Module 4: Section 1 - Disease and the Immune System Flashcards
(97 cards)
1
Q
What is a Disease?
A
Condition that impairs the normal functioning of an organism
2
Q
What is a Communicable diseases?
A
This spread between organisms and caused by a pathogen
3
Q
What is a Pathogen?
A
Organism that causes disease
4
Q
what are Symptoms?
A
A physical/mental sign/feature that indicates a disease
5
Q
Examples of bacterial diseases?
A
Tuberculosis
Bacterial meningitis
Ring rot
6
Q
Examples of viral diseases?
A
HIV/AIDS
Influenza
Tobacco mosaic virus
7
Q
Examples of fungal diseases?
A
Black sigatoka
Ringworm
Athlete’s foot
8
Q
Examples of protoctista?
A
Potato/tomato late blight
Malaria
9
Q
Tuberculosis?
What?
A
Destroys lung tissue
Weakens immune system
Coughing & sneezing
10
Q
Who does Tuberculosis affect?
A
Animals such as human and cattle
11
Q
What is Bacterial meningitis?
What?
A
A serious infection of the lining of brain and spinal cord
12
Q
Who does Bacterial meningitis affect?
A
Humans
13
Q
Ring rot?
What?
A
Incurable & devastating
Damages leaves, tubers & fruit
14
Q
What does Ring rot affect?
A
Potatoes tomatoes
15
Q
What does HIV/AIDS do ?
A
Weakens immune system
Damage T helper cells, leads to AIDS
16
Q
Who does HIV/AIDS affect?
Who
A
Humans
17
Q
Influenza?
What?
A
Contagious respiratory illness causing fever, aches and tiredness (flu)
18
Q
Influenza?
Who?
A
Animals such as humans
19
Q
Tobacco mosiac virus?
What?
A
Incurable
Devastating
Damages leaves and fruit
Mosaic like motting
20
Q
Tobacco?
Who?
A
Many plants
21
Q
Black sigatoka?
What?
A
Incurable
Hyphae enter cells
Digests leaves cause black spots
22
Q
Black sigatoka?
Who?
A
Banana plants
23
Q
Ringworm?
What?
A
Skin infection causing crusty circular areas
Not damaging
24
Q
Ringworm?
Who?
A
Cattle
25
Athele's foot?
What?
Common infection causing itchy white and cracked skin
26
Athlete's foot?
Who?
Humans
27
Potato/tomato late blight?
What?
Incurable
Hyphae enter host cells
Destroys leaves
Tubers & fruit
28
Potato/tomato late blight?
Who?
Potatoes/tomatoes
29
Malaria?
What?
Serious tropical disease spread by mosquitoes
Infects RBCs (fever)
30
Malaria?
Who?
Animals such as humans
31
What is transmission?
the transfer of pathogens from an infected host to an uninfected host
32
what is direct transmission?
transmissions through airborne droplets such as coughing/sneezing
or skin to skin cotact such as kissing/intercourse or faeces to hands
33
what is indirect transmission?
diseases is transmitted via an intermediate such as food, water, air or another organism (vector)
FOOD CAN BE BOTH
34
what is a spillover event?
The jump from animal to human
35
give two examples of direct transmission?
Contact with bodily fluids
Inoculation via an animal bite
Skin to skin contact
36
give two examples of indirect transmission?
Fomites (e.g. objects such as bedding, cosmetics)
Vectors (e.g. animals or water)
Ingestion of contaminated food or drink
37
What increases the probability of catching a communicable disease?
minimum 3
Overcrowded living and working conditions
Poor nutrition
A compromised immune system
e.g. having HIV/AIDS or needing immunosuppressant drugs after a transplant surgery
Poor disposal of waste, providing breeding sites for vectors
Climate change: this can introduce new vectors and diseases
e.g. spread of malaria
Culture and infrastructure
e.g. traditional medical practises
Socioeconomic factors
e.g. lack of trained health workers, insufficient public warning of an outbreak, limited access to good healthcare, good health education.
38
give an example of direct transmission in plants?
Contact between plants
39
give an examples of indirect transmission in plants?
Soil contamination (fungal or protoctista spores or pathogens themselves can infect the next crop)
vectors such as wind, water, animals
40
What increases the probability of transmission of plant diseases?
Overcrowding
Planting varieties susceptible to disease
Poor mineral nutrition reduces resistance of plants
Damp, warm conditions increases survival and spread
Climate change (e.g. malaria)
N.b. drier conditions may actually reduce the spread
41
what are the relative sizes of viruses and bacteria
flu virus - 0.1 mm MICRO
bacteria - 1mm
42
what are symptoms?
the organism's response to pathogens damaging tissues directly
43
virus structure?
same genetic material (DNA OR RNA) surrounded by protien
non-living
non cellular
44
how do viruses replicate?
AKA mode of attack 2
1. invade cells
2. insert genome into host genome
3. host cell machinery makes viruses
4. viruses invade more 'burst'
45
what are bacteriophages?
these are viruses that infect bacteria by taking over bacterial cells destroying them and also using them to replicate
46
what are protoctista?
uni or multicellular organisms
can be pathogenic or parasitic
eukaryotic with a wide range of feeding meths
47
describe mode of attack 1?
bacteria producee toxins that either cause breakdown of cell membranes, inactive enzymes or stop cell division causing disease
48
describe mode of attack 3?
they attack cells, digest and use the cell's contents as they reproduce and break open the host cell
49
what are fungi?
eurokaryotic organisms
majority multicellular
can photosynthesis so digest food extracellularly
these are saprophytes or parasitic
50
fungi's mode of attack?
they affect the leaves of a plant by stopping photosynthesis which kills the plant quickly
they also produce millions of spores spread across long distances which form hyphae
51
what is the difference between physical and mechanical defences?
mechanical defences cause harm whereas physical defences act as a barrier
52
give two examples of physical defences in plants?
- cellulose cell walls
- tough waxy cuticle on leaves
- layers of dead cells aroud stems like bark which fall off
53
give two examples of chemical defences in plants?
- antibacterial chemicals
- toxins like histimines
- poisons
54
give two examples of mechanical defences in plants?
thorns
hairs
leaves which drrop/curl when touched
mimicry to trick animals
55
Why don’t plants heal diseased tissue?
Plants are continually growing at the meristems so they can replace damaged parts.
Instead, plants
Make polysaccharides to seal off or sacrifice diseased tissue
Make chemicals to deter insects or kill pathogens
Undergo abscission (dropping of diseased leaves) or necrosis (controlled cell death)
56
how do plants detect pathogens?
Detection
Chemicals released by pathogens (e.g. enzymes that break down cell wall) may bind to receptors in the cell membrane
57
State two made chemicals by plant cells in response to pathogens?
Response
Signalling molecules in the cell first ‘switch on’ genes so that the following are made:
Defensive chemicals that attack the pathogen
Defensive chemicals that give the alarm to other cells
Polysaccharides secreted to strengthen the cell wall
58
what else is synthesised and deposited in response to pathogens being detected in plants?
Callose:
in cell walls
over sieve plates
in plasmodesmata
why? blocks the pores creating seal/barrier
Lignin:
in cell walls
59
what are non-specific defences?
Non-specific defences = defences that act against all pathogens, are present all the time or are activated easily
60
what are primary defences?
they are there to stop pathogens entering
61
GCSE btw examples of primary defences?
skin
respiratory system
stomach
62
what are secondary defences?
they are there to destroy pathogens once inside the body e.g. WBCs
63
what are specific responses?
target against a specific pathogen; in doing so this takes longer
64
what is skin flora?
a primary defence that outcompetes harmful bacteria for space
65
what is sebum?
a primary defence that inhibits growth of pathogens
66
what is mucus?
a primary defence that is located in the airways and lined in body tracts by mucous membranes
contain lysozymes
67
describe blood clotting as a primary defence?
exposure of platelets to collagen in a damaged blood vessel causes many secretions and reactions leading to blood clot formation, a mesh of protein fibres that traps cells and platelets, also called a thrombus.
Vessels also narrow (vasoconstriction) to reduce blood flow to the area.
This is followed by wound repair, where it dries to form a scab. New skin cells seal the wound, preventing blood loss and pathogen entry (infection).
68
describe the inflammatory response?
Localised response to pathogens/irritants at a wound causing inflammation
Activated mast cells (WBCs) in connective tissue release these chemicals:
Histamines make blood vessels dilate and leaky, to allow phagocytes (WBCs) to enter tissue fluid
Cytokines attract phagocytes
69
what is a phagocyte?
WBCs that engulf and destroy pathogens
70
what is a pathogen?
disease causing organism
71
what is a non self antigen?
foreign protein or polysaccharides on the surface of pathogens
72
what is a phagosome?
vesicle containing pathogen
73
what is a lysosome?
vesicle containing digestive enzymes
74
describe phagocytosis - excluding macrophages
1. phagocyte are attracted by chemicals produced by a pathogen
2. phagocyte recognises the pathogen as a non-self and binds to it
3. phagocyte engulfs the pathogen to form phagosome and lysosome moves towards phagosome and combines with it, forming phagolysosome
4. Break down of the pathogen occurs
75
Describe the structure of an antibody (3)
Due to antibodies being a Quaternary protein they consist of 4 polypeptide chains 2 being heavy and the other being light. They also have 2 binding sites within the variable region which are complementary to a specific antigen. There is a hinge region which provides the antibody with flexibility and strength through disulfide bridges and the bottom half of the antibody is known as the constant region as the structure does not change.
76
Humoral response?
Humoral response involves antibodies and B cells. Humor meaning bodily fluids where antibodies are soluble and transport in.
77
Describe when antibodies bind to a flagellum
this is when antibodies bind to the bacteria's flagellum thus making the bacteria less mobile. This in turn prevents bacteria from invading tissues and making you ill.
78
Give the function of the hinge region (1)
To provide flexibility when binding site binds to pathogen and strength via disulfide bridges formed within the region.
79
Inhibition of a binding to a receptor?
this is the prevention of a virus/toxin binding to a site on another cell as the antibody instead binds to the virus/toxin also preventing virus from endocytosing into a cell.
80
Opsonisation?
this is when antibodies mark the pathogen for phagocytes to perform phagocytosis.
81
Agglutination?
this is when antibodies which are binded to antigens clump together forming antibody antigen complexes for phagocytes to perform phagocytosis.
82
Neutralisation?
this is when an antibody which is an antitoxin binds to a toxin creating an antitoxin toxin complex.
83
Describe B cell activation
SPECIFIC IMMUNE RESPONSE
Antigens in the blood collide with their complementary antibody on a B cell. The B cell takes in the antigen
by endocytosis and then presents it on its cell surface membrane as MHC molecules (antigen fragments)
This attracts the helper T cell receptor that secretes interleukins that activate the B cell to go through clonal expansion
and differentiation
B cells undergo mitosis to make plasma cells or memory B
cells
Plasma cells make antibodies
B memory cells can divide rapidly into plasma-cells
when re-infected with the same pathogen to make large
numbers of antibodies rapidly.
84
What is active immunity?
Memory B cells divide by mitosis and make
plasma cells rapidly if they collide with an
antigen they have previously encountered.
This results in large numbers of
antibodies being produced so rapidly that
the pathogen is destroyed before any
symptoms can occur.
85
Describe phagocytosis including macrophages
1. phagocyte are attracted by chemicals produced by a pathogen
2. phagocyte recognises the pathogen as a non-self and binds to it
3. phagocyte engulfs the pathogen to form phagosome and lysosome moves towards phagosome and combines with it, forming phagolysosome
4. Break down of the pathogen occurs
5. Antigens from the digested pathogen combine
with special proteins called MHCs (major
histocompatibility complex) in the cytoplasm
6. MHCs present the antigen to the specific
immune system
86
What are opsonins?
Opsonins: chemicals (e.g. antibodies IgG & IgM) that bind to pathogens,
tagging them so they are more easily recognised by phagocytes
87
What are cytokines?
Family of cell signalling molecules
88
T helper cells?
Recognise antigens on antigen-presenting cells (APCs) and release
cytokines (interleukins) to activate T killer cells, B cells (increase
antibody production) and stimulate macrophages.
89
T killer cells?
Kill infected cells and pathogens directly using perforin (chemical
that creates holes in membranes and pathogens)
90
T memory cells?
If the body is re-infected with the same pathogen these cells divide
rapidly to form clones of T killer cells.
91
T regulatory cells?
Prevent autoimmune disease - they suppress the immune system after
pathogens have been destroyed. This helps to prevent the immune system
from mistakenly attacking the body cells.
92
What are the modes of direct transmission in plants
Direct contact between different plants?
93
What are the modes of indirect contact is plants
Vectors, contaminated soil
94
What are autoimmune diseases? Examples?
This is when there is a abnormal immune response against cells normally found in the body.
Type 1 diabetes
Lupus
95
What is immunity? + immunisation
The ability of an organism to resist a particular infection
The development of immunity
96
Describe the cell mediated response?
1. Macrophages engulf pathogen and presented as an APC and respond to a changed host cell.
2. APC activates a T helper cell with a specific receptor to the antigen.
3. T helper then produces interleukins which stimulates the cell to rapidly divide (clones).
4. These clones can develop into T killer cells to destroy infected cells
97
What is the difference between active and passive immunity? Examples?
Active immunity is when the body actively produces antibodies/memory cells to destroy pathogens whereas passive does not.
Vaccination
Colostum
