4.1 - Communicable diseases Flashcards

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1
Q

What is disease?

A

A condition that impairs the normal functioning of an organism

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2
Q

Which types of organisms get diseases?

A

Animals and plants

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3
Q

What are communicable diseases?

A
  • diseases that can be transferred from one infected organism to another
  • can be the same or different species
  • caused by pathogens
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4
Q

What is a host?

A

An organism in which a pathogen lives

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5
Q

What is a vector?

A

Carries a disease and spreads it

Eg water, insects

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6
Q

What is a pathogen?

A

An infectious microorganism that causes disease

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7
Q

What are the different types of host-pathogen interactions?

A
  • mutualistic
  • commensal
  • parasitic
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8
Q

What is a mutualistic relationship?

A
  • both organisms benefit

- eg bacteria in stomachs of domestic ruminants (bacteria digests cellulose for host, gets nutrition and environment)

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9
Q

What is a commensal relationship?

A
  • where one species lives harmlessly on the body of a larger species
  • eg microbial flora on skin, mouth etc
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10
Q

What is a parasitic relationship?

A
  • only benefits the parasite
  • some can become pathogenic if there are changes to a hosts health or if they infect an unnatural host (eg rabies virus)
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11
Q

What are the different types of pathogen?

A
  • bacteria
  • virus
  • protoctista (Protista)
  • fungi
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12
Q

What are bacteria?

A
  • prokaryotes
  • a small proportion of bacteria are pathogens
  • will damage hosts by releasing waste products/toxins or by attacking the cells
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13
Q

How can bacteria be classified?

A

By their basic shapes

By cell walls:
- GRAM POSITIVE BACTERIA - look purple/blue under light microscope when Gram stained

  • GRAM NEGATIVE BACTERIA - appear red under light microscope when Gram stained
    Useful as cell wall affects how bacteria react to antibiotics
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14
Q

What are viruses?

A
  • non-living pathogens
  • 0.02-0.30 micrometers (50x smaller than typical bacteria)
  • basic structure = genetic material (DNA or RNA) surrounded by protein coat
  • cant reproduce without cells
  • invade cells and take over genetic machinery/ biochemistry of host cell
  • causes cell to manufacture more copies of the virus
  • host cell eventually bursts, releasing many new viruses which infect healthy cells
  • they reproduce rapidly and evolve by developing adaptations to host
  • this makes them very successful pathogens
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15
Q

What are bacteriophages

A
  • viruses that attack bacteria

- people use bacteriophages to identify and treat some diseases, making them important in scientific research

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16
Q

What are protoctista

A
  • aka Protista
  • eukaryotic organisms
  • have a wide variety of feeding methods
  • include single-called organisms and cells grouped into colonies
  • a small percentage of protoctista act as pathogens, causing diseases in plants and animals
  • usually cause harm by entering host cells and feeding on contents as they grow. Then they break open cell as new generation emerges
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17
Q

What are fungal parasites

A
  • fungal diseases aren’t a major problem in animals but can be devestating for plants
  • fungi are eukaryotic
  • usually multicellular, but some unicellular (eg yeast)
  • cant photosynthesise
  • digest food extracellularly before absorbing nutrients
  • many are saprophytes(feed on dead/decaying matter)
  • some are parasitic - feed on living plants and animals (these are pathogenic)
  • often affect leaves of plants, stopping them photosynthesising and killing them.
  • when they reproduce they release millions of spores which can spread over crops, killing them.
  • below surface of fungo there’s are fine filaments called hyphae, which together form mycelium
  • fungal infections in animals involve mycelium growing under skin surface
  • either digests living cells or produces toxins
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18
Q

Which diseases are caused by bacteria?

A
  • tuberculosis (TB)
  • bacterial meningitis
  • ring rot
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19
Q

Which diseases are caused by viruses?

A
  • HIV/AIDS
  • Influenza
  • tobacco mosaic virus (TMV)
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20
Q

Which diseases are caused by fungi?

A
  • black sigatoka
  • ringworm
  • athletes foot
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21
Q

Which diseases are caused by protoctista?

A
  • potato/tomato late blight

- malaria

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22
Q

What is tuberculosis (TB)?

A
  • caused by bacteria: mycobacterium tuberculosis and M. bovis
  • affects animals (typically humans and cattle)
  • affects many parts of the body, killing cells and tissue
  • lungs most often affected
  • in ppl it’s both curable (antibiotics) and preventable (improving living standards and vaccination)
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23
Q

What’s bacterial meningitis?

A
  • caused by bacteria: neisseria meningitidis or streptococcus pneumonia
  • affects humans (very young children and teens 15-19)
  • infection of the meninges (membranes that surround spinal cord and brain)
  • membranes become swollen and may cause damage to brain and nerves
  • can spread to the rest of the body causing septicaemia (blood poisoning) and death
  • can be cured with antibiotics if delivered early, vaccines can protect against some forms of bacterial meningitis
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24
Q

What is ring rot?

A
  • caused by bacteria by clavibacter michiganesis (gram positive)
  • affects potatoes and tomatoes
  • ring of decay in the vascular tissue of a potato tuber or tomato accompanied by leaf wilting
  • damages leaves, tubers and fruit
  • once it affects a field it cannot be used to grow potatoes again for at least 2 years
  • no cure
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25
Q

What is HIV?

A
  • caused by human immunodeficiency virus, HIV
  • affects humans
  • attacks cells in immune system and compromises the immune response, making people more open to other infections
  • no cure rot vaccine, but anti-retroviral drugs slow process of disease
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26
Q

What is influenza?

A
  • a viral infection caused by orthomyxoviridae
  • attacks ciliates epithelium in gas exchange system
  • affects animals, including humans
  • causes respiratory problems, headaches and muscles
  • can be fatal because it kills ciliates epithelium, leaving animal more vulnerable to secondary infections
  • no cure, but vaccinations available
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27
Q

What is the tobacco mosaic virus (TBV)?

A
  • viral infection caused by tobacco mosaic virus
  • affects many different plants eg tobacco plants, tomatoes, pepper, cucumbers, petunia
  • damages leaves (mottling and discolouration), flowers and fruit, stunting growth + reducing yield
  • resistant crop strains available, but there is no cure
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28
Q

What is black Sigatoka?

A
  • caused by fungus Mycosphaerella fijiensis
  • affects banana plants
  • attacks and destroys leaves: hyphae penetrate and digest the cells, turning leaf black
  • can cause a 50% reduction in yield of plant
  • resistant strains being developed
  • good husbandry and fungicide treatment can control the spread
  • no cure
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29
Q

What is ringworm?

A
  • a fungal disease caused by trichophyton verrucosum
  • affects mammals including cattle
  • growth of fungus in skin with spores erupting through skin to cause grey-white rash
  • cure = anti fungal cream
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30
Q

What is athletes foot?

A
  • fungal disease caused by tibia pedia
  • affects humans
  • form of human ringworm, where fungus feeds on warm, moist skin between toes
  • cure = anti fungal creams
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31
Q

What is malaria?

A
  • caused by protoctista plasmodium
  • spread by bites of infected mosquitos (vector)
  • invades red blood cells, the liver, brain
  • causes headache and fever, which can lead to coma and death
  • no vaccine and limited cure
  • can be prevented by controlling vector (mosquitos) with nets, long sleeves, etc
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32
Q

What is potato/tomato late blight?

A
  • caused by protoctist oomycete phytophthora infestans
  • hyphae penetrates hosts cells, destroying leaves, tubers and fruit
  • no cure
  • resistant strains, careful management and chemical treatments can reduce infections
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33
Q

How can diseases be directly transmitted between animals?

A

DIRECT CONTACT:

  • kissing/ contact with bodily fluid eg in sex
  • direct skin-to-skin contact eg athletes foot,
  • microorganisms from faeces transmitted on hands eg diarrhoeal diseases

INOCULATION:

  • through break in the skin eg during sex
  • from animal bite eg rabies
  • through puncture wound/ sharing needles eg septicaemia

DROPLET INFECTION (INHALATION)

  • minute droplets are expelled from mouth when talking, coughing or sneezing
  • if droplets fall directly onto another organism, it is direct transmission
  • could be indirect if droplets are left in the air
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34
Q

How can diseases be indirectly transmitted between animals?

A

INGESTION:

  • taking in contaminated food/drink
  • transferring pathogens from mouth to hands
  • eg amoebic dysentery, diarrhoael diseases

FOMITES:

  • inanimate objects eg bedding, socks or cosmetics
  • eg athletes foot, gas gangrene, staphylococcus infections

VECTORS:

  • vectors transmit pathogens from one host to another
  • mostly animals, eg malaria in mosquitos, plague in rats, rabies in dogs, foxes, bats
  • water can be a vector eg diarrohoeal diseases
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35
Q

What are the factors affecting the transmition of communicable diseases in animals?

A

The probability of catching a communicable disease is increased by:

  • overcrowding
  • poor nutrition
  • compromised immune system eg immunosuppressant drugs, HIV
  • poor disposal of waste
  • climate change eg higher temp = more mosquitos = promotes spread of malaria
  • culture + infrastructure - traditional medicial practices can increase transmission in some countries
  • socioeconomic factors - lack of trained health workers and insufficient public warnings of outbreak can increase rates
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36
Q

How are diseases directly transmitted between plants?

A

Direct contact of a healthy plant with and any part of a diseased plant

Eg ring rot, TMV, black Sigatoka, late tomato blight

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37
Q

How are diseases transmitted indirectly between plants?

A

SOIL CONTAMINATION:

  • infected plants may leave bacteria and virus pathogens or reproductive spores from protoctista or fungi in soil
  • these can affect the next crop
  • some (mainly spores) can survive the composting process

VECTORS:

  • wind: bacteria, viruses and fungal/oomycete spores can be carried through wind
  • water: spores swim in the surface film of water on leaves, raindrop splashes carry pathogens and spores
  • animals: insects and birds carry pathogens and spores from one plant to another as they feed, and may inoculate pathogens directly into plant tissue
  • humans: pathogens + spores area transmitted through hands, clothing, fomites, farming practices and transport of crops around the world
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38
Q

What are the factors affecting the transmission of diseases in plants?

A
  • planting crops which are susceptible to disease
  • overcrowding increases likelihood of contact
  • poor mineral nutrition reduces resistance of plants
  • damp, warm conditions increase survival and spread of pathogens and spores
  • climate change: increased rainfall and wind promote spread of diseases, changing conditions allows animal vectors to spread to new places. (However, during conditions may reduce the spread of disease)
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39
Q

What are the physical barriers that plants use to defend themselves against pathogens?

A
  • waxy cuticle prevents pathogens coming into direct contact with epidermal cells
  • bark contains lignin. it becomes rigid and woody by deposition of lignin in cell walls. Bark prevents pathogens from coming into direct contact with pathogens
  • before a leaf falls off, fatty material is deposited, sealing off vascular bundles
  • cellulose cell walls are a structural barrier made up of cross-linked cellulose fibres
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40
Q

How do pathogens get through physical barriers in plants?

A
  • natural openings eg stomata
  • mechanical damage (eg wounds, damage when animals feed on plants)

These allow pathogens to enter the plant and infect it.

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41
Q

How do plants recognise an attack?

A
  • some molecules from the pathogen are recognised directly by the plant
  • alternatively, when pathogenic enzymes breakdown the cell wall, the breakdown products are recognised
  • signalling molecules alert the nucleus that the plant is under attack
  • polysaccharides (cal lose and lignin) are made tho strengthen the cell walls
  • defensive chemicals signal to the other cells that they are under attack
  • some defensive molecules directly attack pathogens
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42
Q

What are the mechanical responses to infection in plants?

A
  • guard cells close stomata

* callose is produced and deposited

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43
Q

What is callose?

A

A polysaccharide containing β-1,3 and β-1,6 glycosidic bonds between glucose monomers

Important in the pant response to infection

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44
Q

What does current research suggest the role of callose is in a plants response to infection?

A
  • its a rapid, unspecific response to invasion by a pathogen
  • callose is synthesised and deposited between the cell wall and cell membrane, as well as at the plasmodesmata to prevent the spread of pathogens to adjacent cells
  • large amounts of callose and lignin are deposited in the cell walls to thicken and strengthen the cell wall, increasing the effectiveness of the mechanical barrier
  • callose blocks sieve plates in phloem, sealing off infected cells and preventing spread of pathogens via the transport system
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45
Q

What is necrosis?

A

When injury activates intracellular enzymes in plants that kills cells near the suite fo infection.

This is to prevent pathogens from spreading

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46
Q

What are some examples of chemical defences against pathogens in plants?

A

INSECT REPELLENTS
•citronella (lemongrass)
• pine resin (pine trees)

INSECTICIDES
• pyrethrin (chrysanthemums)
• caffeine, mint, cinnamon
• ricin (caster oil beans)
• cyanide (even lethal to humans)
ANTI-FUNGAL
• gossypol
• phenols
• saponins
• chitinases
ANTIBACTERIAL
• phenols 
• gossypol
• defensins
• lysozymes

ANTI-OOMYCETES
• glucanases

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47
Q

What are terpenoids?§

A
  • range of essential oils that have antibacterial and anti-fungal properties
  • may also create a scent
  • eg menthols from mint
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48
Q

What are phenols?

A
  • have antibacterial and antifungal properties
  • tannins found in bark inhibit attack by insects (bind to salivary proteins and digestive enzymes like trypsin and chymotrypsin, deactivating enzymes)
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49
Q

What are alkaloids?

A
  • nitrogen-containing compounds
  • give bitter taste to inhibit insects from feeding
  • act on metabolic reactions by either inhibiting or activating enzyme action.
  • some inhibit protein synthesis
  • eg caffeine, nicotine, cocaine, morphine, solanine
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50
Q

What are defensins?

A
  • small cysteine-rich proteins that have broad anti-microbial activity
  • act on small molecules in the plasma membrane of pathogens, inhibiting the action of ion transport channels
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51
Q

What are hydrolytic enzymes?

A

Found in spaces between cells

Include :
•chitinases (breaks down chitin I’m fungal cell walls)
• glucanases (hydrolyse glycosidic bonds in glucans)
•lysozymes (degrade bacterial cell walls)

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52
Q

What physical barriers prevent infection?

A
  • skin is a tough keratin layer which prevents pathogens entering. produces sebum, an oily substance that inhibits pathogen growth
  • blood clotting prevents pathogens from entering the skin through lesions
  • hydrochloric acid in stomach kills bacteria.
  • mucous membranes trap pathogens and may secrete anti microbial enzymes
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53
Q

What are expulsive reflexes?

A

When body attempts to force foreign substances out.
• irritation of mucous membranes in nostrils causes sneezing
• irritation of ciliated epithelium in respiratory tract causes coughing
• vomiting and diarrhoea expel contents of cut as well as infective pathogens

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54
Q

How do blood clots form?

A

When platelets come into contact with the collagen in skin or the wall of a da,aged blood vessel, they stick to it and start to secrete several substances.

The blood clot prevents pathogens from entering the wound.

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55
Q

What is thromboplastin?

A

Secreted by platelets when there is a wound.

Enzyme which triggers a cascade of reactions, resulting in a blood clot forming (thrombus)

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56
Q

What is serotonin?

A

Secreted by platelets when there is a wound.

Makes the smooth muscle in the walls of the blood vessel contact, so they narrow and reduce the blood supply to the area of damage

57
Q

Describe the blood clotting cascade

A

1) Injured tissues and platelets release thromboplastin and Ca2+ ions.
2) The thromboplastin catalyses the reaction of prothrombin and Ca2+to make thrombin
3) Thrombin catalyses fibrinogen to form fibrin
4) Fibrin forms from a mesh over the wound, trapping red blood cells and platelets. A blood clot is formed.

58
Q

What happens after a blood clot has been formed?

A

Bleeding stops.

The clot dries out, forming a hard, tough scab that keeps pathogens out

New epidermal cells grow via mitosis to repair the wound site + blood vessels regrow

Collagen fibres are deposited to give the new tissue strength

The clot hardens and becomes smaller

The enzyme plasmin is released to dissolve the clot

59
Q

Name 4 ways the non-specific immune system responds to infection

A
  • inflammation
  • phagocytosis
  • digestive action of lysozymes
  • fever
60
Q

What is inflammation?

A

Biological response of vascular tissues to pathogens, damaged cells or irritants.

Characterised by pain, heat, redness and swelling of tissue

61
Q

What are mast cells?

A
  • produced by the bone marrow and are transported via blood vessels.
  • they release mediators (histamine and cytokines) which cause inflammation, helping your body heal from an injury or infection
62
Q

What are histamines?

A

Mediator released by mast cells.

Has 2 main functions:

1) makes blood vessels dilate, causing localised heat and redness. The raised temperature helps prevent pathogens from reproducing
2) makes the blood vessel more leaky so blood plasma is forced out (once forced out, it is known as tissue fluid). Tissue fluid causes swelling (oedema) and pain

63
Q

What are cytokines?

A

Mediator released by mast cells

They attract white blood cells (phagocytes) to the site.

Phagocytes dispose of pathogens by phagocytosis

64
Q

Outline the process of inflammation.

A

1) damaged blood vessels cause mast cells o release histamines and cytokines
2) histamines cause vasodilation, which causes heat and redness.
3) histamines also make blood vessels more leaky
4) cytokines attract white blood cells (phagocytes) to the damaged site.
5) white blood cells and blood plasma move from the blood vessel into the infected tissue.
6) blood plasma causes swelling, and phagocytes dispose of pathogens by phagocytosis.

65
Q

What are phagocytes?

A

Specialised white blood cells which engulf and destroy pathogens

There are two types - neutrophils and macrophages

66
Q

What are neutrophils?

A
  • the most abundant type of phagocyte
  • has lobed nuclei to allow for it to change shape more readily
  • manufactured in the bone marrow
  • can move around in the blood and are able to ‘crawl’ out of capillaries into tissue fluid
  • can be found in high concentrations along epithelial layers (eg in lungs)
  • short lived
  • released in very large numbers as a response to infection (forms pus)
67
Q

What are macrophages?

A
  • phagocytes that are fixed in place
  • undergo phagocytosis
  • form part of both the non-specific and specific response to infection
  • can become antigen-presenting cells
68
Q

What is phagocytosis?

A

The process by which phagocytes recognise non-self cells, engulf them and digest them.

69
Q

Outline the process of phagocytosis

A

1) phagocytes are attracted to the site of infection by cytokines or chemicals released from pathogen
2) phagocyte recognises pathogen as non-self due to non-human proteins on pathogen membrane. Phagocytes binds to pathogen
3) phagocyte engulfs the pathogen via endocytosis to form a phagosome. A lysosome movies towards the phagosome and binds to it, forming a phagolysosome
4) lysozymes are released into the phagolysosome, breaking down the pathogen.

70
Q

What are MHCs?

A

Major histocompatability complex

When a macrophage has digested a pathogen, it combines antigens from the pathogens surface membrane with glycoproteins in the cytoplasm (MHCs)

The MHC complexmoves the pathogen antigens to the macrophages cell surface membrane.

The macrophage becomes an antigen presenting cell

71
Q

What is an APC?

A

Antigen-presenting cell

A cell that displays foreign antigens complexed with MHCs on their surfaces.

72
Q

What are opsonins?

A

Chemicals which bind to pathogens and tag them, so they are recognised more easily recognised by phagocytes

Eg antibodies

73
Q

What are fevers?

A

A non-specific defence against pathogens

When a pathogen invades, cytokines stimulate the hypothalamus to increase the body temperature. This is helpful because:
• most pathogens reproduce at or below 37ºC. Higher temperatures inhibit pathogen reproduction
• the specific immune system works faster at higher temperatures

74
Q

What is the specific immune system?

A

Aka adaptive response, active/acquired immunity

Is pathogen specific and diverse

Is slow the first time, but very quick if the same pathogen invades again.

75
Q

What are lymphocytes?

A

White blood cells that make up the specific immune response.

2 main types:
• T lymphocytes - mature in thymus gland
• B lymphocytes - mature in bone marrow

76
Q

What are the main types of T lymphocytes?

A
  • T helper
  • T killer cells
  • T memory cells
  • T regulator cells
77
Q

What are T helper cells?

A
  • have CD4 receptors on their cell-surface membranes, which bind to surface antigens on APCs
  • produce interleukins, a type of cytokines (cell signalling molecule)
  • interleukins made by T helper cells stimulate activity of B cells
78
Q

What are T killer cells?

A
  • destroy the pathogen carrying the antigen
  • they produce a chemical called performing, which kills pathogen by making holes in the pathogen’s cell membrane, making it freely permeable
79
Q

What are T memory cells?

A
  • produced from the primary immune response
  • live for a long time and are part of the immunological memory
  • if they meet an antigen for a second time, they divide rapidly to form a large number of T killer cells that destroy the pathogen
80
Q

What are T regulator cells?

A
  • suppress the immune system, acting to control and regulate it.
  • they stop the immune response after a pathogen has been eliminated, and make sure the body recognises self antigens and doesn’t set up an autoimmune response
  • interleukins are important in this role
81
Q

What are main types of B lymphocyte?

A
  • plasma cells
  • B-effector cells
  • B-memory cells
82
Q

What are plasma cells?

A
  • type of B lymphocyte
  • produce antibodies to a particular antigen and release them into circulation
  • an active plasma cell only lives for a few days but produces around 2000 antibodies a second while alone and active
83
Q

What are B-effector cells?

A

• divide to form plasma cell clones

84
Q

What are B memory cells?

A
  • live for a very long time and provide the immunological memory
  • they are programmed to remember a specific antigen and enable there body to make a very rapid response when a pathogen carrying that antigen is encountered again
85
Q

What is clonal selection?

A

There are around 100 million different types of lymphocytes, each with an antigen receptor complimentary to a specific type of antigen

However, there are only around 100 of each type.

Clonal selection is the process of identifying an antibody-producing cell with the complementary receptors to the shape of a specific antigen

86
Q

What is clonal expansion?

A

The mass proliferation of specific antibody-producing cells by clonal selection

87
Q

What is the cell mediated response?

A

Aka cell mediated immunity

Where T lymphocytes respond to cells of an organism that have been hanged in some way, eg
• by a virus infection
• by antigen processing/mutation (eg cancer cells)
• cells from transplanted tissue

The cell mediated response is particularly important against viruses and early cancers

88
Q

Outline the process of the cell mediated response

A

1) in the non-specific defence system, macrophages/dendritic cells engulf and digest pathogens in phagocytosis. They process the antigens from the surface of the pathogen to form APCs
2) T cells with complimentary antigen-receptors to the antigen bind to the MHC-antigen complexes. This activates the T cell (clonal selection) and it produces interleukins

3) The interleukins stimulate the T cells to divide via mitosis (clonal expansion). These cells will then differentiate into:
• T memory cells which will give a rapid response if a pathogen with that antigen is encountered again
• T helper cells, which will secrete cytokines to attract phagocytes and produce interleukins that stimulate B cells to divide
• T killer cells, which secrete perforin to destroy infected cells

89
Q

What is the humoral response?

A

Aka humoral immunity

Responds to antigens found outside of cells, eg:
• bacteria
• fungi
• APCs

The humoral immune system produces antibodies that are soluble in the blood and tissue fluid and are not attached to cells

90
Q

What are the 3 main functions of B lymphocytes?

A
  • as antigen presenting cells for T lymphocytes to attach to
  • to react to interleukins
  • to produce antibodies as part of the humoral immune response
91
Q

How does a B lymphocyte become an APC?

A

A B-lymphocyte with antigen-receptors complimentary in shape to an antigen binds to the antigen on a pathogen and destroys it

The B lymphocyte brings the antigen into the cell via endocytosis for processing

An MHC combines with the antigen to form an antigen-MHC complex, which moves to the B-cells cell surface membrane to be presented.

The B-lymphocyte is now an antigen-presenting cell.

92
Q

Outline the process of the humoral response

A

1) Antibodies on a B cell attach to complimentary antigens on a pathogen and destroy it
2) The B cell takes in the antigens via endocytosis, processes and presents them. The B cell is now an APC.
3) T helper cells attach to the antigen-MHC complex and release interleukins which activate the B cell. This is clonal selection
4) The activated B cell divides by mitosis - this is called clonal expansion
5) The clones then differentiate to form plasma cells or B memory cells
6) plasma cells secrete lots of antibodies to fight the antigens. this is the primary immune response
7) B memory cells divide rapidly if the body is infected with the same pathogen again. this is the secondary immune response.

93
Q

What is the primary immune response?

A

The response of the immune system to a pathogen when it is first encountered.

A small number of antibodies are produced slowly.

94
Q

What is the secondary immune response?

A
The response of the immune system to a pathogen when it is encountered for a second (third, fourth...etc.) time. 
Immunological memory (T memory and B memory cells) gives a rapid production of a large number of antibodies.
95
Q

What is an antigen?

A

A chemical present on the surface of a cell that induces an immune response

96
Q

What is an antibody?

A

​Y-shaped glycoproteins called immunoglobulins produced by B-lymphocytes in response to the presence of a specific antigen

They bind to to a specific antibody or toxin that has triggered an immune response.

There are millions of different antibodies, and there is a specific antibody for each antigen

97
Q

What is the general structure of an antibody?

A
  • have 2 long identical polypeptide chains called the heavy chains
  • have 2 much shorter chains called the light chains
  • disulphide bridges hold chains together
  • the bottom of the branches of the Y shape is called the hinge region, which allows for some flexibility
  • the top of each branch is known as the antigen-binding site. there are 2 of them so each antibody can hold 2 antigens
  • there is a constant region, which is the same in each antibody
  • there is a variable region, which is different on different antibodies
98
Q

What is an antigen-antibody complex?

A

The complex formed when an antibody binds to an antigen

99
Q

How do antibodies work?

A
  • neutralisation
  • agglutination
  • opsonins
  • lysis
100
Q

What is neutralisation?

A
  • the antibody attaches to an antigen to form an antigen-antibody complex.
  • this prevents the antigen from binding to host cells

• antibodies can also act as anti-toxins, binding to the toxins produced by pathogens and neutralising them (making them harmless)

101
Q

What is agglutination?

A
  • antibodies act as agglutinins, causing pathogens carrying antigen-antibody complexes to clump together.
  • this helps prevent them spreading through the body and males it easier for phagocytes to engulf a number of pathogens at once.
102
Q

What is opsonisation?

A
  • antigen-antibody complexes can act as opsonins

* the complex is easily identified by phagocytes to engulf and dispose of

103
Q

What is lysis?

A
  • antibodies bind to antigens, activating proteins in the blood plasma which then digest bacterial/fungal walls
  • water then enters the pathogen, making it swell up and burst
  • this will kill the pathogen
104
Q

What is immunity?

A

The ability of an organism to resist a particular infection or toxin by the action of specific antibodies or sensitized white blood cells.

105
Q

What is active immunity?

A
  • resistance in an organism that has developed through the production of specific antibodies in response to a pathogen.
  • it provides long-lasting immunity as memory cells are produced.
106
Q

What is passive immunity?

A
  • resistance in an organism acquired via the transfer of antibodies.
  • it provides short-term immunity as no memory cells are produced.
107
Q

What is natural active immunity?

A

Immunity which results from the response of the body to the invasion of a pathogen

Eg when your body produces T memory and B memory cells which recognise pathogens if they invade the body a second time

108
Q

What is natural passive immunity?

A

The immunity given to an infant mammal by the mother through the placenta and colostrum (first milk a mammalian mother makes, which is very high in antibodies)

109
Q

What is artificial active immunity?

A

The production of antibodies by the immune system following the exposure to a weakened, attenuated or dead pathogen, e.g: by vaccination

110
Q

What are autoimmune diseases?

A

A condition or illness resulting from an autoimmune response

111
Q

What is an autoimmune response?

A

Response when the immune system acts against its own cells and destroys healthy tissue in the body

112
Q

What causes autoimmune diseases?

A

scientists aren’t fully aware, however:

  • appears to be a genetic tendency in some families
  • sometimes the immune sisters reacts abnormally to a mild pathogen/normal body microorganisms
  • T regulator cells may bit work effectively
113
Q

How can autoimmune diseases be treated?

A

Immunosuppressant drugs which prevent the immune system working

However, they deprive the body of its natural defences against communicable diseases

114
Q

What is type 1 diabetes?

A

Autoimmune disease

Body part affected = insulin-secreting cells of the pancreas

TREATMENT:
• insulin injections
• pancreas transplants
• immunosuppressant drugs

115
Q

What is rheumatoid arthritis?

A

Autoimmune diseases

Body parts effected = joints (esp hands, wrists, ankles, feet

TREATMENT:
• no cure
• anti-inflammatory drugs
• steroids
• pain relief
• immunosuppressants
116
Q

What is lupus?

A

Autoimmune disease

BODY PARTS AFFECTED:
• often affects skin and joints, and causes fatigue
• can attack any organ in body including kidneys, liver, lungs or brain

TREATMENT:
• no cure
• anti-inflammatory drugs
• steroids
• immunosuppressants 
• various others
117
Q

What is a vaccine?

A

A safe form of an antigen, which is injected into the bloodstream to provide artificial active immunity against a pathogen bearing the antigen

118
Q

How can antigens be made safe for a vaccine?

A

Pathogens can be:
• killed/inactivated bacteria and viruses
• attenuated (weakened) strains of love bacteria or viruses
• toxin molecules can be altered and detoxifies
• isolated antigens can be extracted from the pathogen
• genetically engineered antigens can be produced

119
Q

How to vaccinations work?

A

1) vaccine containing safe antigens is administered
2) the primary immune response is triggered by the foreign antigen. B cells recognise the antigen and reproduce. Antibodies are produced which destroy the pathogen and memory cells are produced which remain in the bloodstream
3) if the body comes into contact with the live pathogen, the secondary immune response is triggered and you destroy the pathogen rapidly before you suffer any symptoms.

120
Q

What are booster vaccines?

A

Vaccinations that may be given several years after the first vaccine has been given to ensure the body is still making memory cells

121
Q

What is an epidemic?

A

When a communicable disease spreads rapidly to a lot of people at a local or national level

122
Q

What is a pandemic?

A

When a communicable disease spreads rapidly to lots of people across a number of countries

123
Q

How can vaccinations be used to prevent epidemics?

A

At the beginning of an epidemic, mass vaccination can prevent the spread of the pathogen to the wider population

When vaccines are being deployed to prevent epidemics, they often have to be changed regularly to remain effective

124
Q

What is herd immunity?

A

When you vaccinate most people in a population, so there is minimal opportunity for an outbreak to occur.

This is important for people whop cannot have the vaccine eg those on immunosuppressants

125
Q

Why can can it be difficult to create vaccines for some diseases?

A

Antigenic variation

Vaccines work on the principle that antigens of a pathogen remain the same.

However, some pathogens can mutate and their antigens may change - this is called ANTIGENIC VARIATION

Therefore, your body would have to carry out the primary response for the new antigens, which takes time and you fall ill again.

This means it can be difficult for vaccines to be developed which stop the spread of some pathogens

HIV, influenza virus and S.pneumonia bacteria all show antigenic variation

126
Q

What are some drugs sourced form living organisms?

A

PENICILLIN
• source: commercial extraction, originally from mould growing on melons
• action: antibiotic

DOCETAXEL/PACLITAXEL
• source: originally derived form yew trees
• action: treatment of breast cancer

ASPIRIN
• source: based on compounds from sallow (willow) bark
• action: painkiller, anti-coagulant, anti-pyretic, anti-inflammatory

PRIALT
• source: derived from venom of a cone snail from oceans around australia
• action: pain killing drug 1000x more effective than morphine

VANCOMYCIN
• source: soil fungus
• action: very powerful antibiotic

DIGOXIN
• source: based on digitoxin originally extracted from foxgloves
• action: powerful heart drug used to treat atrial fibrillation and heart failure

127
Q

Why is it important for us to maintain biodiversity?

A

We derive a lot of our medicine from living organisms

Scientists have only explored a fraction of all life on earth

It is important that we maintain biodiversity so that we do not destroy an organism which could give us the key to a life-saving drug

128
Q

What is personalised medicine?

A

A form of medical care that enables doctors to provide healthcare that is customised to an individual’s genotype

The human genome can be analysed relatively rapidly and cheaply, giving a growing understanding of the genetic basis of many diseases

The science of interweaving knowledge of drug actions with personal genetic material is known as pharmacogenomics

129
Q

What is synthetic biology?

A

The design and construction of new biological entities, as well as the reconstruction of pre-existing natural biological systems

Is used to produce drugs what would otherwise be too rare, expensive or not available.

Eg DNA of bacteria can be modified so that it produces a specific chemical that would otherwise need to be extracted from a rare animal/plant

130
Q

What is selective toxicity?

A

The ability to interfere with the metabolism of a pathogen without affecting them cells of the host

131
Q

What are antibiotics?

A

A chemical or compound that kills or inhibits the growth of bacteria

They have been used widely since the discover of penicillin in the 20th century

However, due to the overuse of antibiotics, bacteria is becoming resistant ant antibiotics are becoming less effective

132
Q

How do antibiotics work?

A

Selective toxicity

They may:
• attack wall/coating surrounding bacteria
• interfere with bacteria reproduction
• block protein production in bacteria

133
Q

What are antibiotic-resistant bacteria?

A

Bacteria that undergo mutation yo become resistant to an antibiotic and then survive to increase in number

134
Q

How does antibiotic resistance in bacteria occur?

A
  • random mutations during bacterial reproduction can produce a bacterium that is not affected by the antibiotic
  • the bacterium survives and reproduces, passing on its antibiotic resistance to its offspring
  • as the resistant bacteria’s competition is killed off by antibiotics, the resistant bacteria population quickly increases
  • a large population of the antibiotic-resistant bacteria now exist in the body
135
Q

What is the effect of antibiotics on commensal (helpful) bacteria?

A
  • antibiotics may kill other bacterial populations in the body
  • this can upset the natural balance if bacterial populations within the body
  • with the reduced competition, some bacterial species can flourish and cause problems
136
Q

What is MRSA?

A
  • Methicillin resistant Staphylococcus aureus (antibiotic-resistant bacteria)
  • carried by up to 30% of the population on their skin/nose
  • in the body it can cause boils, abscesses and potentially fatal septicaemia
  • was treated effectively with methicillin, but mutation has produced methicillin-resistnat strains
137
Q

What is C.difficile?

A
  • Clostridium difficile (antibiotic-resistant bacteria)
  • bacterium in the guts of about 5% of teh population
  • produces toxins that damage the lining of intestines, leading to diarrhoea, bleeding and even death
  • not a problem for healthy people, but when antibiotics are used, commensal bacteria in gut dies and C.difficile survives. It can then reproduce and takes hold rapidly
138
Q

What measures can be take to reduce antibiotic-resistant infections?

A
  • minimising the use of antibiotics
  • ensuring every course of antibiotics is completed to reduce the risk of resistant individuals surviving and developing into a resistant strain population
  • good hygiene in hospitals, care homes and in general - has a major impact on the spread of all diseases, including antibiotic-resistant strains