B12 - Communicable diseases Flashcards

1
Q

What are communicable diseases?

A
  • diseases that are caused by pathogens (infective microorganisms)
  • vectors carry pathogens between organisms
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2
Q

What are the types of pathogens?

A
  • bacteria
  • viruses
  • fungi
  • protoctista
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3
Q

What is bacteria?

A
  • prokaryotes
  • do not have membrane-bound organelles or a nucleus
  • can be classified by:
    • shape = rod, spherical, comma, spiralled, corkscrew
    • cell walls = react differently with Gram staining (affects how bacteria reacts to diff. antibiotics)
    • +ve = purple-blue
    • -ve = red
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4
Q

What are viruses?

A
  • non-living infectious agents
  • much smaller than bacterium
  • structure:
    • DNA/RNA is surrounded by protein
  • invade living cells and genetic material of virus takes over biochem of host cell to produce more viruses
  • bacteriophages = attack bacteria
    • use bacteria to replicate/destroy them
    • they can be used to treat some diseases
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5
Q

What is protoctista/protista?

A
  • group of eukaryotic organisms
  • single-celled/colonies
  • small % act as pathogens
    • pathogenic protists = need vector to transfer them to their host
    • e.g. malaria
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6
Q

What is fungi?

A
  • not a major problem in animals
  • eukaryotic organisms (multicellular)
  • cannot photosynthesise and digest food extracellularly
    • most are saprophytes (feed on dead/decaying matter)
  • some are parasitic and can cause plants to stop photosynthesising (leaves affected)
  • produce tiny fungal spores which can spread over large distances
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7
Q

How can pathogens cause damage?

A
  • viruses:
    • take over cell metabolism
    • genetic material inserted into host DNA
    • uses cell to make new viruses
  • protoctista:
    • take over cells and break them open
    • digest and use cell contents to reproduce
  • fungi:
    • digest living cells and destroy them
    • some produce toxins that affect host cells
  • bacteria:
    • produce toxins that damage/poison host cells causing disease
    • some break down cell membranes, inactivate enzymes, interfere with genetic material
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8
Q

What are the different plant diseases?

A
  • ring rot (b)
  • tobacco mosaic virus (v)
  • potato blight (p)
  • black sigatoka (f)
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9
Q

What is ring rot?

A
  • bacterial disease of potatoes, tomatoes, aubergines
  • caused by Gram +ve bacterium
  • damages leaves, tubers, fruit
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10
Q

What is Tobacco Mosaic Virus (TMV)?

A
  • caused by virus that infects tobacco plants
  • damages leaves, flowers and fruit
  • stunting growth and reduces yields
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11
Q

What is potato blight?

A
  • caused by fungus-like protoctist oomycete
  • hyphae penetrate host cells and destroy leaves, tubers, fruit
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12
Q

What is black sigatoka?

A
  • banana disease caused by fungus which attacks/destroys leaves
  • hyphae penetrate/digest cells
  • fungicide can control spread
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13
Q

What are the different animal diseases?

A
  • tuberculosis
  • bacterial meningitis
  • HIV/AIDS
  • influenza
  • malaria
  • ring worm
  • athlete’s foot
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14
Q

What is tuberculosis (TB)?

A
  • bacterial disease that destroys lung tissue and suppresses immune system
  • TB is curable (antibiotics) and preventable (vaccination)
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15
Q

What is bacterial meningitis?

A
  • bacterial infection of the meninges of the brain
  • can spread to the rest of the body causing septicaemia (blood poisoning)
  • antibiotics can cure it
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16
Q

What is HIV/AIDS?

A
  • caused by virus which targets T-helper cells
  • gradually destroys immune system over time (open to other infections)
  • spread through bodily fluids
  • no vaccine or cure
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17
Q

What is influenza?

A
  • viral infection of ciliated epithelial cells in gas exchange system
  • leaves airways open to secondary infection
  • affects mammals and birds
18
Q

What is malaria?

A
  • caused by protoctista Plasmodium and is spread by mosquito bites
  • reproduce in female mosquito and is spread when female takes blood meals
  • invades red blood cells, liver and the brain
19
Q

What is ring worm?

A
  • fungal disease affecting mammals
  • causes grey-white, crusty infectious areas of skin
  • not damaging but may be itchy
20
Q

What is Athlete’s foot?

A
  • human fungal disease
  • grows on and digests warm, moist skin between toes
  • causes cracking and scaling
  • antifungal creams are an effective cure
21
Q

How can pathogens directly be spread?

A
  • direct contact:
    • kissing, or contact with bodily fluids
    • skin-to-skin contact
    • microorganisms from faeces
  • inoculation:
    • break in the skin
    • e.g. animal bite
  • ingestion;
    • taking in contaminated food/drink
    • transferring pathogens from hands to mouth
22
Q

How can pathogens be indirectly spread?

A
  • fomites:
    • bedding, socks, cosmetics (inanimate objects)
  • inhalation:
    • minute droplets of saliva/mucus
    • when healthy individuals breathe them in, they become infected
  • vectors:
    • transmit communicable pathogens from one host to another
    • include: mosquitoes, water, rat fleas
23
Q

What are the factors affecting communicable diseases in animals?

A
  • over crowded living/working conditions
  • poor nutrition
  • compromised immune system
  • poor disposal of waste
  • climate change (can introduce new vectors/diseases)
  • culture/infrastructure (traditional medical practises)
  • socioeconomic factors (lack or trained workers)
24
Q

How are pathogens transmitted between plants?

A
  • direct contact between a healthy/infected plant
  • soil contamination:
    • infected plants may leave pathogens/reproductive spores in the soil
  • vectors:
    • wind
    • water
    • animals
    • humans
25
Q

What are the factors affecting communicable diseases in plants?

A
  • planting varieties of crops that are susceptible to disease
  • over-crowding
  • poor mineral nutrition
  • damp, warm conditions
  • climate change (e.g. increased rainfall promotes spread of diseases)
26
Q

How do plants recognise an attack?

A
  • receptors in cells respond to molecules from pathogens/chemicals produced
  • stimulates release of signalling molecules
27
Q

What are the physical defences of plants?

A
  • callose is synthesised/deposited between cell walls/membrane
    • prevents pathogens from entering
  • lignin is added making the mechanical barrier
  • callose blocks sieve plates and plasmodesmata
    • seals them off from healthy cells and prevent spread of pathogens
28
Q

What are the chemical defences of plants?

A
  • insect repellents
  • insecticides
  • antibacterial compounds (antibiotics)
  • antifungal compounds
  • anti-oomycetes
  • general toxins
29
Q

What are the non-specific defences (preventing pathogens) of animals?

A
  • skin:
    • covers body and prevents entry of pathogens
    • produces sebum that inhibits pathogen growth
  • mucous membranes:
    • secretes mucus which traps microorganisms
  • lysozymes (urine/tears)/stomach acid
30
Q

How does blood clotting/wound repair prevent pathogens enetring?

A
  • when platelets come into contact with collagen, they secrete:
    • thromboplastin = enzyme that triggers the formation of a blood clot
    • serotonin = makes smooth muscle in blood vessels contract
  • clot dries and forms a scab preventing pathogens
  • collagen is deposited to give new tissue strength
31
Q

What is the inflammatory response?

A
  • localised response that leads to pain, heat, redness, swelling
  • mast cells are activated and release histones/cytokines
    • histamines = dilate blood vessels (increase in temp. prevents pathogens reproducing)
    • also make blood vessels more ‘leaky’ to force out blood plasma (tissue fluid)
    • cytokines = attract wbcs (phagocytes)
    • they dispose of pathogens by phagocytosis
32
Q

What are the non-specific defences (removing pathogens) in animals?

A
  • fevers:
    • normal body temp. = 37 degrees C
    • cytokines stimulates hypothalamus to increase temp.
    • most pathogens reproduce best at 37 degrees C/under (higher temps. inhibit this)
    • specific immune system works better at higher temps.
  • phagocytosis:
    • specialised wbcs (phagocytes) engulf and destroy pathogens
    • types of phagocytes = neutrophils and macrophages
33
Q

What are the stages of phagocytosis?

A
  • pathogens produce chemicals to attract phagocytes
  • phagocytes recognise them as ‘non-human’ (non-self)
  • phagocyte engulfs the pathogen and encloses it in a vacuole (phagosome)
  • it then combines with a lysosome to form a phagolysosome
  • enzymes from the lysosome digest and destroy the pathogen
  • neutrophil = 10 mins to engulf
  • macrophages have a more complex process:
    • after digesting, they combine the pathogen antigens with special glycoproteins (MHC = major histocompatibility complex)
    • it then moves the antigens to the macrophage and becomes an antigen-presenting cell
    • the antigens stimulate others cells in the specific immune response
34
Q

What are useful chemicals in non-specific animal defences?

A
  • cytokines:
    • act as cell-signalling molecules
    • inform other phagocytes about pathogen invasion
    • increase body temp./stimulate SIR
  • opsonins:
    • bind to pathogens and ‘tag’ them to be more recognisable
    • phagocytes have receptors on cell membranes that bind to common opsonins
    • antibodies such as immunoglobulin G (IgG) and immunoglobulin (IgM) have the strongest effect
35
Q

What is the specific immune system?

A
  • active/acquired immunity
  • much slower than non-specific responses (can take up to 14 days)
    • immune memory cells helps to speed up reaction
36
Q

What are antibodies?

A
  • Y-shaped glycoproteins called immunoglobulins
  • they bind to specific antigens on a pathogen/toxin
  • they have two identical long polypeptide chains (heavy) and two shorter ones (light)
  • disulfide bridges hold them together
  • antibodies bind to antigens with lock-and-key mechanism
  • variable region = binding site (top of Y shape)
  • constant region = the rest of the shape
  • antibody + antigen = antigen-antibody complex
  • the hinge region allows for flexibility
37
Q

How do antibodies defend the body?

A
  • antibody of a-a complex acts as opsonin so it is easily engulfed/digested
  • most pathogens cannot effectively invade host cells once part of a-a complex
  • antibodies act as agglutinins which cause a-a complexes to clump together
    • makes it easier for phagocytes to engulf multiple at a time
  • antibodies can act as anti-toxins and bind to them making them harmless
38
Q

What are the types of T lymphocytes?

A
  • T helper:
    • CD4 receptors allow them to bind to antigens on APCs
    • produce interleukins (type of cytokine) to stimulate the production of other T cells
    • attracts/stimulates macrophages to ingest pathogens with a-a complexes
  • T killer:
    • destroy pathogen with antigen
    • produce perforin which kills pathogen by making membrane permeable
  • T memory:
    • part of immunological memory
    • divide rapidly when they meet antigen second time (form clones of T killer cells)
  • T regulator:
    • suppress immune system (interleukins)
    • stop immune response to ensure body recognises self antigens and does not set up autoimmune response
39
Q

What are the types of B lymphocytes?

A
  • plasma:
    • produce antibodies to a particular antigen
    • lives for only a few days
  • B effector:
    • divide to form plasma cell clones
  • B memory:
    • provide immunological memory
    • remember a specific antigen and enable body to make rapid response
40
Q

What is cell-mediated immunity?

A
  • T lymphocytes respond to changed cells
  • important against viruses and early cancers
  • macrophages engulf/digest pathogens in phagocytosis
    • process antigens to form APCs
  • receptors on T helper cells fit antigens (activate and form interleukins)
    • stimulates production of more T cells
  • cloned T cells may:
    • form T memory cells
    • produce interleukins (stim. phagocytosis)
    • produce interleukins (stim. B cells to divide)
    • stim. development of clone T killer cells specific for presented antigen and destroy infected cells
41
Q

What is humoral immunity?

A
  • body responds to antigens outside cells/APCs
  • produces antibodies soluble in blood/tissue fluid
  • activated T helper cells bind to B cell APC (clonal selection)
  • interleukins produced by T helper cells activate B cells
  • those B cells divide by mitosis and produce plasma cell clones/B memory cells (clonal expansion)
  • cloned plasma cells produce antibodies
    • bind to antigens
    • act as opsonins/agglutinins
    • ** primary immune response **
  • cloned B cells can develop into B memory cells
    • divide rapidly to form plasma cell clones
    • wipes out pathogens before symptoms are shown
    • ** secondary immune response **
42
Q

What is the action of opsonins, agglutinins and anti-toxins?

A
  • opsonins:
    • chemicals that bind to pathogens and tag them so they are recognised more easily by phagocytes
  • agglutinins:
    • chemicals that cause pathogens to clump together so they are easier for phagocytes to engulf/digest
  • anti-toxins:
    • chemicals that bind to toxins produced by pathogens so they no longer have an effect