Module 4.1 - Communicable Diseases Flashcards
1
Q
What is a pathogen and how do they live?
A
- an organism that causes disease
- live on or in a host organism
- take nutrients from the host ( causes damage )
2
Q
Explain bacteria
A
- prokaryote kingdom
- reproduce rapidly
- damage cells/ release waste or toxins ( e.g in plants, live in vascular tissue and cause it to die )
3
Q
Explain fungi
A
- can live in skin of animals and where its hyphae which form a myecilium, grow under skin. Sends out special reproductive hyphae which release spores- causes irritation and redness
- can live in vascular tissue in plants to gain nutrients, hyphae release extra cellular enzymes (e.g cellulases) to digest surrounding tissue causing decay and death. Fruit and storage organs turn black and decay, leaves become mottled in colour, shriven and curl up.
4
Q
Explain viruses
A
- Invade cells, take over genetic machinery and organelles
- cause cell to make copies of virus
- host cell bursts releasing more viruses which infect healthy cells
5
Q
Explain proctoctista
A
Usually enter host cells and feed in contents and grow
-e.g plasmodium ( causes malaria) has forms that feed on haemoglobin in red blood cells
6
Q
What causes tuberculosis and what are its characteristics?
A
- bacteria: mycobacterium tuberculosis and M. Bovis
- kills cells and tissues in the body, affects the lungs the most
7
Q
What causes bacterial meningitis and what are its characteristics?
A
- bacteria: neisseria menigitidis or streptococcus pneumonia
- infection of meninges - membranes that surround brain and spinal cord, become swollen and damage brain and nerves
8
Q
What causes ring rot and what are its characteristics?
A
-Bacterium: clavibacter michiganesis subsp. sepedonicus
9
Q
What causes HIV/ AIDS and what are its characteristics?
A
Virus: human immunodeficiency virus
-attacks cells in immune system and compromises immune response
10
Q
What causes influenza and what are its characteristics?
A
- Virus: from family orthomyxoviridae
- attacks respiratory system, causes muscle pain and headaches
11
Q
What causes tobacco mosaic virus and what are its characteristics?
A
- Virus: tobacco mosaic virus
- causes mottling and discolouration of leaves
12
Q
What causes black Sigatoka and what are its characteristics?
A
- fungus : mycospharella fijiensis
- causes leaf spots on banana plants, reducing yield
13
Q
What causes blight (tomatoes and potatoes) and whT are its characteristics?
A
- proctoctistan: phytophthora infestans
- affects leaves and potato tubers
14
Q
What causes ringworm ( cattle ) and what are its characteristics?
A
- fungus: trichophyton verrucosum
- fungus growth in skin with spores causes erupting through skin, causes a rash
15
Q
What causes athletes foot and what are its characteristics?
A
Fungus: trichophyton rubrum
-growth under skin of feet, between toes
16
Q
What causes malaria and what are its characteristics?
A
Proctoctistan: plasmodium vivax
- carried by a vector: female Anopheles mosquito
- causes headache and fever which can cause a coma and death
17
Q
What is the life cycle of a pathogen?
A
- travel from one host to another (transmission)
- enter a hosts tissue
- reproduce
- leave the hosts tissue
18
Q
Describe the 4 main means of transmission
A
-direct physical contact
touching infected person or contaminated surface ( e.g HIV, bacterial meningitis, ringworm, athletes foot ). Affected by hygiene- wash hands, clean surfaces, clean cuts, sterilise surgical instruments, use condoms.
-faecal-oral transmission
eating or drinking contaminated things ( e.g cholera, food poisoning ). Treat waste and drinking water to reduce risk, wash dress food with clean water, carefully prepare food.
-droplet infection
pathogen carried by water droplets in air ( e.g tuberculosis, influenza )
Catch it, bin it, kill it. Cover mouth when coughing or sneezing, use tissue and dispose
-spores,
resistant stage of pathogen, carried in air or on soil surfaces ( anthrax, tetanus) use masks and wash skin after soil contact
19
Q
What social factors affect transmission?
A
- overcrowding
- poor ventilation
- poor health e.g HIV/aids
- poor diet
- homelessness
- living or working with people who have migrated from areas where the disease is more common
20
Q
What is direct transmission?
A
Pathogen passes from host to host
21
Q
What is indirect transmission?
A
Pathogen passed from host to host via a vector
22
Q
What is transmission
A
Passions a pathogen from an infected host to an uninflected individual
23
Q
Explain the transmission of plant pathogens
A
- direct and indirect
- some in soil, taken up by roots ( esp if damages by replanting, burrowing animals or storm)
- fungi produce spores ( sexual or asexual ) carried by wind = airborne transmission
- infects vascular tissue, when leaves shed, pathogen in leaves carried to soil and can infect another plant
- enter fruit and seeds, distributed with seeds, infecting offspring
- indirect - insect attack, spores or bacteria attach to burrowing insect, when it attacks another plant, it transmits the pathogen. E.g beetle, the insect acts as a vector
24
Q
How does climate affect disease?
A
- pathogens grow and reproduce more rapid when warm and moist so more common in these climates
- cold climates damage or kill pathogens or reduce ability to grow and reproduce.
- greater variety of diseases in warmer climates
25
(MA -ext) Why are the rates if HIV/AIDS higher in sub-Saharan Africa than in the rest of the world?
- poverty
- less education about means of transmission
- could be more promiscuity/more working in sex industry
- lower availability of condoms
- religious reasons for not wearing condoms
- many countries have promoted denial of existence
- fewer medical facilities for screening etc
- less screening of blood for transfusions etc
- more infected mothers have to breast feed - no alternative
- more cases of rape
- more intravenous drug abuse
- more use of shared needles
26
(MA -ext) Why hasn't TB been eradicated?
- LEDCs can't afford vaccines/antibiotics
- vaccine isn't 100% effective
- bacteria have become antibiotic resistant
- people don't finish long course of antibiotics
- lack of education about TB
- people still drink unpasteurized milk (LEDCs)
- migration of carriers (no symptoms)
27
(MA) Describe phagocytosis (non-specific immune response).
- phagocytes: engulf and digest pathogen
- receptor on phagocyte's cell surface membrane binds to antigen on pathogen's cell surface membrane
- pathogen engulfed by endocytosis
- this produces a phagosome (phagocytic vesicle)
- lysosomes fuse with phagosome, releasing enzymes (lysins) into it
- the pathogen is digested into amino acids and fatty acids etc
- products are absorbed into cytoplasm by diffusion
28
(MA) What are the roles of antibodies?
-bind to antigens on pathogen
-neutralization of pathogens
> antibodies cover binding site of pathogen
> which prevents their entry to host cell
-agglutination of pathogens
> multiple variable regions allow antibodies to clump/bind together many pathogens
> clump too large to enter host cell and increases likelihood of being consumed by (named) phagocyte
29
(MA) Describe the immune response of T lymphocytes (cellular response).
- macrophages engulf + digest pathogens incorporating pathogen's antigens into their own cell surface membrane; now antigen presenting cell
- this helps select the right specific T lymphocytes with receptors complementary in shape to antigens; clonal selection
- once the correct T lymphocytes are selected, they divide by mitosis in clonal expansion
- T helper cells release cytokines with specific shapes which bind to complementary receptors on the cell surface membrane in B lymphocytes, stimulating them, to divide by mitosis and differentiate. They also stimulate macrophages to carry out more phagocytosis
- T killer cells kill infected host cells by secreting protease enzyme into them
- T memory cells stay in the blood in case there's a secondary infection by the same pathogen. They allow a faster secondary response as they recognize the antigen + can make clones + differentiate to form new T cells more quickly than in the primary response
30
(MA) Explain examples of cell signaling in the immune response.
- pathogen's antigens communicate to body cells that they are foreign
- infected with foreign antigens on surface communicate to lymphocytes to be selected in clonal selection + to T killer cells that they need to be killed
- macrophages engulf + digest pathogens + incorporate the pathogen's antigens on their cell surface membrane; communicates to T lymphocytes to be selected in clonal selection
- T helper cells release cytokines; bind to receptors on B cells + stimulate them to divide by mitosis and differentiate
31
(MA) Describe the changes and roles of B lymphocytes in an immune response.
- humoral response
- specific B lymphocytes w/ receptors complementary in shape to antigens on invading pathogen's surface are selected: clonal selection
- cytokines released by T helper cells stimulate B lymphocytes to divide by mitosis: clonal expansion, then differentiate into plasma cells + B memory cells
- plasma cells produce and secrete antibodies complementary in shape to the antigen, causing agglutination or neutralisation of pathogens
- B memory cell stay in blood in case there's a secondary infection by the same pathogen. Allow faster secondary response as they recognise antigen + can make clones to form new plasma cells so antibodies are made more quickly than in the primary response
32
(MA) What examples of cell signalling can be seen in the immune response?
- pathogen's antigens communicate to body cells they're foreign
- infected cells w/ foreign antigens on surface communicate to lymphocytes to be selected in clonal selection + to T killer cells that they need to be killed
- macrophages engulf + digest pathogens + incorporate pathogen's antigens into cell surface membrane. Communicates to T lymphocytes to be selected in clonal selection
- T helper cells release cytokines: bind to receptors on B cells + stimulate them to divide by mitosis + differentiate
33
(MA) Describe the difference in speed between the primary and secondary immune response against a pathogen.
First infection + primary response
-time delay to trigger immune response after first infection
-no B memory cells so slow antibody production + few produced
Secondary infection/response
-shorter delay before response. Reponse is much quicker
-B memory cells specific to the antigen of pathogen have remained in blood after being produced in primary response. Can clone + differentiate to make plasma cells to make more antibodies much more quickly. Give immunity to a disease
34
What's the main difference between animal and plant pathogen response?
Plants don't have an immune system
35
What are the passive plant defences?
- cellulose cell wall- physical barrier and chemical
- lignin thickening of cell walls- waterproof and indigestible
- waxy cuticle-prevents water collecting, pathogens collect in water and need it to survive
- bark- chemical and physical
- stomata closure- entry point for pathogens, controlled by guard cells, close stomata when pathogens detected
- callose- deposited in sieve plates, blocks flow in sieve tube, prevents pathogen spread
- tylose- balloon like swelling fills xylem, plugs vessel so xylem can't carry water. High terpenes ( chemicals ) that are toxic to pathogens
-chemical- ( e.g terpenoids, phenols,alkaloids, hydrolytic enzymes)
36
(MA) Which groups of people should be immunised and why?
- elderly/young children: weak immune systems/young children have had little time to build up natural immunity to many diseases
- HIV/AIDS sufferers: weak immune systems so can't produce many antibodies themselves
- pregnant women: foetus has undeveloped immune system
- health workers: more likely to be at risk of getting disease
- those with chronic diseases like TB/autoimmune disease: already in poor health + bodies may be unable to withstand further disease
37
(MA) Why do some people choose not to get immunised?
- too busy/can't be bothered to go to the doctors
- media scare stories
- concerned about side effects
- allergic to vaccine
- fear of needles
- religious reasons
- cost of vaccine is too expensive
38
(MA) Why, other than the direct health benefits, does the government want people to be vaccinated?
- prevention of disease can save days lost at work by many people, prevents harm to the economy
- costs less to immunise people than to treat them
- health service may not be able to cope if large numbers of people became infected
39
(MA) Why are the elderly (and others) encouraged to get a vaccine for the influenza virus every year?
- vaccine is changed evert year
- different strains of virus each year as it has mutated from previous year
- new strains have different antigens
- old antibodies from previous year aren't complementary to new antigen + new vaccination will encourage new antibodies to be made
40
(MA) How do governments go about vaccinating people to control disease?
```
-herd vaccination
> vaccinate all people at risk
> stops infection spreading
-ring vaccination
> requires people to report victims
> vaccinate all people living with or near victim
> contains spread within ring
```
41
(MA) Why has it not been possible to produce an effective vaccine for malaria?
- different strains of the protoctist each year as it has mutated from previous year
- new strains have different antigens
- more than one stage in its life cycle + different stages have different antigens + would require different vaccines
- Plasmodium concealed in liver cells + RBCs so only exposed to immune system for a short period of time
42
(MA) Describe the life cycle of malaria.
- person w malaria has gametes of P. vivax in blood
- person bitten w female Anopheles mosquito + gametes in blood go into its stomach
- gametes fuse + zygotes of P. vivax develop in stomach
- develop into infective stages + migrate to salivary glands of mosquito
- mosquito bites uninfected person + injects in some of its saliva containing infective P. vivax
- infective stages of P. vivax enter new host's liver + divide (by mitosis)
- enter blood to feed on Hb in RBCs + make more gametes in process
43
(MA) Describe the effects on the body of HIV (human immunodeficiency virus).
- causes AIDS (acquired immune deficiency disease)
- HIV positive = inactive version of virus present (no symptoms of AIDS), can go unknown for a long time (during which time it can be transmitted)
- active version of virus destroys T helper cells
- lowers ability to destroy pathogens
- increased likelihood of contracting (AIDS related) diseases e.g. pneumonia
44
(MA) What is TB and how is it transmitted?
- bacteria: Mycobacterium tuberculosis + M. bovis
- transmitted by droplet infection (e.g. droplets from coughs/sneezes being inhaled)
- TB usually found in lungs
- can also be transmitted through milk/meat of infected cattle
45
(MA) What factors are likely to increase the transmission of pathogens e.g. TB?
- overcrowded living conditions
- poor ventilation
- poor health (or impaired immune system)
- poor diet
- homelessness
- living or working w people who have migrated from areas w high prevalence of TB
46
(MA) What is the structure of antibodies and what is the function of each structure?
- 4 polypeptide chains held together by disulphide bonds. Y shaped molecule
- constant region: for binding to phagocytes
- variable region: complementary in shape to antigen, binds to antigens
- more than one variable region: allows attachment to more than one antigen (hence attaching to more than one pathogen, agglutination)
- hinge region: allows flexibility for branches of Y shaped molecule to move closer/further apart to bind to more than one antigen
47
What is direct transmission?
Passing a pathogen from host to new host, with no intermediary
48
What is indirect transmission?
Passing a pathogen from host to new host, via a vector
49
What is transmission?
Passing a pathogen from an infected individual to an infected individual
50
What is a vector?
An organism that carries a pathogen from one host to another
51
How can pathogens be passed through direct transmission?
- direct physical contact, touching an infected person/infected surface
- faecal-oral transmission, mostly food/drink infected w pathogen
- droplet infection: pathogen caused by tiny droplets in the air
- spores: resistant stage of pathogen, carried in air or reside on surfaces/in the soil
52
What pathogens are spread through direct physical contact and what factors affect this type of transmission?
- HIV, bacterial meningitis, ringworm, athlete's foot
- hygiene: wash hand regularly, keep surfaces clean, cleaning + disinfecting cuts + abrasions, sterilising surgical instruments, condoms during sexual intercourse
53
What pathogens are spread though faecal-oral transmissions and what factors affect this transmission?
- cholera, food poisoning
- human sewage to fertilise crops, treatment of waste water + drinking water to reduce risk, washing of all fresh food, careful prep/thorough cooking of food
54
What pathogens are spread via droplet infection and what factors affect this transmission?
- TB, influenza
| - cover mouth when sneezing/coughing, dispose of tissue
55
What pathogens are spread by spores and what factors affect this transmission?
- anthrax, tetanus
- use a mask
- wash skin after contact w soil
56
How can disease be passed through indirect transmission?
-transmission via vectors/vehicles (non living things that cause disease)
57
How are pathogens spread in plants?
- directly or indirectly
- most common: through roots, particularly when damage around roots (direct)
- air borne transmission: fungi release spores carried by wind
- once pathogen infects may affect all vascular tissue. When leaves shed pathogen spread into soil to infect other plants
58
How are pathogens spread through indirect transmission in plants?
- result of insect attack: spores become attached to insect. Insect transfers pathogen from plant to plant
- e.g. dutch elm disease caused by beetle vector
59
Why is the transmission of particularly diseases, like malaria, lower in the UK than elsewhere in the world and why is there worry that malaria will become more of a pandemic in the future?
- moist warm conditions needed
- pathogens killed in colder climates
- global warming
60
What are the 2 types of plant defences?
- passive
| - active
61
What are the passive plant defences?
- cellulose cell wall: physical barrier. Has tannins: chemical defences activated if pathogen detected
- waxy cuticle: prevent water collecting which contains pathogens
- bark: physical barrier, contains chemicals that work against pathogens
- tylose: balloon-like projection fills xylem, acting as plug to prevent xylem carrying water preventing pathogen spread. Contains high levels of terpenes: toxic to many pathogens
- callose: large polysaccharide molecule deposited within sieve tube elements when pathogen detected. Blocks flow in tube + at Add to dictionary preventing pathogen spread into cells
62
What are the chemical passive plant defences?
- cellulose cell wall: Has tannins: chemical defences activated if pathogen detected
- bark: contains chemicals that work against pathogens
- tylose: contains high levels of terpenes: toxic to many pathogens
63
What are the physical passive plant defences?
- cellulose cell wall: physical barrier
- waxy cuticle: prevent water collecting which contains pathogens
- bark: physical barrier
- tylose: balloon-like projection fills xylem, acting as plug to prevent xylem carrying water preventing pathogen spread
- callose: large polysaccharide molecule deposited within sieve tube elements when pathogen detected. Blocks flow in tube + at Add to dictionary preventing pathogen spread into cells
64
What are the active plant defences?
- cellulose cell walls thicken w more cellulose
- callose deposit
- necrosis: deliberate death of infected cells to stop spread
- increase in production of chemicals (terpenoids, phenols, alkaloids, defensis, hydrolytic enzymes)
- oxidative bursts producing highly reactive oxygen molecules, damaging pathogens
65
What is a primary defence?
prevent pathogens from entering body (not part of the immune system)
66
What are some primary defences of animals?
- skin
- mucous membranes
- coughing + sneezing
- inflammation
- HCl
- ear wax
- lysosomes and antibodies in tears in eyes
- blood clotting + skin repair
- female reproductive system- mucus plug and acidic conditions
67
How do mucous membranes act as a primary defence against disease?
- specialised epithelial cells covered in mucus
- at exchange surface diff distance small so more susceptible to infection from pathogen
- mucous membranes coat these surfaces
68
How does coughing and sneezing act as a primary defence against disease?
- coughing, sneezing + vomiting are expulsive reflexes
- initiation caused by microbes/their toxins
- expulsion carries microbes with it
69
How does inflammation act as a primary defence against disease?
- swelling + redness of tissue caused by infection
- microbes detected by mast cells which release histamine
- histamine causes vasodilation: makes capillaries more permeable so more WBCs can leave
- more tissue fluid forms as more plasma leaves
- causes swelling (oedema)
- tissue fluid can drain into lymph vessels so pathogens may come into contact w lymphocytes (WBCs) + cause specific immune response
70
What is a non specific defence?
don't target specific pathogens, target every pathogen in the same way
71
How does blood clotting and skin repair occur, and therefore how does it act as a primary defence?
- damage to blood vessel
- platelets bind to exposed collagen to form a temporary platelet plug
- platelets release clotting factors activating an enzyme cascade
- enzymes cause fibrinogen to form which attach to plug
- RBCs are also trapped, causing a clot
- clot dries + forms scab that pulls skin closer together
- under the skin collagen is deposited
- stem cells in epidermis divide by mitosis + differentiate forming new skin cells at edge of cut
- new blood vessels form
- when edges of cut are drawn together the repair is complete
72
What is a secondary defence?
attempt to kill pathogens after they've entered the body (phagocytes attempt to kill pathogens before they can reproduce + cause any symptoms: non specific)
73
What are the main types of phagocytes?
- neutrophils
- macrophages
- (antigen presenting cell)
74
What is an antigen?
- proteins on cell surface membrane of cells
| - specific to each individual so antigens on pathogens surface recognised as foreign + produce response
75
What is an opsonin?
- type of antibody (protein) which attach to antigens onc ell surface membrane of pathogens
- not specific
- make it easier for phagocytes to bing to + engulf pathogen
76
What feature of neutrophils aids in their function of undergoing phagocytosis?
-lots of mitochondria as endocytosis uses microtubules which uses ATP
77
What is the function of neutrophils in the non specific response?
- most common phagocytes
- made in bone marrow + travel in blood
- can pass into tissue fluid as they can change shape + have multilobed nucleus so can fit between gaps in endothelium
- job is to engulf + digest pathogens
78
How does phagocytosis occur with the aid of opsonin?
- opsonin binds to antigen on pathogen's cell surface membrane
- receptor on neutrophil's cell surface membrane binds to opsonin
- pathogen engulfed by endocytosis (membrane invaginates, requires ATP from microtubules, membrane fuses w itself)
- produces a phagosome (vesicle w pathogen inside)
- lysosome w lysin in fuses w phagosome, releasing lysin enzyme into phagosome (lysosome moved towards phagosome by cytoskeleton w ATP)
- pathogen digested into amino acids + fatty acids etc
- products are absorbed into cytoplasm by diffusion
79
What is a macrophage, where is it made?
- made in bone marrow + travel in blood as monocytes
- settle in lymph nodes (via tissue fluid) + mature into macrophages
- initiate immune response
80
How would you recognise RBCs, neutrophils, monocytes and lymphocytes on a micrograph?
- RBC: majority of cells, look pink/red
- neutrophil: multilobed nuclei
- monocytes: largest WBC, large nucleus (kidney shaped)
- lymphocytes: smaller, nuclei almost fill cell
81
What do B and T lymphocytes differentiate from?
WBCs made in the bone marrow
82
Where are macrophages found?
lymph node
83
How is a specific immune response triggered?
- antigens on pathogen's surface communicate to body cell's it's foreign
- to initiate an immune response pathogens have to be detected by B + T lymphocytes w correct complementary receptors to pathogen's antigens
- infected cells sometimes get pathogen's antigens on surfaces helping select right B + T lymphocytes
- macrophages in lymph nodes engulf + digest pathogens incorporating antigens onto cell surface membrane: antigen presenting cells (increase chances of correct B + T lymphocytes locating foreign antigens)
- selection of correct lymphocytes w receptors w complementary shape to antigens: clonal selection
- more of these lymphocytes needed to fight pathogens so divide by mitosis: clonal expansion
84
What examples of cell signalling are there in the immune response?
- pathogen's antigens communicate to body cells they're foreign
- infected cells w foreign antigens on surface communicate to lymphocytes to be selected in clonal selection + to T killer cells they need to be killed
- antigen presenting cells communicate to T lymphocytes to be selected in clonal selection
- macrophages release monokines (cytokines) to attract neutrophils + stimulate B lymphocytes to differentiate into plasma cells
- T helper cells release interleukins that bind to receptors on B lymphocytes + stimulate them to divide by mitosis + differentiate
85
What is the role of T helper cells in the immune response?
rlease cytokines w specific shapes which bind to complementary receptors on cell surface membrane of B lymphocytes stimulating them to divide by mitosis + differentiate. Stimulate macrophages to carry out more phagocytosis
86
What is the role of T killer cells in the immune response?
search for + kill infected host cells by secreting protease enzymes into them
87
What is a canker?
A sunken necrotic lesion in plant tissue- stem or branch- causes death of cambium in the bark
88
What is the role of t memory cells in the immune response?
Provide long term immunity
89
What is the role of t regulator cells in the immune response?
Shut down the response once the pathogen has been removed, prevent autoimmunity
90
What is the role of plasma cells?
Circulate in blood and make and secrete antibodies
91
What is the role of b memory cells in the immune response
Act as immunological memory
92
Give examples of cell signalling in th immune response using cytokines
- macrophages release monokines. Some attract neutrophils by chemotaxis, others stimulate B cells to differentiate and release antibodies
- t cells and macrophages release interleukins, stimulate colonial expansion (proliferation) and differentiation of b and T cells
- cells release interferon, inhibits virus replication and stimulates activity of t killer cells
93
What are the non cytokine examples of cell signalling in the immune response?
- pathogens antigens communicate to body cells that they are foreign
- infected cells with foreign antigens on surface communicate to lymphocytes to be selected in colonial selection and to t killer cells that they need to be killed
- antigen presenting cells communicate to t lymphocytes to be selected in clonal selection
94
What is an autoimmune disease?
- immune system attacks part of the body
- normally lymphocytes specific to our own antigens are destroyed when immune system develops
- antibodies attack our antigens
95
Give examples of autoimmune diseases
- arthritis- joint inflammation, antibodies attack membranes around joint
- lupus- swelling and pain, antibodies attack proteins in nucleus of affected cells and affected tissues
96
What type of cells mature in the thymus?
T lymphocytes
97
What type of cells mature in the bone marrow?
B lymphocytes
98
What are antibodies?
Proteins which identify and neutralise antigens. Each antibody is specific to a particular antigen due to the complementary shapes of the antigens + variable region of the antibody
99
How do opsonins cause the neutralisation of pathogens?
- antibodies cover binding site in pathogens
- which prevents entry to host cells
- uncovered antigens would be used by pathogens as binding site to to enter host cells
100
Give 3 examples of antibodies.
- opsonins
- agglutinins
- antitoxins
101
What is the action of agglutinins?
- cause agglutination of pathogens
- multiple variable regions allows antibodies to clump/agglutinate together many pathogens
- clump too large to enter host cells + increases likelihood of being consumed by (named) phagocytes
102
What is the role of antitoxins?
Antibodies which bind to toxins produced by pathogen, making them harmless
103
What is autoimmune disease?
When the immune system attacks the body
104
What causes autoimmune diseases?
Antibodies start to attack our own antigens
105
Give an example of an autoimmune disease.
Arthritis - antibodies attach membranes around joints causing painful inflammation
106
Why is the term immunity incorrect when referring to bacteria and antibiotics?
- resistant
| - immune implies they have an immune system which they don't as they're single celled organisms
107
What is an epidemic?
A disease that spreads quickly and affects a large proportion of the population
108
What is a pandemic?
A disease which spreads worldwide over many countries + continents
109
What kind of immunity comes about from an infection (e.g. chicken pox)?
Natural active
110
What kind of immunity comes about from an injection of a weakened version of a disease (e.g. influenza vaccine)?
Active artificial
111
What kind of immunity comes about from transfer across the placenta or via breast milk?
Natural passive
112
What kind of immunity comes about from injections of antibodies (e.g. tetanus vaccine)?
Artificial passive
113
What are the reasons for changes to vaccines and vaccination programmes?
- once eradicated, routine vaccines can be relaxed as not likely to spread (e.g. small pox)
- governments stockpile vaccines for diseases which could potentially cause epidemics (e.g. swine flu)
- routine vaccinations need to be changed each year for some diseases by quickly mutating pathogens (e.g. influenza)
- vaccinating 'at risk' groups can avoid epidemics/pandemics for new strains of bacteria
