Communicable diseases, disease prevention, and the Immune system.

Question 1

What are communicable diseases caused by?

Answer 1

Pathogens

Question 2

Give examples of pathogens? How do they cause harm?

Answer 2

Virus, bacteria, protoctista and fungi. They cause harm through directly damaging the tissue or via release of toxins.

Question 3

What diseases does bacteria cause in animals?

Answer 3

Tuberculosis in mammals in their lung tissue. It suppresses immune system. Cure via antibiotics and prevent via vaccination.
Bacterial meningitis infects the brain. CAN use antibiotics to cure before too much damage done.

Question 4

What is an infectious disease?

Answer 4

Disease caused by a pathogen that passes from infected individuals to uninfected individuals. Aka communicable disease.

Question 5

What are non-infectious diseases?

Answer 5

Long-term disease not caused by pathogens. Eg lung cancer, depression, vitamin deficiencies and cardiovascular disease.

Question 6

What disease does bacteria cause in plants?

Answer 6

Ring rot in potatoes and tomatoes is caused by gram positive bacteria. Damages leaves, tubers and leaves.

Question 7

What are viruses?

Answer 7

Non living and acellular. Consist of genetic material (DNA/RNA), a capsid and attachment proteins. They replicate inside host cells, and injecting nucleic acid into the cell

Question 8

What diseases do viruses cause in humans?

Answer 8

HIV/AIDS. Aids is when the replicating viruses in the helper T cells interfere with normal functioning of immune system, eventually causing death due to inadequate immune response.
Influenza. It kills ciliated cells, causing secondary infections, e.g. (pneumonia).

Question 9

What disease do viruses cause in plants?

Answer 9

Tobacco mosaic virus. Damages leaves = mosaic patten. This affects photosynthesis. No cure but resistant strains have been developed.

Question 10

What disease does protoctista cause in animals?

Answer 10

These are eukaryotes that exist as single celled organisms or cells grouped into colonies. They are dangerous.
They cause malaria, spread via mosquito vectors. They reproduce sexually and asexually. Infects RBCs, liver and brain.

Question 11

What disease does protoctista cause in plants?

Answer 11

Potato blight. Hyphae enter plant and damage leaves & fruit. Resistant plant strains exist.

Question 12

What are fungi?

Answer 12

Eukaryotes, mainly cause disease in plants. Multi cellular or single cells. Release enzymes that digest host’s tissue and feed off of it.

Question 13

What disease do fungi cause in plants?

Answer 13

Black Sigatoka in plants (bananas), causing black leaves and preventing photosynthesis. Fungicides can kill and resistant strains exist.

Question 14

What disease do fungi cause in animals?

Answer 14

Ring worm. Itchy, not harmful.
Athlete’s food ONLY humans. A type of ringworm that thrives in warm, damp reigons. Cured using antifungal creams.

Question 15

List all modes of transmission of communicable disease.

Answer 15

Direct:
-touching, kissing, contact with cuts, sexual contact.
-inoculation (animal bites, sharing needles, cuts)
-ingestion (drinking and eating contaminated)
-Contact between plants with disease.

Indirect :
-Vectors (wind, water, animals and humans)
-Droplets, pathogens transmitted inside (e.g saliva and mucus)
-Fomites - dry bedding, socks, cosmetics
-Contaminated soil, pathogens and their spores can remain in the soil and infect roots of plants.

Question 16

How does climate impact transmission of disease?

Answer 16

Hot climate - increased heat = more KE for chemical reactions and reproduction.

Question 17

How do social factors impact disease transmission?

Answer 17

Poverty/developing countries.
Eg: poor sewage infrastructure, lack of fresh food or water, poorer sanitation, overcrowded living quatres. Medicine and vaccines are less readily available to prevent the spread

Question 18

List the 3 plant responses to pathogens.

Answer 18

-Barriers to prevent entry (waxy cuticle)
-Antibacterial chemicals and proteins against bacterial infections - repels insects (vectors and kills pathogens)
-Physical defences - e.g callose production to stop pathogens spreading between cells

Question 19

What is the non-specific line of defence in animals?

Answer 19

It is the primary response that is the same regardless of infection.

Question 20

List the first non-specific responses.

Answer 20

-The skin = a barrier. Contains skin flora (healthy microorganisms) that can outcompete pathogenic bacteria
-blood clots form if skin is cut to form new barrier
-mucus membranes line body tracts. Traps pathogens and cilia sweep away from lungs.
-lysozymes digest pathogens (in tears and phagocytes)
-expulsive reflexes - sneezing coughing and vomiting force pathogen out of body.
-localised inflammation where cell damage is detected. Red, hot, sore, swollen and itchy.

Question 21

How does the primary response (non specific) of inflamation occur?

Answer 21

When cell damage is detected, mast cells release histamines and cytokines. Histamines cause vasodilation by increasing blood vessel permeability. So more WBCs can be delivered to site of damage. Phagocytes are attracted by cytokines to engulf and kill pathogens. The increase in temperature from blood can kill pathogens.

Question 22

Explain the process of phagocytosis.

Answer 22

Via phagocytes (macrophages or neutrophils). they can squeeze out of capillaries to engulf and digest pathogens. Non-specific.
1. Damaged cells release cytokines that attract phagocytes to site of infection.
2. Opsonin protein attach to pathogens to mark, making engulfing easier.
3.Phagocytes have receptors that attach to surface of pathogen.
4.Phagocyte changes shape to engulf pathogen and puts it in vesicle called phagosome.
4.Lysosomes full of lysozymes (hydrolytic enzymes) inside phagocyte fuse with phagosome = phagolysozyme.
5.Pathogen hydrolysed. Any useful soluble molecules absorbed into phagocyte cytoplasm.
6. The antigen of pathogen is presented on phagocyte cell surface = antigen presenting cell

Question 23

What is the second line of defence during infection of animals?

Answer 23

Specific response to antigens via 2 types of lymphocytes.
B and T lymphocytes which are made in bone marrow.
B mature in bone marrow and T mature in the thymus.

Question 24

Explain the cell mediated response up to clonal expansion. (T Cells)

Answer 24

1. Receptors on T cells bind to antigens on APC, causing T cell to divide rapidly by mitosis (clonal expansion) = large number of clones.
2. Cloned T helper cells differentiate into:
   -TT helper cells that produce interleukins to activate B lymphocytes.
   -Produce interleukins that stimulate macrophages to perform more phagocytosis
   -T memory cells that retain shaped antigen
   -T killer cells (cytotoxic t cells)
   -T regulator cells, suppress immune response to ensure the cell mediated response only occurs when pathogens are detected.

Question 25

What are antigen presenting cells?

Answer 25

Cells that present a non-self antigen on their surface.
Eg:
-Infected body cells
-Macrophage
-Cells on transplanted organ (different antigen to your self antigens)
-Cancer cells (abnormal shape)

Question 26

How are T killer cells involved in the cell mediated (specific) immune repsonse?

Answer 26

They destroy abnormal or infected cells.
They release a protein, PERFORIN, which perforates the cell surface membrane creating a pore so any substances can leave or enter. This causes cell death.
These are most common in viral infections because viruses infect body cells. They are sacrificed to prevent viral replication.

Question 27

Explain the process of blood clotting and scab formation

Answer 27

A break in the skin membranes or mucous membranes causes a chemical cascade caused by platelets. This causes thrombokinase (protein) to convert prothrombin to thrombin. Thrombin converts soluble fibrinogen to insoluble fibrin fibres. The platelets also secrete prostaglandins which constrict blood vessels to lessen blood loss. Fibrin fibres form a network of fibres that trap platelets and blood cells under the wound, forming a clot which dries to form a scab.

Question 28

How does wound repair occur?

Answer 28

Underneath the scab, stem cells divide by mitosis to heal the wound.
New blood vessels form
Collagen is produced
Granulation tissue forms to fill the wound
Stem cells move over the new tissue and divide to produce epithelial cells
Contractile cells cause wound contraction
Unwanted cells die

Question 29

What are the similarities and differences between neutrophils and macrophages during the immune response?

Answer 29

Similarities:
-Both engulf phagocytes and digest them with hyrolytic enzymes
-Detect phagocytes via the presence of non-self antigens
Attracted by cytokines and histamines
Differences:
-Neutrophils are have a lobed nucleus (can be used to identify them in blood smears)
-Macrophages don’t digest the entire phagocyte
-Only macrophages (and other infected body cells) become APCs

Question 30

How are B lymphocytes involved in the specific immune response?

Answer 30

T helper cells release interleukins, stimulating B cells. This causes the humoral response, involving antibodies.
1. Activated T helper cells bind to B cells with complimentary shaped antibody to antigen on T helper cell = CLONAL SELECTION
2. The B cell is activated by release of interleukins from T helper cell.
3.B cell rapidly divides via mitosis which differentiate into B memory or plasma cells = CLONAL EXPANSION
4. Plasma cells make antibodies.
This happens in the primary immune response.

Question 31

What are antibodies?

Answer 31

Globular, quaternary proteins with 2 binding sites complementary in shape to antigens. They are made up of 2 long polypeptide chains and 2 light polypeptide chains.
Bonding site = variable region. AA sequence her is different from each one.
Antigen + antibody = antigen-antibody complex.
Hinge region gives flexibility so antigen bonding site can be placed at different angles when binding to antigens

Question 32

What are the 3 ways antigens help to destroy pathogens?

Answer 32

1. Agglutination = pathogens clump together so phagocytes can locate and engulf.
   2.Opsonin = when antibody-antigen complex is marking pathogen, so they’re more succesptible to phagocytosis.
2. Bind to toxins, preventing them from entering cells = ANTI-TOXIN

Question 33

What happens in the secondary immune response?

Answer 33

B memory cells remain in the blood and are long-living. If reinfected by a pathogen, B memory cells collide with it and rapidly produce large amounts of antibodies by differentiating into plasma cells.

Question 34

Why are you more likely to show symptoms during the primary response?

Answer 34

As this is the first infection, there are no B memory cells for it. So it takes days for the lymphocytes to create enough of the antibodies to destroy the pathogen. So the pathogen is able to cause damage, making you ill.

Question 35

Why are you less likely to show symptoms in the secondary immune response?

Answer 35

Because you are reinfected with the same pathogen. B memory cells are present so produce large amounts of antibodies rapidly, destroying the pathogen before symptoms can be caused. = ACTIVE IMMUNITY.

Question 36

What is passive immunity?

Answer 36

Antibodies introduced directly into your body. The pathogen itself doesn’t enter your body so there is no long term immunity.
Natural passive immunity = antibodies passed to foetus via placenta, or to baby via breast milk.

Question 37

What is active immunity?

Answer 37

Involves exposure to the pathogen/antigen.
Natural = following infection and creation of your own antibodies via B memory and plasma cells.
Artificial = introduction of weakened version of the pathogen/antigen via a vaccine.

Question 38

What is an autoimmune diease?

Answer 38

Your immune system identifies body cells as non-self, triggering the immune response so WBC attacks your own body cells.
Sometimes the immune system responds to good microorganisms or overreacts to milk pathogens.
Sometimes T regulator cells don’t work properly, so immune system isn’t regulated.

Question 39

Explain two autoimmune diseases.

Answer 39

Rheumatoid Arthiritis - immune system attacks cartilage in joints = inflammation and pain.
Lupus = inflammation to joins, skin, organs and fatigue.
No cure, but anti-inflammatory drugs (steroids), pain relief and immunosuppressant drugs taken to relieve symptoms.

Question 40

Describe passive and artificial active immunity.

Answer 40

Passive immunity = antibodies directly injected into you.
Artificial active immunity = antigens/weakened pathogen injected or taken orally. Triggers a primary immune response with few symptoms. When reinfected you will rapidly produce antibodies via secondary immune response.

Question 41

Why are vaccines not always effective long-term?

Answer 41

Pathogens’ genetic material can mutate, so antigen is different shape,
Antigen variability = B memory cells receptor is no longer complimentary to new antigen, so you are no longer immune.
So we take boosters - eg annual flu vaccine because influenza mutates rapidly.

Question 42

What is an epidemic?

Answer 42

When a disease spreads rapidly on a national level.

Question 43

What is a pandemic?

Answer 43

When a disease spreads rapidly on a global level. Mass vaccine programmes prevent further spread of pathogen causing the disease. These are frequently updated (booster vaccines) to account for antigen variability.

Question 44

What is herd immunity?

Answer 44

If a large enough proportion of the population are vaccinated, spread of pathogen is stopped. This reduces the chance that those to vulnerable to have the vaccine are still protected.

Question 45

Why is biodiversity important for access to medicine?

Answer 45

Many medicines are sourced from microorganisms and plants. There are many we have not discovered, if they go extinct, we can’t discover it.

Question 46

What is an antibiotic?

Answer 46

A medicine produced by a microorganism that inhibits growth of and kill other microorganisms.
1. Preventing cell wall synthesis - inhibit enzymes that make molecules in cell walls. The bacteria then dies from leakage or too much water moving in = bursting (lyse)
2. Disrupting cell membranes - antibiotic binds to phospholipids, distorting structure so it is too permeable.
3. Interfering with protein synthesis - antibiotic attaches to bacterial ribosomes, preventing protein synthesis.

Question 47

Explain antibiotic resistance.

Answer 47

Due to random mutations in bacterial genetic material. Could result in mutation that codes fro a new protein that provides selective advantage against antibiotic. These are more likely to survive and reproduce, passing on mutated allele to population. Eventually whole population is resistant.

Question 48

Why is antibiotic resistance spreading?

Answer 48

This is increasing due to the widespread use and misuse of antibiotics. The antibiotic is the selection pressure. It kills only non-resistant bacteria, leaving those with the resistant gene in their plasmids no competition for resources. Therefore, they are free to reproduce until a resistant strain of bacteria has been made.
Eg. MRSA

Question 49

What is the difference between old and new medicines?

Answer 49

Old medicines sourced from plants include aspirin from willow bark.
New medicines:
- Personalised. Everyone is different so our response to medicine varies. Gene technologies enabled us to identify the most suitable drug and dose for someone to have based on their genes = Pharmacogenetics.
-Synthetic biology is using bacteria as medicine factories. Can also be used to research chemical pathways and mechanisms so tissue engineering, replacement and regeneration of medicines may be possible.