Chapter 12 - Communicable Diseases Flashcards
(305 cards)
1
Q
Define disease
A
an illness or disorder of the body or mind that leads to poor health
2
Q
What are communicable diseases caused by
A
Pathogens
3
Q
4 types of pathogens
A
Bacteria
Virus
Fungus
Protoctists
4
Q
What type of cells are bacteria
A
Unicellular prokaryotic
5
Q
What are bacterial cell walls made of
A
Peptidoglycan
6
Q
Size of bacteria
A
0.2 – 2 micrometres
7
Q
How do bacteria move
A
Flagella
8
Q
How do bacteria reproduce
A
Asexually = binary fission
9
Q
Can bacteria exchange DNA
A
Yes
10
Q
How can bacteria exchange DNA
A
through conjunction = two cells temporarily fuse + transfer DNA (beneficial traits)
11
Q
How do bacteria cause disease
A
produce toxins ( metabolic waste products) + cause symptoms by cell damage
12
Q
What type of cell damage do bacteria do
A
- damage cell membranes / enzymes / genetic material
13
Q
Do bacteria always cause disease
A
No - can remain within body cavities or spaces
14
Q
Draw a diagram of a bacteria
A
15
Q
Structure of a virus
A
- No cellular structure
16
Q
What makes viruses controversial
A
Are they living or not = No cellular structure + can’t produce ATP without living cells
17
Q
How do viruses infect a host
A
- Attach to receptors on surface of host cell + penetrate its genetic material via endocytosis
- Virus uses host cells machinery to replicate DNA
18
Q
Two ways virus cause disease / replicate
A
- Lytic / lysogenic cycle
19
Q
Why are viruses likely to mutate
A
- RNA = more likely to mutate = as only one strand
20
Q
Structure of a virus
A
- Nucleic aid core + capsid = DNA/RNA enclosed in protein coat
21
Q
Draw the structure of a virus
A
22
Q
How do viruses replicate their DNA / RNA
A
reverse transcription
23
Q
What is reverse transcription
A
- single stranded RNA instead of DNA = reverse transcriptase enzymes use RNA as a template to make single stranded DNA
- DNA polymerase enzymes makes double stranded DNA
- Attached to the host DNA
- Host cell now able to make new viruses which travel to the host membrane to be released
24
Q
What is a bacteriophage
A
virus that attacks bacteria
25
What is the lytic cycle
involves the reproduction of viruses using a host cell to manufacture more viruses = then burst out of the cell.
- With lytic phages, bacterial cells are broken open (lysed) and destroyed after immediate replication of the virion. As soon as the cell is destroyed, the virus can find new hosts to infect
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What is the lysogenic cycle
- viral genome will integrate with host DNA and replicate along with it fairly harmlessly = may even become established as a plasmid.
- virus remains dormant until host conditions deteriorate = e.g depletion of nutrients = at some point switches from lysogenic to lytic
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Is the lysogenic cycle itself dangerous
No - dormant
Only dangerous when switches to lytic cycle + bursts
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What type of cells are fungus
- Multicellular or unicellular saprophytes
EUKARYOTIC
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Cell walls of fungus
Chitnin
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Structure of fungus
- Filamentous body = mycelium / hyphae
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How do fungus reproduce
sexually + asexually = gametes + spores
32
Draw structure of a fungus
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What type of cells are protoctists
- Eukaryotic – unicellular or multicellular
- Heterotrophic / autotrophic
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How do protoctists reproduce
- Asexual or sexual reproduction
- Sexual = budding in yeast
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Draw structure of protoctists
36
How to calculate number of cells after dividing for a set amount of time
Number of original X 2^number of cycles
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What is TB caused by
Bacteria
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Organisms affected by TB
Humans / cows / pigs / badgers / deer
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Transmission of TB
Direct – airborne droplets
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How does TB manifest
Damages + destroys lung tissue
Supresses immune system
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How is TB treated
Antibiotics
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What causes bacterial meningitis
Bacteria
43
Who is effected by bacterial meningitis
Humans
44
Transmission of bacterial meningitis
Direct – airborne droplets
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What is bacterial meningitis
Infection of the meninges of the brain
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What is the meninges
protective membrane on brains surface
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How does bacterial meningitis cause death
nfection can spread to rest of body = causing septicaemia = blood poisoning = leads rapid death
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What causes ring rot
Bacteria
49
Organisms effected by ring rot
Potato
50
Transmission of ring rot
Direct – contact with other infected tubers
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Effects of ring rot
Damages leaves / tubers / fruit
Prevent soil use for at least 2 years
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What is AIDS / HIV caused by
Virus
53
Organisms effected by AIDS / HIV
Humans + non-human primates
54
Transmission of HIV
Direct – transfer via bodily fluids
Sharing needles / sex / mothers to babies in pregnancy / breastfeeding
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How does HIV work
Targets T helper cells in the immune system = gradually destroys the immune system = more vulnerable to other infections = TB + flu
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What type of virus is HIV
retrovirus with RNA as genetic material
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How is HIV treated
Anti-retroviral drugs
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What causes influenza
Virus
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Organisms effected by influenza
Mammals
60
Transmission of influenza
Direct – airborne droplets
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How does influenza work
Viral infection of the ciliated epithelial cells in gas exchange system = kills cells = leaving airways open to secondary infections
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What causes tobacco mosaic virus
Virus
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Organisms effected by TMV
Tobacco + 150 other species
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Transmission of TMV
Direct – contact with leaves of infected plants
Indirect – vectors - aphids
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Effects of TMV
Damages leaves / flowers / frui
Stunts growth
Reduces yield
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What causes malaria
Protoctist
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Organisms effected by malaria
Humans
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Transmission of malaria
Indirect – female mosquito
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How does malaria spread
Parasite = has 2 hosts = mosquitos + humans = reproduce inside female mosquitos
Female needs to take 2 blood meals before lays eggs = where transmission occurs
Invades red blood cells / liver / brain
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What causes Potato / tomato blight
Protoctist
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Organisms effected by Potato / tomato blight
Potato / tomato
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Transmission of Potato / tomato blight
Direct – spread via spores = wind
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Effected of Potato / tomato blight
Destroys leaves / tubes / fruits
Penetrate host cell
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What causes black Sigatoka
Fungus
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Organisms effected by black Sigatoka
Bananas
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Transmission of black Sigatoka
Direct – dispersion of spores
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How does black Sigatoka work
Attacks + destroys leaves
Hyphae penetrate + digest cell = turning leaves black
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What causes ring worm
Fungus
79
Organisms effected by ring worm
Mammals
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Transmission of ring worm
Direct – contact with infected organisms
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What causes athletes foot
Fungus
82
Organisms effected by athletes foot
Humans
83
Transmission of athletes foot
Direct – contact with items touched by infected individuals = warm / moist environments
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What must be true in order for pathogens to survive
must successfully transfer from host to host
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Define disease transmission
defined as the transfer of pathogens from an infected host to an uninfected host
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Direct transmission
from one host to another host
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Indirect transmission
second organism (vector) that is unaffected by the pathogen transfers it to a new host
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Examples of direct transmission
• Physical contact
• Inoculation
• Ingestion
• Close proximity
• Spores
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Ingestion
contaminated food + drink / pathogens from hand to mouth
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Inoculation
break in skin/animal bite/puncture wound
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What are spores
small reproductive structures
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How do sores spread
via wind or water
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How are spores produces
• Depending on the organism, spores can be produced via mitosis or meiosis so they can be haploid or diploid
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What type of virus is HIV
Retrovirus
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What are retroviruses
a group of viruses that has the ability to make DNA from RNA because they have the enzyme reverse transcriptase
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How is HIV transmitted
Exchange of bodily fluids
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When does TB spread more quickly
Overcrowded conditions
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How can TB be Transmitter other than airborne droplets
form of TB = occurs in cattle but is spread to humans through contaminated meat + unpasteurised milk
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Examples of indirect transmission
Fomites
Droplet infections
Vectors
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What are fomites
inanimate objects = bedding / socks / cosmetics
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Why are insects ideal vectors
reproduce in large numbers which increases the likelihood of pathogen transmission
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Example of a disease transmitted via a vector
Malaria
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How is malaria Transmitted to humans
o Female Anopheles mosquitoes feed on human blood to obtain the protein they need to develop their eggs
o If the person they bite is infected with Plasmodium, the mosquito will take up some of the pathogen with the blood meal
o When feeding on the next human, Plasmodium pass from the mosquito to the new human’s blood
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Factors that effect disease transmission = overall
presence of the pathogens
= If the pathogen is not present in the population then it cannot spread
o The presence of susceptible individuals
= A high number of immune or resistant individuals in a population will reduce the likelihood of transmission
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Factors that effect direct disease transmission
• Overcrowding
• Lack of ventilation
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Factors that effect indirect disease transmission
• Population of vectors = influenced by weather + climate
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Explain the distribution of malaria
• Caused by insect vector (female Anopheles mosquitoes)
• mosquitoes favour habitats that have high rainfall, high temperatures and high humidity
• Therefore = tropics + sub tropics = AFRICA
• Social factor = migration due to war
• migration happens due to war the parasite can be transferred from areas that have the infection to new region
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What is an endemic
a disease that is always present in a population (even if very low numbers)
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What is an epidemic
a large increase in the number of cases in a population (an outbreak)
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What is a pandemic
an epidemic occurs on a large scale and crosses international boundaries.
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Symptoms of TMV
discolouration in leaves
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How does TMV cause stunted growth
• Less chlorophyll = less photosynthesis = less growth
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How to stop spread of TMV
Burn plant
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What type of pathogen causes barley powdery mildew
Fungus
115
What causes crown gall disease
Bacteria
116
What are passive defence mechanisms
mechanisms are always present
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What’s re active defence mechanisms
activated when pathogens invade
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Plant physical passive defences (6)
• cellulose cell walls
• lignin thickening of cell walls – lignin is water proof + indigestible
• waxy cuticle – prevent water collecting on cell surface = absence of water is passice defence
• stomatal closure – guard cells close when pathogens detected
• bark
• casparian strip = some fungi can invade all the way to endodermis but through this strip
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Physical active plant defences
Reinforced cell walls
Necrosis
Cal lose deposited
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How does depositing callose act as a physical active plant defence
strengthens cell wall + blocks plasmodesmata + blocks sieve plates = limiting spread
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How does reinforcing cell walls act as a physical active plant defence
invasion of pathogens stimulates the release of compounds callose and lignin = molecules are deposited between the cell surface membrane and the cell wall
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What is necrosis and how is it an active physical plant defence
deliberate cell suicide = few cells sacrificed = limits the pathogens access to water + nutrients
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Chemical passive defences in ola ts
• Toxic compounds
• Sticky resin found in the bark
• Compounds that encourage the growth of competing microorganisms
• Enzyme inhibitors
• Receptor molecules
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Example of toxic compounds = chemical passive plant defences
Catechol
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How does sticky resin act as a chemical passive plant defence
traps the pathogens so they can't spread
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Example of enzyme inhibitors in plants
Tannins
127
Chemical active plant defences
• Antibiotic / antifungals = tannins in back inhibit attack by insects = bind to salivary proteins + digestive enzymes to deactivate them = insects to ingest large amount of tannins = no growth / die
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Cell signalling in plants
• Pathogens possess cellulase enzymes that digest the cellulose in plant cell walls
• The molecules produced from this breakdown of cellulose act as signals to cell surface receptors
• By stimulating these receptors they cause the release of defence chemicals
- phytoalexins / Salicylic acid / ethylene
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What do Phytoalexins do
o Disrupting pathogen metabolism
o Delaying pathogen reproduction
o Disrupting bacterial cell surface membranes
o Stimulating the release of chitinases (enzymes that break down the chitin cell walls in fungi)
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What does salicylic acid do
migrates through the plant to uninfected areas. Once there it activates defence mechanisms that protect the plant against pathogens for a period of time
o This long-term protection is called systemic acquired resistance
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What does ethylene do
ethylene vaporises, stimulating other leaves on the same plant to react (as well as other plants)
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Four types of non specific immune responses
Physical
Cellular
Chemical
Commensal
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physical non specific immune responses
body tissues act as barriers, preventing the entry of pathogens
o E.g. skin, mucous membrane of the alimentary canal
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Cellular non specific immune responses
cells detect and signal the presence of pathogens.
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Chemical non specific immune responses
secreted substances generate an inhospitable environment for the growth of pathogens. trap pathogens, cause them to burst / prevent them from entering cells and reproducing
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Commensal organisms non specific immune responses
harmless bacteria and fungi present on and in the body compete with pathogens for nutrients
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How does the skin act as first line of defence
Physical barrier
Skin flora
Secretes antiseptics
Colleges
Sweatv
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How does skin act as a physical barrier
outermost layer = stratum corneum = made of dead skin cells tightly packed together = protective barrier
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How does skin flora act as defence
harmless bacteria prevent harmful bacteria colonising
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What antiseptics does the skin secrete
sebum (produced by sebaceous glands / contains fatty acids that have antimicrobial properties)
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How is sweat a first line of defence
dermcidin = antimicrobial properties that help prevent growth of bacteria
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Where is sebum secreted from
sebaceous glands
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Human first life of defence
Skin
Mucous membranes
Expulsion reflexes
Stomach
Eyes
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What are mucous membranes
• Moist tissue that line the respiratory + digestive tract = bronchi / nose / trachea
• Ciliated epithelial + goblet cells
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How are mucous membranes a first line of defence
• Mucus = secretes thick / sticky fluid = contains antibodies = trap + destroy pathogens
• Helps lubricate + protect tissue from damage
• Cilia = beat in coordinated manner – waft away mucus + pathogens
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Why is mucous sticky
made up of glycoproteins with long carbohydrate chains
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Examples of expulsive reflexes
• Coughing / sneezing/ vomiting
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How are expulsive reflexes first line of defence
• Involuntary responses designed to expel foreign substances / pathogens from body
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How is stomach a first line of defence
• HCL = acidic = kills pathogens
• Lining = produces mucus
• Peristalsis = muscles of stomach + intestines contract / relax to move food + waste materials through digestive system
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How is the gut a first line of defence
• Gut microbiota = beneficial / harmless microorganisms prevent growth of harmful pathogens by competing with them for resources = inhibiting their growth
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Parts of the eyes that are part of the first line of defence
Tears
Eyelashes
Conjunctiva
Cornea
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How are tears first line of defence
lysozymes = break down cell wall of bacteria
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How are eyelashes first line of defence
traps larger particles = dust / dirt
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How are conjunctiva first line of defence
thin layer of tissue that covers front of eye + inside eyelid = produces mucus
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How are cornea first line of defence
covered by layer of epithelial cells = physical barrier
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Second line of defence
o Blood clotting
o Inflammation
o Wound repair
o Phagocytosis
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Describe the clotting cascade
• Damage to skin = exposes collagen = platelets stick = thromboplastin (+ serotonin) released
• Thromboplastin combines with Ca 2+ = calcium deficiency = clotting cascade slows down
• This triggers conversion of prothrombin into thrombin
• Triggers fibrinogen into fibrin
- fibrin forms a network of fibres that traps platelets + blood cells
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Ion needed in blood clotting
Calcium 2+ ion
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What is released / happens when skin is damages + there is exposed collagen
- thromboplastin
- seratonin
- activates mast cells
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What does serotonin do
• causes smooth muscle walls to contract = vasoconstriction = restricts blood flow
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When do activated mast cells carry out their effects
• Later than serotonin effects
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What do mast cells release
Histamine + cytokines
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What does Histamine do
o Vasodilation increases blood flow through capillaries
o "Leaky" capillaries allow fluid to enter the tissues and creating swelling
o A portion of the plasma proteins leave the blood
o Phagocytes leave the blood and enter the tissue to engulf foreign particles
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What do cytokines do
Attract phagocytes
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Put all the second line of defence in one diagram
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What is formed as a result of blood clotting
A scab
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What happens underneath this scab
stem cells that divide by mitosis to heal the wound
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Describe how would healing / repair happens
o Blood clots = to make barrier to keep pathogens out
o Epidermal cells grow beneath cut = seal barrier more effectively
o New blood vessels form
o Collagen is produced / collagen fibres are deposited
o Granulation tissue forms to fill the wound
o Stem cells move over the new tissue and divide to produce epithelial cells
o Contractile cells cause wound contraction
o Unwanted cells die
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Three types of phagocytes
• Neutrophils = Macrophages = Dendritic cells
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Features of neutrophils
• Released in large numbers
• Short-lived cells
• Lobed nucleus
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Purpose of lobed nucleus in neutrophil
Allow for increased flexibility = get through capillaries
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How to identify neutrophils in blood smears
Lobed nucleus
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Features or macrophages
• Larger than neutrophils
• Long-lived
• rather than remaining in the blood, they move into organs including the lungs, liver, spleen, kidney and lymph nodes
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Where are macrophages produced
Bone marrow
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How do macrophages travel in the blood
As monocytes
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Describe phagocytosis = neutrophils
• mast cells secret cytokines
• attract phagocyte + then detects pathogen
• pathogen = antigens = normally glycolipids on surface
• phagocyte grows cytoplasmic extensions + changes shape
• phagocyte engulfs pathogen = via endocytosis
• pathogen = may be coated in opsonin
• phagosome formed
• phagosome fuses with lysosome = phagolysosome
• upon fusion = releases lysozymes = break down pathogen
• absorbs digestive products e.g proteins
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What happens after neutrophils absorb digestive products
GO AND DIGEST SOMETHING ELSE = SHORT-LIVED DUE TO TOXIC WASTE
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What happens in terms of phagocytosis if a macrophage
After absorb digestive products…
• Combines antigen with glycoproteins
• display the antigens of the pathogens on their surface = through a structure called the major histocompatibility complex
• displayed antigens (the cell is now called an antigen-presenting cell) can then be recognised by lymphocytes = T-cells
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What are dendritic cels
• large phagocytic cells with lengthy extensions
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Features of dendritic cells
large surface area to interact with pathogens + lymphocytes
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What do dendritic cells do
• Once they have ingested foreign material they transport it to the lymph nodes
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What is the role of antigen presenting cells
• T-lymphocytes produce an immune response when they are exposed to a specific antigen
• T cells will only bind to an antigen if it is present on the surface of an antigen-presenting cell
• Once the surface receptor of the T cell binds to the specific complementary antigen it becomes sensitised and starts dividing to produce a clone of cells
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Where are T lymphocytes made
Bone marrow
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Where do T lymphocytes mature
Thymus gland
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What type of immunity is carried out by T lymphocytes
Cell - mediated immunity
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What does T lymphocytes respond to (foreign material)
Foreign material INSIDE body cells
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What do T lymphocytes respond to (type of cell)
Own cells = altered by virus / cancer / transplanted tissue
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Where are B lymphocytes made
Bone marrow
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Where do B lymphocytes mature
Bone marrow
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Type of immunity carried out by B lymphocytes
humoral immunity
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What do B lymphocytes respond to (foreign material)
Foreign material OUTSIDE cell
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What do B lymphocytes respond to (type of cell)
Bacteria / virus
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Which type of cell makes antibodies
B lymphocytes
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What are T and B lymphocytes part of
Third line of defence
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Features of the third line of defence
- Specific + adaptive + slower
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What are lymphocytes
type of white blood cell
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How to distinguish between lymphocytes and phagocytes
• Smaller than phagocytes
• have a large nucleus that fills most of the cell
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Process of maturation = T
o T gain specific cell surface receptors = T cell receptors (TCRs)
o A small number of T cells have the same TCRs = a clone
o T cells within each clone differentiate into different types of T cell: T helper cells, T killer cells and T regulator cells after binding to antigen
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Shape of T cell receptors
similar structure to antibodies and are each specific to one antigen
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How do T cells differentiate into helper / killer / suppressor / memory cells
T cell binds to antigen
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How are T helper cells activated
- T cell binds to antigen on antigen presenting cell e.g cancerous cells
- clonal selections
- clonal expansion
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How does clonal selection work in T helper cells
o T helper cells with receptors complementary to the specific pathogenic antigen bind to the APC
o The APC secretes molecules of the cytokine interleukin 1 (IL-1)
IL-1 stimulates the activation of selected T helper cells
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How does clonal expansion work in T helper cells
o Selected T helper cells divide by mitosis to produce larger clones = all clones have complementary antigen
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What do T helper cells secrete
Interleukin 2
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What does interleukin 2 do
- B cells to divide and produce plasma cells
- The T helper cells to become more active and release more cytokines, including interferon (IFN) that stimulates macrophage activity
- The activation of T killer cells
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B cells divide + produce plasma cells. What do these plasma cells do
secrete antibodies specific to the antigen (that belongs to the pathogen)
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How are T killer cells activated
Colonial selection + clonal expansion
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Clonal selection - T killer cells
• When a T killer cell encounters an infected cell that is displaying a foreign antigen complementary to its TCR it becomes activated = clonal selection
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What do T killer cells do after binding to antigen / clonal selection
• attaches to the foreign antigens + secretes toxic substances that kill the body cells + pathogen = e.g = perforins
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What do perforins do
secreted by T killer cells punch a hole in the cell surface membrane of infected cells, allowing toxins to enter
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Clonal expansion - t killer cells
• The IL-2 released by specific T helper cells helps to stimulate the expansion of specific T killer cells = clonal expansion
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Function of T suppressor cells
o Preventing T cells from attacking and killing uninfected host cells
o Shutting down the immune system once the body is cleared of the pathogen
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OVERALL - T CELL MODE OF ACTION
- Antigen presenting cells = ACTIVATES T cells
- T helper = release interleukins = activate T killer cells + B lymphocytes
- T – killer = kills pathogens
- T regulator
- Each T cell = different protein receptors = complimentary to antigen
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Overall how does clonal selection + clonal expansion work in T cells
T helper cells bind to the antigen (clonal selection ) + differentiation + divide (clonal expansion)
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What does humoral mean
Body fluids
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What do B cells produce when they are mature
can make one type of antibody molecule
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How are B cells activated
Clonal selection + clonal expansion
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Clonal selection - B cels
o B cells with B cell receptors complementary to the specific pathogenic antigen bind to it
o clones that have been selected for replication
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Clonal expansion - B cells
elected B cells divide by mitosis to produce larger clones
o T large numbers of identical B-lymphocytes being produced over a few weeks
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What do some B cells differentiate into
Plasma cells or memory cells
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Why do they divide into plasma cells
T helper cells release interleukin 2 (IL-2) which stimulates B cells to divide and produce plasma cells
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Overall - draw out all differentiation of T and B cells
223
Which one produces memory cells - T or B
Both
224
Two types of immune response
Primary + secondary
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What is primary immune response
responding to a newly encountered antigen
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What is secondary immune response
responding to a previously encountered antigen
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Features of the primary immune response
- considerate time delay
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Why is there a considerate time delay in the primary immune system
The clonal selection and expansion of specific T cells and B cells
The synthesis of antibodies
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What does that time delay mean for us
why we get symptoms of a disease when we are first exposed to a pathogen
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Features of plasma cells
Short lived
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What do memory cells do
remain circulating in the blood for a long time and allow for a rapid secondary immune response
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B memory cells and the secondary immune response
• If t same foreign antigen is found in the body a second time = B memory cells recognise the antigen
• B memory cells divide very quickly + differentiate into plasma cells (to produce antibodies) + more memory cells
• very quick = destroyed before the pathogen population increases + symptoms develop
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Why is the secondary immune response quicker
more memory cells present to be selected than there were cells within the original clone(that existed prior to the first infection)
o More memory cells can be selected and so more antibodies are produced within a short time period
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Describe / draw the secondary immune response
235
Name the four types of T cells
Killer
Helper
Suppressor
Memory
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Name the three types of B cells
Memory
Effector
Plasma
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How long do neutrophils last
5 days
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What are antigens
Functional proteins / glycosidic proteins intrinsic to the plasma membrane
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What are T killer cells stimulated by
Interferons
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What cells are most important in cell mediated immunity
T killer cells
241
Draw a graph of antibody concentration against time / days - primary + secondary
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How to identify lymphocytes
very large nuclei that nearly occupy the entire cell.
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How to identify red blood cells
Round shape
244
How to identify platelets
Small size
245
How to identify neutrophils
Lobed nucleus
246
What are immunoglobulins
• Globular glycoproteins produced by plasma cells
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Structure of antibodies
• Quaternary structure = 2 heavy + 2 light polypeptide chains
• Bonded by disulphide bridges
- constant region
- variable region
- antigen binding site
- hinge region
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What is the constant region
does not vary within class / isotype but do vary between classes = determines the mechanism used to destroy pathogen
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What’s the variable region
different for each antibody = where antibody attaches to antigen = antigen – antibody complex
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What’s at the end of the variable region
antigen-binding site
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What is special about the antigen binding site
specific for each antigen = different antibodies need to be produced
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Why is it significant that there are 2 antigen binding sites
aids in agglutination = stops pathogen causing damage
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What’s the hinge region
where disulphide bonds join heavy chains = give flexibility = allows ABS to be placed at diff angles
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Draw an antibody
255
Function of antibodies
• bind to specific antigens = trigger the specific immune response.
• Every antigen has one antibody
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What did antibodies act as
anti-toxins, opsonins and agglutinins
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What region of the antibody does the phagocyte bind to
Constant
258
Why are the ops owning in the specific immune response more effective than those in the moon immune response
They don’t bind tightly to specific antigens
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Primary function of opsonins
Promoting phagocytosis by acting as a marker
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What can’t pathogens do when attached to antibodies
Enter host cells
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How can antibodies act as agglutinins
Each antibody - two binding sites = bind to several pathogens + cross link them =become agglutinated
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How does agglutination help
reduces the chance that the pathogens will spread through the body + makes it possible for phagocytes to engulf a number of pathogens at one time
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How do antibodies act as antitoxins
by binding to toxins produced by pathogens (e.g. the bacteria that cause diphtheria and tetanus) which neutralises them making them harmless
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What else can antibodies do
• can create holes in the cell walls of pathogens causing them to burst (lysis) when water is absorbed by osmosis
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How many polypeptide chains does an antibody contain an
4
266
What allows for sulfide bonding
Amino acid - cysteine
267
What is formed when an antibody binds to an antigen
Antigen-antibody complex
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How do antibodies defend body
- act as opsonins
- acts as antitoxins
- cause agglutination
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When do auto immune diseases occur
When the immune system recognised a ‘self’ antigen as a foreign antigen + attacks healthy body tissue
270
Immunity
Being able to kill pathogens if infected before getting symptoms
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Active immunity
Achieved when the immune system is activated + makes its own antibodies
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Passive immunity
Achieved when antibodies are supplied from another source
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Natural immunity
Achieved through normal life processes
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Artificial immunity
Achieved through medical intervention
275
Natural active immunity
Achieved as a result of infection - individual gets disease + immune system makes memory cells
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Artificial active immunity
= injects inactive pathogen to activate an immune response
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Natural passive immunity
Antibodies provided via the placenta or via breast milk
278
Artificial passive immunity
Injection / infection of antibodies from another animal / individual
279
Examples of artificial passage immunity
o tetanus = antitoxin = antibodies were collected from people whose immune system had been triggered by a vaccination to produce tetanus antibodies
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Are there memory cells in active immunity
Yes
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Are there memory cells in passive immunity
No
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What is a vaccine
a suspension of antigens that are intentionally put into the body to induce artificial active immunity.
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What can vaccines be
Whole live organisms
Dead microorganisms
Attenuated microorganisms
Toxoids
mRNA
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Features of whole live organism vaccines
multiply slowly = allowing body to recognise antigens = stronger + longer-lasting immunity
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Dead microorganisms vaccine
do not trigger a strong or long-lasting immune response like live attenuated vaccines = repeated doses and/or booster doses are often required = Polio vaccine
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Attenuated vaccine
multiply slowly = allowing body to recognise antigens = MMR = stronger + longer lasting immunity
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Toxoid
harmless form of toxin = Diptheria
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Benefits of vaccines
• Highly effective with one vaccination giving a lifetime’s protection(although less effective ones will require booster / subsequent injections)
• Generally harmless as they do not cause the disease they protect against because the pathogen is killed by the primary immune response
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Attenuated
Weakened
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Problems with vaccines
Allergic reactions
Poor response
Antigenic variation
Virus have capacity to change their surface antigens
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What are people allergic to in vaccines
allergic reactions / local reactions (eg. sore arm) to inactivated vaccines as adjuvants (eg. aluminium salts) may be conjugated (joined) to the subunit of the pathogen to strengthen and lengthen the immune response
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Why may people have a poor response to a vaccine
malnourished and cannot produce the antibodies – proteins or their immune system may be defective
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Antigenic variation
variation in antigens of pathogens = vaccines don’t trigger an immune response
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Types of changing surface antigens
Antigenic drift
Antigenic shift
Antigenic concealment
Cross breeding
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Antigenic drift
over time there are small changes in the structure and shape of antigens = same strain
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Antigenic shift
there are major changes in antigens (within the same strain of virus)
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Antigenic concealment
the pathogen ‘hides’ from the immune system by:
Living inside cells
Coating their bodies in host proteins
Parasitising immune cells such as macrophages and T cells (eg. HIV)
Remaining in parts of the body that are difficult for vaccines to reach (eg. Vibrio cholerae – cholera, remains in the small intestine)
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Herd immunity
• 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
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Benefits of here immunity
• allows for the individuals who are unable to be vaccinated (e.g. children and those with weak immune systems) to be protected from the disease
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Ring immunity
• People near a vulnerable / infected person are vaccinated in order to prevent them from catching and transmitting the disease
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Benefits of ring immunity
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
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for a disease to be eradicated by a vaccine it should not:
• Mutate
• Have a life cycle that includes other organisms
• Have symptoms that make it hard to diagnose or trace
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Challenges of eradicating a disease
• some pathogens = complicated a+ present with disease processes that are not straightforward and so a successful vaccine has not been developed
• diseases where a vaccine does exist = not eliminated because too few in the community have been vaccinated = ANDREW WAKEFIELD
• Unstable political situations in areas such as Africa, Latin America and parts of Asia, perhaps resulting in civil unrest or wars
• Lack of public health facilities (poor infrastructure, few trained personnel, limited financial resources)
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Causes of rheumatoid arthritis - read
In RA, the immune system becomes overactive and produces antibodies = rheumatoid factors + anti-cyclic citrullinated peptide (anti-CCP) antibodies, which attack the synovial membrane (lining) of the joints. This causes the synovial membrane to become inflamed and thickened, leading to the formation of a pannus (abnormal tissue growth) and eventually erosion of the cartilage and bone in the joint.
The immune system in RA can also attack other parts of the body such as the eyes, lungs, and heart = can lead to complications such as inflammation of the lung lining, and damage to the heart muscle and blood vessels.
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Why is RNA virus more dangerous
- more easily mutated as only has 1 strand
- keeps mutating - vaccines must keep being updated
