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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
What are the 3 indirect mode of transmission, give a description and example IN ANIMALS
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)
26
What is the direct mode of transmission, give a description and example IN PLANTS
Contact: contact between a healthy plant and a diseased plant eg TMV, potato blight
27
What are the indirect modes of transmission, give a description and example IN PLANTS
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
28
Outline the social and economic factors that increase the risk of a communicable disease being spread (4 marks)
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]
29
Explain what is meant by a fomite and state 2 diseases that are contracted through fomite contact (3 marks)
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
Suggest why potatoes cannot be grown for at least 2 years on land that has supported plants with ring rot (2 marks)
Soil contamination [1] With bacteria [1]
31
What is Callose, what is it an example of
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
What 6 chemical defense mechanisms do plants have, give an example for each one
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
State 2 types of chemical defence produced by plants against pathogens (2 marks)
(Named) antibacterial compounds [1] (Named) anti fungal compounds [1] Anti-oomycetes/ glycanases [1] Cyanide compounds [1]
34
Suggest why Callose is deposited in A: cell walls B: plasmodesmata C: sieve plates During an attack by a pathogen (3 marks)
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
Compare the structure of Callose and cellulose (4 marks)
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
What is a primary defence give some examples
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
What are the 2 secondary defenses called
Inflammation and phagocytes
38
Describe the cascade of reactions that lead to blood clotting
Damaged tissues Platelets activated by damaged tissue Releases thromboplastin Thromboplastin catalyses prothrombin and ca2+ Thrombin Thrombin catalyses fibrinogen Fibrin Fibrin forms clot
39
What is the process of inflammation and how does it help
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
What is the process of phagocytosis and how does it help
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
What are cytokines cells
Cell signaling molecules that attract phagocytes to sites of infection
42
What are opsonins
Bind to pathogens and mark them for phagocytosis, phagocytes have receptors that bind to opsonins
43
Why are primary defenses and phagocytosis known as non-specific defenses (1 mark)
They defend against any pathogen [1]
44
Explain the roles of thromboplastin and thrombin in blood clotting (2 marks)
Thrombin: catalyses the conversion of fibrinogen to fibrin [1] Thromboplastin: catalyses the conversion of prothrombin to thrombin [1]
45
Explain the role played by mast cells in defense against pathogens (3 marks)
Mast cells release histamines [1] Body temp is raised, which inhibits pathogen reproduction [1] And causes inflammation/ swelling [1]
46
What age 3 non specific responses
Barriers, inflammation, phagocytosis
47
What are 2 specific responses
Cell-mediated response using T lymphocytes, humoral response using antibodies
48
What are lymphocytes, what are the 2 types
White blood cells (leukocytes) that perform a variety of roles within the specific immune system T and B lymphocyte
49
What are the 4 types of T lymphocytes and what is there role
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
What are the 3 types of B lymphocytes and what is there role
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
What happens in cell-mediated immunity and what are there typical targets
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
What is humoral immunity and what is it’s typical targets
Clonal selection of antigen-specific B cell Clonal expansion to produce plasma cells and B memory cells Antibody production Bacteria and fungi
53
What is an antigen
A molecule that triggers an immune response (ie antibody production)
54
What is an antibody
A glycoprotein produced in response to the presence of an antigen
55
What are the 3 types of antibody defense and what happens
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
What is an autoimmune disease
Immune system malfunction and stop recognizing self antigens. Body cells are attacked by its own immune system
57
Give 3 examples of autoimmune disease and symptoms
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
describe the structure of an antibody
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
Outline the role of T killer cells (2 marks)
Perforin production [1] Disruption of pathogen cell membranes [1]
60
Explain how agglutination limits bacterial infection of cells (3 marks)
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
Suggest someone with HIV/AIDS may not exhibit a secondary immune response despite already encountering a pathogen (2 marks)
T helper lymphocytes infected/ destroyed [1] Cytokines not produced to activate specific B memory cells [1]
62
Describe active:natural and artificial ways in which a person can gain immunity
natural: memory cells produced following pathogenic infection Artificial: memory cells produced following a vaccination
63
passive:natural and artificial ways in which a person can gain immunity
Natural: fetal immunity (maternal antibodies cross the placenta) Artificial: antibodies are injected into a person, providing temporary immunity
64
What is the principle of vaccination
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
What are the 4 types of vaccines, how do they work, example and advantage and disadvantage
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
What are 3 medicines from natural sources, what properties and uses do they have
Quinine, cinchona spp, antimalarial, painkilling Aspirin, willow, anti-inflammatory, painkillling Penicillin, penicllium fungi, antibiotic
67
What is antibiotic resistance bacteria
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
Explain why artificial passive immunity does not provide long term immunity (2 marks)
Antibodies are injected into a person [1] No memory cells are developed [1]
69
Explain why herd immunity reduces spread of a disease (2 marks)
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
Suggest why vaccinations against tetanus require booster injections (3 marks)
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 (8 decks)

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