1. Communicable Diseases Flashcards
Reasons for rapid spread of fungus between trees
Mobile vector Moving from tree to tree
Overcrowding of trees
Fungal spores carried by wind
Ways to minimise outbreak of bacteria
Increase ventilation
Measures to kill rats
Immediate quarantine for persons w symptoms
How to clone vegetables
Tissue culture
Why is asepsis important
Reduces contamination
Variables that would be controlled by planting clones in adjacent fields
Temperature, wind speed, rainfall, light intensity, soil pH, humidity
Factors that affect spread of communicable diseases
- lack of trained health professionals so lack of vaccinations
- poor sanitation so easy to pick up pathogen from lack of hand washing
- overcrowded living conditions = pathogens spread more easily by coughing
How does a virus enter a plant cell
Wound, carried by vector
How to observe callose production
- use a microscope
- take tissue samples from diff sites
- use a stain
Why does cells recognising and destroying incorrectly formed mRNA counteract infection.
Virus RNA recognised + destroyed and virus replication stopped
Benefit: faulty mRNA destroyed
How do malarial parasites bypass the body’s primary defences
Mosquito mouthparts pierce skin
Pathogen injected into blood
Role of opsonin
Binds to antigen on pathogen and assists binding to pathogycte (increase recognition by phagocytes)
Neutrophil adaptations
Many lysosomes
Many mitochondria
Multi Lobed nucleus
Well developed cytoskeleton
Role of cytokines
Attract phagocytes
Process that leads to production of antibodies against an unfamiliar bacterium
- b lymphocytes have antigen receptor on surface complementary to only one antigen
- activated b cell proliferates and differentiates into plasma cells which secrete antibodies complementary to antigen
How do t helper cells speed up production of antibodies
Stimulated by antigen presenting cells
Release interleukins that stimulate b cell proliferation
Why are diff strains immunologically distinct
- toxins produced by each strain will be different
- each toxin will have diff 3d shape
- toxin acts as antigen
- immune response determined by shape of antigen
Why is immune response faster when you get a disease for the second time
- first time = slower response because of clonal selection
- 2nd time = quicker response = more antibodies produced because of memory cells
Bond found between light and heavy region on antibody
Disulfide = to hold polypeptides together
What is Autoimmune disease
Abnormal immune response against tissues normally in the body (own tissue)
Why are antibodies specific to nuclear proteins not normally made
Nuclear proteins normally not exposed to tissue fluids
Agglutination
Clump pathogens and stop pathogens reproducing.
Help phagocytes engulf pathogens
Affect of overuse of antibiotics
- antibiotic is selective pressure
- bacterial gene pool has variation l- only some bacteria have resistance
- when exposed most resistant survive
- surviving bacteria continue to reproduce tp make a resistant population p- antibiotic becomes ineffective
Pathogens
organisms that can cause disease = bacteria, fungi, viruses, proctoctista
Bacteria
- can cause diseases by damaging your cell or releasing toxins
- Prokaryotic
Fungi cell wall
Chitin
Fungi
- Cause diseases that you can find on the surface of a plant
- Form spores = dormant stage of their life cycle
- Divide by budding?
- Release hyphaes = structure that releases the spores. From the hyphae they can release spores and form mycelium = ‘root’ keeps spores grounded (bundles of hyphaes make a mycelium
Viruses
- not living
- Hijack a cell and make use of the cell’s organelles to create more viral particles
Protoctist
- Parasites that enter the host and feed off them
Example of protoctista
Malaria is caused by a parasite called plasmodium
Diseases caused by bacteria
Tuberculosis, bacterial meningitis, ring Rot
Diseases caused by virus
HIV/AIDS, influenza, tobacco mosaic virus
Diseases caused by fungus
Black Sigatoka, ringworm, athletes foot
Diseases caused by protoctists
Blight, malaria
2 forms of transmission
Direct and indirect
Direct transmission
From one host to the next w nothing in between can pass on disease by physical touch, fecalo-oral, droplet infection, through spores
How to prevent disease transmission by physical touch
can be prevented by washing hands + cleaning surfaces + using protection for sexual intercourse
What is fecalo oral transmission caused by
Contaminated food e.g. cholera + food poisoning
What can fecalo oral transmission be prevented by
treating water + washing all fresh food = careful preparation of food
Droplet infection
pathogen is found inside water droplets
What can droplet infection be prevented by
covering mouth and nose when sneezing, using tissues and disposing of the properly
Spores
can be carried in the air or found in soil
What can spores be prevented by
wearing masks and washing skin after contact with soil
Other factors that affect transmission
Climate factors, social factors
Climate factors affecting transmission
increase in global warming = increasing temperatures so certain diseases can grow in different parts of the world
Social factors affecting transmission
overcrowding, poor education, poor ventilation, homelessness
Indirect transmission
when a pathogen is transmitted by a vector
Is malaria direct or indirect transmission
Indirect
What is malaria transmitted by
female mosquitos known as anopheles mosquito and the parasite being transmitted is plasmodium
Transmission of malaria
Plasmodium travels in the blood to the liver where it then further replicates and migrates to the blood again. Person = infected w/ malaria and if another female mosquito feeds from that blood the plasmodium replicates in her saliva and the second she bites someone else it spreads.
Direct transmission in plants
pathogens found in the soil can enter from the roots. Fungi produces spores = airborne + can affect plants directly, if spores are attached to an insect then it becomes
Indirect transmission of plants
pathogen transferred through insects
2 maintain types of responses against pathogens in plants
Chemical and non chemical
Physical defences in plants (passive)
Cell wall
Lignin
Waxy cuticles
Bark
Stomatal closure
Callose
Tylose formation
Cell wall
Acts as a physical barrier
Lignin
waterproof + can’t be digested = no pathogens can grow on it
Waxy cuticles
waterproof + prevents pathogens from growing on it
Bark
contains chemical defences and act as a physical barrier
Stomatal closure
if pathogens detected the guard cells will tell the stomata to close
Callose
sugar (polysaccharide) that is deposited around the sieve plates which blocks the flow in the sieve tube so the pathogens cannot spread around the plant
Tylose formation
swelling in xylem by forming a plug which prevents the spread of pathogens
Active defences in plants
- cell wall becomes thicker
- Callose deposition increases
- Oxidative bursts = reactive oxygen species that can damage cells
- An increase in production of chemicals
Chemicals used in plant defences
Terpenoids, phenols, alkaloids, hydrolytic enzymes
Terpenoids
oils that create a scent to prevent insects from biting + can have antibacterial and anti fungal properties
Phenols
e.g. tannins = found in bark + inhibit attack by insects by deactivating the salivary enzymes if the insects, causing them to die
Alkaloids
can activate or inhibit enzymes of the attacking animal or insect = can kill the attacking animal or insect by inhibiting processes such as protein synthesis which are vital for the animal/insect
Hydrolysis enzymes
enzymes produced by the plant that can affect the structure of the pathogen
Necrosis
deliberate cell suicide = to prevent pathogen from affecting neighbouring cells
Primary defences against disease
defences that prevented entry of the pathogen = non-specific
Primary defences in animals
Skin, blood clotting, mucous membranes, coughing and sneezing and vomiting, inflammation
The skin
acts as a physical barrier = made up of dead cells on the surface and prevents the entry of pathogens
Blood clotting
prevents entry of pathogens = needs calcium ions and 12 clotting factors + cell needed for clotting = platelets. First step = clot then after you form a scab = a seal which underneath the cells are working to regenerate that skin (skin repair = mitosis occurs + new cells are made)
Mucous membranes
made by goblet cells which trap the pathogens which is moved by cilia to the trachea. Mucus can either be spat out or swallowed where it will then be destroyed by the hydrochloric acid in the stomach. Mucus membranes are found in any openings of the body.
Coughing and sneezing and vomiting
aim is to get rid of the pathogen
Histamine
type of signalling molecule that has many effects e.g. vasodilation
Vasodilation
when the arterials dilate = allows more blood to reach the site of damage = causes redness and heat , can make the walls of the capillaries more permeable = more white blood cells can reach the site of damage which means that we get more tissue fluid = causes swelling (oedema)
Inflammation
performed by immune cells - in inflammation master cells (type of immune cell) are the first cell to detect the pathogen in the blood and they release histamine = causes all the symptoms of inflammation e.g. heat, swelling, pain, redness and loss of function.
Excess tissue fluid
drained into lymphatic system which has lymphocytes (type of white blood cells) therefore allowing more white blood cells to come into contact w/ the pathogen
Other primary defences in animals
- eyes protected by enzymes and antibodies in tear fluid
- Ear Canal is lined by wax which traps pathogens
- Acidity in stomach and vagina
Secondary defences
Non specific = used to combat pathogens that have entered the body.
What can phagocytosis be performed by
Neutrophils and macrophages
What reaches site of infection first
Neutrophils
Phagocytosis w neutrophils
detect the antigens on the pathogen and the pathogen is then engulfed, forming a phagosome. The phagosome then fuses with a lysosome allowing the pathogen to be digested and the harmless products can be absorbed into the cell of the neutrophil however the neutrophil dies soon after.
Phagocytosis w macrophages
carry out phagocytosis however at the end they can prevent the antigens on their surface and become antigen presenting cells (antigen presentation).
Neutrophils need for lots of mitochondria’s
Need for Endocytosis
Neutrophils need for ribosomes
Needed to produce lysosomes
Macrophages
type of white blood cell which travel in the blood as monocytes and when they reach the tissue they become known as macrophages. The best way to identify them is that they’re big and a big portion of the cell is made up of the nucleus. Dendritic cells = another type of macrophage
Secondary specific defence
specific immune system = every antigen is treated differently
2 types of lymphocytes
T and b lymphocytes
Where are t lymphocytes made
in the bone marrow and mature in the thymus gland
Where are b lymphocytes made
made in the bone marrow and mature in the bone marrow
Stages of specific immune response
Clonal selection, clonal expansion, differentiation
Clonal selection
Upon antigen presentation by the macrophage the t-lymphocytes with the complementary receptor to the antigen binds to it
Clonal expansion
Upon clonal selection the t-cells under mitosis/proliferation, where multiple copies of the t-cells are made.
What can T cells differentiate into
Killer, memory, helper, regulatory
T killer cells
attack the pathogen with the complementary antigen
T memory cells
remain in the blood until the same pathogen enters again + remember the antigen
T helper cells
release interleukins (type of cytokine) (to activate the B cells
T regulatory cells
stop the immune system when it’s no longer needed, preventing auto immune diseases from happening
What happens once b cells are activated
T helper cells prevents the antigens to the B cells and the B cells with the complementary antibodies to the antigen are activated, this is known as clonal selection. The B cells proliferate/expand through mitosis, this is known as clonal expansion. B cells have an antigen receptor that can detach which results in antibodies floating around in your blood.
What can b cells differentiate into
Plasma cells and memory cells
B plasma cells
release antibodies that are complementary to the antigen)
B memory cells
remain in the blood until the same pathogen enters + remember the antibody
Autoimmune diseases examples
Arthritis and lupus
Shape of antibodies
Y shaped
What are antibodies made up of
- Made up of 4 polypeptide chains, 2 heavy on the bottom and 2 light on the top
- Polypeptide chains are held by disulphide bonds
What is between light and heavy chains of antibodies
hinge regions which allows for flexibility (antibody can bend around antigen)
Variable region
At top of each peak of the y = actual receptor that binds to antigen
Wats antibodies can act
Opsonin
Agglutination
Anti toxin
Anti toxin
Neutralises toxins released by bacteria
Primary response
first time your body sees a pathogen
Secondary response
Second time your body sees a pathogen
Vaccination
dead pathogen or harmless pathogen or antigen only vaccine or harmless version of toxins to trigger the body’s primary immune system to create b and t memory cells against the antigen.
Can be live organisms
Vaccination programmes
Herd vaccination, ring vaccination
Herd vaccination
aim is to vaccinate all of the people at risk so that the disease can’t spread between people
Ring vaccination
vaccinating everyone in immediate proximity of the case.
Epidemic
rapid spread of disease through a population
Pandemic
rapid spread of disease globally
Routine vaccination
Viruses such as influenza require a new vaccination every year because they mutate a lot so every year their antigens change so the previous memory cells are no longer effective.
Global issues of vaccines
Not everyone can have access to vaccines
Vaccines can be really expensive
4 types of immunity
Active, artificial, natural, passive
Active immunity
- when your body produces its own antibodies
Artificial immunity
- when the body doesn’t see the pathogen itself, but develops immunity. E.g. vaccines
Natural immunity
- No medical intervention = happens over the course of someone’s life
Passive immunity
When the antibodies are given to the body (patient isn’t producing antibodies
Natural active
- immunity provided by antibodies made in immune system as result of infection
Example of natural active
Immunity to chickenpox (person suffers from disease once and is then immune)
Natural passive
when the antibodies are given through breast milk or placenta to the baby. Short lived = no antigens/no immune response,cannot make new antibodies
Artificial active
Antibodies given through vaccination = injected w dead or similar pathogen or antigen = activates immune system
Example of artificial active
Immunity to TB and influenza
Artificial passive
antigodies injected in the person made by another individual
Artificial passive immunity example
Dog bite - tetanus
Sources of new medicine needed bc
- new diseases are emerging
- antibiotic resistance is increasing
What are antibiotics used to treat
Bacteria and fungi but not viruses
Selection pressure
forces evolution + survival of the fittest. Factor that promotors survival of the fittest in bacteria.
Main reasons for antibiotic resistance
- misuse of antibiotics
- Course of taking the antibiotics stops earlier than you should have stopped it = causes the alive bacteria to survive and reproduce
Implications of antibiotic resistance
more people are going to suffer from complications after surgery, more people are going to suffer from infections that can’t be treated.
MRSA
methicillin-resistant staphylococcus aureus
^found in hospitals
Clostridium difficile (C. Diff)
When someone has these diseases it is harder for them to be treated = high antibiotic resistance
How are medicines discovered
Accidental discovery
Tradition remedies
Observation of wildlife
Accidental discovery
- antibiotics can be produced by bacterias themselves to try and kill the bacteria next to it
- E.g. penicillin is an antibiotic which comes from the fungus penicillium
Traditional remedies
- e.g. ibuprofen and aspirin come from willow bark trees
- Morphine comes from poppy seeds
- Traditional medicine has now been manufactured into
Observation of wildlife
E.g. monkeys rub citrus oil on their coats
Ways to personalise medicine
Synthetic biology
Synthetic biology
making a drug from scratch.
Personalised medicine
making a drug that treats a specific persons disease and how it affects their body.
Why are vaccinations an example of active immunity
Antibodies produced by person being vaccinated.
Memory cells remain in person
Why can’t one vaccine protect against more than one pathogen
different pathogens have different aftigens (1)
antigens have specific shape (1)
shape of antibody must be complementary to (specific) antigen (1)
any of the above linked to different antibody needed for each pathogen (1)
2 groups vulnerable to infection
Babies and elderly
ii.
Name the process that increases the proportion of penicillin-resistant bacteria in the population.
Natural selection
Macrophages engulfing bacteria
- antigens on the bacteria are detected by receptors on phagocytes
- Phagocytosis - phagocyte engulfs the bacteria which forms a phagosome
- Phagosome fuses w lysosome
- Lysosome contains hydrolytic enzymes which digest the pathogen
- Useful products are recycled and the antigens are presented on the surface of the macrophage and the macrophage becomes an antigen presenting cell
Monocytes vs macrophage
Monocytes = when macrophage is in blood
Macrophages: when in tissue
Does phagocytosis require energy
Yup
