Communicable Diseases (watered down)

Question 1

Bacteria

Answer 1

• Mode of action: disease symptoms are often caused by toxin production
• Appearance: prokaryotic cells, shapes include rod (bacilli), spherical (cocci) and spiral
• Examples of diseases: tuberculosis (TB), bacterial meningitis, ring rot

Question 2

Fungi

Answer 2

• Mode of action: they secrete enzymes that digest living cells, enabling the fungus to spread through tissue
• Appearance: eukaryotic organisms
• Examples of diseases: ring worm, black sigatoka

Question 3

Protoctista

Answer 3

• Mode of action: they often consume the cell material of the host
• Appearance: eukaryotic cells
• Examples of diseases: malaria, potato blight

Question 4

Viruses

Answer 4

• Mode of action: they insert genetic material into their host’s DNA, taking control of cell metabolism
• Appearance: usually considered non-living, protein coat enclosing genetic material
• Examples of diseases: influenza, tobacco mosaic virus

Question 5

Communicable disease

Answer 5

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

Question 6

Pathogen

Answer 6

A disease-causing organism

Question 7

What traits do viruses lack that define many living organisms?

Answer 7

They can’t grow, synthesise proteins, or reproduce independently

Question 8

Potato blight

Answer 8

• Pathogen: 𝘗𝘩𝘺𝘵𝘰𝘱𝘩𝘵𝘩𝘰𝘳𝘢 𝘪𝘯𝘧𝘦𝘴𝘵𝘢𝘯𝘴 (protoctista)

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

Question 9

Ring rot

Answer 9

• Pathogen: 𝘊𝘭𝘢𝘷𝘪𝘣𝘢𝘤𝘵𝘦𝘳 𝘮𝘪𝘤𝘩𝘪𝘨𝘢𝘯𝘦𝘯𝘴𝘪𝘴 (bacterium)

- Symptoms: destroys vascular tissue in leaves and tubers

Question 10

Tobacco mosaic virus

Answer 10

• Pathogen: TMV (virus)

- Symptoms: mosaic patterns of discolouration on leaves, flowers, and fruit

Question 11

Black sigatoka

Answer 11

• Pathogen: 𝘔𝘺𝘤𝘰𝘴𝘱𝘩𝘢𝘦𝘳𝘦𝘭𝘭𝘢 𝘧𝘪𝘫𝘪𝘦𝘯𝘴𝘪𝘴 (fungus)

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

Question 12

Malaria

Answer 12

• Pathogen: 𝘗𝘭𝘢𝘴𝘮𝘰𝘥𝘪𝘶𝘮 𝘴𝘱𝘱. (protoctista)

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

Question 13

Tuberculosis (TB)

Answer 13

• Pathogen: 𝘔𝘺𝘤𝘰𝘣𝘢𝘤𝘵𝘦𝘳𝘪𝘶𝘮 𝘵𝘶𝘣𝘦𝘳𝘤𝘶𝘭𝘰𝘴𝘪𝘴 (bacterium)

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

Question 14

HIV/AIDS

Answer 14

• Pathogen: Human immunodeficiency virus (HIV)
• Symptoms: infects T helper cells, thereby inhibiting the immune system
• retrovirus

Question 15

Athlete’s foot

Answer 15

• Pathogen: 𝘛𝘪𝘯𝘪𝘢 𝘱𝘦𝘥𝘪𝘢 (fungus)

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

Question 16

Retrovirus

Answer 16

• Contains RNA rather than DNA
• Contains an enzyme called reverse transcriptase, which produces a DNA copy of its RNA genome
• The viral DNA is incorporated into the DNA of a T helper cell, which allows copies to be produced

Question 17

Modes of direct transmission between animals

Answer 17

• Contact - contact with skin, or body fluids; e.g. bacterial meningitis
• Entry through skin - e.g. wounds, bites, or infected needles; e.g. HIV/AIDS and septicaemia
• Ingestion - consumption of contaminated food or drink; e.g. amoebic dysentery

Question 18

Modes of indirect transmission between animals

Answer 18

• Fomites - inanimate objects (e.g. bedding or clothes) that transfer pathogens; e.g. athlete’s foot
• Inhalation - breathing in droplets containing pathogens; e.g. influenza
• Vectors - anything that carries a pathogen from one host to another is a vector (e.g. water, and many different animals); e.g. malaria (vector = mosquitoes)

Question 19

Mode of direct transmission between plants

Answer 19

Contact - contact between a healthy plant and a diseased plant; eg. TMV, potato blight

Question 20

Modes of indirect transmission between plants

Answer 20

• Soil contamination - pathogens, or reproductive spores, move into the soil from infected plants; e.g. black sigatoka and ring rot
• Vectors - wind, water, and animals can act as vectors to transmit plant pathogens; e.g. 𝘗.𝘪𝘯𝘧𝘦𝘴𝘵𝘢𝘯𝘴 spores can be carried by air currents, causing blight to spread

Question 21

Physical defense of plants

Answer 21

Callose - a polysaccharide formed from β-glucose monomers, joined with 1,3 glycosidic bonds (and some 1,6 linkages). It is largely linear (with a few branches), but helical. It is produced in response to pathogenic attacks and deposited in cell walls, plasmodesmata (i.e. pores in the cell walls), and in sieve plates. It acts as a barrier to prevent further infection

Question 22

Chemical defence in plants (6)

Answer 22

• Insect repellents - e.g. citronella, produced by lemon grass
• Insecticides - e.g. pyrethrins, produced by chrysanthemums
• Antibacterial compounds - e.g. glossypol, produced by cotton
• Antifungal compounds - e.g. saponins, produced by many species (e.g. soapworts)
• Anti-oomycetes - e.g. glucanase enzymes, which destroy cell walls in 𝘗.𝘪𝘯𝘧𝘦𝘴𝘵𝘢𝘯𝘴
• General toxins - e.g. cyanide compounds

Question 23

Primary defences

Answer 23

• Primary defences are the barriers that prevent pathogens from entering the body
• They include: the skin, the conjunctiva (membrane covering the eye), mucus, and ciliated epithelia in airways, and the mucus layer and acidic conditions in the stomach and vagina

Question 24

Repairing the primary defences

Answer 24

Blood clotting - cuts to the skin leave an organism open to infection. The evolution of a blood clotting system enables repairs to be made to primary defences whenever they’re damaged

Question 25

Inflammation (secondary defence)

Answer 25

- Mast cells (leucocytes) release histamines, which dilate blood vessels and cause more plasma to move into tissue fluid - this raises temperature and causes swelling - How does it help? - high temperature reduces the rate of pathogen reproduction. Inflammation is thought to be protective (e.g. isolating pathogens)

Question 26

Phagocytosis (secondary defence)

Answer 26

1. The phagocyte engulfs the pathogen 2. The pathogen is enclosed in a vacuole (phagosome) 3. Lysosome fuses with phagosome (forms a phagolysosome) 4. Enzymes released by the lysosome digest the pathogen - How does it help? - destruction of pathogenic cells - Assisted by cytokines (cell-signalling molecules that, among other roles, attract phagocytes to sites of infection) and opsonins (bind to pathogens and mark them for phagocytosis, phagoctes have receptors that bind to opsonins) * non-specific

Question 27

Lymphocytes

Answer 27

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

Question 28

T helper cells

Answer 28

*T lymphocyte | Produce cytokines, which stimulate B cells and other T cells

Question 29

T killer cells

Answer 29

*T lymphocyte | Produce perforin, which damages the cell membranes of the pathogen

Question 30

T memory cells

Answer 30

*T lymphocyte | Recognise antigens from previous infections (immunological memory)

Question 31

T regulator cells

Answer 31

*T lymphocyte | Control the immune system (preventing autoimmune responses)

Question 32

Plasma cells

Answer 32

*B lymphocyte | Produces antibodies

Question 33

B effector cells

Answer 33

*B lymphocyte | Divide to form plasma cell clones

Question 34

B memory cells

Answer 34

*B lymphocyte | Remember specific antigen (enables rapid secondary immune response)

Question 35

Cell-mediated immunity

Answer 35

- What happens? - antigen-presenting cells (e.g. phagocytes) activate T-helper cells, which stimulate phagocytosis, and T memory and killer cell production, no antibodies - Typical targets - viruses and cancerous cells

Question 36

Humoral immunity

Answer 36

- What happens? - clonal selection of antigen-specific B cell, clonal expansion to produce plasma cells and B memory cells, antibody production - Typical targets - bacteria and fungi

Question 37

Antigen

Answer 37

A molecule (on the surface of an invading pathogen) that triggers an immune response (i.e. antibody production)

Question 38

Antibody

Answer 38

A glycoprotein produced in response to the presence of an antigen

Question 39

Opsonisation

Answer 39

*method of antibody defence | What happens? - antibody acts as an opsonin (speeding up phagocytosis)

Question 40

Agglutination

Answer 40

*method of antibody defence What happens? - antigen-antibody complexes clump together. This clump is too large to enter cells and enables phagocytes to engulf several pathogens at once

Question 41

Neutralisation

Answer 41

*method of antibody defence | What happens? - antibodies bind to toxins, rendering them harmless

Question 42

Autoimmune diseases

Answer 42

The immune system can malfunction and stop recognising self antigens. The body's cells are attacked by its own immune systems. This is known as an autoimmune disease

Question 43

Grave's disease

Answer 43

* Autoimmune disease - Thyroid gland affected - Symptoms - overactive thyroid, causing weight loss and muscle weakness

Question 44

Vitiligo

Answer 44

* Autoimmune disease - Melanocytes affected - Symptoms - loss of skin pigmentation

Question 45

Type 1 diabetes

Answer 45

* Autoimmune disease - Pancreatic β-cells affected - Symptoms - lack of insulin production; loss of blood glucose regulation

Question 46

Structure of an antibody

Answer 46

Antigen binding sites, light and heavy chain, receptor binding site, variable region and constant region

Question 47

Vaccination

Answer 47

The principle of vaccinations is to persuade the body to produce antibodies and memory cells against a particular pathogen without a person contracting the disease. Vaccination of many people in a population can prevent a disease spreading; this is called herd immunity and prevents epidemics

Question 48

Natural active immunity

Answer 48

Memory cells produced following pathogenic infection

Question 49

Natural passive immunity

Answer 49

Fetal immunity (maternal antibodies cross the placenta)

Question 50

Artificial active immunity

Answer 50

Memory cells produced following a vaccination

Question 51

Artificial passive immunity

Answer 51

Antibodies are injected into a person, providing temporary immunity

Question 52

Weakened, live pathogen (vaccine)

Answer 52

- How does it work? - modified pathogen that is alive but not pathogenic - Examples of diseases - mumps, polio, measles, TB - Advantages/disadvantages - strongest response and long-lasting immunity, but (rarely) organism may revert and become pathogenic

Question 53

Dead/inactivated pathogen (vaccine)

Answer 53

- How does it work? - pathogen is killed but its antigens are still present - Examples of diseases - influenza and whooping cough - Advantages/disadvantages - stable and safer than live vaccines, but response is weaker (boosters required)

Question 54

Toxoids (vaccine)

Answer 54

- How does it work? - modified toxins - Examples of diseases - tetanus and diphtheria - Advantages/disadvantages - safe, but may not give strong response

Question 55

Subunits (vaccine)

Answer 55

- How does it work? - isolated antigens - Examples of diseases - HIB - Advantages/disadvantages - vaccines for several strains produced

Question 56

Quinine (medicine)

Answer 56

- Source - 𝘊𝘪𝘯𝘤𝘩𝘰𝘯𝘢 spp. | - Properties and uses - antimalarial, painkilling

Question 57

Aspirin

Answer 57

- Source - 𝘚𝘢𝘭𝘪𝘹 𝘢𝘭𝘣𝘢 (willow) | - Properties and uses - anti-inflammatory, painkilling

Question 58

Penicillin

Answer 58

- Source - 𝘗𝘦𝘯𝘪𝘤𝘪𝘭𝘭𝘪𝘶𝘮 fungi | - Properties and uses - antibiotic

Question 59

Antibiotic resistance

Answer 59

- Mutation can result in the evolution of bacterial that are resistant to antibiotics (e.g. methicillin-resistant 𝘚𝘵𝘢𝘱𝘩𝘺𝘭𝘰𝘤𝘰𝘤𝘤𝘶𝘴 𝘢𝘶𝘳𝘦𝘶𝘴, or MRSA) - The spread of antibiotic-resistant infection can be reduced by minimising the use of antibiotics (as overuse can accelerate natural selection of resistant strains) and using good hygiene practices