Communicable diseases Flashcards
1
Q
bacteria as pathogens
A
- most common organism for infection
- not all bacteria are pathogens
- prokarytotes - no membrane bound organelles
- most produce toxins that damage host cells - break down cell membrane, inactivate enzymes, interfere with DNA so they cannot divide
- eg. tuberculosis (animal), ring-rot (potatoes, tomatoes, aubergines)
2
Q
tuberculosis
A
- bacterial
- destroys lung tissue
- suppresses immune system
- people with HIV/AIDS more likely to get TB
- cured by antibiotics
3
Q
viruses as pathogens
A
- non-living
- consist of DNA or RNA surrounded by a protein
- can’t reproduce outside host cell
- to reproduce, it inserts itself into host DNA, uses host cell to make new viruses
- then it bursts out the host cell, destroying it and spreads to infect other cells
- prevent host cell functioning normally
- eg. HIV (human), influenza (animal), tobacco mosaic virus (plant)
4
Q
HIV/AIDS
A
- targets T helper cells to destroy immune system
- HIV - contains reverse transcriptase which transcribes its own RNA to a strand of DNA which interacts with DNA of host cell
5
Q
fungi as pathogens
A
- obtain nutrients by releasing enzymes and digesting material around them
- saprophytes - digest dead material
- parasitic - feed on living plants and animals
- products of digestion absorbed back into fungal cells
- digestion causes damage to host cells and tissues
- when they reproduce they release lots of spores so reproduce rapidly
- in plants they infect leaves preventing photosynthesis
- eg. athlete’s foot (human), black sigotoka (banana)
6
Q
protists as pathogens
A
- eukaryotic cells
- often require a vector to transfer disease - use a host
- some take over cells and digest contents for reproduction
- eg. malaria, potato/tomato late blight
7
Q
malaria
A
- caused by the protoctista Plasmodium and spread by mosquitos
- Plasmodium reproduces in female mosquito and is passed on when she takes 2 blood meals to lay eggs
- no cure, butmany preventatives - insecticides, mosquito nets, window and door screens
8
Q
examples of direct transmission
A
- direct contact eg. kissing, skin to skin
- inoculation - break in skin eg. animal bite
- ingestion
9
Q
examples of indirect transmission
A
- fomites - inanimate objects eg. bed, floor, products
- droplet infection eg. coughing, sneezing
- vectors
10
Q
factors affecting transmission of communicable diseases in animals
A
- overcrowding
- poor nutrition
- compromised immune system
- climateg change - new vectors
- traditional medical practises
- lack of trained health workers
11
Q
transmission of pathogens between plants
A
- direct contact
- soil contamination - pathogens or spores infect next crop
- vectors - wind, water, animals, humans
Factors affecting it: - planting crops susceptible to disease
- overcrowding
- poor mineral nutrition
- damp, warm conditions
- climate change
12
Q
skin - non-specific defences for animals
A
- protective layers - difficult for pathogens to penetrate
- covered in oily sebum - prevents growth of harmful bacteria
- covered in skin flora - harmless microorganisms - reduce growth of pathogens by competing for resources
13
Q
openings to body - non-specific defences for animals
A
- lined with mucous membrane - produces mucous that traps pathogens
- mucous contains lysozymes - destroys bacteria by digesting cell wall
- tears, urine and stomach acid contain lysozymes
14
Q
expulsive reflexes - non-specific defences for animals
A
- sneezing, coughing, vomiting, diarrhoea
- body tries to expel pathogen
15
Q
blood clotting - non-specific defences for animals
A
- endothelium surrounding blood vessel is damaged, platelets exposed to collagen in skin or blood vessel wall
- platelets form plug around damaged area:
1. release thromboplastin - thromboplastin and calcium ions convert prothrombin into thrombin
- thrombin converts soluble fibrinogen into insoluble fibrin
- fibrin forms a mesh trapping RBC and forming a clot
2. platelets also release serotonin - causes smooth muscle cells in blood vessel wall to contract - narrows it, reduces blood flow to area - scab formed keeping pathogens from entering while epidermal cells divide underneath
16
Q
inflamation - non-specific defences for animals
A
- tissue is damaged - activates mast cells - release histamines and cytokines
- histamine causes blood vessels vasodilation - increased blood flow to area - red and hot - reduces pathogen ability to reproduce
- histamine makes blood vessel walls more permeable - more blood plasma leaves making more tissue fluid - swelling, is painful
- swelling is called an oedema
- cytokines - attract WBC to carry out phagocytosis of pathogens
17
Q
fever - non-specific defences for animals (cause and reason)
A
- increase in body temperature caused by cytokines going to hypothalamus
- reduces ability of pathogens to reproduce
- increases effectiveness of immune system
18
Q
stages of phagocytosis - neutrophil
A
- blood has opsonins (eg. antibodies) that recognise foreign antigen on pathogen
- they stick to the pathogen, tagging it as foreign
- phagocytes attracted to pathogens and receptor attaches to it
- phagocyte engulfs pathogen - cytokines released, signalling to phagocytes to move to site of infection
- pathogens now in phagosome
- lysosomes move towards phagosome and fuse with it forming phagolysosome
- lysozymes break down pathogen and destroy it
- broken down pathogen moves out cell by exocytosis
19
Q
opsonin function
A
- bind to antigen on pathogen to assist in its binding to a phagocyte
20
Q
adaptations of neutrophil
A
- lobed nucleus - able to deform in shape to fit through narrow capillaries
- specific receptor for specific antigen
- contain many lysosomes
- well developed cytoskeleton for phagocytosis
21
Q
what immune system are lymphocytes part of?
A
specific immune system
B and T lymphocytes
22
Q
antigen
A
- proteins and polysaccharides on surface of pathogen cells - detected by immune cells as foreign
- leads to an immune response - antibodies released
- your own body cell’s antigens are recognised as ‘self’ and don’t produce and immune response
23
Q
antibody structure
A
- glycoproteins with 4 polypeptide chains
- 2 long heavy chains on inside - identical
- 2 shorter light chains - identical
- identical chains held to each other by disulfide bridges
- 2 antigen binding sites (top of Y shape)
- every antibody can bind to 2 identical antigens - antigen-antibody complex
- antibodies specific to antigen they bind to
- hinge region is flexible - allows distance between binding sites to vary
- all antibodies have the same constant region and different variable regions
- variable regions different for antibodies produced by different B lymphocytes
24
Q
function of antibodies
A
- produced by B lymphocytes
- humoral immunity
- act as opsonins - tagging foreign bodies for phagocytes to engulf and digest
- act as agglutins - stick pathogens together preventing them from spreading around body and making it easier for phagocytes
25
agglutination
- antibodies bind to multiple pathogens and clump them together
- this prevents them moving around or reproducing
- phagocytes can engulf multiple pathogens at once
26
where are T lymphocytes produced and released?
- produced in bone marrow
- mature in thymus gland in chest
- released into blood stream
27
cell-mediated response
1. specific T helper cell receptor attaches to antigen on APC
2. T helper cell is activated:
- produces interleukins which trigger more T helper cells to divide by mitosis for more T cells with specific receptor
3. cloned T cells can:
- develop into T memory cells
- produce interleukins to stimulate phagocytosis or B cells to divide
- stimulate development of T killer cells specific for antigen--
28
types of T-lymphocytes
- T-helper - CD4 receptors bind to antigens on APC's, produce interleukins (type of cytokine) to stimulate B cells
- T-killer - produce perforin killing the pathogen
- T-memory - if they meet pathogen for 2nd time, divide rapidly
- T-regulator - suppress immune system once pathogen eliminated, prevents autoimmune response
29
Humoral response
1. B cell with complementory antibody binds to antigen, engulfs and processes it to become an APC
2. clonal selection - activated T helper cell binds to B cell APC with correct antibody
3. interleukins from T helper cells activate B cells
4. clonal expansion - B cells undergo mitosis making clones that differentiate into plasma cells or memory cells
5. plasma cells - produce antibodies that bind to antigen on pathogen and disable them or act as opsonins or agglutins - primary immune response
6. cloned B cells can develop into memory cells - divide rapidly into plasma cells if re-infection of same pathogen occurs to wipe out pathogen before symptoms - secondary immune response
30
types of B-lymphocytes
- plasma cells - produce antibodies
- B effector cells - divide to form plasma cell clones
- B-memory - remember specific antigen for rapid response when antigen encountered again
31
natural active immunity
- normal immune response with B and T lymphocytes
- natural - body brings it about itself
- active - body brings response producing antibodies etc.
32
artificial active immunity
- vaccinations - contain dead or weakened pathogen stimulating release of antibodies and memory cells
33
natural passive
- new born babies don't have developed immune system
- as a fetus, baby receives antibodies from mother through placenta
- breast milk rich in antibodies - pass into bloodstream without being digested
- temporary until immune system makes its own antibodies
34
artificial passive immunity
- injected with antibodies produced by another organism
- eg. tetanus - given antibodies from horses
- temporary
35
vaccinations
- contain antigens from pathogen
- some are weakened strain from bacteria or virus - infects patient but easily fought off by immune system
- some are killed bacterial cells or inactivated virus - doesn't cause infection but does cause immune response
- some contain only antigen molecules
- some contain modified toxin molecules
1. vaccine injected to blood, triggering primary immune response
2. if you come into contact with same pathogen - secondary immune response, pathogen destroyed before symptoms
36
graph showing antibody production and vaccination over time
- vaccine enters body - primary immune response produces antibodies and T and B memory cells
- in second immune response, antibodies produced rapidly and pathogen destroyed before symptoms
37
importance of herd immunity
- vaccinated people can't catch disease and pass pathogen onto unvaccinated people
- if enough population vaccinated, provides protection for unvaccinated people
- vaccinating enough people at start of epidemic can prevent it turning into a pandemic
38
pharmacogenetics
- personalised medicine that works with your individual combinations of genetics
- eg. shutting down a particular gene associated with breast cancer with a drug
39
autoimmunity
- when lymphocytes start attacking self-antigens
- abnormal immune response against the own tissues in the body
- eg. type 1 diabetes - destroys beta cells in pancreas - can't control conc. of glucose in blood, arthritis
- steroids, anti-inflammatory drugs etc. can reduce symptoms
40
why do antibiotics not effect human cells?
- very different to bacterial cells eg. no cell wall, different ribosomes
41
why do antibiotics have no effect on viruses?
- viruses don't contain any target molecules for them to act upon
- they use a host cell to manufacture proteins and reproduce
42
antibiotic resistance
- caused by overuse of antibiotics
- bacterium develops mutation for antibiotic resistance
- in presence of antibiotic, all other bacteria are killed apart from resistant one
- over time, resistant bacterium reproduces and there is large no. of resistant bacteria
- eg. MRSA - staphylococcus bacteria resistant to methicillin
43
ways of reducing antibiotic resistance
- minimising use of antibiotics
- ensuring every course is finished to reduce risk of resistant individuals surviving
- good hygiene in hospitals - reduces spread of infections
44
sources of antibiotics
- penicillin found in a fungus
- aspirin discovered in willow trees
- digoxin discovered in foxgloves
- reduction of biodiversity threatens production of antibiotics
45
synthetic biology
bacteria and other organisms can be genetically engineered to synthesise large quantities of drugs that would otherwise be too rare or expensive etc.
