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A Level Bio > 4.1.1 Communicable diseases > Flashcards

4.1.1 Communicable diseases Flashcards

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1
Q

What are the different types of pathogens?

A
  1. Bacterium
  2. Fungi
  3. Protoctista
  4. Viruses
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2
Q

How do Gram positive bacteria differ from Gram negative bacteria?

A
  1. Gram + look purple/blue under a light microscope, Gram - look red
  2. Gram + are stained with crystal violet, Gram - stained with safranin
  3. Gram + have a thicker peptidoglycan wall and don’t have a lippopolysaccharide wall
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3
Q

What are the different shapes of bacterium? Give examples.

A
  1. Spherical e.g Cocci
  2. Rod-shaped e.g. Bacillus
  3. Curved e.g. Vibrio
  4. Spiral e.g. Spiralli
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4
Q

How do bacteria multiply? What are the implications of this method?

A

Binary fission.

They can reproduce quickly, so spread diseases quickly and food can go off faster.

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5
Q

Name 2 animal diseases and 1 plant disease caused by bacteria, and 2 characteristics of each.

A

Animal: Tuberculosis - coughing up blood & mucus, high temperature
Bacterial meningitis - blotchy rash, pain when exposed to bright light

Plant: Ring rot - damages leaves, tubers (potatoes) and fruit, kills tissues

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6
Q

What are bacteriophages?

A

Viruses that take over bacterial cells and use them to replicate, whilst destroying the bacteria

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7
Q

Compare the ways in which each type of pathogen damages the body.

A

Viruses: take over the cell’s functioning - insert genetic material (enzyme ‘reverse transferase’ changes their RNA to the cell’s DNA) and cell begins to synthesise viral cells that burst out of the cell and spread

Bacteria: produce toxins that poison/damage the host cell by either breaking down the cell membrane, inactivating enzymes, or compromising the genetic material so the cells can’t divide

Protoctista: Some take over cells, but don’t take over the genetic material. They digest the cell’s contents to use them to reproduce

Fungi: They digest living cells and destroy them (saprophytes), but some produce toxins

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8
Q

Name 2 animal diseases and 1 plant disease caused by viruses, and 2 characteristics of each.

A

Animal: HIV/AIDS - suppresses the immune system, joint/muscle pain
Flu Influenza - sudden fever (38c), sore throat

Plant: Tobacco Mosaic Virus - poor yield of fruits, unusual fruit colour

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9
Q

What are the main features within a fungal cell?

A

Nucleus, Mitochondria, Vacuole, Cell wall, Cell membrane and Cytoplasm

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10
Q

What type of fungi cause diseases?

A

Parasitic fungi feed on animals and plants and can reproduce very quickly

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11
Q

Name 2 animal diseases and 1 plant disease caused by fungi, and 2 characteristics of each.

A

Animal: Cattle ringworm - skin lesions, hair loss
Athlete’s foot - dry, red, flaky skin, foot covered in small blisters

Plant: Black sigatoka - tiny, chlorotic (lack of chlorophyll) spots appear on bottom of leaves, spots grow into thin brown streaks

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12
Q

Name 1 animal and 1 plant disease caused by protoctists, and 2 characteristics of each.

A

Animal: Malaria (caused by Plasmodium) - nausea, muscle pain/convulsions

Plant: Tomato/Potato Blight - brown lesions develop on stems/brown patches on green fruit, white fungal growth around edge of lesions on bottom of leaves

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13
Q

State & describe methods of direct and indirect transmission between animals

A

Direct:

1) Direct contact - bodily fluids, skin-to-skin, faeces
2) Inoculation - break in skin, wounds/sharing needles, animal bite
3) Ingestion - contaminated food/drink, pathogens transferred from hand to mouth

Indirect:

1) Fomites - inanimate objects e.g. bedding
2) Droplet infection - droplets of saliva and mucus expelled from the mouth
3) Vectors - transmit disease from host to host

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14
Q

What factors affect the transmission of communicable diseases in animals?

A
  1. Climate change
  2. Diet/Nutrition
  3. Poor conditions e.g. unclean water (cholera)
  4. Compromised immune system (HIV/Aids)
  5. Overpopulation
  6. Culture - some have different practises (e.g. not burying their dead)
  7. Poor waste disposal
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15
Q

State & describe methods of direct and indirect transmission between plants

A

Direct: Infected plant directly contacts healthy plant

Indirect:

1) Soil contamination - infected plant leaves pathogens in soil that affects whole crop
2) Vectors - pathogens carried in wind, water, animals or humans

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16
Q

What factors affect the transmission of communicable diseases in plants?

A
  1. Specific varieties are susceptible to disease
  2. Climate change
  3. Damp, warm conditions
  4. Over-crowding
  5. Poor mineral nutrition
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17
Q

What physical defences do plants have?

A
  1. Callose is synthesised and deposited between cell walls, cell membranes and plasmodesmata of infected cells act as a barrier to the healthy cells.
  2. Callose is deposited in sieve tubes at the end of a growing season to block flow of pathogen
  3. Lignin (large polysaccharide, non-living tissue) synthesised to thicken and strengthen cell walls
  4. Guard cells can close the stomata
  5. Thick cellulose cell wall acts as barrier
  6. Waxy cuticle - prevents water collecting on surface
  7. Transpiration stream - before it enters the xylem, water in apoplast is forced into symplast through selectively permeable membrane
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18
Q

What chemical defences do plants have?

A
  1. Terpenoids - antibacterial & antifungal properties (e.g. caffeine - toxic to fungi & insects, saponins - chemicals in plant membrances that interfere with fungal cell membranes, chitinases - break down chitin in fungi walls, defensins - disrupt bacterial and fungal cell membranes)
  2. Alkaloids - nitrogen-containing compounds with a bitter taste (caffeine, nicotine, cocaine, morphine) - stops herbivores feeding on them so less exposure to pathogens
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19
Q

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

A
  1. Skin produces sebum - oily substance that inhibits pathogen growth
  2. Lysozymes in tears, urine and mucus - destroys bacterial & fungal cell walls
  3. REM in eyes pushes microbes to front of the eye and out, microbes die in salty conditions
  4. Mucous membranes line most body tracts - contain lysozymes and phagocytes to engulf pathogens
  5. Thromboplastin released causes blood to clot that forms tough layer, Serotonin causes vessel constriction, epidermal cells below scab grow to seal wound permanently, collagen fibres deposited
  6. Fever - increased temp inhibit pathogen reproduction & specific immune system works faster at higher temps
  7. Expulsive reflexes
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20
Q

Describe the inflammatory response (non-specific defence)

A

Mast cells (type of wbc) are activated and release histamines and cytokines:
Histamines - make vessel walls more leaky so plasma is forced out as tissue fluid (causes swelling and pain), temp of body increases (causes redness)
Cytokines - attract phagocytes to the site

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21
Q

What are the main two types of phagocytes? What are their functions?

A

Neutrophils (70% of wbcs): rapid acting - first to act, 10 mins to destroy & engulf pathogens
Macrophages (4% of wbcs): slower, form antigen-presenting cells, engulf and digest pathogens

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22
Q

Describe the process of phagocytosis.

A

1) Pathogen produces chemicals that attracts phagocyte
2) Recognises pathogen as non-self so binds to it
3) Phagocyte engulfs pathogen - packages in vesicle, called a phagosome now
4) Lysosomes form phagolysosome with phagosome, lysins & hydrolytic enzymes in the lysosome break down the pathogen
(JUST MACROPHAGES)
5) Phagocyte absorbs digested pathogen - antigens from pathogen combine with MHC (special glycoproteins) in cytoplasm of phagocyte
6) MHC-antigen complex formed on the membrane - phagocyte appears as antigen-presenting cell (APC)

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23
Q

State the different types of B lymphocytes and their functions.

A
  1. Plasma cells - produce specific antibodies, lives a few days
  2. B effector cells - divide to form plasma cell clones
  3. B memory cells - remember a specific antigen and enable quick response - provide immunological memory
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24
Q

Where do B lymphocytes mature?

A

Bone Marrow

25
Q

Explain the process of hummoral immunity.

A
  1. B cells with complimentary antibodies bind to pathogen’s antigens to form APC
  2. Activated T helper cells bind to APC (clonal selection)
  3. Interleukins from T helper cell activate B cell
  4. Activated B cell divides to produce clones of plasma cells & memory cells (clonal expansion)
  5. Plasma cells form antibodies to bind with antigens and disable them (primary response)
  6. In the case of the pathogen returning, the B memory cells rapidly produce plasma cells (secondary response)
26
Q

State the different types of T lymphocytes and their functions.

A
  1. T Helper cells - have CD4 receptors on their surface that bind to APCs, produce interleukins (type of cytokine)
  2. T Killer cells - produce the chemical, perforin, that makes holes in the cell membrane of the pathogen so it’s permeable
  3. T Memory cells - divide rapidly to produce clones of T killer cells
  4. T Regulator cells - suppresses the immune system, stops it when pathogen is killed to make sure body recognises self-antigens - interleukins play an important part
27
Q

Explain the process of cell mediated immunity.

A

(Particularly important against viruses and early cancers)

  1. Receptors on T helper cells fit the antigens from the APCs formed. T helper cells become activated and produce interleukins that stimulate more T cells to rapidly divide. They form clones of the T helper cells with the right antibodies
  2. Cloned T cells either become T memory cells, T killer cells, or produce interleukins to stimulate phagocytosis, or the division of B cells.
28
Q

What are the main parts in the structure of an antibody?

A

Antigen-binding sites, light chain, heavy chain, variable region, constant region, disulphide bonds, hinge region

29
Q

Give three ways antibodies can help to defend the body against pathogens.

A
  1. Opsonins - antibodies bind to antigens and act as markers for phagocytes
  2. Agglutinins - bind to antigens, clump together that prevents them entering body cells
  3. Anti-toxins - bind to toxins to form toxin-antibody complexes, phagocytes engulf these complexes
30
Q

What are antibodies?

A

Y-shaped glycoproteins called immunoglobulins

31
Q

What is an autoimmune disease?

A

When the immune system doesn’t recognise ‘self’ cells and attacks healthy body tissue

32
Q

What are examples of autoimmune diseases?

A

Lupus: Symptoms - rash, fatigue, joint pain/swelling
Treatment - no cure, but immunosuppressants can limit effects

Arthritis: Symptoms - joint pain, inflammation, restricted joint movement
Treatment - no cure, but painkillers can be used alongside physiotherapy

Type 1 Diabetes: Symptoms - increased thirst, frequent urination, weight loss
Treatment - insulin injections, immunosuppressant drugs

33
Q

What is active immunity?

A

When the body itself produces the antibodies

34
Q

What is passive immunity?

A

When the antibodies are supplied to the body

35
Q

What is natural immunity?

A

When the primary antibody response occurs within your body

36
Q

What is artificial immunity?

A

When the primary antibody response occurs elsewhere, and the secondary response occurs withing your body

37
Q

State an example of natural active & artificial active immunity.

A

Natural active:
Obtaining any disease (B & T lymphocytes specific response)

Artificial active:
Vaccine (inject inactive/weakened pathogen antigens to elicit production of memory cells in body)

38
Q

State an example of natural passive & artificial passive immunity.

A

Natural passive:
Breastmilk (colostrum) from mother is high in antibodies that pass into the infant, after some days the antibody level is equivalent to the mother’s

Artificial passive:
Tetanus - antibodies are extracted from another organism (horses) and injected into body for temporary protection

39
Q

What is an epidemic?

A

Widespread occurrence of an infectious disease at a national level

40
Q

What is a pandemic?

A

Widespread occurrence of an infectious disease over countries or continents

41
Q

What is herd immunity?

A

When enough of the population are vaccinated to lower the occurrence of the disease within the population, protecting those who aren’t vaccinated

42
Q

What are the reasons for changes in vaccines?

A
  1. Bacteria can develop resistance to antibiotics, so new ones have to be developed.
  2. High risk individuals have regular vaccinations to keep the immunity
  3. To remain effective, they’re changed regularly
43
Q

Name 6 drugs, their source and function.

A

Penicillin:
Source - mould on melons
Function - (first) antibiotic

Docetaxel:
Source - yew trees
Function - breast cancer treatment

Aspirin:
Source - willow bark
Function - painkiller

Prialt:
Source - venom of cone snail
Function - painkiller

Vancomycis:
Source - soil fungus
Function - antibiotic

Digoxin:
Source - foxgloves (plant)
Function - treats atrial fibrillation and heart failure

44
Q

What is pharmacogenetics?

A

When genetic material is considered to conclude the action the drug will have on the person

45
Q

Give an example of a disease in which drugs and the genome interact.

A

HER2 Breast Cancer - Herceptin is only prescribed to patients in which the cancer cells have receptors complimentary to the drug

46
Q

What is synthetic biology?

A

The process of using genetic engineering to mimic aspects of biology: enzymes, pigments & bacterial cells
e.g. injecting blueberry pigment into tomatoes

47
Q

What is selective toxicity?

A

When antibiotics affect the metabolism of the bacteria and not the human cells

48
Q

Describe the use of antibiotics after its discovery.

A

Death rate was 36% due to communicable diseases before the discovery of penicillin. First medicine effective against bacteria - death rate fell, only 7% due to communicable diseases.

49
Q

What are the issues with antibiotics presently?

A

Bacteria are becoming increasingly resistant - they reproduce quickly so a mutation is quickly spread to daughter cells

50
Q

What is selection pressure?

A

When you change the environment so that one species is able to survive more than others (occurs in bacterial resistance, as resistant gene is successful)

51
Q

What’s the difference between an antibiotic, an antiseptic and an antibacterial?

A

Antibiotic - Medicinal substance that destroys bacteria inside the body
Antiseptic - Antimicrobial substance that kills micro-organisms (viruses, fungi, bacteria) outside the body
Antibacterial - similar to an antiseptic, but used on surfaces instead of the body

52
Q

How does antibiotic resistance develop?

A
  1. Overuse
  2. Not finishing the course
  3. Taking them when it’s unnecessary/Taking other’s prescriptions
53
Q

How can antibiotic resistance be prevented?

A
  1. Finishing the course, so microbes are killed before resistance can develop
  2. Only prescribing when necessary
  3. Good hygiene in hospitals - stop spreading
54
Q

State the name of the only antibiotic discovered since 1987.

A

Teixobactin - works against gram + bacteria e.g MRSA, found in soil

55
Q

Give two resistant strains of bacteria and their features.

A

MRSA: Usually colonises on skin, becomes dangerous when it can enter the skin (cuts)

Clostridium difficile: normally present in gut, but when other bacteria die, due to excessive use of antibiotics, it remains and can release toxins - causing diarrhoea and a fever (no competition)

56
Q

What is the role of cytokines?

A

Cell-signalling molecules - inform phagocytes of pathogen and stimulate them to move to the site of infection

57
Q

What is the role of opsonins?

A

Chemicals that bind to pathogens so they’re easily recognisable by phagocytes to bind to. Most effective are immunoglobin G (IgG) and immunoglobin M (IgM)

58
Q

Give an example of overuse of antibiotics

A

Farmers routinely add antibiotics to animal feed to prevent animals obtaining infections (reduce profit) - accelerates antibiotic resistance

A Level Bio (8 decks)

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