Communicable Diseases (watered down) Flashcards

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1
Q

Bacteria

A
  • 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
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2
Q

Fungi

A
  • 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
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3
Q

Protoctista

A
  • Mode of action: they often consume the cell material of the host
  • Appearance: eukaryotic cells
  • Examples of diseases: malaria, potato blight
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4
Q

Viruses

A
  • 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
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5
Q

Communicable disease

A

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

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6
Q

Pathogen

A

A disease-causing organism

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7
Q

What traits do viruses lack that define many living organisms?

A

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

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8
Q

Potato blight

A
  • Pathogen: 𝘗𝘩𝘺𝘵𝘰𝘱𝘩𝘵𝘩𝘰𝘳𝘢 𝘪𝘯𝘧𝘦𝘴𝘵𝘢𝘯𝘴 (protoctista)

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

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9
Q

Ring rot

A
  • Pathogen: 𝘊𝘭𝘢𝘷𝘪𝘣𝘢𝘤𝘵𝘦𝘳 𝘮𝘪𝘤𝘩𝘪𝘨𝘢𝘯𝘦𝘯𝘴𝘪𝘴 (bacterium)

- Symptoms: destroys vascular tissue in leaves and tubers

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10
Q

Tobacco mosaic virus

A
  • Pathogen: TMV (virus)

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

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11
Q

Black sigatoka

A
  • Pathogen: 𝘔𝘺𝘤𝘰𝘴𝘱𝘩𝘢𝘦𝘳𝘦𝘭𝘭𝘢 𝘧𝘪𝘫𝘪𝘦𝘯𝘴𝘪𝘴 (fungus)

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

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12
Q

Malaria

A
  • Pathogen: 𝘗𝘭𝘢𝘴𝘮𝘰𝘥𝘪𝘶𝘮 𝘴𝘱𝘱. (protoctista)

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

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13
Q

Tuberculosis (TB)

A
  • Pathogen: 𝘔𝘺𝘤𝘰𝘣𝘢𝘤𝘵𝘦𝘳𝘪𝘶𝘮 𝘵𝘶𝘣𝘦𝘳𝘤𝘶𝘭𝘰𝘴𝘪𝘴 (bacterium)

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

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14
Q

HIV/AIDS

A
  • Pathogen: Human immunodeficiency virus (HIV)
  • Symptoms: infects T helper cells, thereby inhibiting the immune system
  • retrovirus
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15
Q

Athlete’s foot

A
  • Pathogen: 𝘛𝘪𝘯𝘪𝘢 𝘱𝘦𝘥𝘪𝘢 (fungus)

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

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16
Q

Retrovirus

A
  • 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
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17
Q

Modes of direct transmission between animals

A
  • 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
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18
Q

Modes of indirect transmission between animals

A
  • 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)
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19
Q

Mode of direct transmission between plants

A

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

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20
Q

Modes of indirect transmission between plants

A
  • 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
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21
Q

Physical defense of plants

A

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

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22
Q

Chemical defence in plants (6)

A
  • 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
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23
Q

Primary defences

A
  • 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
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24
Q

Repairing the primary defences

A

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

25
Q

Inflammation (secondary defence)

A
  • 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)
26
Q

Phagocytosis (secondary defence)

A
  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
27
Q

Lymphocytes

A

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

28
Q

T helper cells

A

*T lymphocyte

Produce cytokines, which stimulate B cells and other T cells

29
Q

T killer cells

A

*T lymphocyte

Produce perforin, which damages the cell membranes of the pathogen

30
Q

T memory cells

A

*T lymphocyte

Recognise antigens from previous infections (immunological memory)

31
Q

T regulator cells

A

*T lymphocyte

Control the immune system (preventing autoimmune responses)

32
Q

Plasma cells

A

*B lymphocyte

Produces antibodies

33
Q

B effector cells

A

*B lymphocyte

Divide to form plasma cell clones

34
Q

B memory cells

A

*B lymphocyte

Remember specific antigen (enables rapid secondary immune response)

35
Q

Cell-mediated immunity

A
  • 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
36
Q

Humoral immunity

A
  • 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
37
Q

Antigen

A

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

38
Q

Antibody

A

A glycoprotein produced in response to the presence of an antigen

39
Q

Opsonisation

A

*method of antibody defence

What happens? - antibody acts as an opsonin (speeding up phagocytosis)

40
Q

Agglutination

A

*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

41
Q

Neutralisation

A

*method of antibody defence

What happens? - antibodies bind to toxins, rendering them harmless

42
Q

Autoimmune diseases

A

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

43
Q

Grave’s disease

A
  • Autoimmune disease
  • Thyroid gland affected
  • Symptoms - overactive thyroid, causing weight loss and muscle weakness
44
Q

Vitiligo

A
  • Autoimmune disease
  • Melanocytes affected
  • Symptoms - loss of skin pigmentation
45
Q

Type 1 diabetes

A
  • Autoimmune disease
  • Pancreatic β-cells affected
  • Symptoms - lack of insulin production; loss of blood glucose regulation
46
Q

Structure of an antibody

A

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

47
Q

Vaccination

A

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

48
Q

Natural active immunity

A

Memory cells produced following pathogenic infection

49
Q

Natural passive immunity

A

Fetal immunity (maternal antibodies cross the placenta)

50
Q

Artificial active immunity

A

Memory cells produced following a vaccination

51
Q

Artificial passive immunity

A

Antibodies are injected into a person, providing temporary immunity

52
Q

Weakened, live pathogen (vaccine)

A
  • 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
53
Q

Dead/inactivated pathogen (vaccine)

A
  • 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)
54
Q

Toxoids (vaccine)

A
  • How does it work? - modified toxins
  • Examples of diseases - tetanus and diphtheria
  • Advantages/disadvantages - safe, but may not give strong response
55
Q

Subunits (vaccine)

A
  • How does it work? - isolated antigens
  • Examples of diseases - HIB
  • Advantages/disadvantages - vaccines for several strains produced
56
Q

Quinine (medicine)

A
  • Source - 𝘊𝘪𝘯𝘤𝘩𝘰𝘯𝘢 spp.

- Properties and uses - antimalarial, painkilling

57
Q

Aspirin

A
  • Source - 𝘚𝘢𝘭𝘪𝘹 𝘢𝘭𝘣𝘢 (willow)

- Properties and uses - anti-inflammatory, painkilling

58
Q

Penicillin

A
  • Source - 𝘗𝘦𝘯𝘪𝘤𝘪𝘭𝘭𝘪𝘶𝘮 fungi

- Properties and uses - antibiotic

59
Q

Antibiotic resistance

A
  • 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