disease and the immune system
pathogens and communicable diseases
disease = a condition that impairs the normal functioning of an organism e.g. plant/ animal
pathogen= an organism which causes disease e.g. bacteria, protosists, fungi and bacteria
communicable disease= a disease that can be spread between organisms
e.g. TB= bacteria, meningitis= bacteria, ring rot= bacteria, HIV/AIDS= virus, flu= virus, tobacco mosaic virus= virus, black sigatoka= fungus, ring worm= fungus, athletes foot= fungus, potato/tomato blight= protoctist, malaria= protoctist
indirect/ direct transmission
direct= when a pathogen is directly transmitted from one organism to another with no intermediary
indirect= when a disease is transmitted from one organism to another via an intermediate
e.g. droplet transmission via sneezing
sexual intercourse
or touching an infected organism
e.g. a vector such as spores or mosquitos
living conditions, climate and social factors affecting transmission
overcrowded living conditions increase transmission of C diseases e.g. TB is spread directly by droplet infection but also indirectly as the bacteria can remain in the air for long periods of time and infect new people
climate e.g. potato blight is more common in wet summers because the spores need water to spread or malaria is most common in hot/ humid countries because it is the ideal condition for mosquitoes to breed
social factors e.g. areas with bad health care have higher levels of HIV as there is less diagnoses and less anti HIV drugs are available or bad health education as people are less aware of symptoms
defence against pathogens
animals have barriers (primary defences)
pathogens need to enter to cause a disease
skin- physical barrier blocking pathogens from entering the body, chemical barrier as produces chemicals that are anti microbial and lower pH, inhibiting pathogen growth, keratinisation
mucous membranes- these protect bodies openings which are exposed to the environment e.g. moth, nostrils, some membranes (goblet cells) secrete mucus which traps pathogens and contains anti microbial enzymes, wafted out by ciliated epithelial cells
blood clotting- a blood clot is a mesh of protein fibres, blood clots prevent pathogen entry and blood loss, theyre formed in enzyme reaction between platelets and damaged blood vessels involving calcium ions and 12 factors, stem cells divide by mitosis to replace, new blood vessels grow to supply oxygen and nutrients
inflammation- the signs of inflammation include swelling, pain, heat and redness, it can be detected by mast cells which release histamine which increases blood vessel permeability causing an increased conc of tissue fluid, this causes swelling and insolates any pathogens which may have entered, the molecules also cause vasodilation which increases blood flow to affected area, this makes area hot and brings wbcs to area to fight pathogens, tissue fluid is later drained by lymphatic system where lymphocytes are stored
wound repair- the skin is able to repair itself in the event of injury and reform a barrier against pathogen entry, the surface is repaired by outer layer of skin cells dividing and migrating to edges of wound, the tissue fluid below wound contracts to bring edges of wound closer, it is repaired using collagen fibres (too many cause a scar)
expulsive reflexes- e.g. coughing/ sneezing, sneezing is caused when mucus membranes in nostrils become irritated by dust/dirt, a cough is caused by irritation in respiratory tract, both attempt to expel foreign pathogens
plant primary defences
waxy cuticle- physical barrier against pathogen entry and stops water collecting on leaf which could reduce risk of infection by pathogens transferred in water
cell walls- physical barrier against pathogens
callose (polysaccharide)- gets deposited between cell walls and plasma membrane during pathogen invasion, makes it harder for pathogens to enter cells, deposition in plasmodesmata may limit spread of viruses between cells
produce antimicrobials- kill pathogens/ inhibit growth
insecticides- reduces risk of infection by viruses carried by insects
the immune system
foreign antigens trigger immune response
antigens are found on cell surface
immune response is specific and non specific
stages of immune response
1) phagocytes engulf pathogens
p recognizes antigens on pathogen
the cytoplasm of p moves around the pathogen engulfing it (aided by opsonins - molecules in blood that attach to foreign antigens to aid phagocytosis)
the pathogen is contained in phagosome (vesicle)
a lysosome fuses with phagosome, the digestive enzymes break down pathogen
the p then presents the pathogen antigens on its surface to activate other immune system cells (antigen presenting cell)
2) phagocytes activate T lymphocytes
a TL is another type of wbc
their surface is covered in receptors
the receptors bind to antigens presented on APC
each TL has different receptor
when the receptor on surface meets complementary antigen it binds to it (clonal selection)
this activates TL and process of clonal selection
the TL undergoes clonal expansion - it divides to produces clones of itself, different types of TLs carry out different functions
T helper= release cytokines substances to activate b lymphocytes and stimulate phagocytosis
t killer cells= attack and destroy host body cells that display foreign antigen
t regulatory cells= supress immune response from other wbcs (stops body attacking hosts body cells) and stop immune response after pathogen has been removed
3) TLs activate BLs which divide into plasma cells
they are covered in antibodies
antibodies bind to antigens to form antigen- antibody complex
each BL has a different shaped antibody on its surface
when the antibody meets a complementary shaped antigen this activates BL and it undergoes clonal selection
the BL divides by mitosis into plasma cells and memory cells (clonal expansion)
4) plasma cells make more antibodies to a specific antigen
Cell signalling
a cell may release/ present a substance that binds to the receptors of another cell causing a response
cell signalling is important in immune response as it activates all wbcs needed
e.g. t helper cells and macrophages release interleukins that can stimulate clonal expansion and differentiation of B and T
plasma cells are clones of BL
they secrete lots of the antibody into blood
these antibodies will bind to antigens and form antigen-antibody complex
antibody structure
variable region= form antigen binding site, the shape is complementary to a specific antigen (differs between antibodies)
hinge region= allows flexibility when antibody binds to antigen
constant region= allow binding to receptors on immune system cells e.g. phagocytes, its the same in all antibodies
disulphide bridges= hold the polypeptide chains of protein together
antibodies clear infection by
agglutinating pathogens- each antibody has 2 binding sites so one antibody can bind to 2 antigens at the same time clumping multiple pathogens together, phagocytes come along as mass phagocytose them (agglutinins)
neutralizing toxins- like antigens, toxins have different shapes, antibodies called anti toxins bind to toxins to prevent them from affecting the human body neutralizing them and are then phagocytosed
preventing the pathogens binding to human cells- when antibodies bind to antigens they block the surface receptors that the pathogen needs to bind to host cells, preventing it from infecting
slow primary response
when the pathogen first enters the body the antigens activate the immune system (primary response)
its slow because theyre not many BLs
eventually the body will produce enough of the right antibody to fight the infection
after being exposed to the antigen, B and TLs produce memory cells which remain in the body for a long time (blood)
memory TLs remember the specific antigen, memory BLs remember the specific antibody needed to bind to antigen of pathogen
this allows immune system to respond faster to a second infection
faster secondary response
clonal selection occurs faster, memory BLs are activated and divide into plasma cells that produce the correct antibody, memory TLs are activated and divide into the correct type of TLs to kill pathogen
secondary response often gets rid of pathogen before symptoms occur
immunity and vaccinations
passive or active
active
= when the immune system makes its own antibodies after being stimulated by antigen
natural= when you become immune after catching the disease
artificial= when you become immune after being given a vaccination containing a harmless dose of antigen
passive
= when you get given antibodies from a different organism
natural= when a baby receives antibodies from mother through breast milk and becomes immune
artificial= when you become immune after being injected with antibodies from someone else e.g. through blood transfusions
active requires expose to antigen, passive does not
passive has immediate protection, active develops slower
active protection is long term, passive is short
in active memory cells are produced, in passive they are not
autoimmune diseases
=when an organisms immune system is unable to recognize its own antigens as 'self' causing it to launch a response on the organisms own tissue
e.g. lupus= caused by immune system attacking cells in connective tissue
vaccines
vaccine contain antigens that cause body to produce memory cells against a particular pathogen without the pathogen causing disease (immunity without symptoms)
if a large majority of a community is vaccinated the disease becomes rare and so unvaccinated people are unlikely to get the disease (herd immunity) preventing epidemics
vaccines contain antigens which are free or still attached to dead/ weakened pathogen
booster vaccines ensure memory cells are produced
vaccination is the administration of antigens into the body, immunization is the process by which you develop immunity (vaccination causes immunization)
flu
antigens on surface of virus change regularly forming new strains which are not recognized by memory cells (the strains are immunologically distinct) so a new vaccine has to be made
antibiotics and other medicines
antibiotics
antibiotics are chemicals that kill/ inhibit the growth of bacteria
treat bacterial infections only as they target the pathogen without damaging the body
penicillin was first
resistance
there is genetic variation in a population of bacteria, genetic mutation scan make some bacteria naturally resistant to antibiotics
the pathogens with the mutation are better adapted to survive as the non resistant bacteria are destroyed by antibiotics allowing them to reproduce with more resources and less competition
this leads to the allele for antibiotic resistance being passed to the offspring and becomes more common in population over time
its caused by over prescribing antibiotics and people not finishing their courses
leads to the production of superbugs which are harder to get rid of
MRSA
protecting sources of medicine
many medicinal drugs are manufactured using natural compounds found in plants/ animals
only a small portion of organisms have been investigated so far so its possible that some contain compounds that could be used to treat incurable diseases e.g. aids
protected by maintaining biodiversity
future of medicine
personalized
personalized medicines are tailored to an individuals dna and doctors will be able to prescribe most effected drugs
genes determine how body responds to certain drugs
synthetic biology
involves using tech to design and make things like artificial proteins, cells etc
faecal- oral transmission e.g. contaminated food
transmission by spores
transmission in plants
indirect= result of an insect attack which transfers pathogen from infected plant to non infected plant, vector
direct= fungi spores (airborne transmission), pathogens enter via roots in infected soil
protoctists, bacteria and fungi are more common grow more rapidly in warm, moist conditions so are more common in warm climates
lignin in cell walls
stomatal closure- possible point of entry for pathogens
tylose formation (projection that fills xylem)- blocks vessel preventing it from carrying water preventing spread of pathogen, contains terpenes which are toxic to pathogens
chemical
terpenoids - antibacterial, anti fungal properties
phenols- have antibiotic and anti fungal properties, tannins inhibit insect attack as they bind to salivary enzymes deactivating them and if ingested in high conc cause insect to die, preventing transmission
alkaloids- e.g. caffeine, nicotine, cocaine give bitter taste to prevent animals feeding, inhibit enzyme controlled reactions e.g. protein synthesis,
defensins- small cysteine rich proteins which are antimicrobial, act on plasma membrane by inhibiting ion channels
hydrolytic enzymes- included chitinases which breaks down chitin in fungal cell walls, glucanases which hydrolyses glycosidic bonds in glucans and lysosomes which degrade bacterial cell walls
necrosis- deliberate cell death around infection to stop spread, controlled by enzymes
canker- a necrotic lesion on stem/bark which causes death of cambium tissue in bark
secondary defences
antigens and opsonins= a pathogen is recognised as foreign by intrinsic glycoproteins/ proteins in plasma membrane, opsonins are a type of antibody which attach to antigens allowing phagocytes to engulf
neutrophils= bind to antibody attached to antigen on pathogen, engulf pathogen by endocytosis forming a phagosome, lysosomes fuse to phagosome and release lytic enzymes which digest contents
macrophages= travel in blood as monocytes, when macrophage engulfs pathogen it doesn't digest all of it, antigen is moved to a special protein complex on cell, becomes an antigen presenting cell, allows other cells to recognise antigen
active immunity
antigen presenting cell moves around body via blood until it comes in contact with t or b lymphocytes which have recognition site for antigen
specific immune response = activation of specific b and T cells is CLONAL SELECTION which leads to production of antibodies and memory cells for long term immunity
t memory cells= provide long term immunity
plasma cells= circulate blood and release antibodies
b memory cells= remain in body for a number of years and act as immunological memory
e.g. macrophages release monokines which attract neutrophils by chemotaxis or stimulate B cells to differentiate
e.g. many cells release interferon which inhibits viral replication and stimulates activity of t killer cells
made of 4 polypeptide chains
ring vaccination= involves vaccinating people in immediate vicinity of new disease
herd vaccination= providing vaccine to all/almost all of population at risk