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BIOLOGY AS > Mod 4 Chap 12: Communicable Diseases > Flashcards

Mod 4 Chap 12: Communicable Diseases Flashcards

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1
Q

Define Health.

A

A state of complete mental, social and physical well being and not merely the absence of disease or infirmity.

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2
Q

Define disease.

A

Anything that impairs the body.

E.g. Mental health diseases / infectious diseases / genetic diseases / lifestyle diseases.

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3
Q

How are infectious diseases caused?

A

By pathogens and parasites
Pathogen: microorganism that causes disease
Parasite: organism that lives in or on a host and causes it harm

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4
Q

Name the four categories / types of pathogens.🌟

A

Bacteria
Viruses
Protoctista
Fungi

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5
Q

Describe bacteria as a pathogen.🌟

A
  • are prokaryotes
  • no membrane bound nucleus / organelles

Classified by either:

  • their basic shapes: either rod shaped, spherical, comma shaped, spiralled, or corkscrew
  • their cell walls: the two types of bacterial cell walls have diff structures + react differently to Gram Staining (gram +ve bacteria = purple-blue, gram -ve bacteria = red). = useful as type of cell wall affects how bacteria react to diff Antibiotics

Examples:

  • tuberculosis
  • bacterial meningitis
  • ring rot (in potatoes / tomatoes)
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6
Q

Describe viruses as a pathogen.🌟

A
  • non living infectious antigens
  • have some genetic material (DNA / RNA) surrounded by protein
  • invade living cells, where they take over biochemistry of host cell to make more viruses
  • successful pathogens as evolve by adapting to host
  • viruses that attack bacteria = bacteriophages

Examples:

  • HIV / AIDS (in humans)
  • tobacco mosaic virus (in plants)
  • influenza (in animals)
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7
Q

Describe Protoctista as pathogens.🌟

A
  • eukaryotic organisms
  • small percentage of them act as pathogens
  • those that cause disease = parasitic
  • use ppl / animals as their host organism
  • pathogenic protests may need vector to transfer them to hosts (e.g. Malaria), or may enter body directly through polluted water

Examples:

  • malaria
  • potato / tomato late blight
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8
Q

Describe fungi as pathogens.🌟

A
  • fungal diseases more problematic in plants
  • eukaryotic organisms, often multicellular
  • digest food extracellularly
  • many are saprophytes (feed on dead decaying matter)
  • some are parasitic (feed on living plants + animals)
  • parasitic are ones that cause communicable diseases

Examples:

  • black Sigatoka (in bananas)
  • ring worm (in cattle)
  • athletes foot (in humans)
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9
Q

Describe how pathogens damage host tissues directly.🌟

A
  • viruses take over cell metabolism
  • some Protoctista take over cells + break them open as the new generation emerge
  • fungi digest living cells + destroy them
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10
Q

Describe how pathogens produce toxins which damage host tissues.🌟

A

Bacteria:
- most bacteria produce toxins to poison / damage host cells, causing disease
- some damage host cells by breaking down cell membranes
- some by inactivating enzymes
- some by interfering w/ host cells genetic material so it cannot divide
- these toxins are a by p-product of the normal functioning bacteria
Fungi:
- some produce toxins, affecting host cell + causing disease

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11
Q

Describe direct transmission of pathogens between animals. 🌟

A

Pathogen is transferred directly from one individual to another by:

  • direct contact (for contagious diseases): e.g. exchange of bodily fluids, skin-to-skin contact, microorganisms from faeces transmitted on the hands
  • inoculation: through a break in skin, from an animal bite, through a puncture wound or sharing needles
  • ingestion: taking in contaminated food, or transferring pathogens from hands to mouth
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12
Q

Describe indirect transmission of pathogens between animals. 🌟

A

Pathogen travels from one individual to another indirectly by:

  • fomites: inaminate objects e.g. bedding can transfer pathogens
  • droplet infection: when healthy individuals breath in minute droplets expelled from mouth of saliva / mucus with pathogens in
  • vectors: transmits communicable pathogens from one host to another, are often animals
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13
Q

Describe the factors affecting the transmission of communicable diseases in animals. 🌟

A

Probability of catch disease increased by:

  • overcrowded living + working conditions
  • poor nutrition
  • poor disposal of waste
  • climate change
  • socioeconomic factors
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14
Q

Describe direct transmission of pathogens between plants.🌟

A
  • involves direct contact of a healthy plant w/ any part of a diseased plant
    E.g. Ring rot
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15
Q

Describe indirect transmission of pathogens between plants. 🌟

A
  • soil contamination: pathogens in soil from infected plants can infect next crops
  • vectors: wind, water, animals, humans
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16
Q

Describe the factors affecting the transmission of communicable diseases in plants.

A

Factors responsible:

  • planting varieties of crops susceptible to disease
  • overcrowding, increasing likelihood of contact
  • poor mineral nutrition, reducing plant resistance
  • climate change
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17
Q

Name plant the methods plants have for defence against pathogens. 🌟

A

Physical defences
Chemical defences
Also Active defences

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18
Q

Describe plants’ physical defences against pathogens. 🌟

A
  • High levels of the polysaccharide callose produced
  • callose quickly synthesised + deposited between cell walls + cell membrane in cells next to infected cells
  • callose papillae act as barriers to prevent pathogens entering plant cells around
  • lignin added to make mechanical barrier to invasion thicker + stronger
  • callose blocks sieve plates in phloem, sealing off infected part + preventing spread of pathogens
  • callose seals off infected cells from healthy cells in plasmodesmata between them, to prevent pathogen spread
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19
Q

Describe plants’ chemical defences against pathogens. 🌟

A
  • Many produce chemicals to repeal insect vectors of disease / kill invading pathogens
  • some so powerful we use / synthesise them to help control insects, fungi + bacteria
    E.g’s:
  • insect repellents
  • insecticides
  • antibacterial compounds e.g. antibiotics, like phenols (antiseptics)
  • antifungal compounds e.g. chitinases (enzymes that break down chitin in cell walls)
  • general toxins e.g. cyanide
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20
Q

Describe plants’ active defences against pathogens, when recognising an attack.

A
  • plants respond rapidly to attach (so not passive)
  • cell receptors respond to molecules from pathogens produced when plant is attacked
  • stimulates release of signalling molecules to switch on genes in nucleus
  • then triggers cellular responses e.g. producing defensive chemicals sending alarm signals to unaffected cells to trigger their defences, + physically strengthening cell walls
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21
Q

Describe the non specific barrier defences against pathogens in animals. 🌟

A
  • the skin: covers body + prevents entry of pathogens, has a skin flora of healthy microorganisms that outcompete pathogens for space on body surface, produces sebum (oily substance to inhibit pathogen growth)
  • many of the body tracts = lined by mucous membranes = secrete sticky mucus = traps microorganisms + contains lysosomes (to destroy bacterial + fungal cell walls) + phagocytes (to remove remaining pathogens)
  • lysosomes in tears + urine, + acid in stomach, prevent entry of pathogens
22
Q

Describe the non specific expulsive reflex defences against pathogens in animals. 🌟

A
  • coughs + sneezes eject pathogen-laden mucus from gas exchange system
  • vomiting + diarrhoea expel contents of gut w/ any infective pathogens
23
Q

Describe blood clotting and wound repair as a non specific defence against pathogens in animals. 🌟

A

When platelets come into contact w/ collagen in skin or the wall of the damaged blood vessel, they secrete substances e.g:

  • thromboplastin: enzyme triggering cascade of reactions to form a blood clot
  • serotonin: makes smooth muscle in walls of blood vessel contract, so narrow, reducing supply of blood to area
24
Q

Describe the cascade of reactions that form a blood clot.🌟

A

Damaged tissue
= platelets activated
= platelets release thromboplastin
= thromboplastin catalyses reaction of / combines w/ prothrombin + Calcium
= makes thrombin
= thrombin catalyses / reacts w/ fibrinogen to produce fibrin
= fibrin forms blood clot

25
Q

Describe the inflammatory response as a non specific defence against pathogens in animals. 🌟

A
  • is a localised response to pathogens resulting in inflammation at site of a wound
  • main symptoms of inflammation: pain, heat, redness, + swelling
  • mast cells activated in damage tissue + release histamine + cytosine chemicals

Histamines:

  • make blood vessels dilate, causing localised heat + redness, raised temp helps prevent pathogens reproducing
  • make blood vessels walls more leaky so blood plasma forced out, to become tissue fluid, which causes swelling (oedema) + pain

Cytokines:
- attract white blood cells (phagocytes) to site, dispose of pathogens by phagocytosis

26
Q

Describe the structure and mode of action of phagocytes (eventually for phagocytosis) as a non specific defence against pathogens in animals.🌟

A
  • phagocytes = specialised white cells that engulf + destroy pathogens
  • two main types: neutrophils + macrophages
  • they build up at site of infection + attack pathogens
27
Q

Describe the process of phagocytosis FOR NEUTROPHILS as a non specific defence against pathogens in animals. 🌟

A
  • pathogens produce chemicals that attract phagocytes
  • phagocytes recognise non human proteins on pathogen (a response to a cell or organism that is non self)
  • phagocyte engulfs pathogen + encloses it in a vacuole called a phagosome
  • phagosome combines w/ a lysosome to form phagolysosome
  • enzymes from lysosome digest + destroy pathogen
  • digested pathogen absorbed by phagocyte-antigens combine w/ MHC in cytoplasm
  • MHC / antigen complex = displayed on phagocyte membrane, making an antigen presenting cell
28
Q

Describe the MHC and its role in the more complex process of phagocytosis FOR MACROPHAGES. 🌟

A

= Major Histocompatibility Complex (MHC)

  • when a macrophage digests a pathogen, it combines antigens from pathogen surface membrane w/ special glycoproteins in cytoplasm called MHC
  • MHC moves pathogen antigens to macrophage’s own surface membrane, becoming an antigen presenting cell
29
Q

Describe the helpful chemicals of cytokines and opsonins that phagocytes produce. 🌟

A

Cytokines: act as cell signalling molecules, informing other phagocytes that body is under attack, to stimulate them to move to site of infection. Can also increase body temp + stimulate specific immune system.

Opsonins: chemicals that bind to pathogens + ‘tag’ them so more readily recognisable by phagocytes.

30
Q

Describe antibodies in the specific immune response system.🌟

A
  • Y shaped glycoproteins called immunoglobulins
  • specific to a particular antigen
  • made of two pairs of polypeptide chains (2 long and heavy, H chains (1 pair), + 2 short and light, L chains (second pair))
  • held together by disulphides bridges
  • know diagram of it containing: variable region, hinge region + constant region
  • when an Antigen binds to an antibody, it forms an antigen-antibody complex
31
Q

Describe how the antibody action defends the body.🌟

A
  • antibody of antigen consoles acts as an opsonins so complex is easily engulfed + digested by phagocytes
  • most pathogens can no longer effectively invade host cells once they’re part of an antigen-antibody complex
  • antibodies act as agglutinins causing pathogens carrying antigen-antibody complexes to clump together (prevents them spreading through body + makes easier for phagocytes to engulf a no. of pathogens at same time
  • antibodies can act as antitoxins, binding to toxins produced by pathogens + making them harmless
32
Q

Describe lymphocytes generally.🌟

A
  • specific immune systems is based on white blood cells called lymphocytes
    Two types:
  • B lymphocytes mature in Bone marrow
  • T lymphocytes mature in Thymus gland
33
Q

Describe T helper cells as T lymphocytes.🌟

A
  • have CD4 receptors on cell-surface membranes that bond to surface antigens on APCs
  • produce interleukins (a type of cytokine (cell signalling molecule))
  • interleukins then stimulate activity of B cells, increasing antibody production, stimulates production of other types of T cells, + attracts + stimulates macrophages to ingest pathogens w/ antigen-antibody complexes.
34
Q

Describe T killer cells as T lymphocytes.🌟

A
  • destroy the pathogen carrying the antigen

- produce a chemical called perforin, which kills pathogens by making holes in cell membrane so it’s freely permeable.

35
Q

Describe T memory cells as T lymphocytes.🌟

A
  • live for long time + part of immunological memory
  • if they meet an antigen a second time they divide rapidly to form huge no. of clones of T killer cells that destroy the pathogen.
36
Q

Describe T regulator cells as T lymphocytes.🌟

A
  • suppress immune system to control + regulate it
  • stop immune response once a pathogen has been eliminated + make sure body recognises self antigens + doesn’t set up auto immune response
  • interleukins important in this control.
37
Q

Describe Plasma Cells as B lymphocytes.🌟

A
  • produce antibodies to a particular antigen + release them into circulation
  • an active plasma cell only lives for a few days but produces around 2000 antibodies per sec while alive + active.
38
Q

Describe B effector cells as B lymphocytes.🌟

A
  • divide to form plasma cell clones.
39
Q

Describe B memory cells as B lymphocytes.🌟

A
  • live for v long time + provide immunological memory
  • are programmed to remember a specific antigen + enable body to make a v rapid response when pathogen carrying that antigen is encountered again.
40
Q

Describe natural active immunity.🌟

A
  • immunity which results from the response of the body to the invasion of a pathogen
  • so for e.g. when the body itself acts to produce antibodies and/or memory cells
  • e.g. Cannot contract measles again in life if you have it as a child
41
Q

Describe natural passive immunity.🌟

A
  • the immunity given to an infant mammal by the mother through the placenta and the colostrum (breast milk)
42
Q

Describe artificial active immunity.🌟

A

Where the immune system if the body is stimulated to make its own antibodies to a safe form of an antigen (a vaccine injected into bloodstream (vaccination)).

43
Q

Describe artificial passive immunity.🌟

A
  • immunity which results from the administration of antibodies from another animal against a dangerous pathogen
  • usually provides only temporary immunity.
  • e.g. Vaccines against rabies delays disease
44
Q

Describe auto immune diseases.🌟

A

A condition or illness resulting from an auto immune response, where the immune systems stops recognising ‘self’ cells and starts to attack healthy body tissue.
- e.g. Arthritis / lupus.

45
Q

Describe the main steps of a vaccine.🌟

A
  • pathogen is made safe (multiple ways of doing this), so antigens are intact, but is no risk of infection
  • small amounts of safe antigen (vaccine) injected into blood
  • primary immune response triggered by foreign antigens + body produces antibodies + memory cells as if infected w/ a live pathogen
  • if you come into contact w/ a live pathogen, secondary immune response is triggered + destroys pathogen rapidly before suffering symptoms of the disease
46
Q

Describe the role of vaccinations in the prevention of epidemics and pandemics.🌟

A

Epidemic: when a communicable disease spreads rapidly to a lot of people at a local / national level.
Pandemic: when the same disease spreads rapidly across a no. Of countries / continents.

  • mass vaccination can prevent spread of the pathogen into wider population at beginning of an epidemic
  • vaccines often have to be changed regularly to remain effective when used to prevent epidemics
  • vaccinating a significant no. of population gives protection to those who do not have immunity (= herd immunity), as there’s minimal opportunity for an outbreak to occur
47
Q

Describe the possible sources of medicines, some examples of them, and why it is therefore important to maintain biodiversity.🌟

A
  • many sources are plants and microorganisms
    E.g. Penicillin obtained from a fungus, soil bacteria is used to make some cancer drugs, daffodils are used to treat Alzheimer’s
  • so, important to protect biodiversity as possible sources of drugs need to be protected
  • if this does not happen, some species could die out before we get chance to study them.
48
Q

Describe the future of medicine in terms of personalised medicines.🌟

A
  • are medicines tailored to an individual’s DNA
  • so if doctors have your genetic info, it can be used to predict how you will respond to diff drugs + only prescribe ones that will be most effective for you
  • hoped that by studying relationship between ones genetic makeup and their responsiveness to drugs, more effective drugs can be produced in future, as genes determine how body responds to certain drugs.
49
Q

Describe the future of medicine in terms of synthetic biology.🌟

A
  • involves using technology to design and make things like artificial proteins, cells + even microorganisms
  • has practical applications in many areas, including medicine
  • e.g. Scientists looking at engineering bacteria to destroy cancer cells, but while leaving healthy body cells in tact.
50
Q

Describe the benefits of using antibiotics, and the discovery of them, to manage bacterial infection.🌟

A
  • antibiotics interfere w/ metabolism of bacteria without affecting metabolism of human cells (= selective toxicity)
  • so antibiotics = widely used in 20th cent as gave doctors medicines effective against bacteria for first time (e.g. Use of penicillin dramatically decreasing death rates from communicable diseases).
51
Q

Describe the risks of using antibiotics to manage bacterial infection.🌟

A

The development of antibiotic resistance
- antibiotics becoming less effective in treatment as bacteria are becoming resistant to more + more antibiotics (started w/ mass use of penicillin)
- genetic variation in a pop of bacteria, so genitive mutations make some naturally resistant to an antibiotic, a big advantage for them
- is now more able to survive in host who’s being treated w/ antibiotics to get rid of infection, so lives longer + reproduces more
- leads to allele for antibiotic resistance being passed on, an example of natural selection, increasing antibiotic resistance over time
E.g.s of antibiotic resistant bacteria:
- MRSA
- Clostridium difficile

52
Q

Describe the implications of antibiotic resistance.🌟

A
  • problem for people infected w/ these bacteria, as can’t easily get rid of them with antibiotics
  • increased use of antibiotics = increased antibiotic resistance
  • ‘superbugs’ (resistant to most known antibiotics) = more common
  • so less able to treat potentially life threatening bacterial infections

BIOLOGY AS (12 decks)

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