B12 - Communicable diseases Flashcards
(42 cards)
1
Q
What are communicable diseases?
A
- diseases that are caused by pathogens (infective microorganisms)
- vectors carry pathogens between organisms
2
Q
What are the types of pathogens?
A
- bacteria
- viruses
- fungi
- protoctista
3
Q
What is bacteria?
A
- prokaryotes
- do not have membrane-bound organelles or a nucleus
- can be classified by:
- shape = rod, spherical, comma, spiralled, corkscrew
- cell walls = react differently with Gram staining (affects how bacteria reacts to diff. antibiotics)
- +ve = purple-blue
- -ve = red
4
Q
What are viruses?
A
- non-living infectious agents
- much smaller than bacterium
- structure:
- DNA/RNA is surrounded by protein
- DNA/RNA is surrounded by protein
- invade living cells and genetic material of virus takes over biochem of host cell to produce more viruses
-
bacteriophages = attack bacteria
- use bacteria to replicate/destroy them
- they can be used to treat some diseases
5
Q
What is protoctista/protista?
A
- group of eukaryotic organisms
- single-celled/colonies
- small % act as pathogens
- pathogenic protists = need vector to transfer them to their host
- e.g. malaria
6
Q
What is fungi?
A
- not a major problem in animals
- eukaryotic organisms (multicellular)
- cannot photosynthesise and digest food extracellularly
- most are saprophytes (feed on dead/decaying matter)
- most are saprophytes (feed on dead/decaying matter)
- some are parasitic and can cause plants to stop photosynthesising (leaves affected)
- produce tiny fungal spores which can spread over large distances
7
Q
How can pathogens cause damage?
A
- viruses:
- take over cell metabolism
- genetic material inserted into host DNA
- uses cell to make new viruses
- protoctista:
- take over cells and break them open
- digest and use cell contents to reproduce
- fungi:
- digest living cells and destroy them
- some produce toxins that affect host cells
- bacteria:
- produce toxins that damage/poison host cells causing disease
- some break down cell membranes, inactivate enzymes, interfere with genetic material
8
Q
What are the different plant diseases?
A
- ring rot (b)
- tobacco mosaic virus (v)
- potato blight (p)
- black sigatoka (f)
9
Q
What is ring rot?
A
- bacterial disease of potatoes, tomatoes, aubergines
- caused by Gram +ve bacterium
- damages leaves, tubers, fruit
10
Q
What is Tobacco Mosaic Virus (TMV)?
A
- caused by virus that infects tobacco plants
- damages leaves, flowers and fruit
- stunting growth and reduces yields
11
Q
What is potato blight?
A
- caused by protoctist oomycete
- hyphae penetrate host cells and destroy leaves, tubers, fruit
12
Q
What is black sigatoka?
A
- banana disease caused by fungus which attacks/destroys leaves
- hyphae penetrate/digest cells
- fungicide can control spread
13
Q
What are the different animal diseases?
A
- tuberculosis
- bacterial meningitis
- HIV/AIDS
- influenza
- malaria
- ring worm
- athlete’s foot
14
Q
What is tuberculosis (TB)?
A
- bacterial disease that destroys lung tissue and suppresses immune system
- TB is curable (antibiotics) and preventable (vaccination)
15
Q
What is bacterial meningitis?
A
- bacterial infection of the meninges of the brain
- can spread to the rest of the body causing septicaemia (blood poisoning)
- antibiotics can cure it
16
Q
What is HIV/AIDS?
A
- caused by virus which targets T-helper cells
- gradually destroys immune system over time (open to other infections)
- spread through bodily fluids
- no vaccine or cure
17
Q
What is influenza?
A
- viral infection of ciliated epithelial cells in gas exchange system
- leaves airways open to secondary infection
- affects mammals and birds
18
Q
What is malaria?
A
- caused by protoctista Plasmodium and is spread by mosquito bites
- reproduce in female mosquito and is spread when female takes blood meals
- invades red blood cells, liver and the brain
19
Q
What is ring worm?
A
- fungal disease affecting mammals
- causes grey-white, crusty infectious areas of skin
- not damaging but may be itchy
20
Q
What is Athlete’s foot?
A
- human fungal disease
- grows on and digests warm, moist skin between toes
- causes cracking and scaling
- antifungal creams are an effective cure
21
Q
How can pathogens directly be spread?
A
- direct contact:
- kissing, or contact with bodily fluids
- skin-to-skin contact
- microorganisms from faeces
- inoculation:
- break in the skin
- e.g. animal bite
- ingestion;
- taking in contaminated food/drink
- transferring pathogens from hands to mouth
22
Q
How can pathogens be indirectly spread?
A
- fomites:
- bedding, socks, cosmetics (inanimate objects)
- inhalation:
- minute droplets of saliva/mucus
- when healthy individuals breathe them in, they become infected
- vectors:
- transmit communicable pathogens from one host to another
- include: mosquitoes, water, rat fleas
23
Q
What are the factors affecting communicable diseases in animals?
A
- over crowded living/working conditions
- poor nutrition
- compromised immune system
- poor disposal of waste
- climate change (can introduce new vectors/diseases)
- culture/infrastructure (traditional medical practises)
- socioeconomic factors (lack or trained workers)
24
Q
How are pathogens transmitted between plants?
A
- direct contact between a healthy/infected plant
- soil contamination:
- infected plants may leave pathogens/reproductive spores in the soil
- vectors:
- wind
- water
- animals
- humans
25
What are the factors affecting communicable diseases in plants?
- planting varieties of crops that are susceptible to disease
- over-crowding
- poor mineral nutrition
- damp, warm conditions
- climate change (e.g. increased rainfall promotes spread of diseases)
26
How do plants recognise an attack?
- receptors in cells respond to molecules from pathogens/chemicals produced
- stimulates release of signalling molecules
27
What are the physical defences of plants?
- callose is synthesised/deposited between cell walls/membrane
- prevents pathogens from entering
- lignin is added making the *mechanical* barrier
- callose blocks sieve plates and plasmodesmata
- *seals them off* from healthy cells and prevent spread of pathogens
28
What are the chemical defences of plants?
- insect repellents
- insecticides
- antibacterial compounds (antibiotics)
- antifungal compounds
- anti-oomycetes
- general toxins
29
What are the non-specific defences (preventing pathogens) of animals?
- skin:
- covers body and prevents entry of pathogens
- produces sebum that inhibits pathogen growth
- mucous membranes:
- secretes mucus which traps microorganisms
- lysozymes (urine/tears)/stomach acid
30
How does blood clotting/wound repair prevent pathogens enetring?
- when platelets come into contact with *collagen*, they secrete:
- *thromboplastin* = enzyme that triggers the formation of a blood clot
- *serotonin* = makes smooth muscle in blood vessels contract
- clot dries and forms a scab preventing pathogens
- collagen is deposited to give new tissue strength
31
What is the inflammatory response?
- localised response that leads to pain, heat, redness, swelling
- *mast cells* are activated and release *histones*/*cytokines*
- histamines = dilate blood vessels (increase in temp. prevents pathogens reproducing)
- also make blood vessels more 'leaky' to force out *blood plasma* (tissue fluid)
- cytokines = attract wbcs (phagocytes)
- they dispose of pathogens by *phagocytosis*
32
What are the non-specific defences (removing pathogens) in animals?
- fevers:
- normal body temp. = 37 degrees C
- cytokines stimulates hypothalamus to increase temp.
- most pathogens reproduce best at 37 degrees C/under (higher temps. inhibit this)
- specific immune system works better at higher temps.
- phagocytosis:
- specialised wbcs (phagocytes) engulf and destroy pathogens
- types of phagocytes = neutrophils and macrophages
33
What are the stages of phagocytosis?
- pathogens produce chemicals to *attract* phagocytes
- phagocytes recognise them as 'non-human' (non-self)
- phagocyte engulfs the pathogen and encloses it in a vacuole (*phagosome*)
- it then combines with a *lysosome* to form a *phagolysosome*
- enzymes from the lysosome digest and destroy the pathogen
- neutrophil = 10 mins to engulf
- macrophages have a more complex process:
- after digesting, they combine the pathogen antigens with special glycoproteins (MHC = major histocompatibility complex)
- it then moves the antigens to the macrophage and becomes an *antigen-presenting cell*
- the antigens stimulate others cells in the specific immune response
34
What are useful chemicals in non-specific animal defences?
- cytokines:
- act as cell-signalling molecules
- inform other phagocytes about pathogen invasion
- increase body temp./stimulate SIR
- opsonins:
- bind to pathogens and 'tag' them to be more recognisable
- phagocytes have receptors on cell membranes that *bind* to common opsonins
- antibodies such as immunoglobulin G (IgG) and immunoglobulin (IgM) have the *strongest* effect
35
What is the specific immune system?
- active/acquired immunity
- much slower than non-specific responses (can take up to 14 days)
- immune memory cells helps to speed up reaction
36
What are antibodies?
- Y-shaped *glycoproteins* called *immunoglobulins*
- they bind to specific antigens on a pathogen/toxin
- they have two identical *long polypeptide* chains (heavy) and two shorter ones (light)
- *disulfide bridges* hold them together
- antibodies bind to antigens with lock-and-key mechanism
- *variable region* = binding site (top of Y shape)
- *constant region* = the rest of the shape
- antibody + antigen = antigen-antibody complex
- the *hinge region* allows for flexibility
37
How do antibodies defend the body?
- antibody of a-a complex acts as *opsonin* so it is easily engulfed/digested
- most pathogens cannot effectively invade host cells once part of a-a complex
- antibodies act as *agglutinins* which cause a-a complexes to *clump together*
- makes it easier for phagocytes to engulf multiple at a time
- antibodies can act as *anti-toxins* and bind to them making them harmless
38
What are the types of T lymphocytes?
- T helper:
- CD4 receptors allow them to bind to antigens on APCs
- produce *interleukins* (type of cytokine) to stimulate the production of other T cells
- attracts/stimulates macrophages to ingest pathogens with a-a complexes
- T killer:
- destroy pathogen with antigen
- produce *perforin* which kills pathogen by making membrane permeable
- T memory:
- part of *immunological memory*
- divide rapidly when they meet antigen second time (form clones of T killer cells)
- T regulator:
- suppress immune system (interleukins)
- stop immune response to ensure body recognises self antigens and does not set up *autoimmune response*
39
What are the types of B lymphocytes?
- plasma:
- produce antibodies to a particular antigen
- lives for only a few days
- B effector:
- divide to form plasma cell clones
- B memory:
- provide *immunological memory*
- remember a specific antigen and enable body to make rapid response
40
What is cell-mediated immunity?
- T lymphocytes respond to changed cells
- important against viruses and early cancers
- macrophages engulf/digest pathogens in *phagocytosis*
- process antigens to form APCs
- receptors on T helper cells fit antigens (activate and form interleukins)
- stimulates production of more T cells
- cloned T cells may:
- form T memory cells
- produce interleukins (stim. phagocytosis)
- produce interleukins (stim. B cells to divide)
- stim. development of clone T killer cells specific for presented antigen and destroy infected cells
41
What is humoral immunity?
- body responds to antigens *outside* cells/APCs
- produces antibodies soluble in blood/tissue fluid
- activated T helper cells bind to B cell APC (*clonal selection*)
- interleukins produced by T helper cells activate B cells
- those B cells divide by mitosis and produce plasma cell clones/B memory cells (*clonal expansion*)
- cloned plasma cells produce antibodies
- bind to antigens
- act as opsonins/agglutinins
- ** primary immune response **
- cloned B cells can develop into B memory cells
- divide rapidly to form plasma cell clones
- wipes out pathogens before symptoms are shown
- ** secondary immune response **
42
What is the action of opsonins, agglutinins and anti-toxins?
- opsonins:
- chemicals that bind to pathogens and *tag* them so they are recognised more easily by phagocytes
- agglutinins:
- chemicals that cause pathogens to *clump* together so they are easier for phagocytes to engulf/digest
- anti-toxins:
- chemicals that bind to toxins produced by pathogens so they no longer have an effect
