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A Level Biology OCR A > 4.1.1: Communicable diseases, disease prevention and the immune system > Flashcards

4.1.1: Communicable diseases, disease prevention and the immune system Flashcards

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1
Q

What are the different types of pathogen that can cause communicable diseases in plants and animals?

A

bacteria – tuberculosis, bacterial meningitis, ring rot

virus – HIV/AIDS, influenza, Tobacco Mosaic Virus

protoctista – malaria, potato/tomato late blight

fungi – black sigatoka, ring worm, athlete’s foot

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2
Q

What organism does tuberculosis infect?

A

humans

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3
Q

What organism does bacterial meningitis affect?

A

humans

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4
Q

What organism does ring rot affect?

A

potatoes

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5
Q

What organism does HIV/AIDS affect?

A

humans

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6
Q

What organism does influenza affect?

A

animals

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7
Q

What organism does tobacco mosaic virus affect?

A

plants

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8
Q

What organism does malaria affect?

A

humans

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9
Q

What organism does late blight affect?

A

potatoes/tomatoes

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10
Q

What organism does black sigatoka affect?

A

bananas

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11
Q

What organism does ring worm affect?

A

cattle

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12
Q

What organism does athlete’s foot affect?

A

humans

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13
Q

Define direct transmission

A

direct contact, inoculation (break in the skin, animal bites and puncture wounds), ingestion – eating contaminated food

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14
Q

Define indirect transmission

A

fomites – (inanimate objects such as bedding and cosmetics), droplet infection (any infection that makes you cough or sneeze), vectors – (something that transmits disease) , spores

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15
Q

What are the means of transmission of animal and plant communicable pathogens?

A

direct transmission, indirect transmission, living conditions (climate, social factors)

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16
Q

What are the primary non-specific defences against pathogens in animals?

A

skin, blood clotting, wound repair, inflammation, expulsive reflexes and mucous membranes

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17
Q

How does blood clotting work?

A

skin is broken, platelets come into contact with the collagen.

causes the release of thromboplastin and serotonin.

thromboplastin triggers platelets in blood to clot

clot contains fibrin and dries to form the scab

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18
Q

What is thromboplastin?

A

the enzyme that triggers blood clotting

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19
Q

What is serotonin?

A

causes smooth muscle to contract and narrow to reduce the blood supply to the area

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20
Q

Describe wound repairing?

A

epidermal layer starts to grow, damaged blood vessels regrow, collagen fibres deposited to give tissue strength
when the new epidermis reaches normal thickness, the scab sloughs off

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21
Q

Direct transmission in plants?

A

a healthy plant having contact with a diseased plant.

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22
Q

Indirect transmission in plants

A

soil contamination

vectors

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23
Q

Transmission by spores

A

spores can be carried by the wind or on the surface of water

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24
Q

Vectors that spread pathogens to plants?

A

wind

water – spores can be carried on the surface of water.

animals – insects can carry pathogens when they feed

humans – transmitted by hands, fomites and transporting crops around the world.

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25
Q

What’s a vector?

A

an organism that does not cause disease itself but spreads infection by moving pathogens from one host to another.

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26
Q

What are plant defences against pathogens?

A

physical: callose
chemical: repellent, insecticide, antibacterial compounds, antifungal compounds, anti oomycetes, toxins

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27
Q

How might a plant recognise and respond to a pathogen?

A

cells respond to pathogens and molecules made by pathogens that break through the cell wall

the response stimulates signals that switch on genes in the nucleus

this triggers defensive chemicals, alarm signals to unaffected cells and strengthening cell walls

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28
Q

How does the body respond to an antigen?

A

specific response: t and b cells

non specific response: lysosomes, inflammation, interferons and phagocytosis

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29
Q

What is an antigen?

A

a molecule (e.g. protein or glycoprotein) on the surface of an organism (e.g. its plasma membrane) which is recognised as ‘non self’ or foreign

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30
Q

Neutrophils- what do they do?

A

carries out phagocytosis of all pathogens

non specific

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31
Q

Lymphocytes- function?

A

produces antibodies against specific pathogens

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32
Q

What are phagocytes?

A

they are non specific and will attack any invading pathogen regardless of its antigens

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33
Q

Types of phagocytes?

A

macrophages and neutrophils

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34
Q

Cytokines- released by?, function?, responsible for what? and involved in the non specific or specific immune response?

A

released by macrophages and signal to phagocytes to move to the site of infection –this is called cytotaxis. also responsible for fevers and are involved in the specific immune response

35
Q

Why do cytokines bind to receptors?

A

because the receptor and cytokine have complementary shapes

36
Q

What are opsonins?

A

protein molecules that attach to antigens. they are a type of antibody but are not specific

37
Q

Receptors on the cell membrane of a phagocyte recognise antibody molecules known as _ _ _ _ _ _ _ _ , which are bound to pathogens and enhance phagocytosis.

Once engulfed by a phagocyte, a pathogen is contained in a vacuole called a _ _ _ _ _ _ _ _ _ _ _ _ .

Organelles called _ _ _ _ _ _ _ _ _ _ _ produce enzymes that digest the pathogen.

A

1) opsonins
2) phagosome
3) lysosome

38
Q

Why do you think the phagocytic response is described as non specific?

A

the non specific response targets a wide range of pathogens e.g. phagocytes engulf and digest many different pathogens

39
Q

Define ‘immune response’

A

a response to an antigen

involves lymphocytes and production of antibodies

40
Q

How does Mycobacterium tuberculosis

cause disease?

A
  1. Triggers inflammatory response by infecting 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
    become active & destroy lung tissue.
41
Q

How does HIV result in the symptoms of AIDS?

A
  1. Attachment proteins bind to complementary CD4
    receptor on T helper cells.
  2. HIV particles replicate inside T helper cells, killing or damaging them.
  3. AIDS develops when there are too few T helper cells for the immune system to function.
  4. Individuals cannot destroy other pathogens & suffer from secondary diseases/ infections. May cause death.
42
Q

How does the tobacco mosaic virus cause disease?

A

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 & phloem.
Causes stunted growth & mottled leaves.

43
Q

How does the influenza virus cause disease?

A

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

Injects viral RNA into ciliated epithelial cells of throat &
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/joint pain.

44
Q

What causes malaria?

A

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.

45
Q

Define lysis

A

the breakdown of a cell caused by damage to its plasma (outer) membrane

46
Q

What causes potato/ tomato late blight?

A

The protoctista Phytophthora infestans behaves

similarly to a fungus. Mainly transmitted via spores

47
Q

What causes ring rot of potatoes?

A

Sepedonicus subspecies of the bacterium
Clavibacter michiganensis. Mainly transmitted by
planting infected seeds/ contact with fomites.
Plant-to-plant transmission is rare.

48
Q

What causes bacterial meningitis?

A

Often meningococcal bacteria A, B, C, W, X, Y, Z. Also
caused by pneumococcal bacteria & Haemophilus
influenzae type b (Hib) bacteria. Affects meninges
(protective membranes around brain).
Transmitted by droplet infection & direct contact with saliva e.g. kissing. Usually spread by carriers of the bacteria who are not ill & occasionally by individuals with meningitis.

49
Q

Name 4 physical barriers to pathogen

entry in plants.

A

● cellulose cell walls
● lignified layer
● waxy upper cuticle
● old vascular tissue is blocked to prevent
pathogens from spreading inside the plant

50
Q

Describe 2 mechanical responses to infection in

plants.

A

Guard cells close stomata.
The thick polysaccharide callose is produced
& deposited between the cell wall & plasma
membrane to increase entry distance/ limit
spread

51
Q

Describe the chemical defences plants use against

pathogens.

A

●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.

52
Q

Name 5 barriers to infection in animals.

A

●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.

53
Q

What are expulsive reflexes?

A

Body attempts to force foreign substances out:
● Irritation of mucous membranes in nostrils
causes sneezing.
● Irritation of ciliated epithelium in respiratory
tract causes coughing.

54
Q

Name 4 ways the nonspecific immune system

responds to infection?

A

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

55
Q

Outline the process of inflammation.

A
  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.
56
Q

How does phagocytosis destroy

pathogens?

A
  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.
57
Q

Explain the role of antigen-presenting

cells (APCs).

A

Macrophage displays antigen from pathogen on its
surface (after hydrolysis in phagocytosis).
Enhances recognition by T(h) cells, which cannot directly
interface with pathogens/ antigens in body fluid.
Secrete cytokines that are involved in stimulating
specific immune response.

58
Q

What are lysozymes?

A

Digestive enzymes. Found in lysosomes

as well as many secretions e.g. tears & mucus. Damage bacterial cell walls, causing osmotic lysis.

59
Q

Outline how to prepare blood to be

observed under a microscope.

A
  1. Smear a drop of blood onto a slide
    using a spreader held at 45°.
  2. Add leishman stain then a buffer.bRinse.
60
Q

Name the 2 types of specific immune response.

A

● cell-mediated

● humoral

61
Q

Outline the process of the cell-mediated

response.

A
  1. Complementary T helper lymphocytes bind to foreign
    antigen on APC.
  2. Cell signalling via secretion of interleukins stimulates:
    a. clonal expansion of complementary T helper cells (rapid mitosis): become memory cells or trigger humoral
    response.
    b. clonal expansion of cytotoxic T cells (T killer) secrete
    enzyme perforin to destroy infected cells.
62
Q

Outline the process of the humoral response.

A
  1. Complementary T helper 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.
63
Q

Describe the structure and function of B

and T lymphocytes.

A

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).

64
Q

What is an antibody? Describe its structure.

A

‘Y’ shaped molecule.
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.

65
Q

How do antibodies lead to the destruction of a

pathogen?

A 
● Agglutinins form antigen-antibody complexes to
enhance phagocytosis.
● Activation of complement.
● Opsonins mark microbes for phagocytes.
● Antitoxins make toxins insoluble via
precipitation/ neutralisation.
66
Q

What are memory cells?

A

Specialised T helper/ B cells produced from primary
immune response.
Remains in low levels in the blood.
Can divide very rapidly by mitosis if organism
encounters the same pathogen again.

67
Q

Contrast the primary and secondary

immune response.

A

secondary immune response has a faster rate of antibody production, has a shorter time lag between exposure & antibody production.
there’s a higher concentration of antibodies in the secondary response
antibody level remains higher after the secondary
response.
pathogen usually destroyed before any symptoms during secondary response

68
Q

Compare and contrast passive and

active immunity.

A

Passive
- involves antibodies
- can be natural/artificial
- no memory cells & antibodies not replaced
when broken down = short-term
- immediate
- antibodies are from an external source
- no direct contact with antigen necessary

Active

 - involves antibodies
 - natural and artificial
 - memory cells are produced = long term
 - time lag
 - lymphocytes produce antibodies
 - needs direct contact with antigen
69
Q

Give examples of active immunity.

A

Active natural: humoral response to infection.

Active artificial: vaccination.

70
Q

Give examples of passive immunity.

A

Passive natural: antibodies in breast milk/
across placenta.
Passive artificial: injection of antibodies

71
Q

Define ‘autoimmune disease’ and give examples.

A

Immune system produces antibodies against its
own tissues.

Rheumatoid arthritis: immune system targets
synovium lined joints, causing inflammation.

Lupus: results in inflammation throughout body.

72
Q

Explain the principles of vaccination.

A
  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.
73
Q

Define endemic.

A

disease occurs routinely in a geographical area.

74
Q

Define epidemic.

A

temporary rapid increase in incidence of disease in a geographical area.

75
Q

Define agglutination.

A

antibodies stick pathogens together so they are too large to enter cell and also are easier to be engulfed by phagocyte.

76
Q

Define neutralisation.

A

antibodies immobilise pathogen by combining with pathogen (e.g by binding to flagella) to stop entry to cell;.

77
Q

Types of antibody: opsonins

A

can attach to lots of different types of pathogens allowing phagocytes to bind and digest the pathogen

78
Q

Types of antibody: agglutinins

A

antibodies with more than one binding site allowing them to bind to more than one antigen so they can bind to more than one pathogen clumping them together

79
Q

Types of antibody: antitoxins

A

are antibodies which combine with toxins secreted by bacteria such as tetanus and diptheria toxins rendering them harmless.

80
Q

What role do vaccines play in preventing epidemics?

A

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.

81
Q

List possible natural sources of

medicines.

A

● microorganisms e.g. streptomycin, neomycin
● fungi e.g. penicillin
● plants e.g. Taxol for chemotherapy = yew, quinine for malaria = cinchona, digoxin for heart arrhythmia = foxglove
Maintaining biodiversity means new natural treatments can
be discovered in the future.

82
Q

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

A

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.

83
Q

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

A

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.

A Level Biology OCR A (24 decks)

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