Module 4 - Communicable Diseases

What are pathogens and the four types?

communicable diseases are those that can be passed from one organims to another caused by microorganisms known as pathogens where organism pathogen lives called host and they live by taking nutrients from host but also causing damage in the process
by-product of pathogen life cycle is that they cause harm to their host which involves following stages travel from one host to another (transmission) - entering host’s tissues - reproducing - leaving host’s tissues
bacteria - produces toxins that damage body cells
viruses - use host cells to replicate before bursting out and destroying cells
protoctists (protists) - take over cells and break them open
fungi - digest living cells to destroy them some also produce toxins

What is bacteria?

belong to prokaryotae where cells are smaller than eukaryotic cells but can reproduce rapidly as quick as every 20 minutes so once in host body albe to multiple rapidly where their presence can cause disease by damaging cells or releasing waste products and or toxins that are toxic to the host and in plants lives in vascular tissue causing blackening and death of these tissues

What is fungi?

commonly fungus lives in skin of animal which form mycelium which grow under the skin and send out specialised reproductive hyphae which grows to skin to relases spores causing redness and irritation
in plants fungus lives in vascular tissue where it gains nutrients + hyphae release extracellular enzymes such as cellulases which causes decay and fruit and storage organs such as tubers will turn black and decay

What is a virus?

invade cells and take over genetic machinery and other organelles of the cell as they can cause cell to manufacture more copies of the virus then host cells eventually burst releasing many new viruses which will infect healthy cells

What are protoctista?

organisms usually cause harm by entering host cells and feeding on the contents as they grow eg malarial parasite feeds on haemoglobin inside red blood cells
some organisms can be difficult to classify where some organisms have many features that do not fit with other organims in previous groups

What is direct transmission?

pathogens transferred directly from one organism to another there is no intermediary and goes from host to new host
direct contact - skin-to-skin contact touching infected person,kissing or sexual intercourse eg HIV,bacterial meningitis,ring worm + athletes foot
risk reduced by better hygiene (washing hands regularly,keep surfaces clean,sterilising surgical instruments and condoms during intercourse)
airborne droplets - coughing or sneezing tiny droplets of mucus or saliva onto someone where pathogen carried in tiny water droplets in the air eg tuberculosis and influenza which can be reduced by covering mouth when coughing and using a tissues and ensure disposed of correctly
oral transmission - usually be eating food or drinking water contaminated with pathogen eg food poisoning and cholera prevented by treating wastewater and careful preparation
transmission by spores - carried in air or residue of surfaces/soil eg tentanus where diesease can be avoided by wearing face mask and washing skin after contras
transmission is passing a pathogen from an infected individual to uninfected individual

What is indirect transmission?

passed from one organism to another using an intermediate which could be:
food and drinking water - ingestion of contaminated food or water can cause disease
vectors - transmit pathogens from one host to another (eg mosquitos transmit malaria)
contaminated objects - pathogens from infected individuals can live on objects for a short time and infect others
an example vector is plasmodium parasite that causes malaria via entering human host via bite from a female mosquito
lifecycle:female mosquito sucks blood from person infected with malaria - plasmodium develops from gametes in infected blood and migrates to salivary glands of mosquito - mosquito bites an uninfected person - plasmodium from mosquito migrates into the person’s liver - then migrates into their blood - person now has malaria

What factors increase the risk of communicable disease?

living conditions - overcrowded areas increase risk of direct transmission
climate - for example warmer temperatures allow mosquitoes to breed and transmit malaria as many protoctists,bacteria and fungi can reproduce more rapidly in warm weather meaning global warming means tropical pathogens able to survive in Europe
social factors - eg lack of health education and healthcare systems increase the risk of communicable disease in poorer countries
weaker immune system eg a person with HIV

What is malaria and bacterial meningitis and more detail?

protocist that affects humans and other mammals as damages red blood cells,liver and brain causing headaches and fevers as is a parasite in blood - transmitted by vectors (mosquitos) where vectors are an organism that carries a pathogen from one host to another
bacterium called which affects young children and teenagers as damages membranes of brain as becomes swollen which damages brain and spinal cord and can cause blood poisoning - transmitted by airborne droplets

What causes malaria?

mosquitos act as a vector for the plasmodium parasite that causes malaria stored in the salivary glands of the mosquito + when the infected mosquito bites the human it passes from the saliva into the blood
plasmodium live in erythrocytes allows them to hide from the immune system + to complete their lifecycle also acts as a source of food for the plasmodium to allow for growth/reproduction
body’s primary defences do not stop Plasmodium from entering as the vector feeds on the blood, and to do so it breaks the skin so the skin cannot act as a barrier as the mosquito pierces the skin
erythrocytes containing plasmodium are more likely to be destroyed by phagocytes than healthy erythrocytes as they release different chemicals to healthy erythrocytes + these chemicals released by infected erythrocytes attract phagocytes

Where does malaria occur?

more common in tropical areas as the climate is more suitable for the vector is suited to living in such conditions, and as tropical areas tend to be relatively poor, so are less able to prevent malaria
other parts of world becoming increasingly worried about malaria as climate change may cause a tropical climate to spread to other parts of the world and the mosquitoes could spread with this, also there could be increased movement of infected people in future - countries also worry as non-malaria affected countries fund anti-malaria measures via international aid + also because mosquitoes are becoming resistant to insecticides

What is HIV/AIDS and influenza and more detail?

virus known as human immunodeficiency virus that affects human and non-human primates as gradually destroys the immune system as attacks cells compromising immune response - transmitted by exchange of bodily fluids - AIDs is caused by HIV and HIV is transmitted in body fluids - take control of the lymphocytes once it enters uses reverse transcriptase on the host nucleus to insert its own viral DNA into the host chromosomes so that viral mRNA can be transcribed in order to produce viral proteins
virus that affects mammals including humans as kills ciliated epithelial cells in gas exchange systems attacking respiratory system - transmitted by airborne droplets and contaminated objects - risk factors for disease add up to more than 100% as individuals often have more than one risk factor
viruses don’t inhabit red blood cells as they can’t reproduce outside of a host cell but erythrocytes have no nucleus so the virus is unable to replicate/ reproduce in this cell as there is no RER for protein synthesis

How is the spread of HIV affected?

higher rates if education less effective or available - having multiple sexual partners is culturally encouraged - if condoms are not easily available (i.e: due to poverty so not being able to afford them) - if there is less primary health care (so people are less likely to be diagnosed so more likely to unintentionally pass it on) - if unscreened blood is used for blood transfusion + unsterilised needles and surgical apparatus are used,if there is no alternative to breastfeeding, if there is no access to drugs for treatment, if there is no vaccine - needle exchange programs reduces the chance of needle sharing between infected and uninfected people
knowledge of the human genome could be used to reduce the spread of HIV as if we find a person who is immune and isolate gene that provides immunity then can use the gene to find the shape of the protein that provides immunity and manufacture the protein to use as vaccination / cure - could also allow us to find the shape of the receptor involved in HIV and develop a drug to block the receptor

What is athlete’s foot and ring worm and more detail?

fungus which affects human as causes cracking and scaling of skin between toes - transmitted by contaminated objects
fungus that affects mammals including cattle and humans as causes spores to erupt through skin causing a circular red rash - transmitted by direct contact

What is tuberculosis and more detail?

bacterium which affects humans and pigs as damages the lungs and suppresses the immune system as kills cells and tissues - transmitted by airborn droplets
is not transmitted easily and often takes living in close proximity to people with disease for a long time before it is transmitted - BCG vaccination given to teenagers successfully reduce prevalence of TB in Western Europe however increase migration and more people living in overcrowded and poorly ventilated conditions meaning TB is rising in many Western cities 
can be spread by an infected individual coughing or sneezing, and the droplets released (containing the pathogen) being inhaled by the uninfected individualRisk factors for TB include not being vaccinated against TB,a weakened immune system, smoking / alcoholism, homelessness, poor ventilation and overcrowding of housing, close contact with people from / visiting, area where TB is common, close / prolonged, contact with individual(s) with TB, and consumption of milk or beef, from infected cattle in developing countries

How are communicable diseases passed between plants?

can happen via direct transmission - involves direct contact of a healthy plant with any part of an infected plant where can enter the roots where once infected will infect all vascular tissue where pathogens in leaves are distributed when leaves shed and carry pathogen back to soil where it can grow and infect another plant + can also enter fruit and will be distributed in the seeds
also can happen via indirect transmission - can take place via soil contamination when infected plants leave pathogens or spores in the soil ready to infect other plants and also takes place using vectors

What are some examples of vectors in plant disease transmission?

wind - bacterial,viral or fungal spores are carried by the wind to uninfected plants
water - spores can travel on surface of water to reach uninfected plants
animals - insects and birds can carry pathogens or spores from one plant to another such as beetles which when attacks another plant pathogen is transmitted to uninfected plant eg fungus that causes Dutch elm disease carried by beetle
humans - pathogens and spores can be transmitted by handling plants,clothing,farming tools and practices

What factors increase the risk of communicable diseases in plants?

crop variety - some crops are more susceptible to disease than others
overcrowding - increases likelihood of direct contact
mineral nutrition - poor nutrition reduces resistance of plants
climate change - increased rainfall and wind increases the spread of disease

What is ring rot and tobacco mosiac virus and more detail?

rr - bacterium that affects potatoes and tomatoes as damages the leaves,tubers and fruit causing a ring of decay in vascular tissue of potato tuber
tmv - caused by virus that affects many plant species including tobacco and tomatoes as damages the leaves,tubers and fruit by molting and discolouration

What is black sigatoka and potato/tomato blight and more detail?

bs - fungus that affects banana plants as attacks and destroys the leaves,turning them black leaving spots reducing yield
p/t b - protoctist that affects potatoes and tomatoes as destoys leaves,tubers and fruit

How are plants used by pathogens?

plants make sugars in photosynthesis anc convert them into compounds like protein and oils therfore is a rich source of nutrients for many organisms such as all the pathogens,insects and vertebrates where the first might be pathogenic and the other two may act as vectors to help transmit these animals
plants don’t have immune system comparable with animals but have developed range of structral,chemical and protein-based defences which can defend invading organims and prevent them causing extensive damage which includes both passive defences to prevent entry and active defences which are induced when pathogen detected
passive defences are present before infection and their role is to prevent entry and spread of the pathogen which includes physical barriers and chemicals

What are some physical plant defences?

waxy cuticles - leave and stems covered in waxy cuticle which provides a physical barrier against pathogens as prevents water collecting on cell surfaces since pathogens collect in water and need it to survive so absence of water is passive defence
bark - most bark contains a variety of chemical defences that work against pathogenic organisms
cellulose cell walls - plant cells are surrounded by cells walls that form a physical barrier against pathogens + contain chemical defences that can be activated when pathogen detected
lignin thickening of cell walls - lignin is waterproof and almost completely indigestible
production of callose - when plants attacked by pathogens they produce a polysaccharide called callose which is deposited in sieve tubes around the sieve plates and blocks the flow in the sieve tube which can prevent a pathogen spreading around the plant
stomata closure - stomata are possible entry points for pathogens and when pathogenic organisms are detected the guard cells will close the stomata in that part of plant

What are the chemical defences?

plant tissues contain a variety of chemicals that have anti-pathogenic properties including terpenoids,phenols,alkaloids and hydrolytic enzymes where some of theses chemicals such as terpenes in tyloses and tannins in bark are present before infection however as production of chemicals requires a lot of energy so many chemicals are not produced until plant detects an infection

What are four production of chemical which act as chemical defences to plants?

insects repellents - reduce number of insect feeding on plants to prevent them from transmitting pathogens
insecticides - kill insects to prevent them from transmitting pathogen
antibacterial substances - chemicals such as antibiotics are produced to kill bacteria or inhibit their growth
toxins - some plants produce chemicals that break down into cyanide which is toxic when plant cells are attacked

What are active defences?

when pathogen attack specific chemicals in their cell walls can be detected by plant cells where these chemicals include specific proteins and glycolipids - respond to pathogenic attack by production callose,release/production of toxic chemicals like tannins, through leaf drop/abscission, and/or via necrosis also responds by fortifying defences already present including increasing physical defences and producing defensive chemicals
cell walls become thickened and strenghthened with additional cellulose - deposistion of callose between plant cell wall and membrane near invading pathogen which impedes cellular penetration at infection site it strengthenes cell wall and blocks plasmodesmata - oxidative bursts that produce highly reactive oxygen molecules capable of damaging cells invading organims - increase in production of chemicals

What are terpenoids,phenols,defensins and hydrolytic enzymes?

t - range of essential oils that have antifungal and antibacterial properties + creates scent eg menthols by mint plants
p - also have same properties
d - small cysteine-rich proteins that have broad antimicrobial activity which appear to act upon molecules of plasma membrane of pathogens possibly inhibitng action of ion transport channels
h - found in spaces between cells including chitinases (break down chitin found in fungal cell walls) . glucanases (hydrolyses glycosidic bonds in glucans) and lysozymes (capable of degrading bacterial cell walls)

What are tannins,alkaloids,necrosis and tylose?

t - found in bark inhibit attack by insects which bind to salivary proteins and digestive enzymes such as trypsin deactivating enzymes where insects that ingest high amounts of this do not grow and die which helps prevent transmission of pathogens
a - nitrogen-containing compounds such as morphine give a bitter taste to inhibit herbivores feeding + if plant can reduce grazing by larger animals then it will suffer damage that can allow pathogens to enter the plant
n - deliberate cell suicide where few cells are sacrified by killing cells surrounding infection the plant can limit pathogens access to water and nutrients stopping it from spreading further around the plant which is bought about by intracellular enzymes that are activated by injury
t - balloon-like swelling that fills xylem vessels when tylose full formed vessel can no longer carry water blocking x vessel preventing pathogen spread which contains lots of chemicals such as terpines which are toxic

What are two groups defence mechanisms be split into and primary defences?

non-specific defences - act quickly to defend the body but responds in same way for all pathogens
specific defences - are slower to defend the body but produce a specific response for each pathogen + provide long-term immunity
primary defences are those that prevent pathogens entering the body and are non-specific as will prevent entry to any pathogen

What are some examples of non-specific barriers to prevent pathogen entry?

skin - mucous membranes - expulsive reflexes - blood clotting and wound repair - inflammation - phagocytosis

How can skin prevent the entry of pathogen?

acts as a physical barrier to block pathogens entering the body - also acts as chemical barrier by producing sebum an antimicrobial substances that lowers pH to inhibit pathogen growth
outermost layer epidermis consists of layer of cells where producec by mitosis at base then migrate out to surface of skin as they migrate they dry out and cytoplasm replaced by protein keratin called keratinisation and no longer alive when they reach surface + layer of dead cells is effective barrier

How can mucous membranes prevent the entry of pathogen?

parts of ears,nose,throat and digestive tract lined by mucous membranes as air and food taken in may contain microorganisms therefore at risk of infection so protected by mm which secrete mucus to trap pathogens and use lysosymes to destroy them - epithelial layer contains goblet cells which secrete mucus where in airway mucus lines passages and traps any pathogens that may be in air - epithelium also has ciliated cells which are hair-like organelles which move in coordinated way to waft layer of mucus along where move mucus up to top of trachea where it can enter oesophagus to be swallowed to digestive system where pathogens killed by acidity denaturies pathogens enzymes

How can expulsive reflexes prevent the entry of pathogen?

coughing and sneezing are methods for expelling foreign objects such as pathogens from gas exchange system in response to irritation where sudden expulsion of air will carry with it the microorganisms causing irritation - vomit and diarrhoea expel contents of gut along with any present pathogens

How can blood clotting and wound repair prevent the entry of pathogen?

cut to skin provides possible entry for pathogens and so blood clots act quickly to seal any wounds where clotting factor activates thrombokinase which with calcium ions able to convert protein Prothrombin into enzyme thrombin which catalyses conversion of soluble fibrinogen into insoluble fibrin - clot dries out to form a scab that blocks entry to body - after scab formed skin is capable of repairing itself to reform its physical barrier - epidermal cells underneath scab divide while damaged blood vessels regrow to provide oxygen and collagen fibres used to provide strength to new tissue under scab - once epidermis is required thickness scab breaks off and wound is healed

How can inflammation prevent the entry of pathogen?

sign tissue is infected is swelling,heat,redness and pain at site of infections or wounds - presence of microorganisms in tissue detected by mast cells which release chemicals (histamine) which has effects on surrounding tissue to help combat infection affecting blood vessels in two ways:blood vessels dilate which increases blood flow to area making it hotter preventing pathogens from reproducing + blood vessel walls become more permeable so they start to leak tissue fluid causing swelling and isolating any pathogens in damaged tissues - blood plasma + phagocytes leave blood and enter tissue fluid which leads to increased tissue fluid causing swelling which is drained into lymphatic system where lymphocytes are stored which can lead to pathogens being into contact lymphocytes intiating specific immune responses

What else can cause inflammation?

If different materials eg foods,other pathogens have a similar antigen (short sequence of amino acids that may be common to more than one polypeptide)  to a pathogen that the body has encountered before then this molecule will bind to the binding sites on the antibody created for the pathogen + we can say that this antibody is not specific to one molecule - the antibody would then bind to a T lymphocyte and histamine would be released causing inflammation

What are some other primary defences?

eyes are protected by antibodies and enzymes in tear fluid (lysosomes) - ear canal lined by wax which traps pathogens - female reproductive system protected by mucus plug in cervix and by maintaining relatively acidic conditions

What are antigens?

unique molecules usually proteins that can be found on surface of cells where these antigens allow immune system to distinguish between body’s own cells (self) and foreign cells (non-self) where any foreign cells can be destroyed whilst leaving body’s own cells unaffected

What various cells can antigens identify?

pathogens - immune system recognises antigen as being foreign and activates cells to destroy the pathogen
abnormal body cells - cancerous or infected cells display abnormal antigens that trigger an immune response
toxins - are antigen molecules themselves and can be recognised by immune system
cells from other organisms of same species - cells may have different antigens to body’s own cells so are identified as being foreign so can cause rejection of transplanted organs

What are phagocytes and main two types?

type of white blood cell that engulf and destoy pathogens and found in blood and body tissues of many organisms - first line of secondary defence
neutrophils - rapidly engulf and destroy pathogens at site of infection - have multi-lobed nucleus and manufactured in bone marrow + often pushed out of blood into tissue fluid and released in large numbers in when infection occurs containing lots of lysosomes as engulf and digest pathogens - trap foreign matter in a large vacuole (phagosome) which fuses with lysosomes to digest matter
macrophages - these engulf and digest pathogens but also present pathogens antigens on its cell surface to activate other cells in immune system - larger cells manufactured in bone marrow and found in lymph nodes where they mature into

What defence are phagocytes?

considered a secondary defence as they are involved after the pathogen has entered the body + a nonspecific response as they are able to able to engulf and digest a range of different pathogens
able to pass from the blood into the tissue fluid as each has a lobed nucleus and can change shape so phagocytes can fit between cells in the walls of the capillary + histamine makes the capillary walls/endothelium leaky

What is the role of macrophages?

play important role in initiating the specific responses to invading pathogens as when m engulfs a pathogen it does not fully digest it - the antigen from surface of pathogen is saved and moved to special protein complex on surface of the cell becoming an antigen-presenting cell which exposes the antigen on its surface so other cells of the immune system can recognise the antigen where the special protein complex ensures antigen-presenting cells not mistaken for a foreign cell and attacked by other phagocytes

What are the steps of phagocytosis?

pathogen releases chemicals that attract phagocyte - phagocyte recognises the pathogen’s antigens as non-self which causes phagocyte to bind to the pathogen - phagocyte engulfs the pathogen via endocytosis - pathogen is now contained within vesicle known as phagosome - lysosome containing hydrolytic enzymes called lysozymes which fuses with phagosome to form a phagolysosome - lysozymes digest and destroys pathogen by secreting lysins + digested/hydrolysed into amino acids, sugars, fatty acids, and glycerol, which are all absorbed into the cytosol of the phagocyte by diffusion, facilitated diffusion, and active transport - phagocyte presents pathogens antigen on its surface to activate other cells in immune system phagocyte then referred as an antigen-presenting cell
any unwanted breakdown products removed by exocytosis + cytoskeleton is involved in the endocytosis and the movement of the vesicles

How are phagocytes specialised to attack specific pathogenic cells?

receptors on plasma membrane that can bind to opsonin or specific antigen - a lobed nucleus that allows cell to squeeze through small gaps - well-developed cytoskeleton which helps cell to change shape to engulf the pathogen and to move lysosomes and vacuoles around cell - many lysosomes contain lysin and lytic enzymes - many mitochondria to release energy from glucose - a lot of ribosomes to synthesise enzymes involved

What are secondary defences?

used to combat pathogens that have entered body where when a pathogen invades the body it is recognised as foreign by chemical markers on its outer membranes called antigens which are proteins or glycoproteins intrinsic to plasma membrane where antigens are specific to the organism where our own cells have antigens but these are recognised as our own and don’t produce a response

What are two molecules that help with phagocytosis?

cytokines are chemicals released by phagocytes that have engulfed a pathogen and act as cell-signalling molecules to trigger the movement of other phagocytes to site of infection + also trigger an increase in body temperature which inhibits reproduction of pathogens and allows specific immune system to work faster
opsonins are chemicals that bind to pathogen by attaching to antigens on its surface to make them easily recognisable where phagocytes contain receptors on their cell-surface which bind to common opsonins making it easier for phagocyte to bind to pathogen and destroy it therefore enhancing - some not very specific so can attach to variety of pathogenic cells where role to enhance ability of phagocytic cells to bind and engulf pathogens

What are antigen presenting cells,cytokines and opsonins?

a cell that isolates the antigen from a pathogen and places it on the plasma membrane so that it can be recognised by other cells in the immune system
hormone-like molecules used in cell signalling to stimulate immune response
proteins that bind to the antigen on a pathogen and then allow phagocytes to bind

How does the specific immune response differ?

depends on type of lymphocyte produced in bone marrow where the two types are:
T lymphocytes - T cells mature in thymus gland and involved in cellular response where they respond to antigens presented on body cells
B lymphocytes - B cells mature in the bone marrow and involved in humoral response where they produce antibodies found in body fluids
both have large nucleus and specalised receptors on plasma membrane which eventually produces antibodies which neutralise foreign antigens and also provides long-term protection from disease as produces immunological memory through memory cell release which circulate body for years
where antigen-presenting cell moves around body where it comes in contact with either if these cells that activate full immune response where may only be one cell with correct recognition site for the antigen so job to increase chances antigens will come in contact with them

What are the four types of T cells?

T helper cells - T killer cells - T regulator cells - T memory cells

What are T helper cells?

have receptors on cell-surface that bind to complementary antigens on antigen-presenting cells and produce interleukons (type of cytokine) which stimulates immune response of B cells or phagocytes and can also form memory cells or T killer cells
T lymphocytes produce cell signalling molecules called cytokines in order to stimulate specific B-lymphocytes to divide - works by the cytokin/interleukin/ receptor on the B lymphocytes having a unique shape so the cytokine/ interleukin binds to the receptor on the cell surface membrane of the B lymphocyte as the receptor and cytokine have complementary shapes + this stimulates clonal expansion in the humoral response

What are T killer cells?

these cells kill abnormal and foreign cells by attacking infected body cells by producing a protein known as perforin and this proteins makes holes in cell-surface membrane causing it to become freely permeable and causing cell death

What are T regulator and memory cells?

these cells supress immune system after pathogens have been destroyed and this helps to prevent immune system from mistakenly attacking body cells
these cells provide long-term immunity against specific pathogens and they provided a rapid response if body is reinfected by same pathogen by remaining in the blood

What is the specific immune response?

activation of specific B and T cells called clonal selection (selection of specific B or T cells that is specific to antigen) which causes series of events that lead to production of antibodies that can produce the specific pathogens and memory cells that will provide long-term immunity where whole series of events is stimulated and coordinated by a number of hormone-like chemicals called cytokines which stimulate differentiation and activity of macrophages,B cells and T cells

What are the stages of the cellular response?

macrophage engulf pathogens which have specific antigens and display their antigens on cell-surface and now known as antigen-presenting cells
T and B lymphocytes with complementary receptors on plasma membrane bind to these antigens known as clonal selection where can be achieved directly when pathogenic cells enter lymph nodes or via action of antigen-presenting cells
on binding after correct lymphocyte activated the T helper cell is activated to divide by mitosis to form genetically identical clone as must increase in numbers to become effective known as clonal expansion
then differentaition occurs as clones of the lymphocytes develop into a range of useful cells

What different functions can cloned T cells carry out?

develop into T memory cells - these circulate in body to provide long-term immunity and a faster secondary response
develop into T killer cells - these destroy infected cells that display foreign antigen
develop into T regulator cells - these shut down immune system after pathogen removed + involved in preventing autoimmunity
stimulate phagocytosis done by T helper cells - cells produce interleukins which stimulate phagocytes to engulf pathogens
stimulate division of B cells done by T helper cells - cells produce interleukins which stimulate B cells to divide and produce antibodies

What is cell signalling?

needed for coordinated action of a range of cells which need to communicate which is achieved through the release of hormone-like chemicals called cytokines where in order to detect a signal target cell must have cell surface receptor of complementary shape to shape signalling molecule
examples of communication using cytokines:
macrophages release monokines where some attract neutrophils and others stimulate B cells to differentiate and release antibodies
T cells and macrophages releases interleukins which are signalling molecules used to communicate between different wbc these can stimulate clonal expansion and differentiation of B and T cells

How do antigens and antibodies work together?

antigens usually proteins in pathogens plasma membrane stimulates immune response where foreign antigens detected stimulates production of antibodies which are specific to the antigen and to the pathogen usually own antigens are recognised by immune system + don’t stimulate immune response - antibodies are immunoglobulins which are complex proteins produced by plasma cells + releasedin response to an infection which have region with specific shape complementary to antigen where immune system must have one type of antibody for every antigen detected + antibodies attach to antigens rendering them harmless

What is the structure of antibodies?

y-shaped glycoproteins made up of four polypeptide chains,two heavy chains and two light chains where polypeptide chains are held together via disulphide bridges
made of various regions:constant region which is the same for all antibodies and binds to receptors on body cells such as B cells,phagoctyes + mast cells
variable region - different for each antibody as its shape is complementary to specific antigen and this part of antibody that binds to antigens has two or more variable regions - the amino acid sequence of the variable region that gives it its complementary/matching, shape
hinge region - allows antibody to be flexible so it can bind to multiple antigens on pathogens at once as more than one variable region

What are the functions of antibodies?

main function is to bind to specific antigens on pathogens surface where each antibody has unique binding site that fits onto specific antigen forming antigen-antibody complex
4 roles to help destroy pathogens: act by agglutination of pathogens which involves clumping pathogens together to enable easier phagocytosis where antibodies cause pathogens to stick together clump is too large to cross the membrane of host cells to enter them and has an increased likelihood of being consumed by a phagocyte such as a monocyte + allows multiple pathogens to be engulfed at once
neutralisation of toxins which is when antibodies bind to toxins to inactivate them using anti-toxins rendering them harmless - locking the pathogen’s binding sites and also binding to toxins to prevent them from binding to and/or entering the host cells
preventing pathogens from binding where antibodies bind to pathogens to stop them from infecting body cells
opsonins which are a group of antibodies that bind to antigens on a pathogen acting as binding site for phagocytes so can more easily bind and engulf the pathogen

What is agglutination of pathogens?

antibodies act as agglutins causing pathogen to clump together which makes it easier for phagocyte to locate pathogens and allows them to engulf number of pathogens at once
each molecule has two identical binding sites so able to crosslink pathogens by binding an antigen on one pathogen with binding site and antigen on another pathogen with other binding site this crosslinking causes the clumping together of pathogens which has two pros of agglutinated pathogens physically impeded from carrying out functions like entering host cells + agglutinated pathogens readily engulfed by phagocytes particularly against viruses

What is neutralisation of toxins and how do antibodies prevent pathogen from binding cells?

antibodies act as antitoxins where they bind to toxins produced by pathogens and this binding neutralises toxins to prevent them from damaging body cells where molecules may be toxic and action renders them harmless
when antibodies bind to pathogens antigens they block cell-surface receptors needed to bind to host cells which means pathogens cannot bind to or invade host cells

What is more details on opsonins?

antibodies also act as opsonins making pathogens easily recognisable by phagocytes
some are not very specific + stick to type of molecules not found in host cells + others are produced as part of specific immune response and bind to very specific antigens where the opsonins bound to antigen renders antigen useless in process known as neutralisation where it assists in phagocytosis but also prevents pathogen entering host cell before it can be attacked by phagocytes

What is the humoral response?

specific defence mechanism used to protect body from disease involves production of specific antibodies to destroy pathogens
involves use of B lymphocytes which produce and are covered in proteins known as antibodies where antibodies are found in body fluid

What is more detail about B and plasma cells?

each B cell has slightly different DNA code so that the antibodies it can produce are slightly different from those of other B cells - plasma cells cloned from one B cell will all make identical antibodies where structure of plasma cells is specialised contain numerous organelles associated with protein synthesis and secretion such as lots of ribosomes,rough ER ,Golgi apparatus and mitochondria
lack of b-lymphocytes leads to fewer plasma cells in the body so fewer antibodies produced so person more susceptible to pathogens and thus infection

What cells are involved in humoral response?

B cells - have antibodies on plasma membranes that bind to complementary antigens and on doing so they engulf antigens and display them becoming antigen-presenting cells and once activated can divide into plasma cells
Plasma cells - type of B cell that produce and secrete antibodies against specific antigen and have a short lifespan of only a few days (manufacture antibodies which when released can attach to pathogenic antigen)
Memory cells - type of B cell that provides long-term immunity against specific pathogens + have much longer lifespan than plasma cells + divide rapidly into plasma cells if body re-infected with same pathogen - recognise pathogens and produce a clone that can become plasma cells on infection which make antibodies against the pathogens antigens - responsible for the secondary response and destroy the virus before symptoms appear 
Helper T cells - cells bind to antigen-presenting cells to activate division of B cells

What are the stages of the humoral response?

involves antibodies found in body fluids - B cell with complementary antibody binds to antigen on pathogen - B cell engulfs pathogen and presents its antigen on cell-surface membrane to become an antigen-presenting cell - clonal selection occurs where activated T helper cells bind to B cell causing activation of this B cell - clonal expansion means activated B cells divide by mitosis to form plasma and memory cell clones - cloned plasma cells produce and secrete the specific antibody complementary to antigen on pathogen’s surface where these antibodies attach to antigen on pathogen and destroy them - memory cells circulate blood and tissue fluid ready to divide if body re-infected

What is the difference of clonal selection and expansion of B cells?

selection - B cell with correct antibody is selected for cloning by being activated by T helper cell
expansion - division of specfic B cells to produce genetically identical clones

What are autoimmune diseases?

diseases where part of the body is attacked by the body’s own immune system as the immune syste mistakes the body cells as non self + so produces B and T lymphocytes that produce antibodies that are complementary to the body’s own tissues which leads to breakdown of healthy tissues where normally any B or T cells specific to own antigens destroyed during early development so occurs when antibodies start to attack own antigens
the body creating antibodies against the antigens on specific body parts (specify which) so that phagocytes such as macrophages, and also T killer cells, attack the affected tissues,leading to fewer (and more damaged) cells of this type and preventing functionality (i.e: saltatory conduction in neurons)

What are examples of autoimmune diseases?

type 1 diabetes - immune system attacks insulin-secreting cells of pancreas,causing a lack of insulin
lupus - immune system attacks cells in connective tissues causing inflammation (swelling and pain)
rheumatoid arthritis - immune system attacks cells in the membrane around the joints causing painful inflammation of a joint
multiple sclerosis - damage to the myelin sheath of neurones so that they have less insulation which interferes/slows the conduction of nerve impulses/action potentials, + can slow or stop saltatory conduction - this occurs in sensory neurones towards brain the brain/CNS from the receptors in the sensory organs 
chronic fatigue syndrome- pyruvate is not efficiently transferred to the mitochondria + overproduce T lymphocytes and cytokines - specific immune response is poor because the B lymphocytes do not respond to the cytokines that have been produced + lack of ATP there is little energy for the clonal expansion of B cells or the production and release of antibodies

What is primary immune response?

takes place when body exposed to pathogen for first time where this response is slow and infected individual experiences symptoms of disease slower due to clonal selection and clonal expansion and then production of antibodies

What is secondary immune response?

takes place when body has been exposed to same pathogen before where this response is much faster and stronger and pathogens are destroyed before any symptoms appear quicker + more antibodies are produced because of the memory cells / immunological memory

Graph

What are the steps of primary immune response?

1.production of antibodies is slow after exposure to the pathogen (longer lag phase) 2.concentration of antibodies increases slowly 3.this is because there are very few B cells that are specific to pathogen’s antigens 4.takes time for B cells to divide into plasma cells to produce correct antibody so individual experiences symptoms of disease so takes few days before number of antibodies in blood rises to level that can combat the infection 5.during this process some B cells divide into memory cells to make individual immune to this disease

What are the steps of secondary immune response?

1.production of antibodies is much quicker after exposure to pathogen as already has memory cells (shorter lag phase) 2.concentration of antibodies increases quickly 3.this is because memory B and T cells recognise pathogen’s antigens and quickly divide into plasma cells 4.these plasma cells secrete larger number of antibodies to quickly as clonal selection and expansion happen quickly destroying the pathogen before individual experiences any symptoms 5.memory T cells also activated to divide into T killer cells to destroy the pathogen
this overall produces antibodies sooner and more rapid so reaches higher concentration usually quick enough to prevent symptoms

What are the differences of primary and secondary immune response?

primary - first exposure - slow speed of response - symptoms experienced - B and T cells activated - low rate of antibody production - only a few antibodies - long time between pathogen exposure and antibody production (4-7 days)
secondary - second exposure - fast speed of response - no symptoms experienced - memory B and T cells activated - high rate of antibody production - large number of antibodies - short time between pathogen exposure and antibody production (1-3 days)

What are the four types of immunity?

active - develops when immune system activated makes its own antibodies and takes a while for immunity to disease but long-term protection as memory cells produced
passive - develops when given antibodies made by different organisms and provides immediate immunity to disease but short-term as antibodies are broken down + memory cells not produced
natural - achieved through normal life processes + artificial - achieved through medical intervention

What are the different immunity pairs?

can be natural active - antibodies made in immune system after infection where person suffers from disease once then immune eg chicken pox
artificial active - antibodies made after vaccination as injected with weaker pathogen form activating immune system
natural passive - antibodies transmitted from mother to baby via placenta or breast milk making baby immune to diseases mother is immune to
artificial passive - antibodies transfused/injected into individuals

What are vaccinations?

introduction of pathogens antigen into body usually injection which stimulates body to produce an immune response to pathogen providing artificial active immunity to specific disease
may contain dead pathogens eg cholera vaccine,isolated antigens from a pathogen eg hepatitis B vaccine or attenuated pathogen strains (DNA removed) eg TB vaccine

How do vaccinations provide immunity?

cause body to produce antibodies against specific antigens with steps being:
1.vaccine containing antigens injected into the blood 2.stimulates primary immune response to produce antibodies against pathogen 3.memory cells capable of recognizing these antigens are produced 4.on second exposure to this pathogen memory cells rapidly divide into plasma cells 5.plasma cells rapidly produce antibodies against the pathogen 6.pathogen destroyed before any symptoms experienced
sometimes booster vaccines need to be given later on to provide longer-lasting immunity

What are the two other types of immunity?

herd immunity - in population when many are vaccinated means most people are immune and cannot transmit pathogen onto others which reduces the chance of non-vaccinated individuals coming into contact with pathogen so fewer individuals are infected so can no longer be spread important as not possible to vaccinate everyone eg babies or people with compromised immune systems
ring vaccinations/immunity - used when new case of disease is reported involves vaccinating all people in immediate vicinity of case also used to control livestock disease

What are the factors that affect how successful a vaccine will be?

availability must be in large amounts for mass immunisation - minimal side effects means better public acceptance - infrastructure needed for producing + storing vaccines such as refrigeration - administration as requires trained healthcare workers - herd immunity with goal to vaccinate majority of the population
most at risk from diseases are the elderly, young children, pregnant women, those with compromised immune systems, those with chronic diseases and those often in contact with sick people such as health workers

Why vaccines may not eliminate a disease?

individual immunity failure as may get disease before immunity develops - pathogen mutations and antigenic variability where rapid antigenic changes due to frequent mutations make them ineffective as no longer recognizes pathogens new antigens - pathogen variety where disease such as cold have lots of pathogen variants so universally effective vaccine impossible - pathogen hiding some can evade immune system by hiding inside cells - vaccine objections where religious,personal or ethical objections to vaccinations can hinder effectiveness

What is antigenic variability?

some pathogens can change their antigens in a process known as antigenic variability as undergo genetic mutations which makes it difficult to develop vaccines against some pathogens because if antigens change enough will no longer be recognised by immune system meaning memory cells produced by vaccine against one strain will not recognize antigens from another strain
as a result vaccines need to be changed frequently to provide protection against most recent strains
flu vaccine changes every year as the virus mutates each year to form new strains + new strains have different antigens so the antibody produced in response to the vaccine needs to match the antigens of the new strain

How do you control epidemics?

are rapid spread of disease through high proportion of the population where once disease eradicated to low incidence unlikely to spread routine vaccination programme can be relaxed
when mutations occur incidence of disease may increase again where certain pathogens eg influenza unstable and regularly undergo antigen changes so epidemics may arise
threats are monitored so new strains identified so health authorities can prepare for impending epidemic and determine which strains most likely will spread by stockpiling suitable vaccines and vaccinating those at risk such as those over 65
useful to collect information about incidence of a disease in different areas as it allows you to find out where rates are highest/people are most at risk - allows you to keep track of infection rates over time, to see where disease is likely to spread - it helps research into how disease is spread/into effectiveness of drugs - it allows organisations to provide aid/health care where it is needed most + it allows organisations to provide education about disease where it is needed most

How do antibiotics work?

drugs that kill or inhibit the growth of bacteria or fungi as they target the bacterial enzymes and ribosomes used in metabolic reactions meaning they do not damage human cells (as contain different enzymes and ribosomes)
examples of how they affect bacteria include preventing synthesis of bacterial cell walls,preventing DNA and protein synthesis
don’t work against viruses as they lack cell structures instead relying on host cells to carry out metabolic reactions meaning antibiotics cannot target and disrupt these reactions
antibiotic resistant pathogens are a concern as they may become untreatable leading to outbreaks of their diseases which could kill many people + developing more powerful antibiotics is expensive and takes time

What can treat viral diseases?

antiviral medication which acts as competitive inhibitors can help reduce the spread of influenza as fewer viruses are produced so there are fewer in the water droplets released when an infected person sneezes or coughs as the viruses cannot leave the cell so cannot infect/spread to other cells

What is antibiotic resistance?

increased use of antibiotics has led to development of antibiotic resistant bacteria meaning antibiotics were once effective against these bacteria no longer work making it more difficult to treat bacterial infections
develops via natural selection: 1.genetic mutations occur making some bacteria resistant to an antibiotic 2.when an infection is treated with antibiotics resistant bacteria are able to survive 3.resistant bacteria reproduce passing on the allele for antibiotic resistance to their offspring
genes often occur on plasmids meaning can be transferred from one bacterium to another in process of conjugation
some bacteria infamous for multiple resistances including C diff and MRSA - leaf-cutter and farm fungi which they feed to their growing larvae where in order to prevent infection so carry symbiotic bacteria which produces antibiotics may be source for new drugs for bacterial infections

What is the impact of antibiotic resistance and how can it be reduced?

some bacteria developed resistance for several different antibiotics: MRSA - these bacteria cause wound infections and are resistant to multiple antibiotics including methicillin + C difficile - these bacteria infect digestive system and can survive and reproduce in presence of many antibodies
following measures help reduce development of antibiotic resistance: 1.choosing appropriate antibiotics for treatment - antibiotics can be tested against bacterium stains to make sure they are effective in treating the disease
2.using antibiotics only when needed - should only be prescribed for bacterial infections not viral
3.avoiding use of wide-spectrum antibiotics - use of antibiotics specific for the infection is less likely to lead to antibiotic resistance
4.ensuring patients complete courses of antibiotic treatment - ensures all bacteria are killed and so does not give them a chance to develop resistance
5.avoiding use of antibiotics in farming - reduced chance of bacterial becoming resistant to antibiotics

What are some sources of medicines?

come from wide range of natural source including plants,animals and microorganisms
scientists not yet discovered or analysed all organisms on earth so may be organisms that can provide treatments to currently incurable diseases,new diseases and antibiotic treatments becoming less effective these sources need to be protected by maintaining biodiversity
plants used in traditional medicine often used to produce drugs as the plants are already identified as having medicinal properties and few side effects which reduces the time and effort in finding plants/active chemicals which reduces the cost of developing the antibiotics

What are the three ways new medicines can be discovered?

1.accidental discovery - antibiotic penicillin was accidentally discovered by Alexander Fleming where fungus Penicillium releases compounds that kill bacteria
2.traditional remedies - many drugs have been used for centuries and used as people have noted certain plants have beneficial effect - India has over 7000 different plants with medical properties - morphine has origins in use of sap from unripe poppy seeds where opiate drugs reduce nervous action in central nervous system and if nerves cannot carry the impulse no pain is felt - medicinal use of willow-bark extract to relieve pain and fever has a long history led to discovery of aspirin + ibuprofen
3.observation of wildlife - many animals make use of plants with medicinal properties eg monkeys rub citrus oils on their coats as insecticides to prevent insect bites + bird line their nests with medicinal leaves in order to protect chicks from mites

What are some examples of medicines and plant research ?

penicillin - an antibiotic extracted from type of mould + aspirin - a painkiller based on compound from willow bark + prialt - a pain-killing drug derived from venom of a cone snail
scientists use traditional plant medicines + animals behaviour as starting points in search for new drugs eg aspirin research into plants used for traditional remedies enables them to isolate active ingredient where molecule can be analysed and similar molecules manufactured recently concentrated on tropical plants

What is the first path of future medicines?

new research focused on used of personalised medicines to treat disease these are medicines tailored to an individuals DNA - meaning patients genome is analysed and sequenced the genes from individuals before given any treatment so specific drugs more likely to be effective and less likely to cause side effects
possible to screen genomes of plants or microorganisms to identify potential medical compounds from DNA sequences

What is the second path of future medicines?

synthetic biology which involves use of genetic engineering to develop artificial proteins,cells and microorganisms overall development of new molecules that mimic biological systems in one form of synthetic biology - bacteria or mammals can be modified to produce therapeutic drugs to treat certain diseases + another way it is used is to design and construct new devices that may be useful in research eg development of tomatoes which contain a pigment with health benefits
re-engineering of biology could be production of new molecules that mimic natural processes or use natural molecules to produce new biological systems that do not exist in nature

What is research into disease-causing mechanisms?

pharmaceutical companies have been conducting research into way microorganism cause disease many make use of receptors on plasma membrane eg HIV binds to CD4 and CCR5 receptors on surface of T helper cells where if binding between pathogen and receptor site can be blocked so disease-causing pathogen cannot gain access to cell - glycoprotein receptor molecules can be isolated + sequenced once amino acid sequence known molecular modelling used to determine shape of receptor and then need to find drug that mimics shape of receptor and could be used to bind virus itself which would block virus from entering T helper cell

What needs to be considered in kidney donations?

donated kidney needs to be a close match as otherwise the donated kidney is more likely to be recognised as foreign/non-self as the glycoprotein antigens on the donated kidney will be different causing rejection due to the response of the by immune system means that the patient will have to take more immunosuppressant drugs - kidney needs to be a suitable size for the recipient (i.e: a small child needs a small kidney)

What is more information about bacteria and antibiotics?

clear areas occur on a petri dish full of bacteria if/when there is a factors (such as an antibiotic) preventing organisms from growing there
hospitals may use a multidisc to select the antibiotic to use against an infection as it is cheap - the test is quick to carry out as it deals with several antibiotics at the same time - allows early treatment of the patient,it is unbiased as a test as it compares antibiotics under the same conditions + it allows you to select the correct antibiotic first time to prevent antibiotic resistance developing