4.1.1 communicable diseases, disease prevention and the immune system Flashcards

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1
Q

what is a communicable disease?

A

disease that can be passed from one organism to another, of same or different species

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2
Q

what is a pathogen?

A

a disease causing microorganisms

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3
Q

how are bacteria classified?

A
  • by basic shape - rod shaped, spherical, comma shaped, spiralled, corkscrew
  • by cell wall - Gram positive and Gram negative
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4
Q

what colour do Gram positive bacteria look under a light microscope after Gram staining?

A

purple-blue

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5
Q

what colour do Gram negative bacteria look under a light microscope after Gram staining?

A

red

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6
Q

what are viruses?

A

non-living infectious agents

viruses invade living cells, the genetic material takes over the host cell

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7
Q

what are types of pathogens?

A

bacteria
viruses
protoctista
fungi

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8
Q

what are parasites?

A

an organism that lives in or on another organism (host)

and gains nutrients from host at hosts expense

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9
Q

what are the modes of action of pathogens?

A
  • damaging host tissues directly

- producing toxins which damage host tissues

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10
Q

how do pathogens damage host tissues directly?

A
  • viruses take over cell metabolism - viral genetic material is inserted into host DNA, the virus uses host cell to make new viruses which burst out of cell then spread to infect other cells
  • protoctista digest and use the cell contents as they reproduce
  • fungi digest living cells and destroy them
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11
Q

how do pathogens damage host tissues with toxins?

A
  • bacteria produce toxins damage host cells by breaking down cell membranes, inactivate/damage enzymes, interfere with host genetic material
  • some fungi produce toxins which affect host cells
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12
Q

what are bacteriophages?

A

viruses that attack bacteria

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13
Q

what plant disease is caused by bacteria?

A

ring rot

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14
Q

what are the characteristics of ring rot?

A

damages leaves, tubers and fruit

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15
Q

what plant disease is caused by virus?

A

tobacco mosaic virus

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16
Q

what are the characteristics of tobacco mosaic virus?

A

damages leaves, flowers and fruit, stunting growth and reducing yields

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17
Q

what plant disease is caused by protoctist?

A

potato blight

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18
Q

what is black sigatoka?

what are the characteristics of black sigatoka?

A

a banana disease caused by fungus Mycosphaerella fijiensis, which attacks and destroys the leaves
the hyphae penetrate and digest cells, turning leaves black

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19
Q

what plant disease is caused by protoctist?

A

potato blight/ tomato blight/ late blight

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20
Q

what is potato blight?

what are the characteristics of potato blight?

A
  • caused by protoctist oomycte Phytophthora infestans

- hyphae penetrate host cells, destroying leaves, tubers and fruit

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21
Q

what animal diseases are caused by bacteria?

A
  • tuberculosis

- bacterial meningitis

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22
Q

what are the characteristics of tuberculosis?

A

damages and destroys lung tissue and suppresses the immune system

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23
Q

what are the characteristics of bacterial meningitis?

A

bacterial infection of the meninges of the brain which can spread to the rest of the body causing septicaemia and rapid death

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24
Q

what animal diseases are caused by viruses?

A
  • HIV (human immunodeficiency virus)

- influenza

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25
Q

what are the characteristics of HIV?

A

targets T helper cells in the immune system

destroys the immune system so affected people are open to other infections

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26
Q

what are the characteristics of influenza?

A

viral infection of ciliated epithelial cells

kills cells, leaving airways open to secondary infection

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27
Q

what animal disease is caused by protoctista?

A

malaria

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28
Q

what are the characteristics of malaria?

A

caused by protoctista Plasmodium and spread by mosquitoes

the Plasmodium invades the red blood cells, liver and the brain

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29
Q

what animal diseases are caused by fungi?

A
  • ring worm

- athlete’s foot

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30
Q

what are the characteristics of ring worm?

A

fungal disease affecting mammals

causes grey-white, crusty, infectious, circular areas of skin

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31
Q

what are the characteristics of athlete’s foot?

A

a human fungal disease caused by Tinia pedia
a form of human ring worm
digests skin on feet, causing cracking and scaling

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32
Q

what are some methods of direct transmission of pathogens between animals?

A
  • direct contact - skin-to-skin, exchange if bodily fluids
  • inoculation - break in skin, animal bite, puncture wound/ sharing needles
  • ingestion - eating contaminated food/drink
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33
Q

what are some methods of indirect transmission of pathogens between animals?

A
  • fomites - inanimate objects can transfer pathogens
  • droplet infection
  • vectors - mosquitoes, fleas, water
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34
Q

factors affecting the transmission of communicable diseases in animals (7)

A
  • overcrowding living and working conditions
  • poor nutrition
  • compromised immune system
  • poor disposal of waste
  • climate change - new vectors/diseases
  • culture and infrastructure - traditional medical practises
  • socioeconomic factors - lack of health professionals
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35
Q

what are some methods of direct transmission of pathogens between plants?

A

direct contact of a healthy plant with a diseased plant

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36
Q

what are some methods of indirect transmission of pathogens between plants?

A
  • soil contamination - infected plants leave pathogens or reproductive spores
  • vectors - wind, water, animals, humans
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37
Q

factors affecting the transmission of communicable diseases in plants (5)

A
  • planting varieties of crops that are susceptible to disease
  • over-crowding
  • poor mineral nutrition - reduces resistance
  • damp, warm conditions increase the survival and spread of pathogens and spores
  • climate change - increased rainfall/wind, changing conditions allow animal vectors
38
Q

physical defences in plants

A
  • cellulose cell wall
  • waxy cuticle
  • stomatal closure
  • callose (polysaccharide)
  • tylose formation
  • necrosis
  • canker
39
Q

effect of callose

A
  • deposited between cell walls and cell membrane in cells next to infected cells
  • lignin added to callose to make barrier stronger
  • callose blocks sieve plates - sealing off infected part of plant
  • callose deposited in the plasmodesmata
40
Q

effect of tylose formation

A
  • swelling that fills xylem vessel
  • prevents spread of pathogens
  • tylose contains chemicals toxic to pathogens
41
Q

what is necrosis?

A
  • deliberate cell suicide of infected cells

- intracellular enzymes are activated by the injury

42
Q

what is a canker?

A

a sunken necrotic lesion on the woody tissue - causes death of cambium tissue

43
Q

chemical defences in plants

A
  • insect repellents and insecticides
  • defensins (defensive proteins) - cysteine rich proteins with antimicrobial action
  • alkaloids - nitrogen containing compounds - bitter tasting, inhibit enzyme action, inhibit protein synthesis
  • phenols - antibacterial/antifungal compounds, tannins -bitter taste, bind to digestive enzymes and inactivate them
  • hydrolytic enzymes - chitinases (breaks down chitin), lysozymes (breaks down bacterial cell walls), glucanase (breaks down glycosidic bonds in glucose - anti-oomycete)
  • terpenoids - essential oils with antibacterial/antifungal properties
44
Q

primary non-specific defences in animals

A
  • skin - barrier preventing entry of pathogens, produces sebum (antibacterial fatty acids) that inhibits growth of pathogens
  • mucous membranes - mucus traps pathogens
  • expulsive reflexes - cough, sneeze, vomit
  • lysozymes in tears and urine
  • hydrochloric acid in stomach
  • blood clotting/wound repair
  • inflammatory response
45
Q

what is the inflammatory response?

A
  • a localised response to pathogens
  • mast cells are activated in damaged tissue and release histamines and cytokines
  • histamines cause vasodilation - causing localised heat and redness
  • histamines cause blood vessels to become more leaky - blood plasma is forced out causing swelling
  • cytokines attract phagocytes to the site
46
Q

how do blood clots form?

A
  • when platelets come into contact with collagen in skin/blood vessel wall, they adhere and secrete substances
  • thromboplastin - triggers a cascade of reaction, resulting in the formation of a blood clot
  • serotonin - vasoconstriction - reduce blood supply to area
  • clot dries forming scab
  • epidermal cells below scab grow
  • collagen fibres are deposited to strengthen tissue
47
Q

secondary non-specific defences in animals

A
  • fevers

- phagocytosis

48
Q

how does fever defend against pathogens

A
  • when a pathogen invades the body, cytokines stimulate hypothalamus to increase temperature
  • high temperatures inhibit pathogen reproduction
  • specific immune system works better at higher temperatures
49
Q

what is phagocytosis?

A

the process by which phagocytes recognise non-self cells and digest them

50
Q

what are the stages of phagocytosis?

A

NEUTROPHILS AND MACROPHAGES
- pathogens produce chemicals that attract phagocytes
- phagocytes recognise non-self proteins on the pathogen and binds to the pathogen
- phagocyte engulfs the pathogen and encloses it in a vesicle called a phagosome
- the phagosome combines with a lysosome to form a phagolysosome
- enzymes from the lysosome digest and destroy the pathogen
ONLY MACROPHAGES
- combines antigens from the pathogen surface membrane with glycoproteins in cytoplasm called major histocompatibility complex (MHC)
- MHC complex moves pathogen antigens to the macrophage’s own surface membrane, becoming an antigen-presenting cell

51
Q

what do cytokines do?

A
  • produced by phagocytes that have engulfed a pathogen
  • act as cell-signalling molecules, stimulating other phagocytes to move move to the site of infection
  • increase body temperature
  • stimulate specific immune system
52
Q

what do opsonins do?

A
  • bind to pathogens so they are more easily recognised by phagocytes
  • phagocytes have receptors on their cell membranes that bind to opsonins and the phagocyte then engulfs the pathogen
53
Q

what are antibodies?

A

Y-shaped glycoproteins which bind to a specific antigen on a pathogen that has triggered an immune response

54
Q

what is the structure on antibodies?

A
  • two identical long polypeptide chains - heavy chains
  • two shorter identical polypeptide chains - light chains
  • chains held together by disulfide bridges
  • hinge region - provides the antibody with flexibility, allowing it to bind to two antigens
  • constant region - same in all antibodies
  • variable region - the binding site which is different on different antibodies, specific to the antigen
55
Q

what is formed when an antibody binds to an antigen?

A

antigen-antibody complex

56
Q

how do antibodies work? (4)

A
  • antibody of antigen-antibody complex acts as a opsonin - so complex is engulfed by phagocytes
  • pathogen unable to invade cells when part of antigen-antibody complex
  • antibodies act as agglutinins causing pathogens with antigen-antibody complexes to clump together
  • antibodies can act as anti-toxins, binding to toxin produced by pathogens and making them ineffective
57
Q

what are T lymphocytes?

A

lymphocytes that mature in the thymus gland

58
Q

what are the types of T lymphocytes?

A
  • T helper cells
  • T killer cells
  • T memory cells
  • T regulator cells
59
Q

what are B lymphocytes?

A

lymphocytes that mature in the bone marrow

60
Q

what are the types of B lymphocytes?

A
  • plasma cells
  • B effector cells
  • B memory cells
61
Q

what do T helper cells do?

A
  • have CD4 receptors on their cell-surface membranes on cell surface membrane which bind to antigens on APCs
  • produce interleukins which stimulate the activity of B cells to increase antibody production, stimulates production of T cells and stimulates phagocytosis
62
Q

what are interleukins?

A

a type of cytokine

63
Q

what do T killer cells do?

A
  • destroy pathogen carrying the antigen

- produce a chemical called perforin - perforin kills pathogen by making holes in the cell membrane

64
Q

what do T memory cells do?

A
  • part of immunological memory
  • live for a long time
  • if they meet an antigen a second time they divide rapidly to form a large number of clones of T killer cells
65
Q

what do T regulator cells do?

A
  • suppress the immune system to control and regulate it

- stop the immune response once a pathogen has been eliminated to prevent an autoimmune response

66
Q

what do plasma cells do?

A
  • produce antibodies to a particular antigen and release them into circulation
67
Q

what do B effector cells do?

A
  • divide to form plasma cell clones
68
Q

what do B memory cells do?

A
  • part of immunological memory
  • live for a long time
  • immunological memory of antibody needed against specific antigen
69
Q

what is cell-mediated immunity?

A

T lymphocytes respond to cells of an organism that have been changed in some way

70
Q

what is humoral immunity?

A

body responds to antigens found outside the cells

71
Q

what is the process of cell mediated immunity?

A

1 - macrophages engulf and digest pathogens by phagocytosis and process the antigens to become antigen presenting cells
2 - receptors on some T helper cells fit the antigens
3 - the T helper cells become activated and produce interleukins, which stimulate more T cells to divide by mitosis
4 - the cloned T cells:
- develop into T memory cells
- produce interleukins that stimulate phagocytosis
- produce interleukins that stimulate B cells to divide
- stimulate development of a clone of T killer cells that are specific for the presented antigen

72
Q

what is the process of humoral immunity?

A

1 - a B cell with the complementary antibodies will bind to the antigen on the pathogen
2 - the B cell engulfs and processes the antigen to become an APC
3 - activated T helper cells bind to B cell APC (clonal selection)
4 - interleukins produced by the activated T helper cells activate the B cells
5 - the activated B cell divides by mitosis to give clones of plasma cells and B memory cells (clonal expansion)
6 - cloned plasma cells produce antibodies that fit the antigens on the surface of the pathogen, bind to them or act as opsonins or agglutinins
7 - some cloned B cells develop into B memory cells

73
Q

what is the primary immune response?

A

the relatively slow production of a small number of the correct antibodies the first time a pathogen is encountered

74
Q

what is the secondary immune response?

A

the relatively fast production of very large quantities of the correct antibodies the second time a pathogen is encountered as a result of immunological memory

75
Q

what is an autoimmune disease?

A

a condition or illness resulting from an autoimmune response

76
Q

what is an autoimmune response?

A

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

77
Q

what is natural active immunity?

A

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

78
Q

what is natural passive immunity?

A

immunity given to an infant mammal by the mother through the placenta and the colostrum

79
Q

what is artificial active immunity?

A

immunity which results from exposure to a safe form of a pathogen by vaccination

80
Q

what is artificial passive immunity?

A

immunity which results from the administration of antibodies from another animal against a dangerous pathogen

81
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

82
Q

what are the steps of vaccination?

A

1 - the pathogen is made safe so that the antigens are intact but there is no risk of infection
2 - small amounts of the safe antigen are injected into the blood
3 - the primary immune response is triggered by the foreign antigens and the body produces antibodies and memory cells
4 - if the live pathogen is encountered, the secondary immune response is triggered and the pathogen is destroyed

83
Q

what can vaccines contain?

A
  • killed or inactivated bacteria and viruses
  • attenuated strains of live bacteria or viruses
  • toxin molecules that have been altered or detoxified
  • isolated antigens extracted from pathogen
  • genetically engineered antigens
84
Q

what is a pandemic?

A

when a communicable disease spreads rapidly across a number of countries and continents

85
Q

what is an epidemic?

A

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

86
Q

what is Penicillin?

A
  • first widely used, effective and safe antibiotic

- from the mould Penicillium chrysogenum

87
Q

what are the sources of medicines?

A
  • nature - bioactive compounds in plants, microorganisms
  • designed using complex computer programmes to build three-dimensional models
  • computers search through libraries of chemicals to isolate potentially useful action against pathogens
88
Q

what is pharmacogenetics?

A

personalised medicine

combination of drugs that work with your individual combination of genetics and disease

89
Q

what is selective toxicity?

A

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

90
Q

what are antibiotic-resistant bacteria?

A

bacteria that have undergone mutation to become resistant to an antibiotic and then survive to increase in number

91
Q

how can antibiotic-resistant infections can be reduced?

A
  • minimising the use of antibiotics
  • ensuring every course of antibiotics is completed to reduce risk of resistant individuals surviving and developing into a resistant strain population
  • good hygiene in hospitals, care homes