Chapter 12 - Communicable Diseases Flashcards
Define disease
an illness or disorder of the body or mind that leads to poor health
What are communicable diseases caused by
Pathogens
4 types of pathogens
Bacteria
Virus
Fungus
Protoctists
What type of cells are bacteria
Unicellular prokaryotic
What are bacterial cell walls made of
Peptidoglycan
Size of bacteria
0.2 – 2 micrometres
How do bacteria move
Flagella
How do bacteria reproduce
Asexually = binary fission
Can bacteria exchange DNA
Yes
How can bacteria exchange DNA
through conjunction = two cells temporarily fuse + transfer DNA (beneficial traits)
How do bacteria cause disease
produce toxins ( metabolic waste products) + cause symptoms by cell damage
What type of cell damage do bacteria do
- damage cell membranes / enzymes / genetic material
Do bacteria always cause disease
No - can remain within body cavities or spaces
Draw a diagram of a bacteria
Structure of a virus
- No cellular structure
What makes viruses controversial
Are they living or not = No cellular structure + can’t produce ATP without living cells
How do viruses infect a host
- Attach to receptors on surface of host cell + penetrate its genetic material via endocytosis
- Virus uses host cells machinery to replicate DNA
Two ways virus cause disease / replicate
- Lytic / lysogenic cycle
Why are viruses likely to mutate
- RNA = more likely to mutate = as only one strand
Structure of a virus
- Nucleic aid core + capsid = DNA/RNA enclosed in protein coat
Draw the structure of a virus
How do viruses replicate their DNA / RNA
reverse transcription
What is reverse transcription
- 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
What is a bacteriophage
virus that attacks bacteria
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
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
Is the lysogenic cycle itself dangerous
No - dormant
Only dangerous when switches to lytic cycle + bursts
What type of cells are fungus
- Multicellular or unicellular saprophytes
EUKARYOTIC
Cell walls of fungus
Chitnin
Structure of fungus
- Filamentous body = mycelium / hyphae
How do fungus reproduce
sexually + asexually = gametes + spores
Draw structure of a fungus
What type of cells are protoctists
- Eukaryotic – unicellular or multicellular
- Heterotrophic / autotrophic
How do protoctists reproduce
- Asexual or sexual reproduction
- Sexual = budding in yeast
Draw structure of protoctists
How to calculate number of cells after dividing for a set amount of time
Number of original X 2^number of cycles
What is TB caused by
Bacteria
Organisms affected by TB
Humans / cows / pigs / badgers / deer
Transmission of TB
Direct – airborne droplets
How does TB manifest
Damages + destroys lung tissue
Supresses immune system
How is TB treated
Antibiotics
What causes bacterial meningitis
Bacteria
Who is effected by bacterial meningitis
Humans
Transmission of bacterial meningitis
Direct – airborne droplets
What is bacterial meningitis
Infection of the meninges of the brain
What is the meninges
protective membrane on brains surface
How does bacterial meningitis cause death
nfection can spread to rest of body = causing septicaemia = blood poisoning = leads rapid death
What causes ring rot
Bacteria
Organisms effected by ring rot
Potato
Transmission of ring rot
Direct – contact with other infected tubers
Effects of ring rot
Damages leaves / tubers / fruit
Prevent soil use for at least 2 years
What is AIDS / HIV caused by
Virus
Organisms effected by AIDS / HIV
Humans + non-human primates
Transmission of HIV
Direct – transfer via bodily fluids
Sharing needles / sex / mothers to babies in pregnancy / breastfeeding
How does HIV work
Targets T helper cells in the immune system = gradually destroys the immune system = more vulnerable to other infections = TB + flu
What type of virus is HIV
retrovirus with RNA as genetic material
How is HIV treated
Anti-retroviral drugs
What causes influenza
Virus
Organisms effected by influenza
Mammals
Transmission of influenza
Direct – airborne droplets
How does influenza work
Viral infection of the ciliated epithelial cells in gas exchange system = kills cells = leaving airways open to secondary infections
What causes tobacco mosaic virus
Virus
Organisms effected by TMV
Tobacco + 150 other species
Transmission of TMV
Direct – contact with leaves of infected plants
Indirect – vectors - aphids
Effects of TMV
Damages leaves / flowers / frui
Stunts growth
Reduces yield
What causes malaria
Protoctist
Organisms effected by malaria
Humans
Transmission of malaria
Indirect – female mosquito
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
What causes Potato / tomato blight
Protoctist
Organisms effected by Potato / tomato blight
Potato / tomato
Transmission of Potato / tomato blight
Direct – spread via spores = wind
Effected of Potato / tomato blight
Destroys leaves / tubes / fruits
Penetrate host cell
What causes black Sigatoka
Fungus
Organisms effected by black Sigatoka
Bananas
Transmission of black Sigatoka
Direct – dispersion of spores
How does black Sigatoka work
Attacks + destroys leaves
Hyphae penetrate + digest cell = turning leaves black
What causes ring worm
Fungus
Organisms effected by ring worm
Mammals
Transmission of ring worm
Direct – contact with infected organisms
What causes athletes foot
Fungus
Organisms effected by athletes foot
Humans
Transmission of athletes foot
Direct – contact with items touched by infected individuals = warm / moist environments
What must be true in order for pathogens to survive
must successfully transfer from host to host
Define disease transmission
defined as the transfer of pathogens from an infected host to an uninfected host
Direct transmission
from one host to another host
Indirect transmission
second organism (vector) that is unaffected by the pathogen transfers it to a new host
Examples of direct transmission
• Physical contact
• Inoculation
• Ingestion
• Close proximity
• Spores
Ingestion
contaminated food + drink / pathogens from hand to mouth
Inoculation
break in skin/animal bite/puncture wound
What are spores
small reproductive structures
How do sores spread
via wind or water
How are spores produces
• Depending on the organism, spores can be produced via mitosis or meiosis so they can be haploid or diploid
What type of virus is HIV
Retrovirus
What are retroviruses
a group of viruses that has the ability to make DNA from RNA because they have the enzyme reverse transcriptase
How is HIV transmitted
Exchange of bodily fluids
When does TB spread more quickly
Overcrowded conditions
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
Examples of indirect transmission
Fomites
Droplet infections
Vectors
What are fomites
inanimate objects = bedding / socks / cosmetics
Why are insects ideal vectors
reproduce in large numbers which increases the likelihood of pathogen transmission
Example of a disease transmitted via a vector
Malaria
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
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
Factors that effect direct disease transmission
• Overcrowding
• Lack of ventilation
Factors that effect indirect disease transmission
• Population of vectors = influenced by weather + climate
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
What is an endemic
a disease that is always present in a population (even if very low numbers)
What is an epidemic
a large increase in the number of cases in a population (an outbreak)
What is a pandemic
an epidemic occurs on a large scale and crosses international boundaries.
Symptoms of TMV
discolouration in leaves
How does TMV cause stunted growth
• Less chlorophyll = less photosynthesis = less growth
How to stop spread of TMV
Burn plant
What type of pathogen causes barley powdery mildew
Fungus
What causes crown gall disease
Bacteria
What are passive defence mechanisms
mechanisms are always present
What’s re active defence mechanisms
activated when pathogens invade
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
Physical active plant defences
Reinforced cell walls
Necrosis
Cal lose deposited
How does depositing callose act as a physical active plant defence
strengthens cell wall + blocks plasmodesmata + blocks sieve plates = limiting spread
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
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
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
Example of toxic compounds = chemical passive plant defences
Catechol
How does sticky resin act as a chemical passive plant defence
traps the pathogens so they can’t spread
Example of enzyme inhibitors in plants
Tannins
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
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
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)
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
What does ethylene do
ethylene vaporises, stimulating other leaves on the same plant to react (as well as other plants)
Four types of non specific immune responses
Physical
Cellular
Chemical
Commensal
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
Cellular non specific immune responses
cells detect and signal the presence of pathogens.
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
Commensal organisms non specific immune responses
harmless bacteria and fungi present on and in the body compete with pathogens for nutrients
How does the skin act as first line of defence
Physical barrier
Skin flora
Secretes antiseptics
Colleges
Sweatv
How does skin act as a physical barrier
outermost layer = stratum corneum = made of dead skin cells tightly packed together = protective barrier
How does skin flora act as defence
harmless bacteria prevent harmful bacteria colonising
What antiseptics does the skin secrete
sebum (produced by sebaceous glands / contains fatty acids that have antimicrobial properties)
How is sweat a first line of defence
dermcidin = antimicrobial properties that help prevent growth of bacteria
Where is sebum secreted from
sebaceous glands
Human first life of defence
Skin
Mucous membranes
Expulsion reflexes
Stomach
Eyes
What are mucous membranes
• Moist tissue that line the respiratory + digestive tract = bronchi / nose / trachea
• Ciliated epithelial + goblet cells
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
Why is mucous sticky
made up of glycoproteins with long carbohydrate chains
Examples of expulsive reflexes
• Coughing / sneezing/ vomiting
How are expulsive reflexes first line of defence
• Involuntary responses designed to expel foreign substances / pathogens from body
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
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
Parts of the eyes that are part of the first line of defence
Tears
Eyelashes
Conjunctiva
Cornea
How are tears first line of defence
lysozymes = break down cell wall of bacteria
How are eyelashes first line of defence
traps larger particles = dust / dirt
How are conjunctiva first line of defence
thin layer of tissue that covers front of eye + inside eyelid = produces mucus
How are cornea first line of defence
covered by layer of epithelial cells = physical barrier
Second line of defence
o Blood clotting
o Inflammation
o Wound repair
o Phagocytosis
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
Ion needed in blood clotting
Calcium 2+ ion
What is released / happens when skin is damages + there is exposed collagen
- thromboplastin
- seratonin
- activates mast cells
What does serotonin do
• causes smooth muscle walls to contract = vasoconstriction = restricts blood flow
When do activated mast cells carry out their effects
• Later than serotonin effects
What do mast cells release
Histamine + cytokines
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
What do cytokines do
Attract phagocytes
Put all the second line of defence in one diagram
What is formed as a result of blood clotting
A scab
What happens underneath this scab
stem cells that divide by mitosis to heal the wound
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
Three types of phagocytes
• Neutrophils = Macrophages = Dendritic cells
Features of neutrophils
• Released in large numbers
• Short-lived cells
• Lobed nucleus
Purpose of lobed nucleus in neutrophil
Allow for increased flexibility = get through capillaries
How to identify neutrophils in blood smears
Lobed nucleus
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
Where are macrophages produced
Bone marrow
How do macrophages travel in the blood
As monocytes
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
What happens after neutrophils absorb digestive products
GO AND DIGEST SOMETHING ELSE = SHORT-LIVED DUE TO TOXIC WASTE
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
What are dendritic cels
• large phagocytic cells with lengthy extensions
Features of dendritic cells
large surface area to interact with pathogens + lymphocytes
What do dendritic cells do
• Once they have ingested foreign material they transport it to the lymph nodes
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
Where are T lymphocytes made
Bone marrow
Where do T lymphocytes mature
Thymus gland
What type of immunity is carried out by T lymphocytes
Cell - mediated immunity
What does T lymphocytes respond to (foreign material)
Foreign material INSIDE body cells
What do T lymphocytes respond to (type of cell)
Own cells = altered by virus / cancer / transplanted tissue
Where are B lymphocytes made
Bone marrow
Where do B lymphocytes mature
Bone marrow
Type of immunity carried out by B lymphocytes
humoral immunity
What do B lymphocytes respond to (foreign material)
Foreign material OUTSIDE cell
What do B lymphocytes respond to (type of cell)
Bacteria / virus
Which type of cell makes antibodies
B lymphocytes
What are T and B lymphocytes part of
Third line of defence
Features of the third line of defence
- Specific + adaptive + slower
What are lymphocytes
type of white blood cell
How to distinguish between lymphocytes and phagocytes
• Smaller than phagocytes
• have a large nucleus that fills most of the cell
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
Shape of T cell receptors
similar structure to antibodies and are each specific to one antigen
How do T cells differentiate into helper / killer / suppressor / memory cells
T cell binds to antigen
How are T helper cells activated
- T cell binds to antigen on antigen presenting cell e.g cancerous cells
- clonal selections
- clonal expansion
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
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
What do T helper cells secrete
Interleukin 2
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
B cells divide + produce plasma cells. What do these plasma cells do
secrete antibodies specific to the antigen (that belongs to the pathogen)
How are T killer cells activated
Colonial selection + clonal expansion
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
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
What do perforins do
secreted by T killer cells punch a hole in the cell surface membrane of infected cells, allowing toxins to enter
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
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
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
Overall how does clonal selection + clonal expansion work in T cells
T helper cells bind to the antigen (clonal selection ) + differentiation + divide (clonal expansion)
What does humoral mean
Body fluids
What do B cells produce when they are mature
can make one type of antibody molecule
How are B cells activated
Clonal selection + clonal expansion
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
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
What do some B cells differentiate into
Plasma cells or memory cells
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
Overall - draw out all differentiation of T and B cells
Which one produces memory cells - T or B
Both
Two types of immune response
Primary + secondary
What is primary immune response
responding to a newly encountered antigen
What is secondary immune response
responding to a previously encountered antigen
Features of the primary immune response
- considerate time delay
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
What does that time delay mean for us
why we get symptoms of a disease when we are first exposed to a pathogen
Features of plasma cells
Short lived
What do memory cells do
remain circulating in the blood for a long time and allow for a rapid secondary immune response
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
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
Describe / draw the secondary immune response
Name the four types of T cells
Killer
Helper
Suppressor
Memory
Name the three types of B cells
Memory
Effector
Plasma
How long do neutrophils last
5 days
What are antigens
Functional proteins / glycosidic proteins intrinsic to the plasma membrane
What are T killer cells stimulated by
Interferons
What cells are most important in cell mediated immunity
T killer cells
Draw a graph of antibody concentration against time / days - primary + secondary
How to identify lymphocytes
very large nuclei that nearly occupy the entire cell.
How to identify red blood cells
Round shape
How to identify platelets
Small size
How to identify neutrophils
Lobed nucleus
What are immunoglobulins
• Globular glycoproteins produced by plasma cells
Structure of antibodies
• Quaternary structure = 2 heavy + 2 light polypeptide chains
• Bonded by disulphide bridges
- constant region
- variable region
- antigen binding site
- hinge region
What is the constant region
does not vary within class / isotype but do vary between classes = determines the mechanism used to destroy pathogen
What’s the variable region
different for each antibody = where antibody attaches to antigen = antigen – antibody complex
What’s at the end of the variable region
antigen-binding site
What is special about the antigen binding site
specific for each antigen = different antibodies need to be produced
Why is it significant that there are 2 antigen binding sites
aids in agglutination = stops pathogen causing damage
What’s the hinge region
where disulphide bonds join heavy chains = give flexibility = allows ABS to be placed at diff angles
Draw an antibody
Function of antibodies
• bind to specific antigens = trigger the specific immune response.
• Every antigen has one antibody
What did antibodies act as
anti-toxins, opsonins and agglutinins
What region of the antibody does the phagocyte bind to
Constant
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
Primary function of opsonins
Promoting phagocytosis by acting as a marker
What can’t pathogens do when attached to antibodies
Enter host cells
How can antibodies act as agglutinins
Each antibody - two binding sites = bind to several pathogens + cross link them =become agglutinated
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
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
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
How many polypeptide chains does an antibody contain an
4
What allows for sulfide bonding
Amino acid - cysteine
What is formed when an antibody binds to an antigen
Antigen-antibody complex
How do antibodies defend body
- act as opsonins
- acts as antitoxins
- cause agglutination
When do auto immune diseases occur
When the immune system recognised a ‘self’ antigen as a foreign antigen + attacks healthy body tissue
Immunity
Being able to kill pathogens if infected before getting symptoms
Active immunity
Achieved when the immune system is activated + makes its own antibodies
Passive immunity
Achieved when antibodies are supplied from another source
Natural immunity
Achieved through normal life processes
Artificial immunity
Achieved through medical intervention
Natural active immunity
Achieved as a result of infection - individual gets disease + immune system makes memory cells
Artificial active immunity
= injects inactive pathogen to activate an immune response
Natural passive immunity
Antibodies provided via the placenta or via breast milk
Artificial passive immunity
Injection / infection of antibodies from another animal / individual
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
Are there memory cells in active immunity
Yes
Are there memory cells in passive immunity
No
What is a vaccine
a suspension of antigens that are intentionally put into the body to induce artificial active immunity.
What can vaccines be
Whole live organisms
Dead microorganisms
Attenuated microorganisms
Toxoids
mRNA
Features of whole live organism vaccines
multiply slowly = allowing body to recognise antigens = stronger + longer-lasting immunity
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
Attenuated vaccine
multiply slowly = allowing body to recognise antigens = MMR = stronger + longer lasting immunity
Toxoid
harmless form of toxin = Diptheria
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
Attenuated
Weakened
Problems with vaccines
Allergic reactions
Poor response
Antigenic variation
Virus have capacity to change their surface antigens
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
Why may people have a poor response to a vaccine
malnourished and cannot produce the antibodies – proteins or their immune system may be defective
Antigenic variation
variation in antigens of pathogens = vaccines don’t trigger an immune response
Types of changing surface antigens
Antigenic drift
Antigenic shift
Antigenic concealment
Cross breeding
Antigenic drift
over time there are small changes in the structure and shape of antigens = same strain
Antigenic shift
there are major changes in antigens (within the same strain of virus)
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)
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
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
Ring immunity
• People near a vulnerable / infected person are vaccinated in order to prevent them from catching and transmitting the disease
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
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
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)
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.
Why is RNA virus more dangerous
- more easily mutated as only has 1 strand
- keeps mutating - vaccines must keep being updated
