Chap 12 - Communicable Diseases Flashcards
1
Q
Define communicable diseases
A
a disease that can be passed from one organism to another due to pathogens
2
Q
Define pathogen
A
microorganism that causes disease
3
Q
Name 4 different pathogens and their examples
A
Virus - Bacteriophage, HIV, SARS‑CoV‑2
Protoctista - Amoebic dysentery, Giardia, Plasmodim
Bacteria - MRSA, E.coli
Fungi - Tinia pedis
4
Q
Describe 4 ways in which pathogens can damage host tissue, causing harm.
A
- viruses take over cell metabolism, using it to make new viruses which burst out of cell, destroying it and spreading to other cells
- some protoctista take over cell but digest and use cell contents as they reproduce - they dont take over genetic material
- fungi digest living cells & destroy them
- most bacteria and some fungi can produce toxins that affect host cells/damage them and cause disease
5
Q
What type of pathogen causes ring rot?
A
gram-positive bacterium
6
Q
What type of pathogen causes TMV?
A
virus
7
Q
What type of pathogen causes potato blight?
A
protoctist
8
Q
What type of pathogen causes black sigatoka?
A
fungus
9
Q
Identify host species of ring rot.
A
potatoes, tomatoes and aubergines
10
Q
Identify host species of TMV.
A
tobacco plant, tomato, peppers, cucumbers, petunias
11
Q
Identify host species of blight.
A
potatoes, tomatoes
12
Q
Identify host species of black sigatoka.
A
bananas
13
Q
What type of pathogen causes tuberculosis?
A
bacterium
14
Q
What type of pathogen causes bacterial meningitis?
A
bacterium
15
Q
What type of pathogen causes AIDS?
A
virus
16
Q
What type of pathogen causes Influenza?
A
virus
17
Q
What type of pathogen causes malaria?
A
protoctist
18
Q
What type of pathogen causes ring worm?
A
fungus
19
Q
What type of pathogen causes athletes foot?
A
fungus
20
Q
Identify host species of TB.
A
cattle, humans, badgers, deer
21
Q
Identify host species of bacterial meningitis.
A
humans
22
Q
Identify host species of AIDS.
A
humans
23
Q
Identify host species of influenza.
A
mammals and birds
24
Q
Identify host species of malaria.
A
humans
25
Identify host species of ring worm.
mammals
26
Identify host species of athletes foot.
humans
27
Define vectors
living or non-living factor that transmits a pathogen from one organism to another
28
Define spores
reproductive cell capable of developing into a new individual without fusion with a gamete
29
Define contagious disease
passed on from one person to another through direct contact
30
Describe what is meant by direct transmission of a pathogen.
pathogen transferred directly from one individual to another
31
Give types and examples of direct transmission.
- direct contact (kissing/body fluid contact, skin-to-skin contact, microorganisms fro faeces transmitted on hands)
- inoculation (break in the skin, animal bite, puncture wound)
- ingestion (taking in contaminated food/drink or transferring pathogens to the mouth from hands)
32
Give types and examples of indirect transmission.
- fomites (inanimate objects such as bedding, socks, cosmetics)
- droplet infection (droplets of saliva and mucus expelled from mouth)
- vectors (mosquitoes and malaria, water and diarrhoeal diseases)
33
How does ring rot spread?
- direct contact between plants
- soil contamination
- human vectors
34
How does TMV spread?
- direct contact
- soil contamination
- human vectors
35
How does potato blight spread?
- soil contamination
- wind vector
- water vector
36
How does black sigatoka spread?
- wind vector
- direct contact
37
How does TB spread?
- droplet infection
38
How does bacterial meningitis spread?
- direct contact from kissing/contact w body fluids
- droplets from sneezing/coughing
39
How does AIDS spread?
through a break in the skin - inoculation of infected blood in contact with non infected blood, sharing needles
40
How does influenza spread?
- droplet infection
41
How does ring worm spread?
- direct contact
- fomites
42
How does malaria spread?
- mosquito vector bite
43
How does athlete's foot spread?
- direct contact
- fomites
44
Describe 7 factors that affect the transmission of communicable diseases in animals.
- overcrowded living and working conditions
- poor nutrition
- compromised immune system
- poor disposal of waste providing breeding site for vectors
- climate change - introduce new vectors and diseases by increasing temperature
- culture and infrastructure - traditional medical practises increase transmission
- socioeconomic factors - lack of trained health workers
45
Describe and explain 6 factors that affect the transmission of communicable diseases in plants.
- planting varieties of crops susceptible to disease
- overcrowding increases likelihood of contact
- poor mineral nutrition reduces resistance of plants
- damp, warm conditions increase the survival and spread of pathogens and spores
- climate change - increased rainfall and wind
45
Describe and explain 6 factors that affect the transmission of communicable diseases in plants.
- planting varieties of crops susceptible to disease
- overcrowding increases likelihood of contact
- poor mineral nutrition reduces resistance of plants
- damp, warm conditions increase the survival and spread of pathogens and spores
- climate change - increased rainfall and wind
46
State 3 examples of barriers to pathogens in plants
- waxy cuticle on leaves
- bark on trees
- cellulose cell wall
47
Describe the major difference between plants response to pathogens and explain why this is a possible successful strategy for plants.
- they do not heal diseased tissue, they seal it off and sacrifice it
- they are continually growing at meristems so they can replace damaged parts unlike animals
48
Describe 2 ways in which a plant cell can detect the presence of a pathogen.
- receptors respond to mols from pathogens
- receptors respond to chemicals produced when cell wall is being broken down/attacked
49
Name two molecules produced by plants to limit the spread of the pathogen.
callose, lignin
50
Describe the strucutre of callose.
- polysaccharide
ß-1,3 linkages and ß-1,6 linkages
51
List 6 different types of plant chemical defences.
- insect repellent
- insecticide
- antibacterials
- antifungals
- anti-oomycetes
- toxins
52
Give example for insect repellents.
pine resin
53
Give example for insecticides.
pyrethrins made by chrysanthemums, act as insect neurotoxins
54
Give example for antibacterials
Phenols - antiseptics made in many different plants
55
Give example for antifungals.
chitinases -break down chitin fungal cell wall
56
Give example for anti-oomycetes.
glucanases - made by some plants that break down glucans - polymers found in cell walls of oomycetes
57
Give example for toxins.
chemicals that can be broken down to form cyanide compounds when the plant cell is attacked
58
Define non-specific defences.
- innate immune system, made up of phagocytes and barriers
- quicker than specific
59
State 4 barriers the human body has to minimise the entry of pathogens into our cells.
- skin
- mucous membranes
- eyelashes & nose hair
- tears
60
Explain how the skin acts as an effective barrier to the entry of pathogens.
- acts as a physical barrier
- skin flora of healthy microorganisms that outcompete pathogens on body surface
- sebum production to inhibit growth of pathogens
61
Explain how mucous membranes act as an effective barrier to the entry of pathogens.
- secrete sticky mucus that traps microorganisms
- contains lysozymes to destroy fungal and bacterial cell walls and phagocytes
62
Name 4 expulsive reflexes and explain their value for protection against pathogens.
- cough & sneeze - eject pathogen-containing mucus from gas exhange system, rapidly and in large quantity
- vomiting & diarrhoea - expel contents of gut along with infective pathogens also rapid and large quantity
63
Explain the importance of blood clotting and the release of serotonin by platelets.
- when there's a cut - pathogens can enter body & cause infection, also blood loss
- serotonin makes smooth muscle in walls of blood vessels contract so they narrow and reduce supply of blood to the area
64
Describe the processes involved in inflammatory response and explain their value for protection against pathogens.
- mast cells activated in damaged tissue and release histamines and cytokines
- histamines make blood vessels dilate, causing localised heat & redness - raised temp prevents pathogen reproduction
- histamines make blood vessels more leaky so blood plasma is forced out - swelling
65
Describe how fever is initiated in response to invasion by pathogens and explain its value for protection against pathogens.
- when infected, cytokines stimulate hypothalamus to reset thermostat and temperature increases
- most pathogens reproduce best at or below 37*C - higher temp inhibits reproduction
- specific immune system works faster at higher temp
66
Define phagocyte
specialised white blood cells that engulf and destroy pathogens
67
Name the two types of phagocytes
neutrophils
macrophages
68
Describe the stages of phagocytosis
- pathogens produce chemicals that attract phagocytes
- phagocytes recognise non-self antigens on pathogen - recognising self or non-self
- phagocyte engulfs pathogen and encloses it in a vacuole - phagosome
- phagosome combines with lysosome to form phagolysosome
- enzymes from lysosome digest and destroy pathogen
69
Describe the role of the major histocompatibility complex in the cytoplasm of macrophages at the end of phagocytosis.
- glycoprotein
- macrophage combines antigens from pathogen surface membrane with MHC
- MHC moves pathogen antigens to macrophage surface membrane becoming an antigen-presenting cell which stimulates
70
Define antigen-presenting cell.
a cell that displays foreign antigens complexed with MHC on their surfaces
71
Describe the role of cytokines in non-specific defences.
- cell signalling molecules informing other phagocytes the body is under attack
- stimulating phagocytes to move to site of infection/inflammation
- increase body temp and stimulate specific immune system
72
Describe the role of opsonins in phagocytosis.
- chemicals that bind to pathogens and tag them so they can be more easily recognised by phagocytes
- antibodies act as opsonins
73
Explain why blood smears need to be stained for viewing under the light microscope and name a stain used for this procedure.
- stains allow for differentiating between white blood cells, red blood cells and platelets
- stain: methylene blue
74
Name diff types of cell found in blood and outline how to identify them on blood smear slides.
- erythrocytes - red, biconcave shape, majority of cells in blood
- macrophages - kidney bean-shaped nucleus, non-grainy cytoplasm
- neutrophils - multi-lobed nucleus and grainy cytoplasm
- lymphocyte - very large nucleus, takes up almost entire cell
75
Define antigen
identifying chemical on the surface of a cell that triggers an immune response
76
Explain the difference between self and non-self antigens.
- self - on surface of your own cells
- non-self - on surface of cells of pathogens
77
Define antibody
y-shaped glycoproteins made by B cells of the immune system in response to the presence of an antigen
78
Define antigen-antibody complex.
complex formed by binding of an antibody to an antigen
79
Define lymphocyte
WBC that make up the specific immune system
80
Define specific immune response.
- acquired immune response triggered by antigens which is able to distinguish between different pathogens
- slower than non-specific
81
Describe & explain the structure of antibodies.
- glycoproteins made up of two identical long pp chains - heavy chains and 2 shorter identical chains - light chains
- chains held together by disulfide bonds
- hinge region provides flexibility - allowing one antibody to bind to two separate antigens, one at each binding site
82
Describe and explain 4 ways in which antibodies defend the body.
- opsonins - antigen-antibody complex easily engulfed and digested by phagocytes
- pathogens can no longer effectively invade host cells when they are part of antigen-antibody complex
- agglutinins - cause pathogens carrying complexes to clump together - prevents them from spreading and easier to engulf multiple at same time
- anti-toxins - make toxins harmless
83
Explain why B lymphocytes are called B whereas T lymphocytes are called T.
- B lymphocytes mature in Bone marrow
- T lymphoctes mature in the Thymus gland
84
Name 4 main types of T lymphocytes.
- T helper cell
- T killer cell
- T memory cell
- T regulator cell
85
Describe the role of T helper cells.
- produce interleukins (type of cytokine) that:
- stimulate activity of B cells - increasing antibody production
- stimulate production of other T cells
- attract and stimulate macrophages to ingest pathogens with antigen-antibody complexes
86
Describe the role of T killer cells.
produce perforin that kills pathogen carrying the antigen by making holes in the cell membrane
87
Describe the role of T memory cells
- live for long time, part of immunological memory
- if they meet an antigen a second time they divide rapidly to form many clones of T killer cells to destroy the pathogen quickly
88
Describe the role of T regulator cells.
- suppress the immune system once a pathogen has been eliminated
- make sure the body recognises self-antigens and does not perform an autoimmune response
89
Name 3 main types of B lymphocytes.
- B plasma cells
- B effector cells
- B memory cells
90
Describe the role of B plasma cells.
produce antibodies to a particular antigen and release them into circulation
91
Describe the role of B effector cells.
Divide to form plasma cell clones
92
Describe the role of B memory cells.
- live for long time, provide immunological memory
- if they meet a specific antigen a second time they enable the body to make a rapid response
93
Define cell-mediated immunity
T lymphocytes respond to cells of an organism that have been changed in some way
94
Suggest what it cell-mediated immunity is particularly effective against.
- effective against virus infection & early cancers
95
Describe the process of cell mediated immunity.
- in non-specific defence macrophages phagocytosed pathogens, process their antigens and form antigen-presenting cells
- T helper cell with complementary surface receptors to non-self antigens binds to APC
- T helper cell is stimulated to divide by mitosis to form many clones that differentiate into:
- T killer cells - destroy pathogen using perforins and toxins that trigger apoptosis
- T helper cells - secrete interleukins to stimulate phagocytosis and B cell division
- T memory cells - immunological memory of pathogen
- T regulator cells - suppress immune respomnse when pathogen removed
96
Define humoral immunity
B lymphocytes produce antibodies in response to antigens pathogens outside of cells
97
Suggest what humoral immunity is particularly effective against.
effective against bacteria and fungi
98
Describe the process of humoral immunity.
- B cell with complementary surface receptor to pathogen binds to it and engulfs
- antigens are processed, B cell becomes APC
- T helper cell with complementary receptor to presented antigen binds to the APC - clonal selection
- T helper cells induced to secrete interleukins
- interleukins stimulate B cell to divide by mitosis, produce many clones of that B cell variant - clonal expansion
- the B cell then differentiates into:
- plasma cells - secrete antibodies that fit the antigens on pathogens
- B memory cells - retain immunological memory of that pathogen, stored in lymphatic tissue
- secretion of many specific antibodies by plasma cells that circulate in blood and act as: opsonins, agglutinins, anti-toxins act against pathogens - defence
99
Define clonal selection
theory that exposure to a specific antigen selectively stimulates the proliferation of the cell with the appropriate antibody to form numerous clones of these specific antibody-forming cells
100
Define clonal expansion
mass proliferation of antibody-producing cells by clonal selection
101
Summarise the role of antigen presentation in specific immune response.
ensures that specific immune response can be initiated through recognition by T cells
102
Describe the role of cell signalling in the specific immune response.
cell signalling that occurs - interleukins
103
Define primary immune response.
relatively slow production of small number of correct antibodies the first time a pathogen is encountered
104
Define secondary immune response.
relatively fast production of very large quantities of the correct antibodies a second time a pathogen is encountered as a result of immunological memory
105
Define active immunity.
exposure to antigen, triggering specific immune response, antibodies made by individual
106
Define passive immunity
no exposure to antigen, pre-made antibodies received by individual
107
Define artificial passive immunity
results from administration of antibodies from another animal against a dangerous pathogen
108
Define artificial active immunity
results from exposure to a safe form of a pathogen like in vaccination
109
Define natural active immunity
results from response of body to invasion of a pathogen
110
Define natural passive immunity
given to an infant mammal by the mother through the placenta/breast milk
111
Define autoimmune disease
condition/illness resulting from the immune system acting against its own cells and destroying healthy tissue in the body
112
Name 3 examples of autoimmune diseases.
- type 1 diabetes
- rheumatoid arthritis
- lupus
113
Describe type 1 diabetes
- affects insulin-secreting cells of pancreas
- treated with insulin injections, pancreas transplants and immunosuppressant drugs
114
Describe Rheumatoid arthritis
- affects joints (esp. hands, wrists, ankles, feet)
- treated with anti-inflammatory drugs, steroids, immunosuppressants, pain relief
115
Describe Lupus
- affects skin and joints causing fatigue
- treated with anti-inflammatory drugs, steroids, immunosuppressants
116
Suggest how autoimmune diseases may occur.
when the immune system recognises 'self' antigens as 'non self', triggering immune response against its own cells
117
Define vaccine
safe form of an antigen which is injected into the bloodstream to provide an artificial active immunity against a pathogen bearing the antigen
118
Describe 5 ways in which antigens can be obtained for use in vaccines.
- killed/inactivated bacteria and viruses
- weakened strains of live bacteria/viruses
- toxin molecules that have been altered/detoxified
- isolated antigens extracted from the pathogen
- genetically engineered antigens
119
Describe how vaccination results in artificial active immunity.
- small amount of safe antigen-containing vaccine is injected into blood
- primary immune response triggered by foreign antigens and body produces antiodies and memory cells as if infected by live pathogen
- if in contact with that pathogen, but live, secondary immune response triggered and pathogen destroyed rapidly before suffering symptoms of disease
120
Define epidemic
when a communicable disease spreads rapidly to a lot of people at a local/national level
121
Define pandemic
same disease spreads rapidly across number of countries and continents
122
Define herd immunity
large part of population of an area is immune to a disease making the chances of an outbreak very low
123
Explain how vaccination of a significant number of people in a population can provide protection for unvaccinated people.
if there are enough vaccinated people, herd immunity is reached. less transmission = less likely for disease to reach unvaccinated person - it cannot spread through a population that is already immune
124
Suggest which members of a population are likely to need protection through herd immunity.
- people allergic to the vaccine
- people with weakened immune system that maybe take immunosuppressants
125
Give 3 examples of vaccination programmes that aim to provide herd immunity.
- COVID-19
- measles
- polio
126
Suggest why the influenza vaccine needs to be redeveloped and people need to be revaccinated each year.
- virus causing flu mutates regularly - its antigens on surface change too
- vaccines redeveloped as people will no longer be able to form secondary response against the mutated variant
127
Name 6 examples of common medical drugs derived from living organisms.
- penicillin
- docetaxel/paclitaxel
- aspirin (acetylsalicylic acid)
- prialt
- vancomycin
- digoxin
128
Describe penicillin
- source: commercial extraction from mould growing on melons
- action: antibiotic - effective against common bacterial diseases
129
Describe Docetaxel/paclitaxel
source: derived from yew trees
action: treatment of breast cancer
130
Describe aspirin
source: compounds from sallow (willow) bark
action: painkiller, anti-coagulant, anti-pyretic, anti-inflammatory
131
Describe prialt
source: derived from the venom of cone snail
action: pain-killer (1000x more effective than morphine)
132
Describe vancomycin
source: soil fungus
action: one of the most powerful antibiotics
133
Describe digoxin
source: extracted from foxgloves
action: powerful heart drug - treats atrial fibrillation and heart failure
134
Explain the need to maintain biodiversity in relation to discovery of new medicines.
- make sure we do not destroy an organism which could be key to a life-saving drug
135
Define personalised medicine.
combination of drugs that work with your individual combination of genetics and disease
136
Give an example of how treatment is being personalised.
- 30% of breast cancer patients have mutation on a certain gene
- activity of that gene can be shut down by a drug to reduce deaths from that type of cancer
137
Suggest the value of personalising medicine to a person's genetic information.
- we can improve how we treat disease by working out the best approach for a specific person
138
Define synthetic biology.
design and construction of new biological parts, devices and systems and re-designing existing natural biological systems for useful purposes
139
Give 3 examples of how synthetic biology may lead to better medical treatments.
- develop bacteria using genetic engineering that can produce drugs that are rare/expensive
- genetically modify mammals to produce therapeutic proteins in milk
- nanotechnology to deliver drugs to very specific sites within cells of pathogens or tumors
140
Define antibiotic.
chemical that kills or inhibits the growth of bacteria
141
Define selective toxicity.
ability to interfere with the metabolism of a pathogen without affecting the cells of the host
142
Suggest ways in which antibiotics may act selectively on bacterial cells but not human cells.
- destroy/affect peptidoglycan production bc humans dont need it - what the bacterial cell wall is made of
- target their metabolic pathways and not human ones
143
Explain why antibiotics do not work on viral infections.
- antibiotics specifically target machinery in bacteria
- they have completely diff structure and are non-living
- do not have a cell wall that can be attacked by antibiotics, instead they have protein coat
144
Outline different ways 4 common antibiotics have their effect.
- penlillin and cephalosporins weaken cell wall - bacterium more easily damaged by immune reaction
- sulfonamides interfere with metabolic reactions
- tetracyclines and streptomycin inhibit protein synthesis
- polymixines make holes in cell surface membrane altering its activity
145
Suggest two ways in which the use of antibiotics may be increasing the likelihood of resistance evolving.
- over-prescribing antibiotics
- giving farm animals antibiotics to prevent them from getting infected and reducing business profits
146
Give two examples of antibiotic resistant bacteria.
- MRSA
- C. difficile
147
Suggest two methods to reduce the likelihood of resistance developing in bacteria.
- minimise use of antibiotics
- good hygiene - inpact on spread of all infections including antibiotic-resistant strains
