Communicable diseases, disease prevention, and the immune system Flashcards
1
Q
Communicable diseases
A
- disease that is caused by a pathogen
- transmitted directly between organisms
2
Q
pathogens
A
a disease causing microorganism
3
Q
types of pathogen
A
- bacteria
- virus
- protoctista
- fungi
4
Q
Bacteria - example
A
- ring rot
- tuberculosis
5
Q
Virus - example
A
- HIV
- Tobacco mosaic virus
- Influenza
6
Q
Protoctista - example
A
- malaria
- potato late blight
7
Q
Fungi - example
A
- athletes foot
- black sigatoka
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Q
Bacteria
A
- prokaryotic cells that have cell walls but lack organelles
- produce toxins which damage host cells
9
Q
Who can tuberculosis infect
A
- humans
- deer
- cows
- badgers
10
Q
Tuberculosis - transmission
A
- airborne droplets
- more likely for those who live in cramped conditions
11
Q
Tuberculosis symptoms
A
- damages lung tissue
- supresses immune system
12
Q
tuberculosis cure
A
prevented - vaccination
cured - antibiotics
13
Q
What can late blight infect
A
- potato
- tomato
- aubergines
14
Q
what does late blight do
A
- damages leaves, tubes, fruit
15
Q
how is late blight transmitted
A
- infected tubers
- micropropagation of plantlets from infected plants
16
Q
effects of late blight
A
- reduces crop of plants
- livelihood of farmers
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Q
Viruses
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- non living and acellular
- smaller than bacteria
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Q
what is a virus made up of
A
- genetic material
- capsid
- attachment proteins
19
Q
where does viral replication occur
A
- inside host cells
- involves injection of nucleic acid into the cells
20
Q
example of a virus which infects bacteria
A
bacteriophage
21
Q
HIV -
A
- transported around in the blood until it attaches to a protein on the T helper cells
- HIV positive = person is infected with HIV
22
Q
Aids
A
- replicating viruses in the helper T cells interfere with normal functioning of immune system
23
Q
effects of aids
A
- T helper cells destroyed
- Host cannot produce an adequate immune response
- vulnerable to infections and cancer
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Q
HIV - transmission
A
- direct contact through sharing / mixing bodily fluids
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Influenza
- infect ciliated cells lining gas exchange surfaces
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Who are more prone to influenza
- young children
- elderly
- anyone with a lowered immunity
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Symptoms of influenza
- headache
- blocked nose
- sore throat
- aches
- extreme muscle tiredness
- vomiting
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how is influenza virus transmitted
- airborne droplets when coughing/sneezing
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Consequences of influenza virus
possibly death
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Tobacco mosaic virus - what infected
tobacco plants
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What does tobacco mosaic virus do
- damage leaves, causing mosaic pattern
- damages the flowers and fruits
- prevents plant growing properly
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how is tobacco mosaic virus transmitted
- infected leaves touch healthy leaves
- gardeners use contaminated tools
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cure - tobacco mosaic virus
- no cure
- resistant strains have been developed though
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protoctista
- eukaryotes that exist as single celled organisms / cells grouped into colonies
- few are pathogenic
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how are protoctista transmitted
via a vector
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what are pathogenic protoctista called
parasites
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Malaria symptoms
- headache
- chills
- fever
- fatigue in muscles
- back pain
- nausea / vomiting
- spleen enlargement
- dry cough
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Malaria
- caused by plasmodium
- spread to humans through mosquitos (vectors)
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Plasmodium
- reproduces sexually and asexually within mosquitos and humans
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how is malaria transmitted
- mosquito bites when taking blood from humans
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what does plasmodium do in humans
- infects red blood cells
- liver
- brain
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Cures - malaria
- no cure/ vaccine
- some preventative medicines
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Late blight -
- caused by fungus like protoctista
- caused in tomatoes / potato
- has hyphae which enters plant and causes damage to leaves and fruit
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how is potato blight transmitted
- spores which travel in wind
- transferred by animals / insects
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cure - potato blight
- no cure
- resistant strains developed
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fungi
- eukaryotes that cause many plant diseases
- multicellular / single cellular
- pathogenic fungi are parasitic
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what does parasitic fungi do
release enzymes to digest hosts tissue
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black sigatoka
- infects bananas
- fungal hyphae causes damage to leaves
- causing them to turn black, preventing growth
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how is black sigatoka transmitted
spores - from 1 plant to the next through the wind
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black sigatoka cure -
- fungicides
- resistant strains
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Athletes foot
- humans
- type of ring worm , thrives in warm, damp, regions
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Athletes foot - effect
- causes skin to crack and become scaly
- causes itchiness / soreness
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Athletes foot - transmission
- direct contact
- e.g, wearing same socks/ shoes as infected person
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Athletes foot - cure
antifungal creams
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What conditions make pathogen transmission more likely
- hot climates
- social factors
-
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hot climates
- increased heat
- more kinetic energy
- more chemical reactions and reproduction
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social factors
- poverty :
- poorer sewage infrastructure
- lack of fresh water / food
- poorer sanitation
- overcrowded living quarters
- medicines / vaccines being less available
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types of transmission
- direct
- indirect
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Direct transmission - animals
- direct contact
- inoculation
- Ingestion
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Direct contact
- touching
- kissing
- contact with cuts in skin
- sexual contact
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Inoculation
- animal bites
- sharing needles
- cuts in skin
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Ingestion
- drinking / eating contaminated food / water
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Indirect transmission - plants
- vectors
- droplets
- fomites
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vectors
- animals that pass the pathogen to humans
- e.g, mosquitos transmitting malaria
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droplets
- pathogens transmitted in droplets of water
- saliva / mucus when sneezing
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fomites
- dirty bedding / socks / cosmetics
- inanimate objects that can carry / transmit pathogens
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Direct transmission - plants
- direct contact
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direct contact - plants
- between different plants
- e.g ring rot
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Indirect transmission - plants
- contaminated soil
- vectors
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contaminated soil
- pathogens and their spores can remain in soil / infect roots of subsequent plants
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vectors
- wind
- water
- animals / humans can carry pathogens and spores from 1 plant to another
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Plant responses to pathogens
- barriers
- antibacterial chemicals
- physical defences
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Barriers - plants
- to prevent entry
- e.g bark
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antibacterial chemicals -
- act as a defence against bacterial infections
- can repel insects / kill pathogens
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physical defences
- prevents pathogens spreading between their cells
- e.g, callose
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Animal responses to pathogens
- primary line of defence
- secondary line of defence
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primary line of defence
- non - specific
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primary lines of defence - examples
- skin
- blood clots
- mucus membranes
- lysozymes
- expulsive reflexes
- inflammation
- histamines
- cytokines
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skin
- acts as physical barrier
- contains skin flora which outcompetes pathogens for space / resources on skin
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blood clots
- form if skin is cut to form a new barrier
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mucous membranes
- line many body tracts
- mucus traps pathogens
- cilia sweep mucus away from lungs
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lysozymes
- hydrolytic enzymes
- digest pathogens
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expulsive reflexes
- sneezing
- coughing
- vomiting
= forces pathogens out of body
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inflammation
- causes area to become red / hot / sore / itchy
- this damage triggers mast cells to release histamines and cytokines
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histamines
- cause blood vessels to dilate
- more blood flows to this area
- increased temperature kills pathogens
- make walls of blood vessels more permeable = more wbc to site of damage
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cytokines
- attract phagocytes
- engulf and destroy pathogens
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Phagocytes
- travel in blood and squeeze out of capillaries to engulf and digest pathogens
- no n specific
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Phagocytosis
- damaged cells and pathogens release cell signalling chemicals that attract phagocytes
- an opsonin protein attaches to pathogens to mark them / make it easier for neutrophils and macrophages to engulf them
- phagocytes have receptors which attach onto chemicals on surface of pathogens
- phagocyte engulfs pathogen into vesicle to create a phagosome
- within phagocyte there are lysosomes which have hydrolytic enzymes
- the lysosome fuses with phagosome to expose pathogen to lysozyme
- lysozyme hydrolyses with pathogen and any soluble molecules absorb into cytoplasm of phagocyte
- phagocytes will present antigen of digested pathogen on their surface = antigen presenting cells
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examples of phagocytes
- macrophages
- neutrophils
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Second line of defence
- specific response to antigens
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2 types of lymphocytes
- B lymphocytes
- T lymphocytes
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how are both lymphocytes created
bone marrow
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difference between b and t cells
- B cells mature in bone marrow
- T cells mature in thymus
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Cell mediated response
- Receptors on T cells bind to antigen on antigen presenting cells
- T cells divide rapidly by mitosis (clonal expansion)
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Antigen presenting cells
cells that present a non - self antigen on their surface
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examples of antigen presenting cells
- infected body cells
- macrophage
- cells of a transplanted organ
- cancer cells
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infected body cells
- present viral antigens on their surface
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Macrophage
- engulfs and destroys a pathogen
- by presenting antigens on their surface
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Cells of a transplanted organ
- have different shaped antigens on their surface compared to your self - cell antigens
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Cancer cells
- have abnormal shaped self antigens
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Cell mediated response - step by step
- once a pathogen has been engulfed and destroyed by a phagocyte the antigens are positioned on the cell surface
- = antigen presenting cell
- T helper cells have receptors on their surface which attach to antigens on APC
- once attached, interleukins are produced which activates the T helper cells to divide by mitosis to replicate and make a large number of clones
- cloned T helper cells differentiate into different types of cells
102
During cell mediated response, what type of cells do T helper cells differentiate into
- Produce interleukins to activate B - lymphocytes
- Produce interleukins to stimulate macrophages for more phagocytosis
- T memory cells for that shaped antigen
- T killer cells
- T regulator cells
103
T regulator cells - role - cell mediated response
- supress immune response
- ensuring cell mediated response only occurs when pathogens are detected
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T killer cells
- destroy abnormal / infected cells
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how do T killer cells perform their role
- release a protein
- which embeds in cell surface membrane
- makes a pore
- so any substances can enter or leave the cell
- causing cell death
106
why are T killer cells most commonly used in viral infections
- viral infections infect body cells
- they are sacrificed to prevent viral replication
107
how is the humoral response activated
- T helper cells stimulate B cells by producing interleukins
108
what does the humoral response involve
antibodies
109
Antibodies - structure
- globular, quaternary proteins
- have binding sites complementary in shape to antigens
- made up of 4 polypeptide chains
- 2 heavy polypeptide chains
- 2 light polypeptide chains
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Antibody - binding site
- Variable region
- antibody binds to complementary antigen
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Antibody - constant region
rest of antibody
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Antigen - antibody complex
- formed when an antigen binds to an antibody
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Antibody - hinge region
- gives them flexibility
- allowing them to bind to multiple pathogens
114
How do antibodies work
- agglutination
- marking pathogens
- anti - toxins
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Agglutination
- clumping together pathogens
- making it easier for phagocytes to locate and engulf them
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Marking pathogens
- Antibodies act as opsonin when an antigen - antibody complex forms
- antibodies are marking the antigen making them more susceptible for phagocytosis
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Antibodies acting as anti - toxins
- bind to toxins
- preventing them from entering cells and causing harm
118
Process of humoral response
- Clonal selection
- B cell is activated by the release of interleukins from T helper cell
- Clonal expansion
- Plasma cells produce antibodies which attach to antigens on pathogen to help destroy them by agglutination and marking them for phagocytes
- Primary immune response
119
Clonal selection
- activated T helper cells bind to B cells with complementary antibody to antigen
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Clonal expansion
- B cells rapidly divide by mitosis to make clones
- these differentiate into memory B cells or plasma cells
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B memory cells - humoral response
- remain in blood after infection
- can rapidly produce large amounts of antibodies if there is reinfection with the same pathogen
122
Primary immune response
- first exposure to a pathogen
- it can take a few days for lymphocytes to create enough of the complementary antibodies to destroy the pathogen
- you suffer symptoms before pathogen is destroyed
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Secondary immune response
- when you are re-infected with same pathogen
- B memory cells can help produce large amounts of antibodies rapidly
- pathogen is destroyed before causing any symptoms = active immunity
124
Passive immunity
- antibodies are introduced into the body
- pathogen does not enter body
- plasma and B - memory cells are not made
- No long term immunity
125
Natural passive immunity
- antibodies passed to a foetus through placenta
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Artificial passive immunity
- transfusion / injection of antibodies as a part of medical treatment for a disease
- e.g hepatitis B
127
Active immunity
- Immunity is created by your own immune system
- following exposure to the pathogen
128
Natural active immunity
- following infection by a pathogen
129
Artificial active immunity
- following introduction of a weakened version of the pathogen via vaccine
130
How do we prevent lymphocytes from destroying our own body cells
- cells are labelled with proteins for recognition
- each is labelled a unique shape protein
- lymphocytes recognise these as self cells
131
Non - self cell
- any other type of protein detected on the surface of a cell
- recognised as non self
- destroyed
132
example of non self cells
- abnormal body cells, e.g cancer
- toxins produced by pathogens
- pathogens
- cells from other organisms of the same species
133
Antigen
- a protein on the cell surface membrane of non self cells
- their presence triggers an immune response and production of antibodies
134
Autoimmune diseases
- immune system identifies your own body cells as non - self and therefore harmful
- recognises antigens on some body cells/tissues as non self and produces antibodies against them
- cells are then attacked damaged / causing symptoms of the disease
135
How are autoimmune responses triggered
- immune system responds to abnormally healthy microorganisms in the body
- overreacts to mild pathogens
- T regulator cells do not work properly, so immune response isn't regulated
136
Example of an autoimmune disease
Rheumatoid arthiritis
137
Rheumatoid arthiritis
- immune system attacks cartilage in joints
- causes inflammation and pain in joints
138
Cure Rheumatoid arthiritis
- no cure
- anti-inflammatory durgs
- steroids
- pain relief
- immunosuppressant drugs can be taken to relieve symptoms
139
Immunisation
- can induce passive / artificial active immunity
- disease prevention method
140
Artificial active immunity
- antigens or small amounts of an attenuated pathogen are injected
- triggering a primary immune response with few symptoms
- so if re-infected by same pathogen antibodies will be produced much quicker
- due to secondary immune response
141
Vaccination - uses
- protection against disease
142
Passive immunity
- antibodies are injected directly into you to help destroy the pathogen
143
Vaccines - disadvantage
- not always long term effective
- due to antigen variability
144
Antigen variability
- pathogens genetic material can mutate
- resulting in a pathogen producing a different shaped antigen
145
epidemic
a disease spread rapidly on a national level
146
pandemic
disease spreads rapidly on a global level
147
what can prevent epidemics/pandemics
- mass vaccination programmes
- prevent further spread of pathogen
- vaccines are frequently updated
- giving booster vaccines, accounting for antigen variability
148
herd immunity
- if a large enough proportion of population are vaccinated
- most are immune
- it is unlikely a susceptible individual will encounter an infected individual
149
Sources of medicine
- microorganisms
- plants
- why maintaining biodiversity is important
- generally safer and cheaper than synthetic drugs
150
Antibiotics
- produced by microorganisms that inhibit the growth of other microorganisms
151
examples - antibiotics from microorganisms
- penicillin
- vancomycin
152
example - antibiotics from plants
- aspirin
- digitoxin
- quinine
153
aspirin source
willow bark
154
digitoxin source
foxglove
155
quinine source
cinchona tree
156
importance of maintaining diversity
- many drugs originate from plants/ microbes
- increasing chance of finding new drugs
- we maintain genetic resource for future
- once a species is extinct its genetics and potential medicines are lost forever
157
Antibiotic resistance
- random mutations
- a mutation could code for a new protein that provides the bacterial with a selective advantage
- making bacteria more likely to survive
158
what did the widespread use, misuse of antibiotics do
- strengthened selection pressure
- resulting in antibiotic resistance
- which spreads rapidly amongst bacteria
159
where is the mutated gene for antibiotic resistance found
- plasmid
- can be exchanged between bacteria
- resistant strain can reproduce rapidly until a resistant strain of bacteria is created
160
Old medicines
- sourced from plants / microorganisms
- e.g aspirin
161
New medicines - pharmogenetics
- personalised medicines
- link to gene technology
- allowing scientists to work out why certain levels are more/less effective for different people
162
Pharmacogenetics uses
- identify most suitable drug/ dosage for someone to have
163
synthetic biology
- includes synthetic manufacture of medicines
- e.g, genetic engineering of insulin
- using cells as medicine factories
164
what does synthetic biology combine
- gene sequencing
- bioinformatics
- computational biology
- this is to find base sequence of proteins
- store data digitally
- make 3-D models and simulations before physically producing a medicine
