Communicable diseases, disease prevention and the immune system Flashcards
(32 cards)
ring rot
- caused by gram positive bacteria
- affects potatoes, tomatoes
- damages leaves, tubers and fruit
- bacteria infect the vascular tissue and prevent the transport of water, causing the plant to wilt and die
- infection spreads into the potato tubers where the vascular tissue is arranged in a ring=black ring of rot
- infected tuber can lead to the growth of infected new plants
- spread by contaminated soil, water and equipment
- no cure
Tobacco mosaic virus (TMV)
- caused by a virus
- affects a lot of species of plants eg peppers
- damages leaves, flowers and fruit=less yields+cand lead to crop loss
- causes a distinct yellowing of the leaves which produces a mosaic pattern
- no cure but there are some reistant strains
- transmitted by leaf-to-leaf contact between plants+humans touching different plants
Potato/tomato late
blight
- caused by a fungus-like protist
- protist destroys potato and tomato crops leaving them completely inedible
- symptoms=small, dark brown marks on the leaves which quickly increase in size and number
- no curebut there are resistant strains
- careful management and chemical treatments can lower infection risk
- transmitted via spores carried by wind from plant to plant
Black sigatoka
- caused by fungus
- affects bananas
- transmitted leaf-to-leaf contact+ spread of spores by humans or within infected plant matter
- hyphae penetrate+digest the cells=prevent plant photosynthesising=parts of leaf die=producing black streaks
- good husbandry+fungicide treatment can control spread of disease but x cure
- whole leaf dies eventually
Tuberculosis
- bacteria infect the lungs+suppresses immune system=chronic cough+bloody mucus
- transmitted via airborne droplets
- associated with poor hygiene+sanitation
- M. Tuberculosis=TB in humans
- M. Bovine in cows can transmit to humans=cause TB
HIV/AIDS
- enveloped retrovirus
- viral enzyme (reverse transcriptase) produces single-stranded DNA from its viral RNA
- DNA polymerase synthesises double stranded DNA from the single strand=inserted into host
- DNA provirus used to synthesise new viruses
- transmitted by body fluids
- no vaccine+cure
Influenza
- caused by a virus
- infect ciliated epithelial cells in gas exchange system
- 3 types (A, B and C)
- cause high temp+body aches+fatigue
- influenza a is the most common+virulent & classified by proteins on their surface
- transmitted by airborne droplets
- mutate regularly
Athlete’s foot
- caused by fungus
- form of human ring worm that grows on+digests warm & moist skin between toes
- causes cracking+scaling=itchy+sore
- transmitted by skin-to-skin contact with an infected individual+contact with an item of clothing
- anti fungal creams=effective cure
Ringworm (cattle)
- caused by a fungus
- affects mammals eg cattle
- symptoms: grey-white, crusty, infectious, circular areas of skin which can be itchy
- anti fungal creams are an effective cure
Malaria
- caused by protoctista
- transmitted by infected anopheles mosquitoes=vector
- symptoms: fever, chills, fatigue
- complex life cycle with 2 hosts=reproduce inside female mosquito=needs 2 blood meals=protein to lay eggs
- invade rbc, liver, brain
- x vaccine+limited cures
- lots of effective preventative measures
Bacterial meningitis
- caused by a bacteria
- affects meninges (protective membranes of the brain), can be spread to the rest of the body=septicaemia=blood poisoning+rapid death
- affects very young children+teens
- symptoms: blotchy red/purple rash that doesn’t disappear
- antibiotics will cure the disease if given early
- vaccines protect against some forms of it
How are animal diseases transmitted?
direct transmission
- direct contact eg skin to skin, sharing bodily fluids
- inoculation eg animal bite, sharing needles, break in skin, puncture wound
- ingestion eg from hands to mouth, contaminated food/drink
indirect transmission
- fomites=inanimate objects that transfer pathogens
- droplet infection (inhalation)=droplets of saliva+mucus expelled when you cough sneeze, cough, etc=contain pathogens can be passed to those close to you
- vectors=transmit pathogens from one host to another eg mosquitoes
- spores=small reproductive structures released into environment via wind/water=reach food source ie host=start growing
Factors affecting transmission in animal diseases
- high population densities+poor housing=close proximity=high infection rate
- poor nutrition=lead to compromised immune system=easier to get a disease
- poor disposal of waste
- weather+climate=vary the incidence+location of disease
- social factors eg migration due to war=people transfer disase from infected area to a new area=up sprea of disease
How are plant diseases transmitted?
direct
- direct contact=healthy plant contacts diseased plant
indirect
- spores=small reproductive structures released into environment via wind/water=reach food source ie host=start growing
- soil contamination
- vectors=wind, water etc
Factors affecting transmission in plants
- planting varieties that are susceptible to disease
- overcrowding
- poor mineral nutrition
- damp/warm conditions
- climate change
How do plants recognise attacks?
- receptors=respond to molecules from the pathogen/chemicals produced when cell wall is attacked=stimulates release of signalling molecules=alert nucleus to attack=triggers response eg producing defensive chemicals, physically strengthening cell wall
Plant defences
physical
- production of callose=polysaccharide of B-glucose w 1,3 and 1,6 glycosidic bonds=quickly synthesised+deposited bw cell wall+plasma membrane in cells next to infected cells=act as barrier=prevents pathogens entering plant calls around site of infection
- Lignin is added=mechanical barrier is thicker +stronger
- Callose blocks sieve plates in phloem=seals infected part=prevent spread+deposited in plasmodesmata bw infected cells+their neighbours=seals them off from nealthy cells=prevent spread
- tyloses created=ingrouths into xylem → cytoplasm of nearby cell grows into xylem to create a cell wall of callose.
chemical
- produce chemicals that repel insect vectors of disease or kill invading pathogens eg. some are extracted+used/synthesised to help us control insects, fungi etc
- some have strong flavours=used as herbs and spices
- some examples are insect repellents in pine resin, general toxins eg cyanide
passive
- some physical barriers=waxy cuticle, closed stomata, bark cell wall, casparian strip=hard for pathogens to enter
- some chemical defences=toxic compounds eg catechol+sticky resin in bark=traps pathogens=x spread, compounds that encourage growth of competing organisms
What are animal non-specific defences?
- keeping things out=skin, mucus, lysozymes (tears), blood clots
- getting rid of pathogens=fever, phagocytes
- mucus=contains lysozymes=break down bacterial+fungal cell wall & phagocytes
- expulsive reflexes=coughing, sneezing=remove mucus=contains trapped microbes & diarrhoea+vomiting=remove gut contents=contains pathogens
Blood clot formation+wound repair
- platelets activated by damaged tissue=release thromboplastin=catalyses reaction bw prothrombin+Ca 2+=form thrombin=catalyses fibrinogen —> fibrin=sticky, meshy substance=forms a network=traps platelets=forms a thrombus/bld clot
- serotonin is also released=contracts smooth muscle in the bld vessel walls=reduce bld flow to wound area
- clot dries out=hard+tough scab=keeps pathogens out
- epidermal cells under scab grow while damaged bld vessel
- collagen fibres deposited=give new tissue strength
- once epidermis reaches normal thickness=scab comes off=wound healed
Inflammatory response
- consists of pain, heat, redness, swelling
- mast cells=activated at damaged tissue+produced histamines+cytokines
- histamines=cause bld vessels to dilate=increases bld flow=more wbc reach wound site=encourages redness and heat & up temp=prevents microbial reproduction+makes bld vessels leaky=plasma forced out to form tissue fluid=swelling+pain
- cytokines=attract wbc (phagocytes) to wound site
Phagocytosis
- phagocyte (neutrophil+macrophage) is attracted by chemicals produced by pathogen
- phagocyte recognises antigen on pathogen=phagocyte engulfs pathogen+encloses it in a phagosome
- lysosome moves towards phagosome+combine w it=forms phagolysosome
- lysosome in phagolysosome release digestive enzymes=breakdown pathogen
- digested pathogen absorbed by phagocyte
- antigens from pathogen combine w MHC (glycoproteins in cytoplasm)=form MHC-antigens complex moves to phagocyte’s plasma membrane=makes it an antigen presenting cell (APC)=stimulate other cells involved in specific immune system to respond
Cells involved in specific immune response
T lymphocytes=produce in bone marrow+mature in thymus gland
- T helper (T h)=receptors on plasma membrane=bind to complementary antigens on APC & produce interleukins=stimulate B lymphocytes+phagocytes & differentiate into memory cells or T killer cells
- T killer (T k)=kill abnormal/foreign cells by producing perforin=perforates plasma membrane=freely permeable=causes cell death
- T regulator (T r)=suppress immune system after pathogens are destroyed=prevents immune system accidentally attacking body cells
- T memory (T m)=provide long-term immunity against specific pathogens=rapid response if body is re-infected by the same pathogen
B lymphocytes=produced+mature in bone marrow
- B lymphocytes=have antibodies on plasma membrane=bind to complementary antigens=engulf antigens+present them on plasma membrane=become APC & when activated differentiate into plasma+memory cells
- plasma cells=produce+secrete antibodies against a specific antigen (short life span)
- B memory (B m)=long-term immunity against specific pathogens+rapidly divide into plasma cells if body is re-infected by the same pathogen
Specific immune response
cellular
- macrophage spots pathogen=phagocytosis occurs=turns it into an APC
- T helper cells with complementary receptors binds to antigen which activates them (clonal selection)
- clonal expansion (mitosis) occurs to the activated Th cells
- proliferation occurs=Th cells differentiate into Tk cells, Tr cells, Tm cells, Th cells
- Th cells also release interleukins=communicate which B lymphocyte is needed+stimulates their division=produce antibodies & attract phagocytes+stimulate them to engulf pathogens
humoral
- pathogen gets into body fluids
- b lymphocyte engulfs pathogen+presents its antigen on plasma membrane=becomes APC
- activated T h cells bind to B lymphocyte=activates B lymphocytes (clonal selection=B lymphocyte w correct antibody selected by being activated by T h cells= done via interleukins)
- clonal expansion=mitosis=activated B lymphocytes divides
- clonal differentiation occurs=B lymphocytes differentiate into B m cells or plasma cells
- plasma cells=produce antibodies=complementary to antigen on pathogen’s plasma membrane=attach to them+destroy pathogen
infected body cell (part of cellular)
- pathogen enters body cell=killed by enzymes in cell=cell becomes an APC
- T k cells release perforin=perforates plasma membrane=water can get in via osmosis=lysis occurs
How do antibodies work+their function
They can act as opsonins, agglutinins or anti-toxins
- opsonisation=antibodies surface coat pathogens=easier for phagocytes to recognise pathogen
- agglutination=antibodies clump pathogens tgt=easier for phagocyte to find pathogens+can engulf multiple pathogens at once
- anti-toxins=bind to toxins=neutralises them=harmless
functions
- agglutination of pathogens
- neutralisation of toxins
- preventing pathogens from binding=antibodies bind to pathogens=block receptors needed to host cells=stop them from infecting body cells
