Communicable diseases Flashcards

1
Q

Describe pathogens

A
  • organisms that cause disease
  • the organism they live in is called a host
  • a host body creates a good habitat in which microorganisms can live
  • live by taking nutrition from their host, but also causing damage in the process- can be considerable
  • 4 types- bacteria, fungi, viruses, protoctista
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2
Q

Describe bacteria

A
  • in prokaryotae kingdom
  • smaller cells than eukaryotic
  • can reproduce rapidly- up to every 20 mins in right conditions
  • once in host body, can reproduce rapidly
  • presence can cause disease by damaging cells or releasing waste products and/or toxins that are toxic to the host
  • ## in plants, the bacteria often live in the vascular tissues and cause blackening and death of these tissues
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3
Q

Examples of diseases caused by bacteria- including characteristics

A
  • tuberculosis- affects many parts of body- killing the cells and tissues- lungs most often infected
  • Bacterial meningitis- infection of the meningis- the membranes that surround the brain and spinal cord become swollen- can cause damage to brain and nerves
  • ring rot (plants)- ring of decay in vascular tissue of a potato tuber or tomato, accompanied by leaf wilting
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4
Q

Describe fungi

A
  • can cause a variety of disease in both plants and animals
  • common fungal infections in which the fungus luves in the skin of an animal where its hyphae, which form a mycelium, grow under the skin surface
  • the fungus can send out special reproductive hyphae, which grow to the surface of the skin to release s[pres- causes redness and irritation
  • in plants, the fungus iften lives in the vascular tissue, where it can gain nutrients
  • the hyphae release extracellular enzymes, such as cellulase, to digest the surrounding tissue which causes decay
  • leaves will often become mottled in colour, curl up and shrivel before dying
  • fruit and storage organs, such as tuvers ([potatoes) will turn black and decay
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5
Q

Describe fungi

A
  • can cause a variety of disease in both plants and animals
  • common fungal infections in which the fungus luves in the skin of an animal where its hyphae, which form a mycelium, grow under the skin surface
  • the fungus can send out special reproductive hyphae, which grow to the surface of the skin to release s[pres- causes redness and irritation
  • in plants, the fungus iften lives in the vascular tissue, where it can gain nutrients
  • the hyphae release extracellular enzymes, such as cellulase, to digest the surrounding tissue which causes decay
  • leaves will often become mottled in colour, curl up and shrivel before dying
  • fruit and storage organs, such as tuvers ([potatoes) will turn black and decay
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6
Q

Examples of diseases caused by fungi- including characteristics

A
  • black sigatoka (bananas)- causes leaf spots on banana plants reducing yield
  • ringworm (cattle)- growth of fungus in skin with spore cases erupting through skin to cause a rash
  • Athletes foot (humans)- growth under skin- particularly between the toes
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7
Q

Describe viruses

A
  • can cause many diseases in plants and animals
  • invade cells and take over the genetic machinery and other orgalles of the cell
  • then cause the cell to manufacture more copies of the virus
  • host cell eventually bursts, releasing many new viruses which will infect healthy cells
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8
Q

Examples of diseases caused by viruses- including characteristics

A
  • HIV/AIDS- attacks cells in the immune system and compromises the immune response
  • influenza- attacks respiratory system and causes muscle pains and headaches
  • tobacco mosaic virus- causes mottling and discoloration of leaves
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9
Q

Describe protoctista

A
  • usually cause harm by enterinh hos cells and feeding on the contents as they grow
  • the malarial parisite plasmodium has immature forms that feed on the haemoglobin inside red blood cells
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10
Q

Examples of diseases caused by protoctista - including characteristics

A
  • blight (potatoes and tomatoes)- affects both leaves and potato tubers
  • malaria- parisite in the blood that causes headache and fever and may progress to coma and death
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11
Q

stages of a pathogens life cycle

A
  • travelling from 1 host to another (transmission)
  • entering the hosts tissues
  • reproducing
  • leaving the hosts tissues
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12
Q

2 types of pathogen transmission- define

A
  • direct- passing a pathogen from one host to another with no intermediary
  • indirect- passing a pathogen from one host to another via a vector (an organism that carries a pathogen from one host to another)
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13
Q

4 means if direct transmission with factors that affect these

A
  • direct physical contact, such as touching a person who is infected or touching contaminated surfaces(including soil) that harbour the pathogen
  • e.g. HIV, bacterial meningitis, ringworm, athletes foot
  • Hygiene- washing hands regularly- especially after tuning the toilet. Keeping surfaces clean- especially door handles etc- cleaning and disinfecting cuts and abrasions. Sterilising surgical instruments, using condoms during sexual intercourse
  • faecal-oral transmission- usually by eating food or drinking water contaminated by the pathogen
  • e.g. cholera, food poisoning
  • using human sewage to fertiliuse crops is a common practice in some parts of the world. Treatment of waste water and drinking water can reduce risk. Thorough washing and cooking/preoaraton of fresh food.

Droplet infection in which the pathogen in carried in tiny water droplets in the air

  • e.g. tuberculosis, influenza
  • catch it- bin it- kill it- cover mouth while coughing/sneezing- use a tissue and ensure its disposed of correctly
  • transmission by spores- resistant stage of pathogen- can be carried in air or reside in surfaces or in soil
  • e.g. anthrax, tetanus
  • use of a mask, washing skin after contact with soil
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14
Q

Social factors which can affect direct pathogen transmission

A
  • overcrowding (many people sleeping/living in one house)
  • poor ventilation
  • poor health- particularly if a person has HIV/AIDS as they are more likely to contact other diseases
  • poor diet
  • homelessness
  • living/working with people who have migrated from areas where a disease is more common
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15
Q

describe indirect transmission

A
  • transmitted by a vector which may be used by organism to gain access to the primary host
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16
Q

Describe an example of indirect transmission

A

Transmission of malaria:

  • person with maria
  • has gametes of plasmodium in blood
  • female anopheles mosquito (vector) sucks blood
  • plasmodium develops and migrates to mosquitos salivary glands
  • an uninfected person is bitten
  • plasmodium migrates to liver
  • plasmodium migrates to blood- the person now has malaria and cycle repeats
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17
Q

Describe direct transmission in plants, and what happens once the pathogen has entered the plant

A
  • pathogens present in the soil- infect plants by entering the roots- especially if these have been damaged as a result of replanting, burrowing or movement because of a storm
  • many fungi produce spores as a means of sexual or asexual reproduction- may be carries in the wind- airborne transmission

Once inside:

  • pathogen may infect all the vascular tissue
  • pathogens in the leaves are distributed when the leaves are shed and carry the pathogen back to the soil- can grow and infect another plant
  • pathogens can also enter fruit/seeds- distributed with the seeds- many/all offspring infected
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18
Q

Describe indirect transmission in plants

A
  • often occurs as result of insect attack
  • spores or bacteria become attached to a burrowing insect, such as a beetle- attacks an infected plant
  • then attacks another plant- pathogen is transmitted to uninfected plant- beetle is acting as vector
  • e.g. fungus that causes Dutch Elm disease is carried by the beetle Scolytus multistriatus
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19
Q

What is a factor that can affect transmission in plants and animals

A

Climate:
Many protoctists, bacteria and fungi can grow and reproduce more rapidly in warm and moist conditions
- therefor, they tend to be more common in warmer climates
- in cooler climates, these pathogens may be damaged or even killed by cold winter weather- will definitely reduce their ability to grow and reproduce
- greater variety of disease in warmer climates- animals and plants living in these regions more likely to become infected
- climate change- tropical diseases may become more common in Europe

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20
Q

Why are plants vulnerable to communicable disease

A
  • Plants manufacture sugars in photosynthesis and convert those
    sugars to a wide variety of compounds such as proteins and oils.
  • Therefore they represent a rich source of nutrients for many organisms such as bacteria, fungi. protoctists, viruses, insects and
    vertebrates.
    -The bacteria, fungi, protoctists and viruses may be pathogenic, and the insects and vertebrates may act as vectors to help transmit these pathogens
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21
Q

Summarise how plants defend against disease

A
  • do not have an immune system comparable with animals
  • have developed a wide range of structural, chemical and
    protein-based defences which can detect invading organisms and
    prevent them from causing extensive damage
  • includes passive and active
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22
Q

What are passive plant defenses

A
  • defences present before infection, and their role is to prevent entry and spread of the pathogen.
  • includes physical barriers and chemicals.
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23
Q

Describe physical, passive plant defenses

A
  • Cellulose cell wall - physical barrier, most plant cell walls contain a variety of chemical defences
    that can be activated when a pathogen is detected.
  • Lignin thickening of cell walls - lignin (a phenolic compound)
    is waterproof and almost completely indigestible.
  • Waxy cuticles - prevents water collecting on the cell surfaces. Since pathogens collect in water and need water to survive, the absence of water is a passive defence.
  • Bark - most bark contains a variety of chemical defences that
    work against pathogenic organisms.
  • Stomatal closure - stomata are possible points of entry for
    pathogens. Stomatal aperture is controlled by the guard cells.
    When pathogenic organisms are detected, the guard cells will
    close the stomata in that part of the plant.
  • Callose - large polysaccharide that is deposited in the sieve tubes at the end of a growing season. It is deposited around the sieve plates and blocks the flow in the sieve tube. This can prevent a pathogen spreading around the plant.
  • Tylose formation - a balloon-like swelling or projection that fills the xylem vessel. When a tylose is fully
    formed, it plugs the vessel and the vessel can no longer carry watre. Prevents the spread of pathogens through the heartwood. The tylose contains a high concentration of chemicals such as terpenes that are toxic to pathogens .
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24
Q

Describe plant passive chemical defences

A
  • plant tissues contain a variety of chemicals that have anti-pathogenic properties
  • include terpenoids, phenols, alkaloids and hydrolytic enzymes
  • some of these chemicals, such as the terpenes in tyloses and tannins in bark are present before infection
  • however, because the production of chemicals requires a lot of energy, many chemicals aren’t produce till a plant detects an infection
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25
Q

What is active defence in plants

A
  • when pathogens attack, specific chemicals in their cell walls can be detected by the plant cells- these chemicals include specific proteins and glycolipids
  • the plant responds by fortifying the defences already present
  • includes increasing the physical defenses and producing defensive chemicals
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26
Q

Describe types of active defence in plants

A
  • cell walls become thickened and strengthened with additional cellulose
  • deposition of callose between the plant cell wall and cell membrane near the invading pathogen. Callose deposits are polysaccharide polymers that impeded cellular penetration at the site of infection. Strengthens the cell wall and blocks plasmodesmata
  • oxidative bursts that produce highly reactive oxygen molecules capable of damaging the cells of invading organisms
  • an increase in the production of chemicals
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27
Q

Name Chemicals that are used in plant defence

A
  • terpenoids
  • phenols
  • alkaloids
  • defensive proteins (defensins)
  • hydrolytic enzymes
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28
Q

Describe how terpenoids work (plant defence)

A
  • A range of essential oils that have antibacterial and antifungal properties.
  • They may also create scent, for example, the menthols and menthones produced by mint plants.
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29
Q

Describe how phenols work (plant defence)

A
  • These also have antibiotic and antifungal properties
  • Tannins found in bark inhibit attack by insects
  • These compounds bind to salivary proteins and digestive enzymes such as trypsin and chymotrypsin, deactivating the enzymes
  • Insects that ingest high amounts of tannins do not grow and will eventually die- helps to prevent the transmission of pathogens.
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30
Q

Describe how alkaloids work ( plant defence)

A
  • Nitrogen-containing compounds such as caffeine, nicotine, cocaine, morphine, solanine
  • give a bitter taste to inhibit herbivores feeding
  • also act on a variety of metabolic reactions via inhibiting or activating enzyme action
  • Some inhibit protein synthesis.
  • If the plant can reduce grazing by larger animals, then it will suffer less damage that can allow pathogens to enter the plant.
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31
Q

Describe how defensive proteins (defensins) work (plant defence)

A
  • These are small cysteine-rich proteins that have broad anti-microbial activity
  • appear to to act upon molecules in the plasma membrane of pathogens, possibly inhibiting the action of ion transport channels
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32
Q

Describe how hydrolytic enzymes work (plant defence)

A
  • found in the spaces between cells
  • include chitinases (which break down the chitin found in fungal cell walls), glucanases (which hydrolyse the glycosidic bonds in glucans) and lysozymes (which are capable of degrading bacterial cell walls).
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33
Q

Describe 2 other ways plants defend against disease

A
  • necrosis- deliberate cell suicide- a few cells are killed to save the rest of the plant- by killing cells surrounding the infection, the plant can limit the pathogens access to water and nutrients and therefor stop it spreading further around the plant. Necrosis is brought about by intracellular enzymes that are activated by injury- these enzymes destroy damaged cells and produce brown spots on leaves or dieback
  • Canker- a sunken necrotic lesion in the woody tissue such as the main stem or branch- causes death of the cambium tissue in the bark
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34
Q

What are primary defences

A
  • Stop pathogenic organisms entering the body of their host.
  • evolution has selected hosts adapted to defend themselves against such invasions
  • non specific as will prevent the entry of any pathogen
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35
Q

Name the main human primary defences

A
  • skin
  • blood clotting and skin repair
  • Mucous membranes
  • Coughing and sneezing
  • inflammation
  • others
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36
Q

Describe the skin as a primary defence

A
  • the body is covered by skin- the main primary defence
  • outer layer of the skin is called the epidermis, consists of layers of cells
  • most of these cells are called keratinocytes- these cells are produced by mitosis at the base of the epidermis- then migrate out to the surface of the skin- as they migrates, they dry out and the cytoplasm is replaced by the protein keratin
  • this process is called keratinisation and it takes about 30 days
  • by the time the cells reached the surface, they are no longer alive
  • the keratinised layer of dead cells act as an effective barrier to pathogens
  • eventually, the dead cells Slough off
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37
Q

What must happen when an abrasion or laceration damages the skin and why

A
  • the skin is only protective if it is complete
  • say open the body to infection- the body must prevent excess blood loss by forming a clot, making a temporary seal to prevent infection, and repairing the skin
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38
Q

What is involved in blood clotting

A
  • calcium ions and at least 12 clotting factors
  • many of the clotting factors are released from platelets and from damaged tissue- these factors activate an enzyme cascade
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39
Q

Describe the enzyme cascade of blood clotting

A
  • damage to blood vessel wall exposes collagen and releases clotting factors
  • platelets in the blood bind to the collagen and to release clotting factors
  • a temporary platelet plug is formed
  • the clotting factors cause inactive thrombokinase in blood to lead to active thrombokinase (an enzyme)
  • this causes prothrombin in blood, with the help of Ca2+ ions, to convert to active thrombin (an enzyme)
  • this turn soluble fibrinogen in plasma to turn to insoluble fibrin
  • these fibres attach to platelets in the plug
  • red blood cells and platelets also get trapped
  • all leads to blood clot
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40
Q

What happens once a blood clot has formed

A
  • it begins to dry out and form a scab
    the scab shrinks as it dries, drawing the sides of the cut together
  • this makes a temporary seal, under which the skin is repaired
  • the first stage is the deposition of fibrous collagen under the scab
  • stem cells in the epidermis then divide by mitosis to form new cells, which migrate to the edges of the cut and differentiate to form new skin
  • new blood vessels grow to supply oxygen and nutrients to new tissues
  • the tissues contract to help draw the edges of a cut together so that the repair can be completed
  • ask the new skin is completed, the scab will be released
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41
Q

Which areas in the body are at risk of infection and why

A
  • the Airways, lungs and the digestive system
  • certain substances, such as oxygen and the nutrients in our foods, must enter our blood
  • the exchange surface is where this occurs must be thinner and are less well protected from pathogens
  • the air and foods that we take in from our environments may harbour microorganisms
  • theerfor, these areas are protected by mucous membranes
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42
Q

Describe how mucous membranes provide protection against disease

A
  • the epithelial layer contains mucus secreting cells that are called goblet cells
  • the also extra mucus secreting glands under the epithelium
  • in the Airways, the mucus lines the passages and traps any pathogens that may be in the air
  • the epithelium also has ciliated cells
  • the cilia are tiny, hairlike organelles that can move
  • they move in a coordinated fashion to waft the layer of mucus along- they move the mucus up to the top of the trachea, where it can enter the oesophagus
  • it is swallows and passes down the digestive system- most pathogens in the digestive system are killed by the acidity of the stomach, which can be pH 1-2
  • this denatures the pathogens enzymes
  • Mucous membranes also found in the gut, genital areas, anus, ears and nose
43
Q

Describe coughing and sneezing as a defence against disease

A
  • areas that are prone to attack are also sensitive
  • they respond to the irritation that may be caused by the presence of microorganisms or the toxins that they release
  • these reflexes includes coughing, sneezing and vomiting
  • in a cough or sneeze the sudden expulsion of air will carry with it the microorganisms causing the irritation
44
Q

Describe inflammation as a defence against disease

A
  • one of the signs that a tissue is infected is swelling and redness known as inflammation- the tissue may also feel hot and painful
  • the presence of microorganisms in the tissue is detected by specialised cells called mast cells
  • these cells release a cell signalling substance called histamine
  • histamine has a range of effects on the surrounding tissue, which help to combat the infection- the main effect is to cause vasodilation and make the capillary walls more permeable to white blood cells and some proteins
  • blood plasma and phagocytic white blood cells leave the blood and enter the tissue fluid
  • this leads to increased production of tissue fluid, which causes the swelling (oedema)
  • excess tissue fluid is trained into the lymphatic system where lymphocytes are stored
  • this can lead to the pathogens coming into contact with the lymphocytes and initiating specific immune responses
45
Q

Describe other primary defences against disease

A
  • the eyes are protected by antibodies and enzymes in tear fluid
  • the ear canal is lined by wax, which traps pathogens
  • the female reproductive system is protected by a mucus plug in the cervix and by maintaining relatively acidic conditions in the vagina
46
Q

What are secondary defenses

A
  • used to combat pathogens that have entered the body
47
Q

How are pathogens recognised, describe this

A
  • antigens
  • chemical markers on outer membrane
  • specific to the organism
  • made of protein or glycoprotein
  • our own cells have antigens, but these are recognised as our own and don’t produce a response
48
Q

What attaches to the antigen on the surface of a molecule, describe this

A
  • opsonins
  • protein molecules
  • type of antibody
  • some not very specific- can attach to variety of pathogenic cells
  • role is to enhance the ability of phagocytic cells to bind and engulf the pathogen
49
Q

Types of white blood cells- categories, specifics

A

Phagocytes (non-specific)- neutrophils, macrophages

Lymphocytes- specific- smaller- B and T cells

50
Q

Briefly describe phagocytes

A
  • first line of secondary defence is phagocytosis

- in blood and tissue fluid

51
Q

Describe neutrophils

A
  • most common phagocytes
  • multilobed nucleus
  • manufactured and matured in bone marrow
  • travel in blood, often squeeze out into tissue fluid
  • short lived but released in large numbers as result of infection
  • large numbers of lysosomes
  • engulf and digest pathogens
  • usually die soon after ingesting a few pathogens
  • dead neutrophils may collect in area of infection, to form pus
52
Q

Describe how neutrophils work

A
  • bind to opsonin attached to the antigen of the pathogen
  • pathogen engulfed by endocytosis forming a phagosome
  • lysosomes fuse to the phagosome and release lytic enzymes into it
  • after digestion, the harmless products can be absorbed into the cell
53
Q

Neutrophils specialisations

A
  • receptors on plasma membrane that can bind to the opsonin or a specific antigen
  • a lobed nucleus allows the cell to squeeze through narrow gaps
  • well developed cytoskeleon helps the cell to chnage shape to engulf the pathogen and to move vacuole and lysosomes around inside the cell
  • many lysosomes containing lysin
  • many mitochondria to release energy from glucose
  • a lot of ribosomes to synthesis the enzymes involved
54
Q

describe macrophages

A
  • larger cells
  • kidney shaped nucleus
  • manufactured in bone marrow
  • travel in blood as monocytes before settling in body tissues
  • many found in lymph nodes where they mature into macrophages
  • dendritic cells (type of macrophage) found in more peripheral tissues
55
Q

describe how macrophages work

A
  • play important role in initiating the specific responses to invading pathogens
  • when a macrophage engulfs a pathogen, it does NOT fully digest it
  • the antigen from the pathogen in saved and is moved to a special protein complex on the surface of teh cell
  • the cell becomes an antigen-presenting cell
  • it exposes the antogen on its surface, so that other cells of the immune system can recognise the antigen
  • the special protein complex ensures that the antigen presenting cell is not mistaken for a foreign cell and attacked by other phagocytes
56
Q

Describe the specific immune response

A
  • Involves T and B lymphocytes (B/T cells)
  • white blood cells- smaller, large nucleus
  • special receptors on plasma membrane
  • produces antibodies- neutralise the foreign antigens
  • provides immunological memory through memory cells
57
Q

What are the phases of the spcific immune response

A
  • infection and reproduction of pathogen
  • presentation of antigens
  • clonal selection
  • proliferation
  • differentiation
  • Differentiation
  • Action
58
Q

Diagram of specific immune response

A
59
Q

Describe antigen presentation

A
  • can happen on macrophage, infected cell or pathogen in body fluid
  • the antigen presenting cell moves around the body where it can come into contact with specific cells that can activate the full immune response- T/B cells
  • may only be one T/B cell with correct receptor- therefor role of antigen presenting cell is to increase the chances of that antigen coming into contact with them
60
Q

Describe the origination and working of B cells

A
  • originated AND matured in bone marrow
  • Mature to have different shaped/specific receptors (proteins that have a complimentary shape to the antigen)
  • antigens must be detected by B cells
  • Clonal selection- B cell with complimentary receptor (to the antigen on pathogen) on plasma membrane identified
  • contact between the antigen and lymphocytes can be achieved directly when pathogenic cells enter lymph nodes or by action of antigen-presenting cells
  • Proliferation (clonal expansion)- once the correct B cell has been identified, they must increase in numbers to become effective- achieved by mitotic cell division
  • differentiation
61
Q

Describe differentiation of B cells

A
  • Plasma cells- circulate in blood- manufacture and release antibodies
  • B memory cells (Bm)- remain in the body for a number of years- act as the immunological memory
62
Q

Describe the origination and working of T cells

A
  • originated in bone marrow
  • matured in thymus
  • usually can only happen when antigen in host cell
  • Mature to have different shaped/specific receptors (proteins that have a complimentary shape to the antigen)
  • antigens must be detected by T cells
  • Clonal selection- T cell with complimentary receptor (to the antigen on pathogen) on plasma membrane identified
  • contact between the antigen and lymphocytes can be achieved directly when pathogenic cells enter lymph nodes or by action of antigen-presenting cells
  • Proliferation (clonal expansion)- once the correct T cell has been identified, they must increase in numbers to become effective- achieved by mitotic cell division
  • differentiation
63
Q

Describe differentiation of T cells

A
  • T helper cells (Th)- release cytokines (chemical messengers) that stimulate the B cells to develop and stimulate phagocytosis by the phagocytes
  • T killer cells (Tk)- attack and kill host-body cells that display the foreign antigen
  • T memory cells (Tm)- provide long term immunity
  • T regulator cells (Tr)- shut down the immune response after the pathogen has been successfully removed. Also involved in preventing autoimmunity.
64
Q

Describe cell signalling in terms of immune response- what it is, how it is achieved and examples of molecules

A
  • the specific immune response involves the coordinated action of a range of cells. In order to work together effectively, these cells need to communicate- cell signalling.
  • this communication is achieved through the release of hormone like chemicals called cytokines. There is a huge range of signalling molecules, each performing a different role. In order to detect a signal, the target cell must have a cell surface receptor complementary in shape to the shape of the signalling molecule.
    Examples of cell communication using cytokines:
  • macrophages release monokines. Some monokines attract neutrophils (by chemotaxis- some movement of cells towards a particular chemical), and others stimulate B cells to differentiate and release antibodies.
  • T cells and macrophages release interleukins, which can stimulate clonal expansion (proliferation) and differentiation of B and T cells
  • Many cells can release interferon, which inhibits virus replication and stimulates the activity of T killer cells
65
Q

Autoimmune diseases- what they are, why they don’t normally occur, 2 examples

A
  • an autoimmune disease occurs when the immune system attacks a part of the body.
  • normally, any B or T cells that have receptors which are specific to our own antigens are destroyed during the early development of the immune system- they have programmed for cell death called apoptosis
  • an autoimmune disease arises when antibodies start to attack our own antigens- possibly because antigens that are not normally exposed to become exposed to attack
  • the causes of autoimmune disease unknown, but seem to include both genetic and environmental factors
  • arthritis- a painful inflammation of a joint. The cause is uncertain, but it starts with antibodies attacking the membranes around the joints
  • lupus- can’t affect any part of the body, causing swelling and painful stop it may be associated with antibodies that attack certain proteins in the nucleus in cells and affected tissues.
66
Q

Describe antigens and antibodies in organisms- what they are, what they are made of, how they interact

A
  • antigens are molecules that can stimulate an immune response. Almost any molecule could act as an antigen, but they are usually proteins or glycoproteins in the plasma membrane of the pathogen. A foreign antigen will be detected by the immune system and it will stimulate the production of antibodies.
  • Antibodies are specific to the antigen and as antigens are specific to the Organism, we can think of the antibody being specific to the pathogen.
  • Our own antigens are recognised by our immune system and do not stimulate any response.
  • antibodies are immunoglobulins- complex proteins produced by the plasma cells in the immune system (B). they are released in response to an infection. They have a region with a specific shape that is complementary to that of a particular antigen.
  • Our immune system must manufacture one type of antibody for every antigen that is detected.
  • Antibodies attach to antigens and render them harmless.
67
Q

Describe the structure of an antibody

A
  • Y- shaped
  • Have 2 distinct regions- one constant region which is the same in all antibodies (it may have a site for the easy binding of phagocytic cells), and one variable region which has a shape specific to the shape of the antigen
  • 4 polypeptide chains- 2 x light and 2 x heavy
  • disulphide links hold polypeptides together
  • there is a hinge region to allow flexibility so molecule can grip more than one antigen
68
Q

What are three types of how antibodies work

A
  • opsonins
  • agglutinins
  • anti toxins
69
Q

Describe how opsonins work

A
  • they are a group of antibodies that bind to the antigens on a pathogen
  • they then act as binding sites for phagocytic cells, so that these can more easily bind and destroy the pathogen
  • some are not very specific and stick to types of molecules that are not found in the host cell, for example the peptidoglycans found in the cell wall of bacteria
  • others are produced as part of the specific immune response and binds to very specific antigens. The pathogen may have another use for this antigen molecule. For example, it’s maybe a binding site used for attachments to the host cell. In this case, the opsonins bound to the antigen renders the antigen useless- a process known us neutralisation. The opsonin assists in phagocytosis, but also prevents the pathogen entering a host cell before it can be attacked by phagocytes.
70
Q

Describe how agglutinins work

A
  • because each antibody molecule has two identical binding sites it is able to cross link pathogens by binding an antigen on one pathogen with one binding site and then an antigen on another pathogen with its other binding sites
  • when many antibodies perform this cross linking they clump together (agglutinate) pathogens
  • has two advantages- the agglutinated pathogens are physically impeded from carrying out some functions, such as entering host cells, and the agglutinated pathogens are readily engulfed by phagocytes. This is particularly effective against viruses.
71
Q

Describe anti-toxins

A
  • some antibodies bind to molecules that are released by pathogenic cells. These molecules may be toxic and the action of anti toxins renders them harmless.
72
Q

Describe primary response

A
  • when infecting agent first detected, the immune system starts to produce antibodies after clonal selection/expansion/ differentiation (B plasma cells)
  • takes a few days before number of antibodies rises enough to combat the infection successfully
  • once the pathogens have been dealt with, the number of antibodies in the blood drops rapidly
73
Q

Describe secondary response

A
  • antibodies dont stay in blood- must be made again
  • however, specific/primary immune response leaves T/B memory cells circulating in blood
  • these cells can recognise the specific antigens and the immune system can swing into action more quickly
  • usually quick enough to prevent any symptoms being detected by the host
74
Q

primary vs secondary response, graph

A
  • primary rises slower and reaches lower concentration than secondary
75
Q

Describe vaccination

A
  • provides immunity to specific diseases
  • created by deliberate exposure to antigenic material that has been rendered harmless
  • antigenic material usually injected, but can be taken orally
    the immune system reacts (primary response- it treats the antigenic material as a real disease
  • immune system is activates- antibodies and memory cells produced- memory cells provide long term immunity
76
Q

Describe different types of antigenic material used in vaccination

A
  • whole, live microorganisms- usually ones which are not as harmful as those that cause the real disease. Must have very similar antigens so the antibodies produced will be effective against the real pathogen- e.g. the smallpox vaccine uses similar virus that causes cowpox
  • a harmless of attenuated (Weakened) version of the pathogen e.g. measles and TB vaccines
  • a dead pathogen (e.g. typhoid and cholera vaccines)
  • a preparation of the antigens from the pathogen (e.g. hepatitis B vaccine)
  • a toxoid, which is a harmless version of a toxin (e.g. tetanus vaccine)
77
Q

Name 2 vaccination strategies

A
  • herd vaccination

- ring vaccination

78
Q

Describe herd vaccination

A
  • using vaccine to provide immunity to all/ almost all of population at risk
  • Once enough people are immune, the disease can no longer be spread through the population and you achieve ‘herd immunity’
  • in order for it to be effective, it is essential to vaccinate almost all of the population- e.g. smallpox- needed 80-85% of the population,
  • estimated that nearly 95% of the population would need to be immunised to prevent the spread of measles
  • UK vaccination program to immunise children against diphtheria, tetanus, whooping cough, polio, MMR- given to majority of children at the appropriate age
79
Q

Describe ring vaccination

A
  • used when a new case of a disease is reported
  • involves vaccinating all of the people in the immediate vicinity of the new cases
  • may mean vaccinating people in the surrounding houses, or even in the whole village/town
  • also used in many parts of the world to control the spread of livestock disease
80
Q

Briefly describe the different categories of immunity

A
  • Natural - achieved through normal life processes
  • artificial- medical intervention
  • active- immune system activates, manufactures own antibodies
  • passive- antibodies supplied from another source
81
Q

Describe natural active immunity

A
  • immunity provided by antibodies made in the immune system as a result of infection
  • a person suffers from the disease once and is then immune
  • e.g. immunity to chickenpox
82
Q

Describe natural passive immunity

A
  • antibodies provided via the placenta or via breast milk
  • makes the baby immune to the diseases to which the mother is immune
  • very useful in first year of babies life when immune system is developing
83
Q

Describe artificial active immunity

A
  • immunity provided by antibodies made in the immune system as a result of vaccination
  • a person is injected with a weakened, dead or similar pathogen, or with antigens- this activates their immune system
  • e.g. immunity to TB and influenza
84
Q

Describe artificial passive immunity

A
  • immunity provided by injection of antibodies made by another individual as faster response
  • no memory cells produced
  • e.g. hepatitis A/B, tetanus when toxoid hasn’t worked well
85
Q

What can happen once a disease has been eradicated or reduced to such a low incidence that it is unlikely to spread

A

The routine vaccination programme can be relaxed

86
Q

What can happen to some pathogens which is an issue for vaccination

A
  • Some pathogens can undergo genetic mutations which change their antigens.
  • The memory cells produced by the vaccination may not recognise the new antigens.
  • When this occurs, the pathogen may be transmitted, and the incidence of the disease increases.
  • certain pathogens such as influenza virus all relatively unstable unregulated undergo changes in their antigens
  • when this occurs, an epidemic may arise
87
Q

Define and describe epidemic’s

A
  • a rapid spread of disease through a high proportion of the population
  • threats from epidemics must be monitored so that new strains of pathogens can be identified. This enables the health authorities to prepare for an impending epidemic by stockpiling suitable vaccines and vaccinating people who who are at particular risk from the disease.
88
Q

What is a pandemic and what is done to avoid one happening?

A

A worldwide epidemic- people at risk of certain diseases are immunised- for example UK vaccination programme to immunise all those over 65 and those at risk for any other reason against influenza. The vaccination changes every year as the strains of flu used in this immunisation programme change every year- worldwide research undertaken to determine which of the strains of the flu are most likely to spread in any given year.

89
Q

Why are new drugs needed

A
  • new diseases are emerging
  • there are still many diseases for which there are no effective treatments
  • some antibiotic treatments are becoming less effective
90
Q

what are 7 ways in which new medicines can be discovered

A
  • accidental discovery
  • traditional remedies
  • observation of wildlife
  • further plant research
  • research into disease causing mechanisms
  • personalised medicine
  • synthetic biology
91
Q

Describe accidental discovery of new medicine

A
  • accidental discovery of the antibiotic penicillin by Alexander Fleming
  • the fungus penicillum releases compounds that kill bacteria- a scientist makes an observation and sets out to explain what he or she has seen
  • Florey and Chain- purified penicillin- demonstrated the potential value of antibiotics- scientists work together
92
Q

Describe traditional remedies as a way of discovering new medicine

A
  • many drugs have been used for centuries- they are used because people have noted that certain plants or extracts have a beneficial effect
  • World health Organisation calculates that 80% of the worlds population relies on traditional medicines
  • India- 7000 different plants used for their medicinal properties, China- 5000 different plants, Europe- many of our modern drugs have their origins in traditional medicine
  • morphine has its origins in the use of SAP from unripe poppy seed heads as long ago as Neolithic times. In the 12th century, opium from poppies was used as an anaesthetic and, by the 19th century, morphine and opium what being used. These opiate drugs reduce nervous action in the central nervous system. If the nerves cannot carry impulses, then no pain is felt.
  • medicine and use of Willow bark extract to relieve pain and fever has a long history. After discovery of its active ingredient, away was later found in 1897 to reduce the size effect of stomach bleeding, by adding an acetyl group. This led to the development of the drugs aspirin and ibuprofen
93
Q

Describe observation of wildlife as a way of discovering new medicine

A

Many animals make use of plants with medicinal properties. For example:

  • monkeys, bears and other animals rub citrus oils on their coats as insecticides and anti septics in order to prevent insect bites and infection
  • birds line their nests with medicinal leaves in order to protect chicks from blood sucking mites
94
Q

Describe further plant research as a way of discovering new medicine

A
  • scientists have used traditional plant medicines and animal behaviour as a starting point in their research for new drugs
  • for example aspirin- research into the plants used for traditional remedies enables scientists to isolate the active ingredient- this molecule can be analysed, and similar molecules can be manufactured
  • in recent decades, discovery of natural drugs has concentrated on tropical plants. Owing to their great diversity, there are hopes that many may contain molecules that could form new medicinal drugs.
  • there may be many potential uses of wild and cultivated plants in the UK
  • new chemical fingerprinting technology is enabling scientists to screen natural chemicals more effectively for their activity as potential medicines
95
Q

Describe research into disease causing mechanisms as a way of discovering new medicine

A
  • pharmaceutical companies have been conducting research into the way that microorganisms cause disease
  • many make use of receptors on plasma membranes- for example the HIV virus binds to the CD4 and CD5 receptors on the surface of T helper cells
  • if the binding between the pathogen and the receptor site can be blocked, then the disease causing pathogen cannot gain access to the cell
  • look like a protein receptor molecules can be isolated and sequenced- once the amino acid sequences known, molecular motor land can be used to determine the shape of the receptor
  • the next step is to find a drug that mimics the shape of the receptor and could be used to bind to the virus itself, which would block the virus from entering the T helper cell
  • in a similar way, drugs that inhibits the action of certain enzymes can also be developed
96
Q

Describe personalised medicine as a way of discovering new medicine

A
  • sequencing technology and molecular modelling have huge potential for future medicines
  • it is possible to screen at the genome’s of plants or microorganisms to identify potential medicinal compounds from the DNA sequences
  • it is hoped that this technology can even be taken a step further- once the technology is fully developed, it may be possible to sequence the genes from individuals with a particular condition and develop scientific drugs for the condition- known as personalised medicine
97
Q

Describe synthetic biology as a way of discovering new medicine

A
  • the development of new molecules, in particular enzymes, that mimic biological systems is one form of synthetic biology
  • another way that synthetic biology is used is to design and construct new devices and systems that may be useful in research, healthcare or in manufacturing- for example, there is the development of tomatoes which contain the pigment anthocyanin- this pigment is found in fruits such as blueberries, and has specific health benefits- antioxidants, help protect against coronary heart disease
98
Q

What are antibiotics

A

Compounds that prevent the growth of fungi or bacteria

99
Q

What was the first antibiotic

A

Penicillin- discovered by Alexander Fleming in 1928

100
Q

Where do most antibiotics come from

A

Most antibiotics currently in use are derivates of a compound made by bacteria from the genus streptomyces- antibiotics have been used widely to treat bacterial infections

101
Q

Weather most antibiotics come from

A

Most antibiotics currently in use are derivates of a compound made by bacteria from the genus streptomyces- antibiotics have been used widely to treat bacterial infections

102
Q

When did antibiotic use become very widespread

A

World war II cheap prevent the infection of wounds

103
Q

What is the current issue with antibiotics, describe how it has happened, why, give examples

A
  • over use of antibiotics- prescribing them for too many things, misuse- not finishing the full course (allow resistant/stronger pathogens to survive)
  • has enabled microorganisms to develop resistance by mutations in their DNA- these resistant bacteria reproduce- many of the current antibiotics have limited effectiveness as a result
  • some of resistance too a range of antibiotics- for example Clostridium difficile, methicillin-resistant Staphylococcus aureus (MRSA)