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4.1.1 Communicable diseases, disease prevention and the immune system Flashcards

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1
Q

Communicable diseases, disease prevention, and the immune system - Topic 1.1

A

Communicable diseases, disease prevention, and the immune system - Topic 1.1

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2
Q

Definition

Disease

A

Impaired functions within the body

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3
Q

Defintion

Health

A

Good mental and physical wellbeing, plus an absence of disease

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4
Q

Defintion

Infectious disease

A

A communicable disease that can be transmitted from one organism to another via a pathogen

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5
Q

What is a communicable disease?

A

They are diseases that can be passed from one organism to another, of the same or different species.

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6
Q

What is a pathogen?
What are the 4 types?

A

Pathogen: a microorganism that causes disease
4 types:
- Bacteria
- Fungi
- Viruses
- Protocista

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7
Q

What are the components of a bacterial cell?

Bacteria diagram

A

Contains: (7)
- plasma membrane
- circular DNA
- peptidoglycan celll wall
- capsule
- ribosomes
- cytoplasm
- flagella

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8
Q

Pathogen 1

What are the shapes and function of bacteria?

A

Cocci (spherical) 🔘:
- has less surface area per volume than bacilli or spirilli so it can survive in denser environments

Vibrio (curved) 🦠:
- has greater S.A:V ratio and can take up nutrients from dilute solutions more efficiently

Bacilli (rod-shaped) ➖:
- has greater S.A:V ratop and can take up nutrients from dilute solutions more efficiently

Spirilli (spiral) 〰️:
- move with a corcscrew motion and therefore meet less resistance from surrouding water

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9
Q

Pathogen 1

Bacteria are characterised by their cell wall

A

The cell wall affects how bacteria respond to antibiotics.
- Gram Positive:
purple/blue under light micrsocope; stain with crystal violet; e.g. MRSA

  • Gram Negative:
    red under light microscope; stai with safranin; e.g. e-coli
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10
Q

Pathogen 1

How do bacteria reproduce?
How do bacteria cause disease?

A

They reproduce via binary fission. To calculate to 2^n. n= no. of divisions

They produce toxins and cause symptoms by cell damage. They damage cell membranes, enzymes, or genetic material.

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11
Q

Pathogen 2

What is the structure of viruses?
What is a bacteriophage?

A

Structure:
-some genetic material (DNA or RNA) surrounded by a protein shell
-non-living as they cannot replicate by themselves

Bacteriophage: a virus that infects bacterial cells

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12
Q

Pathogen 2

Explain the stages of viral reproduction.

A
  1. The virus attaches to a specific host cell
  2. The genetic material from the virus is injected into the host cell
  3. The viral genes causes the host cell to make the new viruses
  4. The host cell splits open releasing the new virus
  5. Process repeats to other cells producing lots of virus cell
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13
Q

What are the components of a fungus celll?

Fungi diagram

A

Contains: (7)
- cell wall
- plasma membrane
- cytoplasm
- ribosomes
- vacuole
- mitochondria
- nucleus

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14
Q

Pathogen 3

Fungi
How do fungi grow?
How do fungi cause disease?

A
  • many fungi are sapotrophic and feed on dead and decaying matter
  • parisitic fungi feed on living organisms; tese ones are pathogenic

Growth:
budding in yeast (unicellular)
in multicellular fungi, growth occurs at hyphal tips

  • they digest living cells and destroy them
  • some produce toxins which affect host cells
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15
Q

Pathogen 4

Protoctists
How are they transmitted?
How do they cause disease?

A

Eukaryotic cells
Protists which cause disease are parisitic

They need a vector to transfer them to their host. They may enter the body directly through water (amoebic dysentry)

They digest and use contents of host cell, then break them open when the new protists emerge. (They don’t take over genetic material)

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16
Q

How do pathogens cause disease?

A
  • travel from host to host
  • get into tissues
  • reproduce
  • cause damage
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17
Q

How are pathogens transmitted?

A
  • vectors
  • physical contact
  • droplet infection
  • non-direct contact
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18
Q

What is direct transmission?

A

When a pathogen is transmitted directly from one individual to another.

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19
Q

What is indirect transmission?

A

When a pathogen travels from one individual to another indirectly.

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20
Q

Why is it important to understand how pathogen are transmitted?

A

It allows us to work out ways to reduce/prevent diseases occuring.

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21
Q

What is a vector?

A

A living or non living factor that transmits a pathogen from one organism to another.

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22
Q

3 types

What types of direct transmission are there between animals?

A

1) Direct contact: Any contact with the body fluids of another person; Direct skin to skin contact; Micoroogranisms from faeces transmitted on hands
2) Inoculation: Through a break in the skin; From an animal bite; Through a puncture wound
3) Ingestion; Taking in contaminated food/drink; Transferring pathogens to the mouth from the hands

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23
Q

What types of indirect transmission are there between animals?

A

1) Fomites: Inanimate objects e.g. bedding socks can transfer pathogens between organsims
2) Droplet infection: Minute drops of saliva and mucus expelled and others breathe in the droplets
3) Vectors: Transmits communicable pathogens from one host to another- usually animals
4) Water: Can act as a vector of diseases

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24
Q

Animals

What are 3 key factors to reduce the spread of disease in humans?

A

1) regular hand washing
2) improvements in living & working conditions
3) disposal of both bodily & household waste effectively

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25
Q

Factors affecting tranmission in animals

A
  • overcorwded living and wokring conditions
  • poor nutrition
  • compromised immune system
  • poor disposal of waste
  • climate change
  • culture + infrastructure
  • socioeconomic factors
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26
Q

Examples of transmission between humans and animals.
How can this be minimised?

A

e.g. bird flu strain; brucellosis

minimised by:
- minimising close contact with animals
- washing hands thoroughly folllwoing any contact

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27
Q

What is direct transmission between plants?

A

Involves direct contact of a healthy plant with any part of a diseased plant.

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28
Q

What types of indirect transmission are there between plants?

A

1) Vectors: e.g
-wind: bacteria, viruses,fungal,or oomycete spores may be carried on the wind
-water: spores swim in the surface film of water on leaves
-animals: insects and birds carry pathogen and spores from one plant to another as they feed
-humans: pathogens ans spores are transmitted by hands, clothing, fomites, farming practice etc.
2) Soil contamination: infected plants often leave pathogens or reproductive spores from protoctista or fungi in the soil. This can infect the next crop which will be planted on the same soil.

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29
Q

Wht are the 5 key factors to reduce the spread of disease in plants?

A

1) leave plenty of room between palnts to minimise the spread of pathogens
2) clear fiels as throughly as possible- remove a traces of plants from the soil at harvesting
3) rotate crops
4) follow strict hygiene practices
5) control insect vectors

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30
Q

Wha are the factors affecting transmission in plants?

A
  • planting varieties of crops that are susceptible to disease
  • over-crowding increases the likelihood of contact
  • poor mineral nutrtion reduces the resistance of plants
  • damp, warm conditions & survival & spread of pathogens
  • climate change
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31
Q

What is an epidemic?

A

When a communicable disease spreads rapidly to a lot of people at a local/national level.

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32
Q

What is a pandemic?

A

When a communicable disease spreads rapidly to a lot of people across a number of countries.

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33
Q

List some bacterial diseases

A

1) Tubercolosis
2) Bacterial meningitis
3) Ring rot

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34
Q

Tubercolosis

A

casual agent: mycobacterium
symptoms: bloody cough, weight loss, ashy skin, chest pain
transmission: air-borne drplets
treatments: antibiotics, vaccines
economic impact: 1% of people every year infected, 10-15% get TB later on

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35
Q

Bacterial Meningitis

A

casual agent: Streptococcus preumoniae
symtpoms: vlotchy rash that doesnt dissapar, temperature, hearing loss, bulging fontanelle, irritability
transmission: nose, thorat, drect, repsiratory
treatments: vaccines, antibiotics
economic impact: 10% of infected die, 25% of infected and recovered have some permenant damage, mainly affects young children an teenagers 15-19

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36
Q

Ring rot

A

casual agent: Clavibacter michiganesis
symptoms: damages leaves, poattoes (udnergorund) and tomatoes
transmission: direct contact, direct handling of infected and non-infected plants, infected seed tubers
treatments: nothing- farmer has to leave field unsued for 2.5 years
economic impacts: big impact by farmer losing field and crops- redundant field and can’t earn anything from it

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37
Q

List some viral diseases

A

1) HIV/AIDS
2) Influenza
3) Tobacco mosaic virus

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38
Q

HIV/AIDS

A

casual agent: human immunodeficieny virus
symptoms: sore thorat, tiredness
transmission: sharing/exchange of bodily fluids, unprotected sex, shared needles, contaminated blood
treatments: anti-retro viral drugs slow down the progress of the disease
economic impacts: ~39 milllion (around 70% of global total) have HIV. 800k people have died due to HIV

HIV: infected AIDS: when you get another illlness due to HIV (weakend immune system)

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39
Q

Influenza

A

casual agent: orthomyxoviridae spp.
symtpoms: headache, fever, muscular pain, coughing, runny/stuffy nose
transmission: dropleta, fomites
treatments: vaccines
economic impacts: poultry and swine can be affected by flu and call destroy all of the animals

40
Q

Tobbaco Mosaic virus

A

casual agent: tobacco mosaic virus
symtpoms: yellow leaves, affects plants leaves, flowers and fruit, stunts growth
transmission: direct contact between leaves, plants, or through farm worker
treatments: no treatment
economic impacts: big economic impacct- can lead to whole crop loss

41
Q

List some protoctista diseases

A

1) Malaria
2) Potato/tomato late blight

42
Q

Malaria

A

casual agent: Plasmodium species (impacts mosquitoes and humans)
symptoms: flu-like symptoms: high temp/fever, headaches, sweats, chills, vomiting
transmission: bites of infected female, pregnant anopheles mosquitoes (vector transmission)
treatments: anti-malarial tablets, no cure/vaccine; preventative measures: cover up arms and legs, insect repellant, mosquito nets, avoid stagnant water
economic impact: leading causes of death in developing countries, ~90% of death due to malaria occur in sub-sahran africa, half of world’s population are living in malaria affected countries

43
Q

Potato/Tomato late blight

A

casual agent: Phytophthora infestans
symptoms: leaves destroyed; damaged fruit, tubers, and leaves due to hyphae
transmission: air-borne spores spread in the wind
treatments: no cure- resistant strains exist
economic impact: causes millions of pounds of damage of crop each year

44
Q

List some fungal diseases

A

1) Black sigatoka
2) Ring worm
3) Athletes foot

45
Q

Black sigatoka

A

casual agent: Mycosphaerella fijensis
symptoms: attacks and destroys leaves, turning them black and reduces their ability to photosynthesise
transmission: spreads through leaves of plant
treatments: good husbandry and fungicide treatment can control disease spread, no cure
economic impact: can cause 50% reduction in yield

46
Q

Ring Worm

A

In cattle:
casual agent: Trichophyton verucosum
symptoms: grey-white, crusty infectious, circular areas of skin, may be itchy
transmission: direct contact with infected cattle
treatments: antifungal creams

47
Q

Athletes foot

A

casual agent: Tinia pedia
symptoms: crackling and scaling skin; may become itchy and sore
transmission: direct skin to skin contact or indirectly with contact with an item of clothing
treatments: antifungal creams

48
Q

How do plants deal with diseased tissue?
What are the 2 types of meristems?

A
  • they seal it off and sacrifice it
  • this is possible bevuase plants grow continuossly at the meristems so thye can replace damaged tissue

apical meristems: causes primary growth at shoots/roots
lateral meristems: causes secondary growth (produes bark on trees)

49
Q

How do plants recognise an attack?

A
  • reccognise pathogens by molecules that are produced
  • this ability heps to prevent widespread infection as defence mechanism can be inititated quickly
  • when a pathogen tries to enter a plant cell, receptors on the plasma membrane bind to either 1) molecules made by pathogens or 2) products of pathogenic enzymes that break down molecules in the cell wall
  • the receptors are activated and cells will then release signalling molecules
  • this switches on defensive genes in the nuclues
  • this triggers cellular repsones such as producing chemicals, sending alarm singals and strengthening the cell wall
50
Q

What physcial defences has a plant got?

A
  1. Cellulose cell wall: physcial barrier, lignin thiclens ell walll- waterproof and indigestable
  2. Waxy cuticle: prevents wtaer from collecting on the sruface (pathogens need water)
  3. Guard cellls: can close the stomata
  4. Callose: large polysaccharide that is deposited to seal of infected cells from neighbouring ones from the phloem
51
Q

When is lignin added and what is its purpose?

A
  • It is added once the nucleus has been alerted
  • thickens cell wall
  • water proof
  • indigestable
52
Q

What is callose?
What is its initial job and purpose for it?
What is the purpose of it in:
- plasmodesmata
- phloem vessels

A
  • A polysaccharide containing beta 1-3 linkages and beta 1 -6 lonkages between the glucose monomers that is important in the plant repsone to infection

Callose is synthesised and depossited between the cell wall and cell membrane in cells next to infected cells.
Done to seal off the infected cells and this prevents pathogens from entering the plant cell around the site of infection

Plasmodesmata: string of cytoplasm through the cell walls
-barrier controlling the movement of molecules between plant cells
-helps in response to various developmental enviromental cues

Phloem vessels:
-blocks sieve plates sealing off infected part and preveting the spread of pathogens

53
Q

What are non-specific defences?

A

Do not distinguish one infectious agent from another- respond in the same way

54
Q

What are specific defences?

A

Recognise specific antigens

55
Q

What are primary defences?

A

1) Barriers to prevent pathogen entry
2) Non-specific
3) Expulsive reflexes

56
Q

What are some non-specific responses?

A

1) blood clotting
2) fever
3) inflammatory response
4) phagocytosis

57
Q

4 barriers

What barriers have we got to prevent pathogen entry?

A

Skin:
- produces sebum which inhibits pathogen growth
- covers whole body and prvents entry of pathogens
- lots of healthy microogranisms on body which outocmpete pathogens for space on body surface
Mucuous membranes:
- body tracts lined by this
- secrete mucus which contains phagocytes which remove remaining pathogens
- traps microorganisms and contains lysozomes which destory bacterial and fungal cell walls
Lysozomes:
- in tears, urine, and stomach acid
- help to prevent a=pathogens getting into our bodies
Expulsive reflexes:
- coughs and sneezes eject pathogen-laden mucus from the gas exchange system
- vomiting and diarrhoea expel contents of gut alogn with any infective pathogens

58
Q

What happens during blood clotting?

A

1) Thromoboplastin is an enzyme that catalyses a cascade of reactons resulting in the fomration of a blood clo/ fibrin formation
2) Serotonin makes smooth muscle in the walls of the blood vessels contract (vasconstriction) so they narrow and reduce the supply of blood to the area

59
Q

What is the procces of inflammation?/ What is the inflammatory response?

A

1) Mast cells are activated in damaged tissue in repsone to pathogens/allergens/irritants and they release chemicals callled histamines and cytokines
2) Histamines make blood vessels dilate causing localsied heat and redness- raised temperature prevents pathogens reproducing. They also make blood vssel walls mroe leaky to let more phagocytes out to form more tissue fluid which leads to swelling
3) Cytokines attract white blood cells (phagocytes) to the site
4) Pathogens are disposed by phagocytosis

60
Q

Why do cytokines encourage the hypothalamus to raise the temperature?

A
  • Most pathogens reproduce best at 37 degrees celcius or lower => higher temperatures inhibit pathogen reproduction
  • the specific immune system works better at higher temperatures
61
Q

What are the different ype of leukocytes? (white blood cells)

A

Specifci defenses:
1) Lymphocyte: a) T lymphcyte b) B lymphocyte

Non-specifc defences
2) Phagocyte: a) Macrophage b) Neutrophil

62
Q

What are phagocytes?
What are the 2 types?

A

Specialised white lood cells that build up at the site of infection
They engulf and destory pathogens

1) Neutrophils: smaller, 60% of all white blood cells, short-lived, multi-lobed nucleus, attracted by histamines
2) Macrophages: larger and involved in antigen presentation, more complex and slower process, round cnulues, cut up pathogen to produce an antigen presenting cell (APC)

63
Q

What is an outline of phagocytosis?
What is an MHC?
What is an APC?

A

A pathogen is engulfed by a phagocyte. Th pathogen is contained within a vauole called a phagosome and this combines with a lyosome to form a phagolysosome which digests and destroys the pathogen

MHC: major histocompatability complex (protein complex that can bind to a number of antigens

APC: antigen- preseting cell, these antigens now stimulate otther cells involced in the specific immune system response

64
Q

What are the steps of phagocytosis?
In both neutrophils and macrophage

A

1) The phagocyte is attracted tot he pathogen by the chemicals it is producing
2) the pahgocyte can recognise th epathogen a being non-self
3) The pahgocyte is able to engulf the pathogen and froms a phagosome
4) A lysosome wil move towards a phagosome and fuse with it fomring a phagolyosome
5) A lysosome contains digestive enxymes
6) The digestive enxymes will then hyrdoluse the pathogen inside the phagolysosome

65
Q

What is the step of phagocytosis if it continues in a neutrophil?

A

The whole process would take 10 minutes and waste materials are pushed out of the body

66
Q

What is the step of phagocytosis if it continues in a macrophage?

A

1) Another process occurs after hyrdolysis of the pathogen
2) The antigens from the surface ofthe pathogen are comibined with the glycoproteins from the cytoplasm of the macrophage
3) The anitgens are combined with a group of glycoproteins known as MHC
4) The MHC complex moves the antigens towards the cell surface membrane of the macrophage
5) When the anitgens are on the cell surface membrane the macrophage becomes an atigen-presenting celll (APC)
6) The APCcan then stimulate the other cellls in the immune system to respond

67
Q

What are cytokines?

A

Phagocytes produce cytokines
Act as self-signalling molecule, infroming other phagocytes that the body is under attack and simulating them to move tp the site of infection/inflammation
Can also increase the body temp and stimulate specific immune system

68
Q

What are opsonins?

A

They bind to pathgoens and ‘tag’ them
This is sot hey can be mor easily recognised by phagocytes. phagocytes have receptrs on their cell membranes that bind to commmon opsonins and the pahgocyte then egulfs the pathogen

69
Q

What are the 2 types of specific immune response?

A

1) cell mediated repsonse
2) humoral immunity

70
Q

What is the process of cell mediated response?

A

1) MAcorphages become APCs during non-spefici immune response
2) Receptors on same T-helper cells fit the antigens Clonal selection
3) 3) T-helper cells become activated, producing interleukins and dividing by mitosis Clonal expansion
4) Creates T-helper clones which have the corrrect receptor to bind to pathgoen
5) Cloned T-helper cells:
- develop into T-memory cells
- produce interleukins to stimulate phaocytosis
- produce interleukins to stimulate B cells
- develop into T killer cells that destroy infected cells

71
Q

What is the process of Humoral immunity?

A

1) Millions of different B lymphocytes exist with different anitbodies in thier plasma membranes
2) when a pathogen/antigen enters the body, a B cell with the complementary antibody binds to it, engulfs it, and processes the antigens to become APCs
3) Activated T-helper cells bind to the APC Clonal selection
4) Interleukins (from activated T-helper cells) activate the B cell
5) Divides by mitosis creating plasma cells Clonal expansion
6) Plasma cells produce antiobides
7) Some B cellls develop into memory cells

72
Q

7 of them ( 4 T, 3 B)

What type of lymphocytes are there in the specific immmune response?

A

1) T helper
2) T killer
3) T memory
4) T regulator
5) Plasma cell (B)
6) B effector
7) B memory

73
Q

What is the role of a T-helper cell?

A

binds to the surface antigens on APC
increases antibody production and attracts and stimulates macrophages
makes interukins (type of cytokines) which stimulate B and T cells and macrophages

74
Q

What is the role of a T-killer cell?

A

destory pathogen carrying antigen
makes perforin (creates holes in pathogen/infected cell membrane)

75
Q

What is the role of a T-memory cell?

A

part pf immunological memory, if near antigen a second time, divide rapidly to form a huge no. of clones

76
Q

What is the role of a T-regulator cell?

A

part of immune system acting to control and regulate it
stops immune repsonse once pathogen is eliminated

77
Q

What is the role of a (B) Plasma cell?

A

releases anibodies into the bloodstream
produces ~2000 antibodies per second whilst alive
make antibodees for particular antigen

78
Q

What is the role of a B-effector cell?

A

divide to from plasma cell clones

79
Q

What is the role of a B memory cell?

A

provide immunological memory
programmd to remember a specific antigen and enable body to make rapid response to pathogen again

80
Q

What are antibodies?

A

produced by plasma cells
Y shaped glycoproteins called immunoglobulins
bind to specific antigens so have a specific, complementary shape

81
Q

Diagram of antibody

A

Y

looks like a Y with double lines at top
- constant portion on bottom- allow antiobodies to bind to immune cells
- variable portion on top
- antigen binding site on the tp
- hinge region between straight and diagonal- creates flexibility when multiple antigens are bound
- ligh polpeptide chain and hevay polypeptide chain held together by disulfide bridge

82
Q

What are the roles of antibodies?
What are agglutins

A

1) antibody is a part of antibody-antigen act as an opsonin (tags the antigen) sp that the pahgocyte can engulf it
2) prevent entry of pathgoens into host cells once bound to its antigen
3) act as agglutins which clump pathogens togther
4) act as antitoxins by binding to toxins and making them harmless

83
Q

What is an autoimmune disease?
Why do they occur?
examples?

A

A condition in which the body’s immune system mistakes its own healthy tissues as foreign and attacks them.

  • not yet fully understood
  • tend to be genetic
  • could be an abnormal response to a pathogen or normal body microorganisms
  • could be T regulator cells not wokring properly
  • immunosuppressants drug can be used to treat them bu they also supress the normal immune system

e.g.: rheumatoid arthiritis, lupus, odisaris syndrome, sjogren’s syndrome

84
Q

What are the symtpoms and treatmnets of rheumatoid arthiritis?

A

symptoms:
- inflammation in joints
- painful deformity and immobility

Treatments:
- no cure
- only treated with immunosuppressants, steroids, anti-inflammtory drug

85
Q

What are the symtpoms and treatmnets of lupus?

A

symptoms:
- headaches
- memroy loss
- scartchy rash
- fatigue
- swelling of legs

TreamtnetS:
- no cure
- treated with steroids, immunosuppresants, and anti-inflammatory drugs

86
Q

What are the symtpoms and treatmnets of odisaris syndrome?

A

symtpoms:
- 70-90% caused by immune system
- weight loss
- hypotension
- vitiligo

Treamtnets:
- no cure
- must take hormones daily for lide e.g. caticosteroids to repalce cortsiol and adrenaline
- may need more salt in diet

87
Q

What are the symtpoms and treatmnets of sjogren syndrome?

A

symtpoms:
- glands ifnlamed
- recues production of tear and saliva causing dry eyes and mouht

Treamtnets:
- no cure
- relive synmptoms with aritificla tears, moisture casuig glasses, chewing sugar free gm, punctal plugs (seal tear ducts)

88
Q

How does autoimmunity happen?

A

Primary response to antigen A: - produces antibodies to antigen A
- slow first response
- ill during this time period
- t helper cells binds to anitgens on surface and increase antibody production
- B plasma cells release antiobides into bloodstream and T killer destroys the pathogen

Secondary response to antigen A: -
- T memory cells meet antigen second time and divide rapidlyto form clones
- B memory cells respond rapidly to pathogen so fells less ill or not ill at all

89
Q

What are vaccines?

A

A way of artificially activating the immune system to produce antibodies
They can contain:
- whole live micoroogranisms e.g. small pox
- killed/inactive bacteria/viruses
- attentenuated versions
- harmless toxin
- antigens extracted from pathogn e.g. fl-changes shape
- geneticlaly engineered antigens e.g. hepititus
- genetically engineered RNA e.g. covid

90
Q

Why are these vaccines effective?

A
  • stable pathgoen - doesnt mutate
  • live vaccine- more effective (c. 100%)
  • easy to produce; cheap; hihg aailability
  • esy storage; freeze dried; heat stable
  • infected people easy to identify and coooperative
  • easy to administer; no ooster needed (only 1 inncoulation)
  • no otehr reservoir of infection- only human host
91
Q

What are two types of eradication programmes?

A

1) Herd vaccination - (vaccinate most/all people)- stops infection spreading iwthin a population
2) ring vaccination- vaccinate all people around victim - contains spred within ring and stops transmission; trace and isolte contacts; trvael restriciton; make disease notifiable

92
Q

What are the different types of immunity?

A

1) Active immunity:
- natural (antibodies developed in resonse to an infection)
- artificial (antiboides developed in response to a vaccination
2) Passive immunity
- natural (antibodies recieved from mother, thorugh breast milk
- artificial (antiobides recieved from a medicine, from a gamma globulin infection or infusion)

93
Q

Active Natural

A

Advantages:
- long term immunity
- make memory cells

Disadvantages:
- side ffects
- takes time for an immune response
- may suffer from severe symtpoms

94
Q

Active Artificial

A

Advantages:
- lasts longer
- memory cell
- no severe symptoms

Disadvantages:
- side effects
- immune response takes time
- may need boosters

95
Q

Passive Natural

A

Advantages:
- immediate protection
- lasts long enough until own made
- relevant to environment

Disadvantages:
- short term effection
- no memory cells produced

96
Q

- immediate pr

Passive Artificial

A

Advantages:
- immediate protection- can be life saving

Disadvantages:
- side effects
- temporary
- no memory cells

Biology- Module 4 (4 decks)

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