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
Q
where are T lymphocytes produced and released?
A
- produced in bone marrow
- mature in thymus gland in chest
- released into blood stream
26
Q
cell-mediated response
A
- specific T helper cell receptor attaches to antigen on APC
- T helper cell is activated:
- produces interleukins which trigger more T helper cells to divide by mitosis for more T cells with specific receptor - 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–
27
Q
types of T-lymphocytes
A
- 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
28
Q
Humoral response
A
- B cell with complementory antibody binds to antigen, engulfs and processes it to become an APC
- clonal selection - activated T helper cell binds to B cell APC with correct antibody
- interleukins from T helper cells activate B cells
- clonal expansion - B cells undergo mitosis making clones that differentiate into plasma cells or memory cells
- plasma cells - produce antibodies that bind to antigen on pathogen and disable them or act as opsonins or agglutins - primary immune response
- 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
29
Q
types of B-lymphocytes
A
- 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
30
Q
natural active immunity
A
- normal immune response with B and T lymphocytes
- natural - body brings it about itself
- active - body brings response producing antibodies etc.
31
Q
artificial active immunity
A
- vaccinations - contain dead or weakened pathogen stimulating release of antibodies and memory cells
32
Q
natural passive
A
- 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
33
Q
artificial passive immunity
A
- injected with antibodies produced by another organism
- eg. tetanus - given antibodies from horses
- temporary
34
Q
vaccinations
A
- 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
35
Q
graph showing antibody production and vaccination over time
A
- 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
36
Q
importance of herd immunity
A
- 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
37
Q
pharmacogenetics
A
- personalised medicine that works with your individual combinations of genetics
- eg. shutting down a particular gene associated with breast cancer with a drug
38
Q
autoimmunity
A
- when lymphocytes start attacking self-antigens
- 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
39
Q
why do antibiotics not effect human cells?
A
- very different to bacterial cells eg. no cell wall, different ribosomes
40
Q
why do antibiotics have no effect on viruses?
A
- viruses don’t contain any target molecules for them to act upon
- they use a host cell to manufacture proteins and reproduce
41
Q
antibiotic resistance
A
- 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
42
Q
ways of reducing antibiotic resistance
A
- minimising use of antibiotics
- ensuring every course is finished to reduce risk of resistant individuals surviving
- good hygiene in hospitals - reduces spread of infections
43
Q
sources of antibiotics
A
- penicillin found in a fungus
- aspirin discovered in willow trees
- digoxin discovered in foxgloves
- reduction of biodiversity threatens production of antibiotics
44
Q
synthetic biology
A
bacteria and other organisms can be genetically engineered to synthesise large quantities of drugs that would otherwise be too rare or expensive etc.
