4.1.1 Communicable diseases, Disease prevention and the Immune System Flashcards
1
Q
Communicable disease
A
- Diseases cased by pathogens that invade the body and disrupt normal function
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Q
Bacteria - Tuberculosis
A
- Infect humans, deer, cows, pigs
- Transmitted through airborne droplets
- Harms by damaging lung tissue and supressing immune system
- Cured using antibiotics an prevented through vaccination
3
Q
Bacteria - Ring rot
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- Infects potatoes, tomatoes + aubergines
- Damages leaves, tubers + fruit
- Transmitted through infected tubers and micropropagation of plantlets from infected plants
- Reduces crop of plant + affects livelihood of farmers
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Q
Viruses
A
- Non-living and acellular
- Smaller than bacteria
- Consists of genetic material, a capsid and attachment proteins
- Viral replication occurs inside host cells + involved injection of nucleic acid into the cell
- Bacteriophage - virus that infects bacteria
5
Q
Viruses - HIV/AIDS
A
HIV - transported around blood then attaches to protein on helper T cells - transmitted through direct contact through sharing/mixing of bodily fluids
AIDS - when replicating viruses in helper T cells interfere with normal functioning of the immune system
- Helper T cells destroyed, host unable to produce an adequate immune response to other pathogens - vulnerable
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Q
Virus - Influenza
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- Infect ciliated cells lining gas exchange surfaces
- Young children, elderly + lowered immune system at higher risk of severe symptoms or dying
- Transmitted by airborne droplets when coughing or sneezing
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Q
Virus - Tobacco Mosaic Virus
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- Infects plants - tobacco
- Damage to the leaves - mosaic patterns
- Damages flowers + fruits
- Prevents plant from growing
- Transmitted when infected leaves touch healthy leaves of contaminated tools
- No cure but made resistant strains
8
Q
Protoctista
A
- Eukaryotes that exist as single celled organisms
- Very few are pathogenic but the few cause extremely dangerous symptoms to the hosts they infect
- Parasites - usually transmitted via a vector - malaria transmitted by mosquitoes
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Q
Protoctista - Maleria
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- Caused by Plasmodium + spread to humans via mosquitoes - vectors
- Reproduces both sexually +asexually within mosquitoes + human hosts
- Passed from mosquitoes to humans when they bite + take blood
- Infects RBC, liver + brain
- Preventative medicines but no vaccine or cure
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Q
Protoctista - Potato blight
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- Caused by fungus-like protoctista
- Causes potato blight + tomato late blight
- Hyphae which enter the plant and cause damage to the leaves and fruit
- Transmitted by spores by wind or animals + insects
- No cure, resistant strains made
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Q
Fungi
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-Eukaryotes that cause many plant diseases
- Multicellular or single-celled
- Pathogenic fungi are parasitic - releasing enzymes to digest the host’s tissue
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Q
Fungus - Black sigatoka
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- Infects bananas
- Hyphae cause damage to leaves - black - preventing plant growth
- Transmitted by spores through the wind
- Fungicides can kill the fungus + resistant strains
13
Q
Fungus - Athlete’s foot
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- Infects humans
- Ring worm that thrives in warm, damp regions between the toes
- Causes skin to crack and become scaly + itchiness + soreness
- Transmitted by direct contact - same socks/shoes
- Cured using antifungal cream
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Q
Modes of transmission - Direct
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Direct contact - touching, kissing. contact with cuts on skin + sexual
Inoculation - animal bites, sharing needles, cuts in skin
Ingestion - drinking, eating contaminated water + food
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Q
Modes of transmission - Indirect
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Vectors - animals that pass the pathogen to humans, mosquitoes
Droplets - pathogens transmitted in droplets of water, saliva + mucus when sneezing
Fomites - dirty bedding, socks, cosmetics - inanimate objects that can carry and transmit pathogens
16
Q
Modes of transmission - Plants
A
- Direct contact - between different plants
- Contaminated soil - pathogens + spores remain in the soil + infect roots of plants
- Vectors - wind, water, animals, humans can carry pathogens + spores from one plant to another
17
Q
Plant responses
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-Barriers to prevent entry - bark, waxy cuticles
- Antibacterial chemicals + proteins - can repel insects and kill pathogens
- Physical defences - producing callose to stop pathogens spreading between cells
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Q
Animal responses - Primary
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- Non-specific
- Skin - physical barrier, skin flora which outcompete pathogens
- Blood clots - form if the skin is cut to form a new barrier
-Mucous membranes - mucus produced traps pathogens + cilia sweep it away from the lungs - Lysozymes - hydrolytic enzymes which digest pathogens
- Expulsive reflexes - sneezing, coughing mechanisms to force pathogens out the body
- Inflammation - localised areas where damage to cells is detected. Causes area to become red, hot, sore, swollen - mast cells release histamines + cytokines
- Histamines - blood vessels dilate, more blood flowing in the area - increased temp from blood can kill pathogens - wall oof BV more permeable - more WBC delivered to site of damage
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Q
Phagocytosis
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- Phagocytes (macrophages, neutrophils)
- Non-specific
1. Damaged cells + pathogens release cytokines that attract phagocytes to site of infection
2. Opsonin protein can attach to pathogens to mark them + easier for phagocytes to engulf
3. Phagocytes have receptors which can attach onto chemicals on surface of pathogens
4. Phagocyte engulfs the pathogen into a vesicle - phagosome
5. Within phagosome - lysosomes containing hydrolytic lysozyme enzymes.
6. Lysosome fuses with phagosome - hydrolyses the pathogen + soluble useful molecules are absorbed into cytoplasm
7. Phagocytes present the antigen of digested pathogen on their surface - antigen-presenting cell
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Q
Second line of defence - lymphocytes
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-Specific response
- B lymphocytes
- T lymphocytes
- Created by bone marrow cells - B cells mature in bone marrow, T cells mature in thymus
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Q
Cell-mediated response - T-cells
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-Receptors on T cells bind to antigens on antigen-presenting cells
- Interleukins produced - activated T helper cells to divide by mitosis rapidly (Clonal expansion)
- Cloned T helper cells differentiate into different cells:
T helper cells produce interleukins to activate B lymphocytes
Some produce interleukins to stimulate macrophages to perform more phagocytosis
T memory cells for that antigen
T killer cells
T regulator cells - supress the immune response to ensure the cell mediated response only occurs when pathogens are detected
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Q
T killer cells
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- Destroy abnormal or infected cells
- Release a protein, perforin, embeds in the cell surface membrane + makes a pore - any substances can enter + leave the cell + cell death
- Common in viral infections - viruses infect body cells - sacrificed to prevent viral replication
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Q
Humoral response
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- T helper cells stimulate B cells by producing interleukins
- Initiates humoral response - antibodies
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Q
Antibodies
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- Globular quaternary proteins, have binding sites complementary in shape to antigens Made up of 4 polypeptide chains, 2 heavy and 2 light
- Binding site - variable region, antibody binds to a complementary-shaped antigen
- Rest of the antibody is the constant region
- Antigen binds to antibody - antigen-antibody complex
- Hinge region gives it flexibility when binding to multiple pathogens
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Agglutination
- Clumping together of pathogens to make it easier for pathogens to locate + engulf
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Acting as opsonins
-Antibodies act as an opsonin when an antibody-antigen complex has been formed
-Antibodies are marking the antigen, making them more susceptible to phagocytosis
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Act as anti-toxins
-Antibodies can bind to toxins, preventing them from entering cells + causing harm
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Process of humoral response
- Activated T helper cells bind to B cells with complementary antibody to antigen (clonal selection)
- B cell activated by release of interleukins from T helper
- B cells rapidly divide by mitosis - make clones that differentiate into memory or plasma cells (clonal expansion)
- Plasma cells produce antibodies - attach to antigens on pathogen - help destroy by agglutination + phagocytosis
- Primary immune response
- B memory cells remain in blood after infection + rapidly produce large amounts of antibodies if reinfection occurs
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Primary + Secondary immune response
- First exposure to a pathogen - primary immune response
- Can take a few days for the lymphocytes to create enough antibodies to help destroy the pathogen - suffer from symptoms before pathogen is destroyed
- Secondary immune response - re-infected with same pathogen. B memory cells help produce large amounts of antibodies rapidly - pathogen destroyed before causing any symptoms (active immunity)
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Passive immunity
- Antibodies introduced to the body, pathogen doesn't enter the body - plasma + memory cells not made
- No long-term immunity
Natural passive - antibodies passed to a foetus through placenta or breast milk to a baby
Artificial passive - Transfusion or injection of antibodies as part of the medical treatment of a disease
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Active immunity
- Immunity is created by your own immune system following exposure the the pathogen or its antigen
Natural active - following infection by a pathogen
Artificial active - following the introduction of a weakened version of the pathogen or antigens via vaccine
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Autoimmune diseases
- When the immune system responds abnormally to healthy 'good' microorganisms within the body or overreacts to mild pathogens
- Recognises antigens on some body cells as non-self + produces antibodies against them
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Rheumatoid arthritis
- Immune system attacks the cartilage in joints
- Can cause inflammation and pain in affected joints
- No cure but anti-inflammatory drugs, steroids, pain relief + immunosuppressant drugs can be taken to relieve symptoms
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Disease Prevention
- Immunisation (vaccine): Can induce passive or artificial active immunity
- Passive immunity: when antibodies are injected into you to help destroy the pathogen
- Artificial active: when antigens or small amounts of an attenuated pathogen are injected or taken orally - trigger a primary immune response but with few symptoms
- If re-infected with the same pathogen, will rapidly produce antibodies - secondary immune response
- Vaccines provide protection for individuals and populations against disease.
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Vaccines
- Not always effective in the long-term
- Pathogens' genetic material can mutate, resulting in a pathogen producing a different shaped antigen - antigen variability
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Epidemic
When a disease spreads rapidly on a national level
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Pandemic
When a disease spreads rapidly on a global level
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Herd immunity
- Mass vaccination programmes prevent further spread of the pathogen causing the disease
- Frequently updated - booster vaccines to account for antigen variability
- If large enough proportion of a population are vaccinated - unlikely that a susceptible individual will encounter an infected individual
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Sources of medicine
- Many medicines have been sourced from microorganisms and plants
- Maintaining biodiversity is key
- Medicines from plants + microbes are generally safer and cheaper than synthetic drugs
- E.g. Microorganisms - many antibiotics including penicillin and vancomycin
Plants - aspirin (willow bark), digitoxin (foxglove), quinine (cinchona tree)
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Importance of maintaining biodiversity
- Many drugs originated from plants + microbes
- Increases chances of finding more new drugs
- Maintain genetic resource for the future
- Many modern drugs have been made using knowledge of traditional remedies
- Once a species is extinct, its genetics and potential medicines would be lost forever
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Antibiotic resistance
- Random mutations occur in bacterial genetic material
- Mutation could code for a new protein that provides the bacteria with a selective advantage
- Widespread use + misuse of antibiotics strengthen selection pressure - antibiotic resistance
- Antibiotics only kill non-resistant bacteria, leaves bacteria with mutated resistance gene to survive with no competition
- Mutated gene found in the plasmid - can be exchanged between bacteria + reproduce rapidly until a resistant strain of bacteria has been created.
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New medicines - Personalised medicines
- Not a new concept but link to gene technology is
- Everyone is different, certain medicines will be more effective for different people - help from advances in gene technology
- Pharmacogenetics
- Analysing DNA - identify drugs that individuals will respond better to
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New medicines - Synthetic biology
- Synthetic manufacture of medicines including genetic engineering of insulin
- Using cells as medicine factories (mostly bacterial)
- Combines gene sequencing, bioinformatics and computational biology
- Find out base sequence of a protein, store data digitally + make 3D models/simulations before producing the medicine.
