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AS biology > 4.1 Communicable diseases, disease prevention and the immune system > Flashcards

4.1 Communicable diseases, disease prevention and the immune system Flashcards

1
Q

pathogen

A

a microorganism that causes disease

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2
Q

host

A

organism in which pathogens live

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3
Q

bacteria

A
  • prokaryotes
  • reproduce v rapidly (20 mins)
  • cause harm by damaging cells/ releasing toxins
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4
Q

where do bacteria tend to live in plants

A

vascular tissues

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5
Q

how do fungi work (animals)

A
  • hyphae form a mycelium, which grow under the surface of skin
  • they send out specialised reproductive hyphae which grow under the skin and release spores
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6
Q

how do fungi work (plants)

A
  • lives in the vascular tissue, and gains nutrients
  • hyphae release extracellular enzymes to digest and decay surrounding tissue
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7
Q

viruses

A
  • invade cells and take over the genetic machinery and other organelles
  • cause the cell to manufacture more copies of the virus
  • host eventually bursts, releasing many new viruses
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8
Q

protoctist

A
  • enter host cells + feed on the contents as they grow
  • eg plasmodium
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9
Q

TB

A
  • bacteria
  • kills cells and tissues. lungs most affected
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10
Q

bacterial meningitis

A
  • bacteria
  • infects meninges (membranes surrounding brain and spinal cord). they become swollen and may cause damage to the brain and nerves
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11
Q

ring rot

A

-bacteria
- ring of decay in the vascular tissue of the potato tuber, accompanied by leaf wilting

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12
Q

HIV/AIDS

A
  • virus
  • attacks cells in the immune system and compromises the immune response
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13
Q

influenza

A

-virus
- attacks respiratory system and causes muscle pains and headaches

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14
Q

TMV

A
  • virus
  • causes mottling and discolouration of leaves
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15
Q

black sigatoka

A
  • fungus
  • bananas
  • cayses leaf spots on banana plants reducing yield
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16
Q

blight

A
  • protoctist
  • potato and tomato
  • affects both leaves and potato tubers
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17
Q

ringworm

A
  • cattle
  • fungus
  • growth of fungus in skin, with spore cases erupting through skin to cause a rash
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18
Q

athletes foot

A
  • humans
  • fungus
  • growth under skin of feet (particularly between the toes)
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19
Q

malaria

A
  • protoctist
  • parasite in the blood which causes headache and fever. may progress to coma and death
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20
Q

life cycle of pathogen

A
  • transmission (travel from one host to another)
  • enter host tissues
  • reproduce
  • leave host tissues
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21
Q

4 means of transmission

A
  1. direct physical contact
  2. faecal-oral transmission
  3. droplet infection
  4. transmission by spores
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22
Q

direct physical contact

A
  • touching a contaminated person or surface
    PREVENT:
  • wash hands regularly
  • clean surfaces
  • disinfect wounds
  • sterilise surgical instruments
  • condoms
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23
Q

faecal-oral transmission

A
  • eating food or drinking water contaminated by pathogen
    PREVENT:
  • treat drinking water
  • wash fresh food
  • thoroughly cook all food
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24
Q

droplet infection

A
  • pathogen carried in tiny droplets in air
    PREVENT:
  • cover mouth when sneeze and cough
  • use a tissue then bin it
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25
Q

transmission by spores

A
  • carried in air, or reside on surfaces or in soil
  • PREVENT:
  • wear a mask
  • wash skin after contact with soil
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26
Q

social factors affecting transmission (6)

A
  • overcrowding
  • poor ventilation
  • poor health (eg if u have aids ur more likely to get TB)
  • poor diet
  • homelessness
  • living or working w people who have migrated from an area where a disease is more common
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27
Q

transmission of malariaifecycle of plasmodium

A
  1. person has malaria
  2. gametes of plasmodium in blood
  3. female mosquito sucks blood
  4. plasmodium reproduces and migrates to a mosquitos salivary glands
  5. uninfected person is bitten by mosquito, enters blood
  6. plasmodium migratres to liver
  7. plasmodium migrates to blood
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28
Q

transmission of pathogens to plants

A
  • spores
  • enter roots through soil
  • insects act as a vector
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29
Q

why more disease when its hotter

A
  • pathogen can grow and reproduce more rapidly in warm and moist
  • global warming, more tropical diseases in europe
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30
Q

cellulose cell wall

A

PHYSICAL
- physical barrier
- contains chemical defences that can be activated when a pathogen is detected

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31
Q

lignin in cell walls

A

PHYSICAL
- waterproof
- indigestibile

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32
Q

waxy cuticles

A

PHYSICAL
- prevent water collectin gon cell surfaces
- pathogens need water to survive. no water = no pathogen. reduces risk of infection by pathogens that are transferred between plants in water

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33
Q

bark

A

PHYSICAL
- contains chemical defences

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34
Q

stomatal closure

A

PHYSICAL
- stomata are possible entry points for pathogens
- stomatal aperture is controlled by guard cells. guard cells close stomata when a pathogen is detected

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35
Q

callose

A

PHYSICAL
- large polysaccharide
- deposited in sieve tubes, around the sieve platses, at the end of a growing season
- blocks flow in sieve tube and prevents a pathogen spreading round the plant

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36
Q

tylose

A

PHYSICAL
- swelling that fills the xylem vessel, blocking it so cant carry water
-prevents spread of pathogens through the heartwood
- tylose contains a high conc of chemicals (eg terpenes) that are toxic to pathogenss

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37
Q

when are plant chemical released

A
  • usually active (except terpenes in tylose) as production of chemicals requires lots of energy
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38
Q

active plant defenses (4)

A
  1. call walls thicken and are strengthened with additional lignin;pathogens cant pass through
  2. CALLOSE DEPOSITION between cell wall and membrane. strenghtens cell wall and plasmodesmata. prevents pathogen spreading between cells
  3. oxidative bursts: produce highly reactive oxygen molecules that damage the cells of invading organisms
  4. increase in chemicals
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39
Q

examples of plant chemicals

A
  1. terpenoids + phenols. antibacterial and antifungal properties
  2. defensive proteins (defensins). inhibit action of ion transport channels in cell membranes
  3. hydrolytic enzymes in cell spaces. break down cell walls
  4. tannins = toxic to insects
  5. alkaloids- contain nitrogen compunds. bitter to prevent herbivories feeding, and some inhibit protein protein synthesis
40
Q

plant necrorsis

A
  • deliberate cell suicide
  • kills cells surrounding infection, prevents pathogens access to water and nutrients eg brown spots
41
Q

canker

A

sunken nectrotic lesion in woody tissue.death of cambium tissue

42
Q

6 animal non specific primary defences

A
  1. SKIN: physical barrier blocking entrance of pathogens. skin flora (microbes) outcompete pathogens. produces antimicrobial pH lowering chemicals
  2. MUCOUS MEMBRANES: protect body openings exposed to environment
  3. BLOOD CLOTTING: plugs wounds to prevent pathogen entry and blood loss
  4. INFLAMMATION: blood vessels more permeable so leak fluid to surrounding areas; swelling and isolated pathogens that entered damaged tissue. vasodilation, makes the area hot and kills pathogens
  5. WOUND REPAIR: skin can re form a barrier against pathogen entry. surface replaced by outer skin layer dividing and migrating to edges of the wound. tissue contracts to bring edges of wound closer together. collagen fibred
  6. EXPULSIVE REFLEXES: coughing and sneezing. expels foreign objects automatically when irritated
43
Q

APC

A

cell that isolates the antigen from a pathogen and places it on the plasma membrane to be recognised by other immune cells

44
Q

clonal selection

A

selection of a specific B or T cell specfiic to the antigen

45
Q

cytokines

A

molecule useed in cell signalling to stimulate immune response

46
Q

opsonins

A

-proteisn that bind to the antigen on a pathogen to mark them, making it easier for phagocytes to bind. INCREASED LIKELIHOOD OF PHAGOCTYSOSIS- phagocytes bind to them

47
Q

first line of defense

A

phagocytosis

48
Q

neutrophils

A
  • most common phagocyte
  • MULTILOBED NUCLEUS
  • manufactured in bone marrow
  • travel in blood and squeeze out into tissue fluid
  • pus is formed by a collection of dead neutrophils
49
Q

phagocytosis process

A
  1. cytokine released by damaged cell and pathogen attracts neutrophils to site of infection
  2. opsonins attach to antigens to mark them to make it easier for receptor on phagocyte to recognise antigen, and for phagcyte to bind to bacteria
  3. cytoplasm of phagocyte changes shape to engulf pathogen into a vesicle (phagosome)
  4. lysosome fuses with phagosome. Secrete hydrolytic lysosyme enzymes which hydrolyse pathogen
  5. pathogen broken down into amino acids, sugars, etc (name some bio mols)
  6. any useful soluble molecules absorbed by DIFFUSION/ACTIVE TRANSPORT into cytoplasm of phagocyte
  7. NEUTROPHIL: apoptosis, dies, dead neutrophils collect and become pus
    MACROPHAGE: doesnt digest fully, presents antigens, APC on top of protein complex
50
Q

MACROPHAGES

A
  • larger cells manufactured in bone marrow
  • travel in blood as monocytes before they mature in lymph nodes
  • doesnt fully digest pathogen- saves the antigen and moves onto a SPECIAL PROTEIN COMPLEX on the surface of the cell, becoming an APC. exposes the antigen so other immune cells can recognise it, but the protein complex ensures the APC isnt mistaken for being foreign
51
Q

dendritic cells

A

type of macrophage found in more peripheral tissues

52
Q

where are both T and B cells made

A

bone marrow

53
Q

T cells mature in

A

thymus

54
Q

B cells mature in

A

bone marrow

55
Q

CLONAL SELECTION + EXPANSION

A

activation of T lymphocytes
- each t lymphocyte surface covered w different specific receptors
- binds to a complementary antigen, activating it
- t cells rapidly mitosis to produce clones

56
Q

T lymphocytes differentiate into

A
  • T helper cells
  • T killer cells
    -T memory cells
57
Q

T helper cells

A

release cytokines (IL) that bind to receptors on the B lymphocytes, ACTIVATING B CELLS

58
Q

What happens once the T helper cells have activated B cells

A

B cells differentiate into plasma cells and memory cells (clonal expansion)

59
Q

plasma cells

A
  • make specific antibodies
60
Q

T killer cells function

A

release toxic substances to kill infected cells and the pathogen within

61
Q

what activates B lymphocytes

A
  • release of IL from T helper cells
  • when the antibody on its surface meets a complementary shaped antigen
62
Q

B memory cells

A
  • remain in blood
  • more antigens produced at a faster rate upon secondary immune response
63
Q

T memory cells

A
  • remain in blood
64
Q

antibody structure

A
  • globular
  • quaternary (4 PPC)
  • binding site is the variable region, complementary to an antigen
  • hinge region allows for flexibility when the antibody binds to the antigen OR binding of 1+ antigen
  • constant region is the same on all antibodies, allow binding to PHAGOCYTES
  • disulfide bridges hold the PPC’s together
  • variable region = allows binding to antigens
65
Q

role of antibody - agglutinins

A
  • each antibody has 2 identical binding sites, so can bind to 2 pathogens at once - crosslinking- they become clumped togeheter
  • physically impedes them from moving and entering host cells
  • more pathogens can be engulfed by phagocytes (extra good for viruses).
66
Q

role of antibody- antitoxins

A

some antibodies can bind to toxins
- prevents the toxins from affecting human cells, so are inactivated (neutralised)
- toxin antibody complex can be phagocytosed

67
Q

role of antibody- opsonins

A
  • bind to antigens on a pathogen
  • becomes binding site for phagocytes, so can bind and engulf more easily.increased likelihood phagocytosis
  • ALSO , some antigens are used by the pathogen as attachment to the host cell. when the opsonin binds to the antigen it renders the antigen useless, so prevents the pathogen entering the host cell
68
Q

primary response

A
  • slow
  • allow for clonal selectrion and expansion and production of antibodies
  • symptoms produced
69
Q

secondary response

A
  • more antibodies produced at a much faster rate
  • memory T cells become t killer
  • memory b differentiate to plasma and release antibodies
  • NO SYMPTOMS
70
Q

active immunity

A

immune system activated and produces its own antibodies

71
Q

artificial immunity

A

immune after vaccination

72
Q

natural immunity

A

immune after catching a disease

73
Q

passive immunity

A

immunity when antibodies are given to u

74
Q

vaccination

A
  • deliberate exposure to antigenic material
  • injected or orally
    involves:
    1. attenuated pathogen
    2. dead pathogen
    3. antigens
    4. toxoid
75
Q

herd immunity

A
  • vaccinating almost 1005 of population
  • disase can no longer be spread and survive as not enough reservoirs of infection
76
Q

ring vaccination

A
  • vaccinate all people in immediate vicinity of new case
77
Q

epidemic

A

rapid spread of disease through national levels

78
Q

pandemic

A

rapid spread of disease internationally

79
Q

why do we need booster vax

A
  • mutation in genetic material causing different shaped of antigens
  • ANTIGEN VARIABILITY, memory B cell receptor no longer complementary so vaccine needs updating
80
Q

colostrum

A
  • natural passive immunity
  • first form of breast milk
  • contains antibodies to the diseases to which the mother is immune
  • v useful when the baby’s immune system is first developing
81
Q

antibiotics

A

chemical which prevents the growth of other microorganisms

82
Q

advantages of antibioitics

A
  • target bacterial cells without damaging body cells
83
Q

antibiotic resistance

A
  • genetic variation in a population due to random mutation means some bacteria have the allele that makes u resistant
  • selection pressure applied (eg taking an antibiotic), those who are resistant survive and reproduce and pass on advantageous allele to offspring
  • over generations, increases and becomes more ocmmon
84
Q

discovery of medicines

A
  1. accidental (fleming)
  2. traditional remedies (willow bark for aspirin, morphine from poppy seeds)
  3. observation of wildlife (animals rub citrus oils on their coats as insecticides\0
85
Q

personalised medicines

A
  • medicine tailored to the genome of na individual
86
Q

synthetic biology

A
  • re engineering of biology
  • production of new molecules that mimic natural processes of use of natural molecules to produce new bioloigcal systems which dont exist in nature
87
Q

problem of MRSA (3)

A
  • might become untreatable
  • potential for epidemic
  • developing new antibiotics is expensive and takes time
88
Q

differentpathogen strains effect on vacine (4)

A
  1. different strains of pathogen
  2. have different antigens
  3. due to mutation
  4. so will need a different vaccine
89
Q

suggest why an adult who survived x disease may lose immunity when they LEAVE the area (4)

A
  1. no repeat infections so no more exposure to pathogen
  2. immunological memory lost
  3. mempry cells lost
  4. no secondary response
90
Q

describe the actions of the B lymphocytes in the immune response

A
  1. humoral response
  2. have an antigen receptor complementary to only one antigen
  3. CLONAL SELECTION: specific B cell activated by T helper cells releasing interleukins / apcs
  4. CLONAL EXPANSION: seleccted cell divides by mitosis
  5. B cell differentiates to form plasma cells which produce antibodies complementary to the antigen
  6. they also form memory cells which remain in blood to provide secondary response
91
Q

how EXACTLY are b cells activated by interleukins

A
  • interleukins receptor has a specific shape complementary to the receptor on the cell surface membrane of the B cell
  • binds to it
  • activates clonal expansion, mitosis
92
Q

factors increasing likelhood of getting a disease (5)

A
  1. not vaxed against it
  2. weakened immune system
  3. poor diet
  4. homelessness
  5. overcrowding
93
Q

why are they looking for medicine in plants

A
  1. reduces cost
  2. reduces time
  3. plants already identified to have medicinal side effects
94
Q

role of B memory cells

A
  • remain in blood
  • recognise pathogen
  • clonal expansion, divide by mitosis
  • differentiate to form plasma cells which PRODUCE antibodies
  • secondary response; destroy pathogen before symptom appears
95
Q

health is (2)

A
  • free from disease
  • physical, mental, social wellbeing
96
Q

explain how bacteria spoils food

A

1.bacteria multiply
2.secrete enzymes
3.digest food
4.eg proteins to amino acids
5.secrete toxins
6.alter texture

97
Q

why does food spoil faster at higher temperatures

A
  1. reproduce faster
  2. more bacteria present
  3. more toxins produced
    (reference enzymes if needed)

AS biology (14 decks)

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