Diseases and the Immune System Flashcards
Pathogen
Organisms that cause disease
- they take nutrition from the host as an energy source (except viruses)
4 types of infectious organisms
- bacteria
- fungi
- viruses
- protoctista
Bacteria
- smaller than eukaryotic cells
- reproduce rapidly
- damage cells through release of toxins
- TB, bacterial meningitis, ring rot
Fungi
- often lives in the skin- hyphae form a mycelium
- reproductive hyphae grow into the skin and release spores
- lives in vascular tissue of plants to gain nutrients
- hyphae release extracellular digestive enzymes to break down cellulose
- black sigatoka, ringworm, athletes foot
Protoctista
- needs a vector to enter the host e.g. mosquito
- enter host cell and feed on the contents of the cell
- malaria parasite plasmodium has immature forms which feed on haemoglobin
- blight, malaria
Virus
• viruses invade host cells and take over genetic machinery and other organelles
• Cause cell to manufacture more copies of the virus
• Host cell eventually bursts, releasing new viruses to invade new host cells
• HIV, influenza, tobacco mosaic virus
Direct transfer
- physical contact
- fecal transmission
- droplet infection
- spores transmission
Indirect transmission
- transmission via vectors
- e.g. malaria via mosquitoes
7 factors which affect transmission
- overcrowding
- nutrition
- compromised immune system
- poor waste disposal
- climate change
- socioeconomic factors
- culture
2 main types of plant defences
- Passive
- Active
Do plants have an immune system
No- plants don’t have an immune system so they use defences to prevent extensive damage
What can passive defences be split into
- Physical
- Chemical
Physical defences
Cellulose cell wall- physical barrier, contains chemicals defences when a pathogen is detected
Waxy cuticle- prevents water collecting, which can contain pathogens
Bark- contains chemicals which will work against pathogens
Tylose formation- is a balloon like projection which fills the xylem, acting as a plug to prevent the xylem from carrying water, so prevents the spread of pathogens. Contains high levels of terpenes which are toxic to many pathogens
Chemical defences
- Hydrolytic enzymes
- Defensive proteins
- Alkaloids
- Phenols
- Terpenoids
Tylose and tannins are in bark before infection, however use lots of energy to create so aren’t made until infection is detected
Chemical defences: hydrolytic enzymes
Widespread throughout all plants and break down the cell wall of invading organisms
Chemical defences: defensive proteins
Destroy pathogens by engulfing and destroying them
Chemical defences: alkaloids
release a strong scent/odour- toxins. Have bitter taste to prevent herbivores feeding on them
Chemical defences: phenols
contain antitoxin properties which help destroy pathogens
Chemical defences: terpenoids
released to signal to the rest of the plant to initiate response. Contain antibacterial properties
Active defences
When a plant becomes infected with a pathogen, proteins and glycolipids in the cell wall of the plant detect the, and signal chemical defences, and increase physical defences
Examples of active defences
- cellulose cell wall thickens
- oxidative bursts that produces highly reactive oxygen molecules which can damage the cells of invading organisms
- increase in production of chemicals
- callose is synthesised and deposited in both sieve plates and between cell wall and cell membranes of surrounding cells, blocking plasmodesmata / flow through the phloem
What are cell walls of bacteria made from
Peptidoglycan
What is gram staining
A method used to distinguish between different groups of bacteria
Gram negative
Appear red under a light microscope
E.g. E-coli
Gram positive
Appear purple/blue under a light microscope
E.g. MRSA
How do pathogens infect hosts
- damage host tissue directly
- produce toxins which damage host tissue (indirectly)
How do viruses, protoctista and fungi damage cells
Directly
How do bacteria and fungi damage cells
Indirectly
Bacteria examples
- Tuberculosis
- Bacterial meningitis
- Ring rot (plants)
TBR
Tuberculosis
Characteristics
Infect lungs - chronic cough, bloody mucus, fatigue
Transmission
Direct
- airborne droplets
Bacterial meningitis
Characteristics
Fever, neck stiffness, headaches, altered mental status
Transmission
Direct
- airborne droplets
Ring rot
Characteristics
Host- potato, tomato
- infects vascular tissue, prevents transport if water, in tubers (causes black ring)
Transmission
Direct
- contact with other infected tubers
Virus examples
HIV/AIDS
Influenza
Tobacco mosaic virus
HIT
HIV / AIDS
Characteristics
Weakens immune system
- fever, diarrhoea, fatigue, weight loss
Transmission
Direct
- transfer of sexual bodily fluids
Influenza
Characteristics
High temperature, body aches, fatigue
- infects cells that line the airway
Transmission
Direct
- airborne droplets
Tobacco Mosaic Virus
Characteristics
Host- tobacco
- yellowing of leaves, produces mosaic pattern
Transmission
Direct- contact with infected leaves
Indirect- vectors (aphids)
Fungi examples
- black sigatoka
- ringworm
- athletes foot
BRA 👙
Black sigatoka
Characteristics
Host- bananas
- leaves can’t photosynthesise
- produce black streaks
Transmission
Direct
- spores (rain splash and wind)
Ringworm (cattle)
Characteristics
Ring shaped rash on skin
Transmission
Direct
- contact with infected cattle
Athlete’s foot
Characteristics
Itchy white patches & cracked skin between toes
Transmission
Direct
- contact with infected items
Protoctista examples
- Blight
- Malaria
Blight
Characteristics
Small, dark brown marks on leaves
- destroys crops - inedible
Transmission
Direct
- spores (windborne)
Malaria
Characteristics
Fever, chills, fatigue, nausea, headaches
Transmission
Indirect
- bite from infected anopheles mosquito
Types of transmission
Direct or Indirect
Types of transmission: direct
Direct contact
- kissing/contact with bodily fluids (HIV)
- skin to skin contact (athlete’s foot)
- microorganisms from faeces on the hands
Inoculation
- broken skin (HIV)
- animal bites (rabies)
- puncture wounds / sharing needles (septicaemia)
Ingestion
- contaminated food or water (dysentery)
- e.g. mould
Types of transmission: indirect
Formites
- inanimate objects that can carry infection- bedding, socks, cosmetics (athletes foot)
Droplet infection (inhalation)
- sneezing, coughing, talking- in saliva & mucus (influenza)
Vectors
- transmits infection from one host to another (malaria by anopheles mosquito)
Direct transmission between plants
- direct contact of a healthy plant with an infected plant
E.g. ring rot, black sigatoka, tobacco mosaic virus, blight (tomato & potato)
Indirect transmission between plants
Soil contamination
• pathogens (bacteria or virus) or spores (fungi) can be left behind in the soil and infect the next crop
• Some pathogens can even survive the composting process, and so compost can carry infection
• E.g.black sigatoka spores, ring rot spores
Vectors
• wind- e.g. black sigatoka carried between Caribbean islands
• Water- spores swim in surface film, raindrop splashes
• Animals- insects and birds carry pathogens as they feed
• Humans- on hands, clothing, formites, farming practices and transporting crops around the world e.g. ring rot can survive in farming machinery
Factors affecting disease transmission
- crop variety (monoculture)
- overcrowding
- poor mineral nutrition
- damp, warm conditions
-climate change - lack of healthcare workers
- *lack of sanitation *
Strategies to prevent spreading of pathogens
- wear masks / cover mouth + nose when cough
- ensure areas are well ventilated / outside where possible
- trained healthcare workers + educate people
- wash hands after toilet / before eat
Non specific defences
- Barriers
- Inflammatory response
- Clotting and wound repair
Barriers to prevent entry
- hair
- skin
- mucus
- tears
- stomach acid- hydrochloric acid
- expulsion reflexes- coughing, sneezing
- cilia- line the airways
- lysozymes- in tears and urine
How do ciliated epithelial cells defend against pathogens
- cilia sweep mucus with trapped pathogens out of the airway
- goblet cells produce and secrete mucus (contains lysozymes)
How does skin protect against pathogens
- microorganism flora outcompetes pathogens for space in the surface of the Boyd
- sebum oil inhibits pathogen growth
- physical barrier between pathogens and body
- waterproof mechanical barrier
How does mucous membranes defend against pathogens
- cilia- contain phagocytes
- produce mucus to trap pathogens to be broken down
How does stomach acid defend against pathogens
- bacteria can’t survive in low pH
- kills bacteria and parasites that have been swallowed
How does lysozymes (in tears and urine) defend against pathogens
Contains enzymes that breaks down the cell wall of bacteria
How do expulsive reflexes defend against pathogens
- expel pathogens back outside the body
- eject mucus containing pathogens from gas exchange system
Inflammatory response
A localised response to pathogens
- coordinated by mast cells
Upon infection they release:
1. Histamines
2. Cytokines
Inflammatory response: histamine function
- histamines cause vasodilation which increases skin temperature
- helps defend against pathogens as the increased temperature means pathogens are less likely to reproduce
- histamines make blood vessels leakier, forcing blood plasma and WBC’s out and into surrounding tissues
- this helps as plasma proteins and WBC’s can migrate to the site of infection quickly
Inflammatory response: cytokines function
Attract phagocytes to site of infection
- phagocytes can engulf and destroy the infecting pathigen
- cytokines also stimulate the hypothalamus to increase body temperature
- this means that pathogens are less likely to reproduce
- the specific immune system works faster at higher temperatures- enzyme activity
Blood clotting and wound repair
When platelets meet collagen in the skin, or a damaged blood vessel wall, they adhere and begin to secrete substances
They secrete:
Thromboplastin- an enzyme that triggers the clotting response
Serotonin- causes smooth muscle in the blood vessel constrict and narrow, reducing blood flow to the area
Eventually, the clot will dry and form a scab. This will trigger epidermal cells underneath to grow and form collagen fibres to give strength to the new tissue
Blood Clotting and wound repair
Clotting response
• calcium ions in the plasma, and thromboplastin trigger the conversion of prothrombin into thrombin (enzyme)
• Thrombin catalyses the conversion of fibrinogen into fibrin
• Fibrin fibres mesh and tangle together, trapping platelets and red blood cells
• Scab is formed
Clotting response diagram
Damaged blood vessel
|
Calcium ions releases thromboplastin
|
Prothrombin —> thrombin
|
Fibrinogen —> fibrin
Fibrin forms a network of fibres that trap platelets and blood cells
- scab forms
Phagocytosis
- Attraction: pathogens produce chemicals which attract phagocytes (chemotaxis)
- Recognition: Phagocytes recognise non human proteins on the pathogen
- Endocytosis: the phagocyte engulfs the pathogen
- Bacteria are enclosed within a vacuole to form a phagosome
- The phagosome combines with a lysosome to form a phagolysosme
- Lysozymes in the lysosome are released to digest and destroy the pathogen
Step only for macrophages
the phagocyte displays the antigens from pathogen on its cell membrane (displayed in MHC complexes in cell membrane)
- phagocyte is now an APC
- antigen is a processes antigen
- APC’s stimulate the T cell response
2 types of phagocyte
- Macrophages
- Neutrophils
Chemicals involves in phagocytosis
Cytokines
- signalling proteins that help control inflammation in the body
- act as chemical messengers that tell cells how to behave
- released by phagocytes to signal to other phagocytes that the body is under attack
- too many cytokines can lead to excess inflammation and conditions e.g. autoimmune diseases
Opsonins
Bind to pathogens and take them, making them more recognisable to other phagocytes
Antigens
All cells have antigens on their cell surface membrane. Antigens that are from pathogens are recognised as ‘non self’ by the immune system
- triggers the production of antibodies which are released from lymphocytes
Antibody structure
- antibodies are Y shaped glycoproteins called immunoglobulins
- they bind to specific antigens on pathogens or toxins
- made up of 2 identical long polypeptide chains (heavy chains) and 2 short identical chains (light chains)
- the chains are held together by disulphide bridges known as the hinge region
- this allows for flexibility, so the antibody can bind to 2 antigens at once
What is it called when an antibody binds to an antigen
Antibody-antigen complex
Opsonisation
- signals the presence of a pathigen
- signals the phagocytes to start phagocytosis
- antibodies act as opsonins
Agglutination
- microbes clump together in the presence of certain antibodies that bind them together
- presence of agglutinins is what makes agglutination by antibodies possible
- pathogens carrying antigens clump together - makes it easier for phagocytes to carry out phagocytosis, and prevents spreading throughout the body
Antitoxins
Binds to toxins and make them ineffective
Neutralisation
Binds to antigens and cover binding sites, preventing pathogens from entering the cell
What are lymphocytes
- type of white blood cells
- smaller than phagocytes
- have a large nucleus that fills most of the cell
- produced in bone marrow before birth
Specific immune responses are slower but more effective than non specific immune responses
What are the 2 types of lymphocyte
T cells- mature in thymus gland
B cells- mature in bone marrow
Maturation of T cells
Maturation means they gain specific cell surface receptors called T cell receptors (TCRs)
Immature form in bone marrow
Mature in thymus gland
- matured T cells remain inactive until they encounter their specific antigen
4 types of T cell
- T helper cells
- T killer cells/ cytotoxic T cells
- T regulator cells
- T memory cells
Role of T helper cells
- binds to cells displaying antigens via major histocompatibility complex (MHC) to be altered for attack, but recognises specifically this is self cell for marker for destruction
- release interleukins:
- stimulate B cells to make antibodies
- T cells to divide
- macrophages (increase phagocytosis)
Role of T killer cells
- patrol body in search of antigen presenting body cells
- attach to foreign antigens in cell surface membrane of infected cells and secrete toxic substances that kill infected cells
- perforins secreted by T killer cells punch a hole in the cell surface membrane of infected cells, allowing toxins to enter
Role of T regulator cells
- suppress immune system
- no direct involvement
- after response, control all T cells and inhibit body from autoimmune response
Role of T memory cells
- immunological memory of Ag- rapid secondary response
- memory cells remain in the blood- if same antigen is encountered again, process of clonal selection occurs quicker
What are interleukins and their role
- made by T helper cells
- cause phagocytosis to increase
- needed to activate B cells and stimulate release of T cells
T cell activation
- Clonal selection
- a T helper cell with a specific complementary receptor to antigen on APC (phagocyte or B cell) will recognise and bind to it - Activation
- T cells increases the size of RER and number of mitochondria - Clonal expansion
- T cells divide rapidly by mitosis - Differentiation
- T regulator, T memory, T helper, T killer
B cell activation
- Clonal selection
- B cells with complementary receptor binds to non self antigen e.g. in bloodstream - B cell internalises and displays antigens to become a type of APC
- Activation
- B cell APC binds to T helper cells: B cell is activated - Clonal expansion
- B cells divide rapidly by mitosis
- They need cytokines from T helper cells to do this - Differentiation
- B memory cells
- Plasma cells — secrete antibodies
Cell mediated response
- Pathogens invade body cells or are taken in by phagocytes
- The phagocyte places the antigen on its own cell-surface membrane (APC)
- Receptors on certain T helper cells fit exactly onto these antigens
- This stimulates other T cells to divide rapidly by mitosis to form a clone
- The cloned T cells:
• develop into memory cells that provide rapid response in the future
• Stimulate phagocytes to engulf the bacteria by phagocytosis
• Stimulate B cells to divide
• Kill infected T cells
Bacteria, virus, fungi, protist
TMR- TB, meningitis, ring rot
HIT- HIV, influenza, tobacco mosaic virus
BRA- black sigatoka, ringworm, athletes foot
BM- blight, malaria
Humoral response
Involves antibodies which are soluble in the blood and tissue fluid
- The surface antigens of the invading pathogens are taken up by the B cells
- The B cells process the antigens and present them on their surface
- T helper cells attach to the processed antigens and B cells, thereby activating them
- The B cells are now activated to divide by mitosis to give a clone of the plasma cells
- The cloned plasma cells produce antibodies that exactly fit the antigens on the pathogens surface
- The antibodies attach to antigens on the pathogens and destroy them (primary)
- Some B cells develop into memory cells. These can respond to future infections by the same pathogen by dividing rapidly and developing into plasma cells that produce antibodies (secondary)
Autoimmune diseases
Autoimmune response- a response where the immune system acts against its own cells, destroying healthy tissue
- Type 1 diabetes
- Rheumatoid arthritis
- Lupus
Type 1 diabtetes
Affected area
- prevents pancreas from making insulin
- insulin secreting cells of the pancreas
Treatment
- insulin injection
- eat sugary foods if low
- blood sugar monitor
- pancreas transplant
- immunosuppressants
Rheumatoid arthritis
Affected area
- causes pain, swelling and stiffness in joints
- usually affects hands, feet and wrists
Treatment
- no cure
- medicine to relieve symptoms and slow the progress of the condition
- surgery to correct any joint problems
- anti inflammatory drugs
- steroids
- immunosuppressants
- pain relief
Lupus
Affected area
- body’s immune system attacks your tissues and organs
- kidneys, brain, CNS, lungs, heart
Treatment
- no cure
- anti inflammatory drugs
- steroids
- immunosuppressants
Immune response
A biological response that protects the body by recognising and responding to antigens and by destroying substances carrying non self antigens
Natural immunity
Acquired from exposure to the disease organism through infection with the actual disease
Natural active- immunity which results from the response of the body to the invasion of the pathogen
E.g. getting ill
Natural passive- immunity given to an infant mammal by its mother- through placenta or colostrum
E.g. breastfeeding
Artificial passive immunity
Artificial passive- antibodies are given as a medication to a non immune individual
E.g. antibody injection
Advantages
- passive immunisation can override a deficient immune system
- quick acting- starts producing immune response within hours or days
Disadvantages
- antibodies are difficult and costly to produce
- can cause serious allergic reactions
- requires intravenous injection- time consuming and complicated procedure
- short lived immunisation and doesn’t lead to memory cells
Future applications of artificial passive immunity
- use of monoclonal antibodies for infectious diseases and non infectious diseases such as cancer, CV disease
- could play a role in emergency response to bio terror threats
Artificial active immunity
Artificial active- the body is stimulated to make its own antibodies
E.g. vaccination
Stages of vaccination
- Pathogen is made safe so there is no risk of serious infection.
Vaccines contain:
- dead/inactive version of the pathogen
- detoxified toxin molecules
- isolated antigens - Small amounts of the safe antigen (vaccine)are injected into the bloodstream
- The primary immune response (mediated and humoral) is triggered, and your body produced antibodies and memory cells
- If you come into contact with a live pathogen, the secondary immune system response is triggered and the pathogen is destroyed rapidly before you feel any symptoms
Immunity summary
Active Passive
Natural: getting ill Breastfeeding
Artificial: vaccination Antibody injection
Epidemic and pandemic
Epidemic- a widespread occurrence of an infectious disease in a community at a particular time
- localised
- region, country, continent
Pandemic- a widespread occurrence of an infectious disease over a whole country or the the world at a particular time
- global
Herd immunity
Indirect protection from an infectious disease that happens when a population is immune either through vaccination or immunity developed through previous infection
Achieving herd immunity through exposing people to a virus is dangerous because they have to let people catch the disease and gain immunity through it as they are still exposed to the dangers and symptoms of the disease.
The immunity may not last long, leads to unnecessary infections, suffering & death
What are the challenges in determining level and duration of immunity to a virus
- different vaccines may be given
- different strains of virus exhibit different symptoms- make it difficult to see how much immunity you get from it
- don’t know the long term immunity
- virus is constantly evolving and mutating
What kind of people wouldn’t be able to vaccinate
- autoimmune disease
- on immunosuppressants or other medication
- age
- pregnant
- risk of blood clots
- allergic
- underlying health conditions
Why do vaccines not always work: malaria, HIV
Malaria: plasmodium (protoctista) is evasive- it spends time inside the red blood cells and so is protected by self antigens from the immune system
HIV: HIV enters the macrophages and T helper cells, and so disables the immune system
Medicinal management
Treat symptoms
- painkillers
- anti inflammatory pies (NSAIDS)
- anti acids (indigestion)
Cure
- chemotherapy
- antibiotics
- antifungals
Drugs and their sources
Penicillin
Action: antibiotic- treats many common bacterial diseases
Source: commercial extraction originally from mould growing on melons
Docetaxel/paclitaxel
Action: used to treat many different cancers including ovarian
Source: bark of yew trees
Aspirin
Action: NSAID used to treat pain, fever, swelling, rheumatoid arthritis
Source: bark and leaves of willow and poplar trees
Antibiotic resistance
- Population of bacteria in the gut, some have antibiotic resistance through random mutation
- When exposed to an antibiotic, bacteria causing illness, as well as healthy gut bacteria are killed
- With reduced competition for nutrients, antibiotic resistant bacteria multiply, forming a larger population that is difficult to control
- must take full course of antibiotics
Pharmacogenetics
Refers to personalised medicine
- combining the effects of drugs with genome analysis and interweaving to create treatment plans
Synthetic biology
Genetically engineering bacteria to produce certain drugs
Sources of antibiotics
- soil microorganism
- honey
- fish blood
