pathogen
  • T and B memory cells
  • Duration: First vaccination will give a few years of immunity and boosters will extend this
141
Q

What is passive natural immunity?

A
  • Antibodies cross placenta to foetus
  • Colostrum in breastmilk is high in antibodies
  • Lasts a few months (no memory cells)
142
Q

What is passive artificial immunity?

A
  • Antibody extraction
  • Injected into persons
  • Temporary as there are no memory cells
143
Q

What routine vaccinations do children in the UK have?

A

First few months- DPT, polio (first and boosters)
15-18 MONTHS- MMR
14 YEARS - girls will have HPV (and now boys)
15 YEARS- DPT (low dose booster)

144
Q

What is a medicine?

A

Any substance containing an active ingredient used in treating a disease and alleviating the symptoms of that disease

145
Q

What are the sources of medicine?

A
  • Fungi (penicillin)
  • Plants (aspirin from willow bark)
  • Digitalis (heart disease medication) from foxgloves
  • Future medicines likely to be found in rainforests (undiscovered areas)
146
Q

How can drugs be administered?

A
  • Orally (pill/liquid)
  • IV
  • Nasal
  • Creams
  • Patches
  • Eyedrops
147
Q

What is pharmacogenomics?

A

Science of interweaving knowledge of drug actions with personal genetic materials

148
Q

What is personalised meication?

A

Tailored treatments to a patient based upon the genome of the patient and pathogen to get the most effective result

149
Q

What is the example of personalised medicine?

A
  • 30% of all breast cancers are caused by a mutation in he HER2 gene
  • Activity of this gene can be shut down by specific drugs herceptin and lapatinib
  • By analysing breast tumours and treating those who have this mutation with the relevant drugs, doctors can reduce deaths from HER2 breast cancer by 50%
150
Q

What is the advantage of antibiotics?

A

Greatly reduced deaths from bacterial infection

151
Q

What is the issue with antibiotics?

A

Overuse of antibiotics in the last years has caused many strains of bacteria to become resistant to antibiotics.

152
Q

What is an example of antibiotic resistant bacteria?

A

MRSA is resistant to several widely used antibiotics. This means that infections with MRSA can be much harder to treat than other bacterial infections. It is a massive problem in hospitals and elderly care homes

153
Q

Where are scientists looking for the next generation of antibiotics?

A
  • Looking in a variety of places such as; soil microorganisms, deep ocean, honey, fish slime
  • Scientist have used Crispr-Cas 9 which are genetic scissors that can edit genes by cutting DNA
  • Companies are exploring Crispr-based antibiotics that might be delivered through a harmless virus
154
Q

How can antibiotic-resistant strains be reduced?

A
  • Minimising use of antibiotics where its not needed
  • Ensuring every course of antibiotic is used to completion
  • Good hygiene in hospitals, care homes and in general to prevent spread of all infections, including antibiotic resistant strains.

Biology (33 decks)

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