4.1 Communicable Diseases, Disease Prevention And The Immune System

Question 1

Name 4 groups of pathogen that can cause communicatble diseases.

Answer 1

• Bacteria
• fungi
• protoctista
• viruses

Question 2

How does mycobacterium tuberculosis cause disease

Answer 2

1. triggers inflammatory response by infectingh phagocytes in lungs.
2. Infected phagocytes are sealed in waxy-coated tubercles so bacteria remain dormant. first infection has no symptoms.
3. if another factor weakens immune system, bacteria becomes active and destory lung tissue.

Question 3

How does HIC result in the symptoms of AIDs.

Answer 3

1. Attachment protein bind to complementary CD4 receptor on Th cells.
2. HIV particles replicate inside Th cells, killing or damaging them.
3. AIDs develops when there are too few Th cells for immune system to function.
4. Individuals cannot destory other pathogens and suffer from secondary diseases / infections. May cause death.

Question 4

How does the tabacco mosaic virus cause disease

Answer 4

Affects plants, mainly transmitted via infected sap.

contains ssRNA, which is directly transcribed by host cell to assemble new virions.
Virions enter other cells via plasmodesmata then enter xylem and phloem.
Causes stunted growth and mottled leaves.

Question 5

How does the influenza virus cause disease

Answer 5

Transmitted via: droplet infectrion, contact with mucas containing virus, zoonotic infection, contact with fomites.

injects viral RNA into ciliated epithelial cells of throat and lungs. Viral RNA hijacks cell biochemistry to produce new virions. Cell lysis releases virions.

5-7 days of headache, coughing, sneezing, sore throat, vomiting, fever, muscular/join pain.

Question 6

What causes malaria

Answer 6

Female Anopheles mosquito acts as vector for plasmodium spp. protoctista when it transfers saliva to another organism during feeding. Parasite reproduces asexually in red blood cells in liver, causing lysis.

Question 7

What causes potato / tomato late blight

Answer 7

The protoctista Phytophthora infestans behaves similarly to a fungus. mainly transmitted via spores.

Question 8

What cause ring rot of potatoes

Answer 8

Sepedonicus subspecies of the bacterium clavibacter michiganensis. Mainly transmitted by planting infested seeds/ contact with formites. Plant-to-plant transmission is rare.

Question 9

What causes bacterial meningitis

Answer 9

Oftern meningococcal bacteria A, B, C, W, X, Y, Z. also caused by pneumococcal bacteria and Haemophilus influenzae type b bacteria. Affects meninges (protective layer around the brain).

transmitted by droplet infection and direct contact with saliva. usually spread by carriers of the bacteria who are not ill and occasionally by individuals with meningitis.

Question 10

Describe 3 fungal infections.

Answer 10

the sac fungus Mycosphaerella fijiensislack causes the leaf-spot disease Black sigatoka in banana plants.

About 40 types of fungi cause ringworm. Transmitted by contact with fomites, zoonotic infection, direct contact with infected individuals. Particularly affects cattle.

Athlete’s foot in humans is caused by a range of fungi which can also affect hands or nails.

Question 11

How are communicable pathogens transmitted directly?

Answer 11

• Inhalation (droplet infection)
• Skin-to-skin contact or exchange of fluids.
• penetrate skin actively using enzymes or passively through wounds, hair follicles or sweat glands.

Question 12

How are communicable pathogens transmitted indirectly?

Answer 12

Consumption of contaminated food and drink.
Via a vector mosquitoes transmit plasmodium parasite.
Spores.

Question 13

How do living conditions affect disease transmission?

Answer 13

Overcrowding increases direct transmission.

Climate determines which organsisms can survive malaria is more prevalent in tropical countries, where mosquitoes can breed.

Socail factors influence how quickly people are treated, which can increase / decrease direct transmission.

Question 14

Name 4 physical barriers to pathogen entry in plants.

Answer 14

Cellulose cell walls.
Iignigiesd layer
waxy upper cuticle
old vascular tissue is blocked to prevent pathogens from spreading inside the plant.

Question 15

Describe 2 mechanical responses to infection in plants.

Answer 15

Guard cells close stomata

The thich polysaccharide callose is produced and deposited between the cell wall and plasmna membrane to increase entry distance and limit spread.

Question 16

What is necrosis.

Answer 16

Injury activates intracellular enzymes in plants that kill cells near the site of infection to prevent pathogen from spreading.

Necrosis of woody tissue is know as canker.

Question 17

Describe the chemical defences plants use against pathogens.

Answer 17

●Terpenoids (essential oils) e.g. menthols act as antibacterials.
●Phenols e.g. tannin inhibit insects from attacking by interfering with digestion.
●Alkaloids e.g. caffeine & morphins deter herbivores from feeding because they taste bitter.
●Defensins (cysteine-rich proteins) inhibit transport channels.
●Hydrolytic enzymes e.g. chitinases break down cell wall of invading organisms

Question 18

Name 5 barriers to infection in animals.

Answer 18

● Skin is tough keratin layer.
● Blood clotting prevents pathogens from entering through skin lesions.
● Hydrochloric acid in stomach kills bacteria.
● Harmless bacteria in gut & on skin surface increase interspecific competition with pathogens.
● Mucous membranes trap pathogens and may secrete antimicrobial enzymes.

Question 19

What are expulsive reflexes?

Answer 19

● Irritation of mucous membranes in nostrils causes sneezing.
● Irritation of ciliated epithelium in respiratory tract causes coughing

Question 20

Name 4 ways the nonspecific immune system responds to infection.

Answer 20

● inflammation
● phagocytosis
● digestive action of lysozymes
● production of interferon (antiviral agent)

Question 21

Outline the process of inflammation.

Answer 21

1. Damaged vessels release histamines, causing vasodilation.
2. Blood flow & permeability of blood vessels increase.
3. White blood cells & plasma move into the infected tissue.

Question 22

How does blood clotting occur?

Answer 22

When the blood vessel is cut it releases clotting factors

1. Blood platelets form plug by binding to collagen & release chemicals that enhance clotting e.g. thromboplastin.
2. clotting factors causes a cascade of enzymes to activate Prothrombin into thrombin, its active form.
3. Fibrinogen changes into insoluble fibrin which attaches to platelets in plug
4. red blood cells and platelets trapped to help clot wound.

Question 23

Name the 2 types of white blood cell involved in phagocytosis

Answer 23

Neutrophils

Macrophages (can become antigen-presenting cells)

Question 24

How does phagocytosis destroy pathogens?

Answer 24

1. Phagocyte moves towards pathogen which may have been marked by opsonins via chemotaxis.
2. Phagocyte engulfs pathogen via endocytosis to form a phagosome.
3. Phagosome fuses with lysosome (phagolysosome).
4. Lysozymes digest pathogen.
5. Phagocyte absorbs the products from pathogen hydrolysis.

Question 25

Explain the role of antigen-presenting cells (APCs).

Answer 25

Macrophage displays antigen from pathogen on its surface (after hydrolysis in phagocytosis).

Enhances recognition by TH cells, which cannot directly interface with pathogens/ antigens in body fluid.

Secrete cytokines that are involved in stimulating specific immune response.

Question 26

What are lysozymes

Answer 26

Digestive enzymes. Found in lysosomes as well as many secretions e.g. tears & mucus. Damage bacterial cell walls, causing osmotic lysis

Question 27

Outline how to prepare blood to be observed under a microscope.

Answer 27

1. Smear a drop of blood onto a slide using a spreader held at 45°.
2. Add leishman stain then a buffer. Rinse.

Question 28

Name the 2 types of specific immune response.

Answer 28

● cell-mediated

● humoral

Question 29

Outline the process of the cell-mediated response

Answer 29

1. Complementary TH lymphocytes bind to foreign antigen on APC.
2. Cell signalling via secretion of interleukins stimulates:
   a. clonal expansion of complementary TH cells (rapid mitosis): become memory cells or trigger humoral response.
   b. clonal expansion of cytotoxic T cells (TC): secrete enzyme perforin to destroy infected cells

Question 30

Outline the process of the humoral response

Answer 30

1. Complementary TH lymphocytes bind to foreign antigen on antigen-presenting T cells.
2. Release cytokines that stimulate clonal expansion (rapid mitosis) of complementary B lymphocytes.
3. B cells differentiate into plasma cells.
4. Plasma cells secrete antibodies with complementary variable region to antigen.

Question 31

Describe the structure and function of B and T lymphocytes.

Answer 31

Many specific receptors & immunoglobulins on surface.

B cells differentiate into plasma cells to secrete antibodies.

3 types of T cell: T helper (secrete cytokines), T killer(secrete perforin), T regulator (suppress other immune cells to prevent autoimmune disease).

Question 32

What is an antibody? Describe its structure.

Answer 32

Proteins secreted by plasma cells.

Quaternary structure: 2 ‘light chains’ held by disulfide bridges, 2 longer ‘heavy chains’.

Binding sites on variable region of light chains have specific tertiary structure complementary to an antigen.
The rest of the molecule is known as the constant region.

Question 33

How do antibodies lead to the destruction of a pathogen?

Answer 33

● Agglutinins form antigen-antibody complexes to enhance phagocytosis.
● Activation of complement.
● Opsonins mark microbes for phagocytes.
● Antitoxins make toxins insoluble via precipitation/ neutralisation.

Question 34

What are memory cells?

Answer 34

Specialised TH/ B cells produced from primary immune response.
Remain in low concentrations the blood.
Can divide very rapidly by mitosis if organism encounters the same pathogen again. (proliferation)

Question 35

Contrast the primary and secondary immune response

Answer 35

secondary response:
● Faster rate of antibody production.
● Shorter time lag between exposure & antibody production.
● Higher concentration of antibodies.
● Antibody level remains higher after the secondary response.
● Pathogen usually destroyed before any symptoms.

Question 36

Compare and contrast passive and active immunity.

Answer 36

Passive:

• both involve antibodies & can be natural or artificial
• no memory cells & antibodies not replaced when broken down = short-term
• immediate
• antibodies from external source
• no direct contact with antigen necessary

Active:

• both involve antibodies & can be natural or artificial
• memory cells produced = long-term
• time lag
• lymphocytes produce antibodies
• needs direct contact with antigen

Question 37

Give examples of passive and active immunity

Answer 37

Passive natural: antibodies in breast milk/ across placenta.
Passive artificial: anti-venom, needle stick injections.
Active natural: humoral response to infection.
Active artificial: vaccination.

Question 38

Define ‘autoimmune disease’ and give examples.

Answer 38

Immune system produces antibodies against its own tissues.
Rheumatoid arthritis: immune system targets synovium lined joints, causing inflammation.
Lupus: results in inflammation throughout body.

Question 39

Explain the principles of vaccination.

Answer 39

1. Vaccine contains dead/ inactive form of a pathogen or antigen.
2. Triggers primary immune response.
3. Memory cells are produced and remain in the bloodstream, so secondary response is rapid & produces higher concentration of antibodies.
4. Pathogen is destroyed before it causes symptoms.

Question 40

Define endemic and epidemic.

Answer 40

Endemic: disease occurs routinely in a geographical area.
Epidemic: temporary rapid increase in incidence of disease in a geographical area.

Question 41

What role do vaccines play in preventing epidemics?

Answer 41

Routine vaccination of 80-90% of population reduces available carriers of pathogen, resulting in herd immunity. Limited by country’s resources.
Vaccinating close contacts of infected individual limits spread of pathogen, but raises issues of distributive justice.
Programs have changed to account for informed consent & maximum beneficence even during epidemic.

Question 42

List possible natural sources of medicines.

Answer 42

● microorganisms e.g. streptomycin, neomycin, chloramphenicol = various species of Streptomyces genus
● fungi e.g. penicillin
● plants e.g. Taxol for chemotherapy = yew, quinine for malaria = cinchona, digoxin for heart arrhythmia = foxgloveMaintaining biodiversity means new natural treatments can be discovered in the future.

Question 43

What is personalised medicine and synthetic biology?

Answer 43

Personalised medicine: genome sequencing has enabled scientists to predict an individual’s response to disease/ certain medicines so prescriptions can be targeted.
Synthetic biology: engineering that targets biochemical processes.

Question 44

What are the benefits of using antibiotics to treat bacterial infection?

Answer 44

Effectively reduce population of bacterial colony. Used widely since discovery of penicillin in mid-20th century.

Bacteriostatic antibiotics prevent protein synthesis/ inhibit formation of nucleic acids = inhibit growth.

Bactericidal antibiotics prevent formation of peptidoglycan cross-links in cell walls = osmotic lysis.

Question 45

What are the risks of using antibiotics to treat bacterial infection?

Answer 45

Overuse of antibiotics increases selection pressure for resistant strains of bacteria. Antibiotic-resistant infections e.g. caused by MRSA & Clostridium difficile are difficult to treat.

Question 46

Define agglutinins

Answer 46

Antibodies that cause pathogens to stick together.

Question 47

define anti-toxins

Answer 47

Antibodies that render toxins harmless

Question 48

define opsonins

Answer 48

antibodies that make it easier for phagocytes to engulf the pathogen.

Question 49

define primary immune response

Answer 49

the initial response caused by a first infection.

Question 50

deffine secondary immune response

Answer 50

a more rapid and vigorous response caused by a second or subsquent infection by the same pathogen.