4.1.1 communicable diseases Flashcards
1
Q
are bacteria prokaryotes or eukaryotes
4.1.1(a)
A
prokaryotes
2
Q
do bacteria have a cell wall
4.1.1(a)
A
yes
3
Q
do bacterial cells have membrane bound organelles
4.1.1(a)
A
no
4
Q
what are the 3 diseases caused by bacteria and where are they found
4.1.1(a)
A
tuberculosis-animals
bacterial meningitis-animals
ring rot-plans
5
Q
what do viruses consist of
4.1.1(a)
A
short section of DNA or RNA surrounded by a protein coat (Caspid)
6
Q
do viruses contain any membrane bound organelles
4.1.1(a)
A
no
7
Q
do viruses contain a cell wall
4.1.1(a)
A
no
8
Q
what are the three disease caused by viruses and where are they found
4.1.1(a)
A
HIV/AIDS-animals
influenza-animals
tobacco mosaic virus-plants
9
Q
how do protists carry diseases
4.1.1(a)
A
through a vector
10
Q
what are two diseases caused by protists and where are they found
4.1.1(a)
A
malaria-animals
potato blight-plant
11
Q
do fungi have a cell wall
4.1.1(a)
A
yes
12
Q
do fungi have membrane bound organelles
4.1.1(a)
A
yes
13
Q
what are the 3 diseases caused by fungi and where are they found
4.1.1(a)
A
athletes foot-animals
ringworm-animals
black sigatoka-plants
14
Q
what is direct transmission
4.1.1(b)
A
This occurs when the pathogen is transferred directly from one infected individual to another susceptible individual
15
Q
what are the 4 types of direct transmission
4.1.1(b)
A
-direct contact
-inoculation
-transmission between animals and humans
-indigestion
16
Q
what is direct contact
(direct transmission)
4.1.1(b)
A
Kissing or any contact with the bodily fluids of another person
Direct skin-to-skin contact e.g. ringworm, athlete’s foot
Microorganisms from faeces transmitted on the hands
17
Q
what is inoculation
(direct transmission)
4.1.1(b)
A
Bodily fluids transmitted through a break in the skin, into the blood:
· during sex (e.g. HIV)
· from an animal bite (e.g. rabies)
· through a puncture wound or through sharing needles (e.g. hepatitis B
18
Q
what is transmission between humans and animals
(direct transmission)
4.1.1(b)
A
Some communicable diseases can be passed from animals to people. These are known as zoonotic disease
19
Q
what is indigestion
(direct transmission)
4.1.1(b)
A
Taking in contaminated food or drink
or transferring pathogens to the mouth from the hand
20
Q
what is indirect transmission
4.1.1(b)
A
Occurs when a pathogen travels from one individual to another indirectly. Contact with the infected individual is not necessary.
21
Q
what are the two types of indirect transmission
4.1.1(b)
A
-fomites
-inhaling droplets
22
Q
what are fomites
(indirect transmission)
4.1.1(b)
A
Inanimate objects such as bedding, socks or cosmetics can transfer pathogens, for example the fungus that causes athlete’s foot can be transferred from a surface infected by fungal spores.
23
Q
what is inhaling droplets
(indirect transmission)
4.1.1(b)
A
Tiny droplets of saliva and mucus are expelled from your mouth as you talk, cough or sneeze. If these droplets contain pathogens, healthy individuals can breathe them in and become infected.
24
Q
what is a vector
4.1.1(b)
A
A vector is (usually) an organism that transmits communicable pathogens from one host to another.
25
4 factor affecting the transmission of communicable disease in animals
4.1.1(b)
Overcrowded living and working conditions make it easier for diseases to spread, and poor sanitation means that it is easier for pathogens to spread through dirty water.
People may have compromised immune systems due to other conditions like AIDS, or due to immunosuppressant drugs. Being malnourished makes it more difficult for the immune system to respond effectively to pathogens.
Climate change can introduce vectors and diseases to areas that would not historically have had them. For example, increasing temperatures promote the spread of malaria as it increases the geographical area that is suitable habitat for Anopheles mosquitos.
Socioeconomic factors can influence the distribution of trained healthcare workers and the ease of spreading information about how to prevent the spread of disease, as well as communicating about outbreaks and delivering treatments or vaccines.
26
how does direct transmission occur in plants
4.1.1(b)
Plant pathogens can spread by direct contact between a healthy plant and any part of a diseased plant
27
how does indirect transmission occur in plants
4.1.1(b)
infected plants leave pathogens or reproductive spores in the soil these can then infect the next plant
28
what are the 4 vectors in plants that can cause diseases
4.1.1(b)
Wind – bacteria, viruses and fungal or oomycete spores can be carried on the wind, e.g. P. infestans sporangia form spores that are carried by the wind to other potato crops
Water – raindrop splashes can carry pathogens and spores from one plant to another
Animals – insects and birds carry pathogens and spores from one plant to another as they feed. Insects like aphids inoculate pathogens directly into plant tissues
Humans – pathogens and spores are transmitted by hands, clothing, fomites, farming practices, and by transporting plants and crops around the world.
29
what are the factors affecting the transmission of communicable diseases in plants
4.1.1(b)
· Planting of varieties that are susceptible to disease – most crop plants have been selectively bred leading to very low genetic diversity, so all of the plants in a monoculture will be susceptible to diseases
· Over-crowding in fields increases likelihood of direct contact
· Poor mineral ion content in soils reduces resistance of plants
· Damp, warm conditions increase survival and spread of pathogens and spores
· Climate change – increased rainfall and wind promote the spread of pathogens; changing conditions allow animal vectors to spread to new areas; drier conditions may reduce the spread of pathogens
30
what do plant cell wall receptor bind to/respond to
4.1.1(c)
1.plant cell wall receptors bind to antigens on the pathogen
2. this stimulates the release of signalling molecules that increase the transcription of defence genes
3.this triggers a cellular response eg-producing defence chemicals + physically strengthening there cell walls
31
what can these chemicals produced by plants do
4.1.1(c)
repel insect vectors
kill invading pathogens
32
what are the chemicals that plants use for defense used as
4.1.1(c)
-human medicines
-others have strong flavour and can be used as herbs, spices
33
what are examples of some of the chemicals produced by the plants
4.1.1(c)
-insect repellents
-insecticides
-antibacterial + antifungal compounds
34
what are some physical defenses plants have
4.1.1(c)
-leaves have a waxy impermeable cuticle acts as a physical barrier also prevents water from collecting on the leaf which could transmit pathogens
-trees have thick bark
-plant cells have cellulose cell walls that act as physical barriers
35
after an initial attack by a pathogen what is deposited
4.1.1(c)
callose is synthesized and deposited
36
where is callose deposited
4.1.1(c)
-between cell wall and cell membrane
-cell membranes in cells next to the infected cells
-in sieve plates in the phloem
-in plasmodestmata
37
after callose is deposited what is deposited next
4.1.1(c)
lignin
this makes the mechanical barrier thicker and stronger
38
why is callose deposited in sieve plates and plasmodestmata
4.1.1(c)
to seal off infected part from neighboring cells and prevent pathogens from spreading
39
what is callose and what is it joined by
4.1.1(c)
Callose is a polysaccharide made of glucose joined together by β-1,3 glycosidic bond
40
if pathogens are detected on leaf surface what may guard cells do
4.1.1(c)
if pathogens are detected on leaf surface guard cells may close stomata to prevent entry
41
what do plants do to infected leafs
4.1.1(c)
plants can drop infected leafs through the process of leaf abscission
42
what is the primary non-specific defence
4.1.1(d)
defends against all pathogens in the same way and is always present.
43
what does skin prevent the entry of pathogens
4.1.1(d)
-its a impermeable barrier
-its covered in a skin flora of healthy microorganisms that
outcompete pathogens for space on the body surface
-secretes sebum-which inhibits pathogen growth. It also seals off hair follicles to prevent pathogen entry
44
when platelets contact collagen in the skin or in the walls of damaged blood vessels what 2 products are secreted
4.1.1(d)
thromboplastin
seratonin
45
what does thromboplastin do
4.1.1(d)
an enzyme that triggers a cascade of reactions resulting in the formation of a blood clot (thrombus)
46
what does seratonin do
4.1.1(d)
which makes smooth muscle in the walls of arterioles contract, so they narrow and reduce the supply of blood to the area
47
what happens to the blood clot
4.1.1(d)
The clot dries out and forms a scab that keeps pathogens out. Epidermal cells below the scab start to divide by mitosis, sealing the wound permanently, while damaged blood vessels are repaired by mitosis. Collagen fibres are deposited, giving the new skin tissue strength.
48
how do expulsive reflexes remove pathogens
4.1.1(d)
Coughs and sneezes eject mucus containing pathogens from the gas exchange system. Vomiting and diarrhoea expel the contents of the gut along with pathogens.
49
how does stomach acid remove pathogens
4.1.1(d)
HCl with a pH of 1.5 – 3.5. Kills pathogens by denaturing their enzymes and destroys viruses by denaturing their protein coats and nucleic acids.
50
how do mucous membranes remove pathogens
4.1.1(d)
protect body openings that are exposed to the environment
goblet cells secrete sticky mucus
-it traps microorganisms
-contains lysozyme which hydrolyses bacterial and fungal cell walls
-contains phagocytes which engulf and digest pathogens
-in the gas exchange surface ciliated epithelial cells waft their cilia to move mucus and trapped pathogens to the oesophagus where its swallowed
51
how does inflammation remove pathogens
4.1.1(d)
The inflammatory response is a local response to pathogens, damage or irritants at the site of a wound. Mast cells are activated in damaged tissues and release histamines and cytokines
52
what is the role of histamines
4.1.1(d)
Histamines make blood vessels dilate, causing localised heat and redness. The high temperature helps to prevent pathogens reproducing.
Histamines make blood vessel walls more leaky, so more blood plasma is forced out, forming more tissue fluid. Tissue fluid causes swelling and pain. However, this also allows more phagocytes to access the site of infection
53
what is the role of cytokines
4.1.1(d)
Act as cell signalling molecules and cause other phagocytes to **move** to the area of infection
54
how does a fever reduce pathogens
4.1.1(d)
Normal body temperature of around 37°C,
During an infection, cytokines stimulate the hypothalamus to increase core body temperature.
Most pathogens reproduce best at around 37°C. Higher temperatures inhibit pathogen reproduction.
The specific immune system works faster at higher temperature
55
what is a phagocyte
4.1.1(e)
a phagocyte is a specialised WBC that engulfs and digests pathogens
56
what are the two main types of phagocyte
4.1.1(e)
neutrophils
macrophages
57
how can macrophages be identified
4.1.1(e)
by there large roughly spherical nucleus
58
what does the pus formed at the sight of infections consist of
4.1.1(e)
dead pathogens and neutrophils
59
Describe the 5 stages of phagocytosis
4.1.1(e)
1. Pathogens produce a chemical that attracts phagocytes
2. Phagocyte recognises antigen on pathogen as non/self/foreign
3. the phagocyte engulfs the pathogen by endocytosis. The pathogen is enclose in the vacuole called the phagosome
4. phagosome combines with a lysosome to form phagolysosome
5. hydrolytic enzymes (lysozyme) from the lysosome digest and destroy the pathogen
60
how does a macrophage become an antigen presenting cell
4.1.1(e)
once a macrophage has digested the pathogen...
1. Combines antigens on the pathogen with MHC (major histocompatibility complex)
2. The MHC moves the pathogens antigen to the macrophage CSM
3. the macrophage become an antigen presenting cell
this stimulates other cells involved in the specific immune system response
61
after engulfing a pathogen what do phagocytes produce
4.1.1(e)
cytokines
62
what is the role of cytokines
4.1.1(e)
Act as cell signalling molecules and cause other phagocytes to **move** to the area of infection
63
what is the role of Opsonins
4.1.1(e)
bind to antigens on the pathogen
making it easer for the phagocyte to recognise and pathogen and engulf it
64
where do T lymphocytes mature
4.1.1(f)
T lymphocytes mature in the thymus gland
65
what is the role of T helper cells
4.1.1(f)
have CD4 receptors on their CSM which bind to antigen on antigen-presenting cells
66
what is the role of T killer cells
4.1.1(f)
produce perforin which kill pathogens by making holes in there CSM
67
what is the role of T memory cells
4.1.1(f)
if they encounter a pathogen a second time T killer cells divide rapidly by mitosis to produce a huge number of clones that kill the pathogen
68
what is the role of T regulator cells
4.1.1(f)
-supress the immune system
-ensure the body does not trigger an autoimmune response to a self-antigen
-interleukins are important in this control
69
where do B lymphocytes mature
4.1.1(f)
bone marrow
70
What is the role of a B plasma cell
4.1.1(f)
produce antibodies to a specific antigen and release them into the blood
71
what is the role of B effector cells
4.1.1(f)
these divide to form plasma clones when activated by a T helper cell
72
what is the role of B memory cells
4.1.1(f)
when responding to a specific antigen again they are programmed to rapidly produce many antibodies
73
outline the 5 stages in the cell mediated response
4.1.1(f)
1. macrophage engulfs a pathogen and becomes an antigen-presenting cell by displaying its antigens on its cell surface membrane
2.T-helper cells contains CD4 receptors which bind to the antigen
3. T-helper cells produce interleukins which stimulates more t-helper cells to to to differentiate into
-t-memory
-t-killer
-b cells
-increase phagocytosis
74
describe what happens in the humoral response
4.1.1(f)
1. B lymphocyte antibody binds to antigen on the pathogen and engulfs it.
2. B cell becomes an antigen presenting cell
3. T-helper cell binds to antigen presenting b cell with the correct antibody. (clonal selection)
4. T-helper cell becomes activated and releases interleukins
5. interleukins cause activate the antigen-presenting B cell to divide to produce (clonal expansion)
B-plasma cells-make the correct antibody (primary response)
B-memory cells-when pathogen attacks again this activates the B memory cell to divide to produce B plasma cells which produce the correct antibody quickly (secondary response)
75
what is the primary immune response
4.1.1(g)
-slower-less antibodies are produced
-involves clonal expansion + selection of a B plasma cell which produces many antibodies against a specific pathogen
76
how many days does it take for the antibody concentration in the blood to peak
4.1.1(g)
10-14 days
77
what is the secondary immune response
4.1.1(g)
-quicker
when an antigen is encountered again it will bind to the antibody on the CSM on the B memory cell
the B memory cells divides and differentiates into B plasma cells
B plasma cells quickly produce many antibodies
78
Draw the structure of an antibody
4.1.1(h)
in booklet
79
What is the structure of antibodies and what are they also known as
4.1.1(h)
antibodies are Y-shape glycoproteins
AKA immunoglobins
80
what is each specific antibody made by
4.1.1(h)
Each specific antibody is made by a B plasma cell
81
what is the binding site an area of
what is it called
4.1.1(h)
the binding site where the antibody binds to the antigen is an area of 110 amino acids so is known as the variable region
82
what is the site called when an antibody binds to an antigen
4.1.1(h)
when an antibody binds to an antigen it forms an antigen-antibody complex
83
what does the hinge region provide
4.1.1(h)
the hinge region provides flexibility so the antibody can bind to 2 separate antigens
84
what are the 3 functions of antibodies
4.1.1(h)
1. can act as **opsonins** bind to antigens on the pathogen
making it easer for the phagocyte to recognise and pathogen and engulf it
2.antibodies act as **agglutinins** which cause pathogens carrying antigen-antibody complexes to clump together this makes it more difficult for pathogens to move through the body (reduces motility) and allows phagocytes to engulf multiple pathogens at once
3.antibodies bind to **free toxins** produced by pathogens so they wont affect body cells
85
what is active immunity and how it is acquired
4.1.1(j)
-the body produces antibodies
-it produces T and B memory cells
-produces a secondary immune response the next time the same antigen is encountered
its acquired through
-exposure to microbes
-through vaccines
86
what is passive immunity and how is it acquired
4.1.1(j)
-occurs without an immune response so doesn't produce antibodies or T or B memory cells so isn't long-lasting
-The person is infected with a virulent pathogen and requires immediate medical attention, because the primary response will take too long or be insufficient to prevent infection. The treatment for these cases is immunoglobulin therapy, where the patient is given an intravenous infusion of antibodies.
o The antibodies are collected from an animal whose immune system had been triggered to produce specific antibodies by a vaccinatio
87
what is the difference between natural and artificial immunity
4.1.1(j)
natural- Natural immunity occurs through contact with a pathogen when the contact was not deliberate.
EG-being infected with a pathogen, or feeding on breastmilk, are not actions that are taken with the intention of developing immunity
Artificial immunity-Artificial immunity develops through deliberate actions of exposure
EG- using an injection or an intravenous infusion, such as a vaccination, or infusion with immunoglobulins.
88
what is an autoimmune disease
4.1.1(k)
when the body fails to recognise a "self" antigen so produces antibodies
89
why could autoimmune disease be a result of
4.1.1(k)
-failure of T regulator cells functioning
--abnormal response to a mild pathogen
90
how could autoimmune disease be treated
4.1.1(k)
using immunosuppressant drugs however these prevent normal response to pathogens
91
what body parts and what is the treatment for the autoimmune disease type 1 diabetes
4.1.1(k)
-B cells in the pancreas are effected
-treatment includes insulin injection, immunosuppressant drugs and pancreas transplantation
92
How does a vaccine work
4.1.1(l)
1. The pathogen is made safe so that the antigens are intact
2. a small amount of the safe antigen is injected into the blood
3. the primary immune response is triggered (cell-mediated response + humoral response)
4.this means if you come into contact with the antigen again B memory cells will produce antibodies to the specific antigen as the secondary immune response is triggered
93
why are new vaccines needed for the flu each year
4.1.1(l)
-pathogens and viruses can mutate and the structure of there surface antigen can change meaning B memory cells would not recognise the new suraface antigen
94
what is an epidemic vs a pandemic
4.1.1(l)
epidemic-local/national level
Pandemic-global
95
what is herd immunity
4.1.1(l)
large amount of the population is vaccinated so there is no susceptible host for the pathogen to spread through
96
What was penicillin and what was it used to cure
4.1.1(m)
penicillin was the first safe antibiotic used to cure bacterial diseases
produced by alexander fleming
97
what does biodiversity mean for discovering new medicines
4.1.1(m)
due to human activity, climate change means loss of habitats for natural ecosystems
this means plant species may become extinct by the time we have chance to discover what drugs they provide
98
what is pharmacogenomics/personalised medicine
4.1.1(m)
using an individuals genome to determine medicine choice
99
what is genetic screening
4.1.1(m)
-another type of personalised medicine
-individuals will be identified as having a high chance of developing a certain disease they can then take preventative measures
100
what is synthetic biology
4.1.2(m)
using genetic engineering, to modify organisms so they can produce useful drugs
101
what are antibiotics
4.1.1(n)
antibiotics are chemical substances that inhibit and kill bacterial cells
102
what is selective toxicity
4.1.1(n)
antibiotics being harmful to prokaryotes but not eukaryotes
103
what can antibiotics be described as
4.1.1(n)
bactericidal (they kill bacteria)
bacteriostatic (they inhibit growth processes)
104
explain how a bacterial population may become resistant to a bacteria
4.1.1(n)
1. at first the population doesn't have an antibiotic resistant bacteria. However the mutation produces an antibiotic resistant allele
2. this mutation produces a selection pressure which means there's a strong natural selection for the bacteria with the gene for antibiotic resistance as these are the bacteria that will survive and reproduce
3. this increases the proportion of resistant alleles in the population
105
how else can the spread of antibiotic resistance occur
4.1.1(n)
bacteria are capable of horizontal gene transfer-where plasmids are passed on from one bacterial cell to another without the need for asexual reproduction
106
why may antibiotics be becoming less effective
4.1.1(n)
-antibiotic being prescribed when not necessary eg-viral infection
-patients failing to complete a full course of antibiotics
-antibiotics are used in farming to prevent diseases even when animals are not ill
107
what is an example of a bacterial that has multiple resistant genes
4.1.1(n)
mRSA
108
describe 3 ways of reducing antibiotic resistance
4.1.1(n)
-requiring a doctors prescription for antibiotics
-antibiotics not being used for viral infections
-finishing a full course of antibiotics so all the bacteria are killed
109
110
