protection against infection (chapter 7) Flashcards

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1
Q

communicable diseases

A
  • a.k.a ‘infectious’ or ‘transmissible’ diseases
  • characteristics:
    - caused by pathogens
    - contagious
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2
Q

pathogens

A
  • organism capable of causing disease
  • commonly:
    - bacteria
    - virus
    - parasite
    - fungi
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3
Q

bacteria

A
  • surrounded by plasma membrane, cell wall and slime
  • no nucleus/membrane bound cells
  • contains only DNA
  • cytoplasm containing ribosomes
  • comparatively larger (can be seen under light microscope)
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4
Q

disease caused by bacteria (cholera)

A
  • bacteria infected intestine; produce cholera toxin
  • causes severe diarrhoea which leads to dehydration
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5
Q

disease caused by bacteria (diphtheria)

A
  • bacteria produces a toxin that affects mucous membranes of mouth and nose
  • general flu symptoms: fever/chills/cough/core that)
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6
Q

disease caused by bacteria (tetanus)

A
  • spores enter body through cuts and develop into bacteria; these spread to CNS and produce toxins (tetanusospasmin)
  • toxins prevent nerve signals to muscles - muscles spasms and stiffness
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7
Q

disease caused by bacteria (tuberculosis)

A
  • bacteria usually attack lungs, symptoms depend on where bacteria grow
  • lungs: bad cough, pain in chest, cough up blood
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8
Q

disease caused by bacteria (whooping cough)

A
  • respiratory tract infection; cold-like symptoms, persistent dry cough
  • bacteria attach to cilia lining upper part of respiratory tract; cilia and airways swell
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9
Q

virus

A
  • enclosed with protein coat
  • no nucleus/membrane bound cells
  • contains RNA
  • no ribosomes
  • smaller (can only be seen under electron microscope)
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10
Q

disease caused by viruses (HIV/AIDS)

A
  • RNA
  • virus attacks CD4 helper (immune) lymphocytes
  • body is unable to fight off infections
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11
Q

disease caused by viruses (ebola)

A
  • RNA
  • virus targets liver, immune and endothelial cells lining blood vessels
  • disrupts cell adhesion; leading to haemorrhaging and internal bleeding
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12
Q

disease caused by viruses (measles)

A
  • RNA
  • virus infects macrophages and dendritic cells, then B and T cells in lymph nodes
  • causes inflammation throughout entire body
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13
Q

disease caused by viruses (influenza)

A
  • RNA
  • virus attacks epithelial cells of nose, throat and respiratory system; infects and kills NK immune cells
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14
Q

transmission of pathogens

A
  • contact (direct or indirect): chicken pox, genital warts
  • transfer body fluids (saliva, mucus, blood): HIV
  • infection by droplets: colds, influenza
  • ingestion (of contaminated food/water): salmonella
  • airborne transmission (can survive even once dried): tuberculosis
  • vectors: malaria (by mozzies), lyme disease (by ticks)
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15
Q

non-specific vs specific defences

A

non-specific:
- works against all pathogens (general)
- body’s first line of defence
- there are:
- external defences
- internal defences
- protective reflexes

specific:
- directed at particular pathogens
- immune system produces antibodies to target pathogens

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16
Q

external defence (skin)

A
  • barrier; prevents entry of micro-organisms
  • large amount of bacteria live on the skin - occupying bacteria make it difficult for new (pathogenic) establishments
  • sebum; an oily secretion which kills some pathogenic bacteria
  • sweat; salts and fatty acids prevent growth of many micro-organisms
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17
Q

external defence (mucous membranes)

A
  • found in digestive, urinary, respiratory and urogenital tracts
  • line body cavity (that open to exterior)
  • secrete mucus; inhibits entry of micro-organisms
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18
Q

external defence (hairs)

A
  • found in nose and ears
  • hair trap micro-organisms
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19
Q

external defence (cilia)

A
  • found in respiratory tract (line nasal cavity, trachea etc.)
  • tiny heir-like projections from cells
  • ‘beating’ motion moves mucus up towards throat (cough up/swallow)
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20
Q

external defence (acids)

A
  • found in stomach and vagina and sweat
  • kills micro-organisms that are ingested with food or in mucus
  • reduces growth of micro-organism
21
Q

external defence (lysozyme)

A
  • found in tears, saliva, sweat, nasal secretions and tissue fluid
  • enzymes kills bacteria
22
Q

external defence (cerumen)

A
  • found in outer ear
  • slightly acidic and contains lysozyme
  • prevents and traps pathogens from entering
23
Q

external defence (flushing action)

A
  • occurs in urine flowing through urethra, tears, sweat, saliva and vagina
  • cleansing action = prevents bacterial growth from travelling through ducts/tracts
24
Q

protective reflexes (sneezing)

A
  • stimulus: irritation of walls of nasal cavity (noxious fumes/dust particles)
  • forceful expulsion of our from lungs, carries mucous/foreign particles/irritation gases out through nose and mouth
25
Q

protective reflexes (coughing)

A
  • stimulus: irritation in lower respiratory tract (bronchi/ols)
  • air is forced from lungs, carried contents up through throat and mouth
26
Q

protective reflexes (vomiting)

A
  • stimulus: psychological; excessive stretching of stomach; bacterial toxins
  • muscles of abdomen and diaphragm contract, contents of stomach are expelled
27
Q

internal defences (phagocytes)

A
  • cells that engulf and digest microorganisms and cell debris (through phagocytosis)
  • monocytes leave blood stream, enter tissue when infected or inflamed - differentiate into macrophages to destroy pathogens as they appear

leucocytes:
- white blood cells
- able to leave blood capillaries; migrate through tissues to place of injury/infection
- some can secrete substances to engulf/destroy bacteria

macrophages:
- large; develop from monocytes (type of WBC)
- some move through tissues to look for pathogens
- some in fixed place - deal with pathogens that come to them by engulfing or releasing of substances

28
Q

internal defences (inflammatory response)

A

response to tissue damage:
- reduce spread of pathogens
- repair damage
- cell debris removal

sign of inflammation; redness, swelling, heat and pain

29
Q

internal defences (fever)

A
  • elevation of body temperature
  • inhibits growth of bacteria and viruses
  • increases rate of metabolism; helps body cells repair themselves more quickly
  • fever harmful/fatal if reaches 44.4-44.5 degrees
30
Q

inflammation

A
  • response to tissue damage
  • signs:
    • redness (increased blood flow)
    • swelling (movement of fluid from blood to tissue)
    • heat (increased blood flow)
    • pain (abnormal condition stimulate pain receptors)
  • inflammatory response:
    1. mechanical damage/local chemical changes (stimulate mast cells to release histamine and heparin into tissue fluid)
    2. histamine increases blood flow (increases permeability of blood capillary walls - more fluid filtered)
    3. heparin prevents clotting (in areas of injury)
    4. mast cells release chemical (which attract phagocytes)
    5. abnormal conditions stimulate pain receptors
    6. phagocytes (containing debris) die, combines with tissue fluid - forming pus
    7. mitosis, production of new cells
31
Q

fever

A
  • it is the elevation pf body’s temperature
  • hypothalamus resets body’s core temperature in response to an infection
  • white blood cells release pyrogens during inflammatory response
  • pyrogens act on hypothalamus
  • high body temperature may inhibit growth of some pathogens
  • heat increases rate of metabolism = increased rate of repair
  • can be harmful it too high
32
Q

the immune response

A

homeostatic mechanisms:
- micro-organisms/foreign substances enter the body, then the immune response deals whit the invasion and restores internal environment to normal conditions

types of immune (specific) responses:
- antibody mediated immunity: production of antibodies; circulate body and attack invaders

  • cell mediated: formation of special lymphocytes (WBC) that destroy invading agents
  • both responses directed at specific invading agents and both involve lymphoid tissue
33
Q

lymphoid tissue

A
  • most tissue in lymph nodes; but also spleen, thymus, tonsils
  • composed of B cells and T cells

B cells:
- a lymphocyte (antibody mediated immunity)
- produced in bone marrow
- matured in bone marrow
- become a part of lymphoid tissue
- attacks invaders outside of cell

T cells:
- lymphocyte (cell mediated immunity)
- produced in bone marrow
- matures in thymus
- becomes a part of lymphoid tissue
- attacks invaders inside of cell

34
Q

antigen

A
  • any substance capable to causing a specific immune response
  • causes body to produce antibodies
  • large molecules; proteins, carbs, lipid or nucleic acids
  • not just associated with pathogens (e.g. blood groups, transplanted tissue, egg white, pollen grain)

self antigen:
- large molecule; produced by own body
- do not cause immune response

non-self antigen:
- ‘foreign compounds’
- do cause immune response

35
Q

antibody

A
  • specialised protein; immunoglobulins
  • produced in response to antigen
36
Q

process of antibody mediated immunity

A
37
Q

antigen presenting cells

A
  • when foreign antigen enters the body, specific cells recognise this and respond = antigen presenting cell
  • these include:
    • dendritic cells
    • macrophages
    • undifferentiated B-cells
  • they engulf pathogen, digest it and small fragments that move to surface of cell
38
Q

memory cells

A
  • cells which remain in the body for long period of time (up to 20 years)
  • enable a quick response in secondary response
39
Q

how antibodies inactivate antigens

A
  • form with antigens to make an antigen-antibody complex (antigen has a specific active site = lock and key)

ways they’re destroyed:
- neutralisation: antibody combines with foreign enzyme/bacterial toxins, inactivate them by inhibiting reaction with other cells or compounds
- binding to surface of virus ; prevents entry into cell
- coat pathogens: enhances consumption by phagocytosis
- agglutination: pathogens clump together, makes it easier for phagocytes to capture)
- dissolve organisms: lysis
- react with soluble substances to make the insoluble more easily consumed by phagocytes (precipitation)

40
Q

T cells

A

killer T-cell:
- migrate to site of infection and attaches to invading cells, secrete a chemical which will destroy antigen
- then goes to search for more antigens

helper T-cells:
- involved in antibody and cell mediated immunity
- bind to antigen presenting cells, their antigens
- stimulating the secretion of cytokines that:

  • attract lymphocytes to the infection site
  • attract macrophages (increase phagocytosis)
    intensity phagocytic activity
  • promote the action of killer T-cells

suppressor T-cells:
- act when excessive immune activity or infection’s been dealt with successfully
- releases substances that inhibit T and B cell actvivity

41
Q

process of cell mediated immunity

A
  • foreign antigen enters body
  • antigen presenting cells recognise engulf and digest pathogens, displaying the antigen on their surface
  • antigen presenting cell reach lymphoid tissue and present the antigen to particular T cell
  • sensitised T cells enlarge and divide, each giving rise to a clone
  • some cells of clone remain in the lymphoid tissue as memory cells
  • T cells that don’t become memory cells develop further producing the different T-cells.
42
Q

immunity

A
  • is a resistance to infection by an invading organism
  • the presence of memory cells allows the body to respond quickly enough to deal with any invasion before symptoms occur
  • natural immunity: occurs without any human intervention
  • artificial immunity: results from injecting antibodies or antigens
43
Q

types of immunity

A

natural passive:
- a person receives antibodies produced by someone else (e.g. mother passing antibodies to baby via placenta)
- short lived

natural active:
- develops from having disease and recovering from it, memory cells are created in this process.
- long-term

artificial passive:
- injection of antibodies are given to combat a particular disease
- given so immunity is given immediately

artificial active:
- injection of antigen associated with disease are given, manufacturing it’s own antibodies in response

44
Q

types of vaccines

A

living attenuated micro-organisms:
- reduces virulence (ability to produces disease symptoms)
- often exposing micro-organisms to high temperatures
- e.g. polio, tuberculosis

inactivated vaccines:
- dead pathogens; unable to produce symptoms
- not as prolonged immunity
- e.g. cholera, typhoid

toxoids:
- filtrate of bacterial cultures containing toxins
- bacteria not necessary as it is toxin that causes symptoms (which are inactive)
- e.g. diphtheria, tetanus

conjugate vaccine:
- pieces of bacterial coat inducing carrier proteins combined together

sub-unit:
- fragments of micro-organism either whole or attenuated
- e.g. HPV, hepatitis B

45
Q

vaccine delivery

A
  • most common method is via syringe
  • others involve fine spray, skin patch, orally, ingestion via food
46
Q

vaccine schedule

A
  • most don’t begin until after 2 moths (due to antibodies from mother - breastmilk/placenta)
  • if it was administered, the vaccine would be ineffective
47
Q

herd immunity

A
  • group immunity; occurs when high proportion of population is immunised
  • reduces chances of disease spreading through population (transmission) especially to those vulnerable
48
Q

concerns with vaccines

A

health issues:
- allergic reactions (may be allergic to how vaccine is administered e.g. influenza is manufactured using egg)
- preservative: some people may react to them, (they’re to increase ‘shelf-life’

social factors:
- ethical concerns with animal products and testing
- informed consent
- availability

cultural factors:
- religious beliefs (that prayer will protect them, concerned with animal products)

economic factors:
- cost of vaccine (AUS government subsidises cost, not all around world)
- commercialisation: company is a business

49
Q

antibodies

A
  • bactericidal antibodies: altering cell membrane structure or disrupting enzyme action
  • bacteriostatic: stop bacteria from reproducing by disrupting protein synthesis