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Biology Year 12 > Communicable Diseases ✅ > Flashcards

Communicable Diseases ✅ Flashcards

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1
Q

What are the 4 types of pathogens

A

Bacteria, fungi, protoctista, viruses

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2
Q

For bacteria what is it’s mode of action, appearance and some examples

A

MoA: disease symptoms are often caused by toxin production

Appearance: prokaryotic cells, shapes include rod (bacilli), spherical (cocci) and spiral

Examples: tuberculosis (TB), bacterial meningitis, ring rot

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3
Q

For fungi what is its mode of action, appearance and examples

A

MoA: they secrete enzymes that digest living cells, enabling the fungus to spread through tissue

Appearance: eukaryotic organisms

Examples: ring worm, black sigatoka

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4
Q

For protoctista what is it’s mode of action, appearance and examples

A

MoA: they often consume the cell material of their host

Appearance: eukaryotic cells

Examples: malaria, potato blight

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5
Q

For viruses what is their mode of action, appearance and examples

A

MoA: they insert genetic material into their hosts DNA, taking control of cell metabolism

Appearance: unusually considered non loving, protein coat enclosing genetic material

Examples: influenza, tobacco mosaic virus

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6
Q

What is a communicable disease

A

A disease caused by a pathogen, which can be transmitted to another organism

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7
Q

What is a pathogen

A

A disease-causing organism

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8
Q

State 2 eukaryotic kingdoms that contain pathogenic species (2 marks)

A

Protoctista [1]
Fungi [1]

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9
Q

Describe the typical cause of symptoms for diseases resulting from
A: bacterial infection
B: fungal infection (2 marks)

A

A: toxin excretion by bacteria [1]
B: enzyme secretion by fungi, causing host tissue to be digested [1]

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10
Q

Evaluate whether viruses should be considered organisms (3 marks)

A

Viruses can reproduce [1]
But not without exploiting the metabolism of host cells [1]
They cannot synthesize proteins or transform energy [1]
They have evolved over time [1]

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11
Q

List 4 common plant diseases

A

Potato blight
Ring rot
Tobacco mosaic virus
Black sigatoka

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12
Q

What pathogens and symptoms are there for potato blight

A

Pathogen: phytophthora infestans (a protoctist)

Symptoms: hyphae (branching structures) penetrate cells, destroying tubers, leaves and fruit

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13
Q

What pathogens and symptoms are there for ring rot

A

Pathogen: clavibacter michiganensis (a bacterium)

Symptoms: destroys vascular tissue in leaves and tubers

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14
Q

What pathogen and symptoms are there for tobacco mosaic virus

A

Pathogen: TMV (virus)

Symptoms: mosaic patterns of discoloration on leaves, flowers and fruit

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15
Q

What pathogen and symptoms are there for black sigatoka

A

Pathogen: mycosphaerella fijiensis (a fungus)

Symptoms: hyphae penetrate and digest leaf cells, turning leaves black

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16
Q

What are 4 common animal diseases

A

Malaria
Tuberculosis (TB)
HIV/AIDS
Athletes foot

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17
Q

What pathogen and symptoms are there for malaria

A

Pathogen: plasmodium spp. (protoctists)

Symptoms: infects erythrocytes and liver cells, causing fever and fatigue

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18
Q

What pathogen and symptoms are there for tuberculosis (TB)

A

Pathogen: mycobacterium tuberculosis (a bacterium)

Symptoms: destroys lung tissue, resulting in coughing, fatigue and chest pain

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19
Q

What pathogen and symptoms are there for HIV/AIDS

A

Pathogen: human immunodeficiency virus (HIV)

Symptoms: infects T helper cells, thereby inhibiting the immune system

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20
Q

What pathogen and symptoms are there for athletes foot

A

Pathogen: tinia pedia (a fungus)

Symptoms: digests skin on people’s feet, causing cracking and itchiness

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21
Q

State 1 similarity and 1 difference between potato blight and black Sigatoka (3 marks)

A

Similarity:
both involve hyphae penetrating plant tissue [1]

Difference: potato blight is caused by a protoctist, whereas black sigatoka caus e by a fungus [1]
Black sigatoka infects only leaves [1]

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22
Q

Describe how HIV is able to replicate (4 marks)

A

In T helper cells [1]
Reverse transcriptase [1]
Converts viral RNA into DNA [1]
Viral DNA integrated into host cell DNA [1]
Viral proteins and RNA replicated using host machinery [1]

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23
Q

A new strain of the H1N1 virus causes a pandemic of influenza in 2009. Suggest why the new strain resulted in a pandemic (2 marks)

A

Genetic mutation resulted in new antigens on the H1N1 virus [1]
New strain not encountered before by human immune systems [1]
No vaccine [1]

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24
Q

What are the 3 direct mode of transmission, give a description and example
IN ANIMALS

A

Contact: contain with skin or body fluids eg bacterial meningitis

Entry through the skin: wounds, bites or infected needles eg HIV/AIDS or septicaemia

Ingestion: consumption of contaminated food or drink eg emoebic dysentery

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25
Q

What are the 3 indirect mode of transmission, give a description and example
IN ANIMALS

A

Fomites: inanimate objects (bedding or clothes) that transfer pathogens eg atheletes foot

Inhalation: breathing in droplets containing pathogens eg influenza

Vectors: anything that Carrie’s a pathogen from one host to another (water and different animals) eg malaria (mosquito is the vector)

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26
Q

What is the direct mode of transmission, give a description and example
IN PLANTS

A

Contact: contact between a healthy plant and a diseased plant eg TMV, potato blight

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27
Q

What are the indirect modes of transmission, give a description and example
IN PLANTS

A

Soil contamination: pathogens or reproductive spores, move into the soil from infected plants eg black Sigatoka, ring rot

Vectors: wind water and animals can act as vectors to transmit pathogens eg p. Infestans spores can be carried by air currents, causing blight to spread

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28
Q

Outline the social and economic factors that increase the risk of a communicable disease being spread (4 marks)

A

High population density/overcrowding [1]
Poor nutrition [1]
Poor hygiene/ waste disposal [1]
Culture/ medical practices [1]
Number of trained health professionals [1]
Lack of public warning systems [1]

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29
Q

Explain what is meant by a fomite and state 2 diseases that are contracted through fomite contact (3 marks)

A

An inanimate object that can harbour and spread pathogens [1]; examples include :
Meningitis’s [1]
Influenza [1]
Athletes foot [1]
Cold sores [1]
Conjunctivitis [1]
(Max 2 examples)

30
Q

Suggest why potatoes cannot be grown for at least 2 years on land that has supported plants with ring rot (2 marks)

A

Soil contamination [1]
With bacteria [1]

31
Q

What is Callose, what is it an example of

A

A physical defense
It’s a polysaccharide formed from beta glucose monomers, joined with 1-3 glycosidic bonds (some 1-6 linkages). Largely linear (a few branches) but helical. Produced in response to pathogenic attacks and deposited in cells walls, plasmodesmata and in siege plates, it acts as a barrier to prevent further infection

32
Q

What 6 chemical defense mechanisms do plants have, give an example for each one

A

Insect repellent: citronella, produced by lemon grass

Insecticides: pyrethrins, produced by chrysanthemums

Antibacterial compounds: gossypol, produced by cotton

Anti fungal compounds: saponins, produced by many species (soap worms)

Anti-oomycetes: glucanase enzymes, which destroy cell walls in p. Infestans

General toxins: cyanide compounds

33
Q

State 2 types of chemical defence produced by plants against pathogens (2 marks)

A

(Named) antibacterial compounds [1]
(Named) anti fungal compounds [1]
Anti-oomycetes/ glycanases [1]
Cyanide compounds [1]

34
Q

Suggest why Callose is deposited in
A: cell walls
B: plasmodesmata
C: sieve plates
During an attack by a pathogen (3 marks)

A

A: provide a physical barrier against pathogens [1]

B: stop pathogens moving through plasmodesmata to infect neighboring cells [1]

C:stop pathogens moving through sieve tubes to other parts of the plant [1]

35
Q

Compare the structure of Callose and cellulose (4 marks)

A

Both are formed from beta glucose monomers [1]
Callose has 1,3 glycosidic bonds/ cellulose has 1,4 glycosidic bonds [1]
Both are (largely) linear (Callose has some branches) [1]
Callose is helical/ cellulose is not [1]
Cellulose has cross links between chains [1]

36
Q

What is a primary defence give some examples

A

The barriers that prevent pathogens from entering the body
Eg: skin, conjunctiva (membrane covering eye), mucus, ciliated epithelia in airways, mucus layer and acidic conditions in stomach and vagina

37
Q

What are the 2 secondary defenses called

A

Inflammation and phagocytes

38
Q

Describe the cascade of reactions that lead to blood clotting

A

Damaged tissues

Platelets activated by damaged tissue

Releases thromboplastin

Thromboplastin catalyses prothrombin and ca2+

Thrombin

Thrombin catalyses fibrinogen

Fibrin

Fibrin forms clot

39
Q

What is the process of inflammation and how does it help

A

Mast cells (which are leucocytes) release histamines, which dilate blood vessels and cause more plasma to move into tissue fluid, this raises temp and causes swelling

High temp reduces rate of pathogen reproduction. Inflammation is thought to be protective (eg isolating pathogens)

40
Q

What is the process of phagocytosis and how does it help

A

Phagocyte engulfs the pathogen. Pathogen is enclosed in a vacuole (phagosome). Lysosomes fuses with phagosome (forms phagolysosome). Enzyme released by lysosome digest the pathogen

Destruction of pathogenic cells

41
Q

What are cytokines cells

A

Cell signaling molecules that attract phagocytes to sites of infection

42
Q

What are opsonins

A

Bind to pathogens and mark them for phagocytosis, phagocytes have receptors that bind to opsonins

43
Q

Why are primary defenses and phagocytosis known as non-specific defenses (1 mark)

A

They defend against any pathogen [1]

44
Q

Explain the roles of thromboplastin and thrombin in blood clotting (2 marks)

A

Thrombin: catalyses the conversion of fibrinogen to fibrin [1]

Thromboplastin: catalyses the conversion of prothrombin to thrombin [1]

45
Q

Explain the role played by mast cells in defense against pathogens (3 marks)

A

Mast cells release histamines [1]

Body temp is raised, which inhibits pathogen reproduction [1]

And causes inflammation/ swelling [1]

46
Q

What age 3 non specific responses

A

Barriers, inflammation, phagocytosis

47
Q

What are 2 specific responses

A

Cell-mediated response using T lymphocytes, humoral response using antibodies

48
Q

What are lymphocytes, what are the 2 types

A

White blood cells (leukocytes) that perform a variety of roles within the specific immune system

T and B lymphocyte

49
Q

What are the 4 types of T lymphocytes and what is there role

A

T helper cells: produce cytokines, which stimulates B cells and other T cells

T killer cells: produce perforin, which damages the cell membranes of pathogens

T memory cells: recognize antigens from previous infections (immunological memory)

T regulator cells: control the immune system (preventing autoimmune responses)

50
Q

What are the 3 types of B lymphocytes and what is there role

A

Plasma cells: produce antibodies

B effector cells: divide to form plasma cell clones

B memory cells: remember specific antigen (enables rapid secondary immune responses)

51
Q

What happens in cell-mediated immunity and what are there typical targets

A

Antigen-presenting cells (eg phagocytes) activate T helper cells, which stimulate phagocytosis, T memory and T killer cell production
No antibodies

Viruses and cancerous cells

52
Q

What is humoral immunity and what is it’s typical targets

A

Clonal selection of antigen-specific B cell
Clonal expansion to produce plasma cells and B memory cells
Antibody production

Bacteria and fungi

53
Q

What is an antigen

A

A molecule that triggers an immune response (ie antibody production)

54
Q

What is an antibody

A

A glycoprotein produced in response to the presence of an antigen

55
Q

What are the 3 types of antibody defense and what happens

A

Opsonisation: antibody acts as an opsonin (speeding up phagocytosis)

Agglutination: antigen-antibody complex’s clump together. This clump is too large to enter cells and enables phagocytes to engulf several pathogens at once

Neutralization: antibodies bind to toxins, rendering them harmless

56
Q

What is an autoimmune disease

A

Immune system malfunction and stop recognizing self antigens. Body cells are attacked by its own immune system

57
Q

Give 3 examples of autoimmune disease and symptoms

A

Graves’ disease: overactive thyroid causing weight loss and muscle weakness

Vitiligo: affects melanocytes, loss of skin pigmentation

Type 1 diabetes: affects pancreatic beta cells, lack of insulin production, loss of blood glucose regulation

58
Q

describe the structure of an antibody

A

Heavy chain=longest chain
Light chain=shortest chain
Variable region=non shaded part of a chain
Antigen binding site=where light and heavy chain end
Constant region=shaded part of a chain (longer then variable region)
Receptor binding site=bottom of heavy chains

59
Q

Outline the role of T killer cells (2 marks)

A

Perforin production [1]
Disruption of pathogen cell membranes [1]

60
Q

Explain how agglutination limits bacterial infection of cells (3 marks)

A

Antibody (complex) with many binding sites for antigen [1]
Pathogens clumped together [1]
Complex is too large to enter cells [1]
Facilitates phagocytosis/ phagocytes can engulf several pathogens at once [1]

61
Q

Suggest someone with HIV/AIDS may not exhibit a secondary immune response despite already encountering a pathogen (2 marks)

A

T helper lymphocytes infected/ destroyed [1]
Cytokines not produced to activate specific B memory cells [1]

62
Q

Describe active:natural and artificial ways in which a person can gain immunity

A

natural: memory cells produced following pathogenic infection

Artificial: memory cells produced following a vaccination

63
Q

passive:natural and artificial ways in which a person can gain immunity

A

Natural: fetal immunity (maternal antibodies cross the placenta)

Artificial: antibodies are injected into a person, providing temporary immunity

64
Q

What is the principle of vaccination

A

To persuade the body to produce antibodies and memory cells against a particular pathogen with one a person contracting the disease, vaccination of many people in a polymath on= herd immunity and prevent epidemics

65
Q

What are the 4 types of vaccines, how do they work, example and advantage and disadvantage

A

Weakened, live pathogen: modified pathogen that is alive but not pathogenic, mumps, ADV:strongest response and long lasting, DIS: organism could revert and become pathogenic

Dead/ inactive pathogen: pathogen is killed but it’s antigens are present, influenza,ADV: stable and safer, DIS: response is weaker

Toxoids: modified toxins, tetanus,ADV: safe, DIS: not five strong response

Subunits: isolated antigens, HIB, ADV:vaccines for several strains produced

66
Q

What are 3 medicines from natural sources, what properties and uses do they have

A

Quinine, cinchona spp, antimalarial, painkilling

Aspirin, willow, anti-inflammatory, painkillling

Penicillin, penicllium fungi, antibiotic

67
Q

What is antibiotic resistance bacteria

A

Mutation causes evolution of bacteria that are resistant to antibiotics, spread can be reduced by minimizing use of antibiotics and using good hygiene practices

68
Q

Explain why artificial passive immunity does not provide long term immunity (2 marks)

A

Antibodies are injected into a person [1]
No memory cells are developed [1]

69
Q

Explain why herd immunity reduces spread of a disease (2 marks)

A

Many people in a population have immunity to a pathogen [1]
A disease carrier is less like to encounter people who lack immunity [1]

70
Q

Suggest why vaccinations against tetanus require booster injections (3 marks)

A

Tetanus vaccine is in form of toxoids [1]
Small amounts of toxin can be very harmful [1]
Boosters maintain high levels of antitoxin antibodies and memory cells in the blood (to maintain immunity) [1]

Biology Year 12 (7 decks)

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