4.1.1 Communicable diseases, disease prevention and the immune system

what are the types of pathogen that can cause communicable diseases in plants and animals (and examples of each)

• bacteria - (tuberculosis and ring rot (potatoes))

• virus - (hiv/aids, influenza, tobacco mosaic virus)

• protoctista - (malaria, potato/tomato late blight)

• fungi - (black sigatoka (bananas), athletes foot)

what are bacteria?

they produce toxins that damage body cells

what are viruses?

use host cells to replicate before bursting out and destroying cells

what are protoctists?

take over cells and break them open

what are fungi?

digest living cells to destroy them and some also produce toxins

what is the definition and some examples of direct transmission (animals)

• direct transmission - pathogens transferred directly from one organism to another

• direct contact - skin to skin, kissing, sex

• airborne droplets - coughing, sneezing

what is indirect transmission and some examples (animals)

indirect transmission - communicable diseases can also be passed between organisms via an intermediate

food transfer - ingestion of contaminated food or drink

vectors - transmit pathogens from one host to another eg mosquitoes transmit malaria

contaminated objects - pathogens from infected individuals can live on objects for a short time and infect others

what factors increase the risk of communicable diseases (animals)

• living conditions - overcrowded areas increase risk of direct transmission

• climate - eg warmer temps allow mosquitoes to breed and transmit malaria

• social factors - eg lack of health education and healthcare systems

what are examples of vectors in plants

• wind - bacterial, viral or fungal spores are carried by the wind to uninfected plants

• water - spores can travel on the surface of water to reach uninfected plants

• animals - insect and bird can carry pathogens or spores from one plant to another

• humans - pathogens/spores can be transmitted by handling plants, clothing, farming tools and practices

what factors increase risk of communicable diseases (plants)

• crop variety - some crops are more susceptible to disease

• overcrowding - increases likelihood of direct contact

• mineral nutrition - poor nutrition reduces resistance of plant

• climate change - increased rainfall and wind increase the spread of disease

what are the physical plant defences

• waxy cuticle - leaves and stems are covered in waxy cuticle that provide physical barrier

• cell wall - plant cells surrounded by cell wall that form physical barrier

• production of callose - when plants are attacked by pathogens they produce a polysaccharide called callose - this is deposited between cell wall and surface membrane to make it harder for pathogens to enter

what are the chemical plant defences

• insect repellents - reduce the number of insects feeding on plants to prevent them from transmitting pathogens

• insecticides - these kill insects to prevent them from transmitting pathogens

• antibacterial substances - chemicals like antibiotics kill bacteria/inhibit growth

• toxins - some plants produce chemical that break down into cyanide when plant cells are attacked

what are the primary non specific defences against pathogens in animals (physical)

• skin

• mucous membranes

• expulsive reflexes

• blood clotting and wound repair

what are the primary non specific defences against pathogens in animals (chemical)

• inflammation triggered by:

• blood vessels dilating - increases blood flow to the area making it hotter which prevents pathogens from reproducing

• blood vessel walls become more permeable so they start to leak tissue fluid causing swelling and isolating any pathogens in the damaged tissue

what are antigens

• usually proteins that let the immune system distinguish between bodys own cell and foreign cells

what do antigens allow the immune system to identify

• pathogens

• abnormal body cells (eg cancerous cells)

• toxins

• cells from other organisms of the same species

what are phagocytes

a type of white blood cell that engulf and destroy pathogens - phagocytosis

what are the 2 main types of phagocyte

• 1) neutrophils - these rapidly engulf and destroy pathogens at the site of infection

• 2) macrophages - these engulf and digest pathogens but also present the pathogens antigens on its cell surface to activate other cells in the immune system

phagocytosis step 1

pathogen releases chemicals that attract a phagocyte

phagocytosis step 2

phagocyte recognises the pathogens antigens as non self. this causes the phagocyte to bind to the pathogen

phagocytosis step 3

phagocyte engulfs the pathogen

phagocytosis step 4

pathogen is now contained within vesicle known as phagosome

phagocytosis step 5

lysosome containing hydrolytic enzymes called lysozymes fuses with the pathogosome to form phagolysosome

phagocytosis step 6

lysozymes digest ad destroy pathogen

phagocytosis step 7

phagocyte presents pathogens antigens on its surface to activate other cells in the immune system then the phagocyte is referred to as an antigen-presenting cell

what are cytokines

• chemical that are released by phagocytes that engulfed a pathogen

• they act as cell signalling molecules to trigger the movement of other phagocytes to the site of infection

• also trigger an increase in body temp to inhibit phagocyte reproduction

what are opsonins

• chemicals that bind to pathogens to make them easily recognisable by phagocytes

• phagocytes have receptors on their cell surface that bind to common opsonins making it easier for phagocyte to bind to pathogen and destroy it

what are the types of lymphocyte

• 1) T cell - mature in the thymus, involved in cellular response where they respond to antigens presented on body cells

• 2) B cell - mature in bone marrow, involved in the humoral response where they produce antibodies

what is a T helper cell

• have receptors on their cell surface that bind to complementary antigens on antigen presenting cells

• they produce interleukins - a type of cytokine- that stimulate B cells or phagocyte

• can also form memory cells or T killer cells

what is a T killer cell

• kill abnormal foreign cells by producing the protein perforin

• perforin makes holes in the cell surface membrane causing it to become freely permeable and causing cell death

what is a T-regulator cell

• they suppress the immune system after apthogens have been destroyed

• helps prevent immune system from accidentally attacking body cells

what is a T memory cell

• provide long-term immunity against specific pathogens

• provide a rapid response if the body is reinfected by the same pathogen

cellular response stage 1

macrophages engulf pathogen and display antigen on the cell surface and are then known as antigen presenting cells

cellular response stage 2

T helper cells with complementary receptors bind to these antigens

cellular response stage 3

on binding, the T helper cell is activated to divide by mitosis to form genetically identical clones

what can cloned T cells do

• develop into memory cells

• develop into T killer cells

• stimulate phagocytosis

• stimulate division of B cells

what is the humoral response

one of the specific immune responses that involves the production of specific antibodies to destroy pathogens

how are B cells involved in the humoral response

• have antibodies on their cell surface membrane that bind to complementary antigens

• they can engulf antigens and display them on their cell membrane to become antigen presenting cells

• once activated, they can divide into pasma or memory cells

how are plasma cells involved in the humoral response

• types of B cells that produce and secrete antibodies against a specific antigen

• have a short lifespan of a few days

how are memory cells involved in the humoral response

• type of B cell that provide long term immunity against specific pathogens

• have much larger lifespan than plasma cells

• they rapidly divide into plasma cells if body is reinfected with the same pathogen

how are helper T cells involved in the humoral response

• bind to antigen presenting cells to activate division of B cells

humoral response stage 1

B cell with complimentary antibody binds to antigen on pathogen

humoral response stage 2

B cell engulfs pathogen and presents its antigens on the cell surface membrane to become an antigen presenting cell

humoral response stage 3

clonal selection - activated T helper cell bind to B cell, causing activation of this B cell

humoral response stage 4

clonal expansion - activated B cell divides by mitosis to form plasma and memory cell clones

humoral response stage 5

cloned plasma cells, produce and secrete the specific antibody which is complementary to the antigen on the pathogens surface - these antibodies then attach to antigens on pathogens and destroy them

humoral response stage 6

memory cells circulate the blood and tissue fluid, ready to divide if the body is reinfected with the same pathogen

what is clonal selection

B cell with the correct antibody is selected for cloning by being activated by a T helper cell

what is clonal expansion

division of specific B cells to produce genetically identical clones

what is the graph showing primary vs secondary response

primary

• longer lag phase

• slower response

• involves symptoms

• very few B cells specific to the antigen

• 4-7 days

secondary

• shorter lag phase

• fast response

• no symptoms

• quickly divide into plasma cells as memory cells already exist

• plasma cells secrete large number of antibodies

• memory T cells are also activated into T killer cells to destroy pathogens

what is an autoimmune disease

when the immune system cant recognise self antigens so starts to attack them and breakdown healthy tissues

what is type 1 diabetes

autoimmune disease where the immune system attacks insulin secreting cells in the pancreas leading to lack of insulin

what is lupus

autoimmune disease where the immune system attacks cells in the connective tissues causing inflamation

what is rheumatoid arthritis

autoimmune disease where the immune system attacks cells in the joints causing pain and inflammation

what is the structure of an antibody

• y shaped and made of 4 polypeptide chains (2 heavy and 2 light) and have 3 regions

• constant region - same for all antibodies and binds to receptors on cells like B cells

• variable region - different for each antibody as its shape is complementary to a specific antigen - its the part of the antibody that binds to antigens

• hinge region - allows antibody to be flexible so it can bind to multiple antigens at once

what is the agglutination of pathogens

• clumping antigens together to enable easier phagocytosis

• makes it easier for phagocytes to locate pathogens and allows them to engulf a number of pathogens at once

• antibodies also act as opsonins making pathogens easily recognisable by phagocyte

what is neutralisation of toxins

• antibodies act as antitoxins where they bind to toxins produced by pathogens

• binding neutralises the toxins to prevent them from damaging body cells

what is preventing pathogens from binding to cells

• when antibodies bind to antigens, they block cell surface receptors needed to bind to host cells

• this means that pathogen cant bind to or invade host cells

what is active immunity

immunity developed after the immune system makes its own antibodies

what are the types of active immunity

• natural - antibodies made after infection

• artificial - antibodies made after vaccine

what is passive immunity

immunity from receiving antibodies from another organism

what are the types of passive immunity

• natural - antibodies transmitted from mother to baby

• artificial - antibodies transfused or injected into individual

what are vaccines

• introduction of a pathogens antigens into body to stimulate the bodies immune response to the pathogen allowing the body to develop active artificial immunity

• vaccines usually contain antigens but also need to be safe to prevent symptoms of disease

what may vaccines contain

• dead/inactive pathogen

• weakened strains

• harmless version of toxin

• isolated antigens from pathogen

• genetically engineered antigens

how do vaccines work

1) vaccine with antigens injected

2) stimulates primary immune response to produce antibodies against antigen

3) memory cells capable of recognising those antigens are produced

4) on second exposure to antigen, memory cells rapidly divide into plasma cells

5) plasma cells rapidly produce antibodies against pathogen

6) pathogen destroyed before any symptom

what are the criteria for successful vaccine

• availability

• minimal side effects

• infrastructure (necessary resources for production, storage etc)

• administration

• herd immunity

what factors may prevent elimination of disease

• individual immunity failure

• pre immunity infection

• pathogen mutation

• pathogen variation

• pathogen hiding

• vaccine objections

what is antigenic variability

• some pathogens can change their antigens in the process of a vaccine

• makes it difficult to develop vaccines against some pathogens because if the antigen change enough they will no longer be recognised by the immune system

• this means memory cells produced from vaccination against one strain wont recognise the antigen from another strain

what are antibiotics

• drugs that kill/inhibit bacteria growth

how do antibiotics work

• preventing synthesis of bacterial cell wall

• disrupting protein activity in cell membrane

• disrupting enzyme action

• preventing dna synthesis

• preventing protein synthesis

how does antibiotic resistance occur via natural selection

1) genetic mutation occur making some bacteria resistant to the antibiotic

2) when an infection is treated with antibiotics resistent bacteria lives

3) resistant bacteria reproduce passing on the allele for resistance to their offspring

what bacteria have developed resistance for many antibiotics

• MRSA

• C. difficile

what can help reduce development of antibiotic resistance

• choosing appropriate antibiotics for treatment

• only use when needed

• avoid use of wide spectrum antibiotic

• ensure you complete the full course of antibiotic

• avoid antibiotic use in farming

what are some examples of medicines from natural resources

• penicillin - type of mould

• aspirin - willow bark

• prialt - venom of cone snail