4.1.1 Communicable diseases, disease prevention and the immune system Flashcards

(123 cards)

1
Q

what are communicable diseases

A
  • diseases that are caused by infective organisms called pathogens + can be spread between organisms via bodily fluids, bodily contacts + intercourse
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2
Q

what are the different types of pathogens

A
  • bacteria
  • virus
  • fungi
  • protoctista
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3
Q

what are pathogens

A
  • microorganisms that attack an organisms + cause disease
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4
Q

are bacteria prokaryote / eukaryote

A
  • prokaryote
    > their cell structure is very different from eukaryotic organisms they infect
  • no membrane bound organelles
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5
Q

what are the diff shapes that bacteria can be

A

rod shaped, spherical, comma, corkscrew

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6
Q

how do bacteria cause disease

A
  • produce toxins that poison/damage the host cells + causes disease
    > does this by breaking down cell membrane
    > damage/inactivate enzymes
    > interfere with hot cell genetic material
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7
Q

what are viruses

A
  • non living infectious agents
  • basic structure is genetic material (R/DNA) surrounded by protein
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8
Q

how do viruses cause disease

A
  • invade living cells by genetic material of virus taking over biochemistry of host cell
  • virus reproduce rapidly + evolve by developing adaptations to their host
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9
Q

what are bacteriophages

A
  • viruses that attack bacteria
    > viruses are known as the ultimate parasite
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10
Q

what are protoctista

A
  • group of eukaryotic organisms with a wide variety of feeding methods
    > some act as pathogens causing devastating communicable dieases
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11
Q

how do protoctista cause disease

A
  • they are parasitic so use animals / people as their host
    > need vectors to transfer them to the host
  • can take over cells + break them open
    > digest + use cell contents
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12
Q

what is fungi

A
  • eukaryotic organisms –> often multicellular
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13
Q

many fungi are saprophytes meaning that

A
  • they feed on dead + decaying matter
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14
Q

some fungi are parasitic meaning that

A
  • they feed on living plants + animals
    > these are the pathogenic fungi that cause communicable diseases
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15
Q

how do fungi cause diseases in plants

A
  • they stop plant from photosynthesising + kill it
    > when fungi reproduce they produce millions of tiny spores that can spread large distances
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16
Q

how do fungi cause disease (general)

A
  • digest living cells + destroy them
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17
Q

what are the two modes of actions pathogens produce

A
  • damaging host tissues directly
  • producing toxins which damage host tissues
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18
Q

which pathogens produce toxins that damage host tissues

A
  • bacteria produce toxins that damage host cells: break down membrane, inactivate enzymes, interfere with genetic material
  • fungi produce toxins that affect host cells + cause disease
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19
Q

what type of pathogen is ring rot + host plant + method of transmission + brief symptoms

A
  • bacterium
  • potato, tomato, aubergines
  • infected soil / seeds
  • damages leaves, tubers and fruit
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20
Q

what type of pathogen is TMV + host plant + method of transmission + brief symptoms

A
  • virus
  • tobacco
  • contaminated tools
  • stunts growth, discolours leaves
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21
Q

what type of pathogen is late blight + host plant + method of transmission + brief symptoms

A
  • protoctista
  • potatoes
  • wind + rain
  • destroys leaves, tubers and fruit
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22
Q

what type of pathogen is black sigatoka + host plant + method of transmission + brief symptoms

A
  • fungus
  • banana
  • wind + rain
  • attack + destroys leaves
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23
Q

what type of pathogen is tuberculosis + method of transmission + brief symptoms

A
  • bacterium
  • airborne
  • damage to lung tissue + suppresses immune system
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24
Q

what type of pathogen is HIV/AIDS + method of transmission + brief symptoms

A
  • virus
  • sexual contact + blood contact
  • weakened immune system
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25
what type of pathogen is influenza + method of transmission + brief symptoms
- virus - airborne droplets - fever, weakness, secondary infection
26
what type of pathogen is malaria + method of transmission + brief symptoms
- protoctista - mosquito vector - fever, chills, nausea
27
what type of pathogen is athletes foot + method of transmission + brief symptoms
- fungus - contact with an infected surface - cracked itchy skin
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what is direct transmission
- pathogens transferred directly from one individual to another
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what are some examples of direct transmission in animals
- direct contact: > bodily fluids, kin to skin - inoculation: through a break in the skin > animal bite, puncture wound - ingestion: taking in contaminated food
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what is indirect transmission
- pathogen travels from one individual to another indirectly
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what are some examples of indirect transmission in animals
- fomites: > inanimate objects like bedding - droplet infection (inhalation): > saliva, mucus, sneeze, cough - vectors: transmits communicable pathogens from one host to another
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what does a vector do
- transmits communicable pathogens from one host to another
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what are some of the factors that effect the transmission of communicable diseases in animals
- overcrowded living + working conditions - poor nutrition - climate change (introduce new vectors + diseases) - culture + infrastructure - socioeconomic factors: e.g. lack of trained health workers - poor disposal of waste - compromised/weakened immune system
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describe an example of direct transmission in plants
- direct contact of healthy plant with any part of a diseased plant
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what are some examples of indirect transmission in plants
- soil contamination > infected plants leave pathogens in soil that can infect next crop - vectors > wind > water > animals > humans
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what are some of the factors that affect the transmission of communicable diseases in plants
- planting variety of crops susceptible to disease - overcrowding inc likelihood of contact - poor mineral nutrition - damp warm conditions - climate change
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what are some passive physical defenses in plants to protect from pathogens
- waxy cuticle - casparian strip in root endodermis - bark - cellulose cell walls - sticky resins in bark
38
what are some passive chemical defenses in plants to protect from pathogens
- secreting toxic compounds - secreting enzyme inhibitors (inhibit enzymes needed by pathogens to enter plant) - stomatal closure - secreting compounds which support growth of competitors of pathogen
39
what is hypersensitivity / necrosis in plants
- an active defence - immediate death of tissues surrounding infection site to prevent spread of infection (cell suicide)
40
what is callose deposition in plants
- an active defence - callose is large polysaccharide that blocks sieve tubes (phloem or plasmodesmata, preventing spread of pathogen > also deposited in cell walls
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what is tyloses in plants
- an active defence - growths (made of chemicals called terpenes) that block xylem
42
what is cell signaling in plants
- active defence - leads to increased production of defence chemicals > e.g. antibiotics, antifungals, toxins e.g. cyanide
43
name some non-specific defenses in animals
- skin - mucous membranes - lysosomes in tears + urine - expulsive refluxes
44
how does skin act as a non-specific defence
- covers body + prevents entry of pathogens - produces sebum that inhibits growth of pathogens > lactic acid + fatty acid produced from sweat/sebaceous glands are acidic - generally impermeable to most pathogens
45
how do mucous membranes act as non-specific defences
- these line parts of body most likely to come into contact with pathogens > airways, digestive / genital tract - mucous secreted traps pathogens + contains lysosomes that destroy bacterial + fungal cell walls > also contain phagocytes
46
how do expulsive refluxes act as non-specific defences
- coughing + sneezing - areas prone to infection are sensitive to dust / microorganisms > these are reflexes that happen automatically to expel foreign bodies
47
what is thromboplastin
- enzyme that triggers a cascade of reactions resulting in formation of blood clot
48
what does serotonin do
- makes smooth muscles in walls of blood vessels contract so they narrow + reduce supply of blood to the area
49
give an overview of wound repair
- clotting factors activate enzyme cascade - mesh forms + traps platelets + forms clot - clot dries out forming scab - epidermal cells below scab grow + collagen deposited - once new skin formed, scan falls off
50
describe the steps in wound repair
- damage to blood vessel wall exposes collagen + releases clotting factors - platelets come into contact with collagen + release mor clotting factors - platelets form temporary plug - inactive thrombokinase activated by clotting factors - active thrombokinase works with calcium to activate prothrombin - thrombin catalyses conversion of soluble fibrinogen in plasma to insoluble - fibrin covers temporary platelet plug forming mesh which traps red blood cells - new cells grow under clot - enzyme plasmin releases to dissolve clot
51
what do mast cells release
- when activated in damaged tissue they release chemicals called histamines or cytokines
52
what do histamines do
- increase permeability of capillaries so blood plasma (fluid) leaks out into surrounding tissue - also dilate blood vessels causing localised heat + redness (prevents pathogens reproducing)
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what do cytokines do
- attract white blood cells (phagocytes) to the site > they dispose of pathogens by phagocytosis
54
what are phagocytes
- specialised white cells that engulf + destroy pathogens > produced throughput life by bone marrow
55
what are the 2 main types of phagocytes
- neutrophil - macrophages
56
what are some features of neutrophils
- lobed nucleus - short lived - die after digesting bacteria - travel in blood + tissue (enter tissue fluid during infections) - large numbers during infections - make up much of pus (dead)
57
what are some features of macrophages
- larger than neutrophils - found in lymph / organs (not blood) - made in bone marrow as monocytes (called macrophages once reached organs) - long lived - display antigens from the pathogens to initiate specific immune response
58
what are some features of dendritic cells
- have long processes that inc SA to interact with pathogens - found in areas near surface, skin, digestive tract - migrate to lymph nodes after phagocytosis - are antigen presenting cells (APC's)
59
describe the steps of phagocytosis
- pathogens produce chemicals that attract phagocytes - ingestion of microbe by phagocyte - formation of phagosome (pathogen enclosed in vacuole) - phagosome combines with lysosome to form phagolysosome - enzyme from lysosome digests + destroys pathogens - residual body containing indigestible material expelled
60
what do APC's do
- they don't fully digest all the pathogen > the antigen combines with special protein complex + placed on APC's own membrane - the APC carries itself to lymph system where lymphocytes produce specific antibodies in response to antigens that are foreign to body
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how are cytokines helpful in phagocytosis
- act as cell-signaling molecules informing other phagocytes that body is under attack + stimulates them to move to site of infection / inflammation
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how are opsonins helpful in phagocytosis
- they're chemicals that bind to pathogens + 'tag' them so they are more easily recognisable by phagocytes > phagocytes have receptors that bind to common opsonins
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what is the specific immune response
- refers to production of specific antibodies by lymphocytes to combat infection by specific pathogens
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what are white blood cells
- cells in blood that protect against infection > specific immune system based on white blood cells called lymphocytes
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what are phagocytes
- white blood cells responsible for non specific immune response > they engulf + destroy pathogens and present antigens to trigger the specific immune response
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what are lymphocytes
- white blood cells responsible for the specific immune response > they produce antibodies which help prevent pathogens causing disease through agglutination, labeling, attaching to flagella, antitoxin action and neutralisation
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what are B + T cells
- both types of lymphocytes > B mature in Bone marrow + T mature in Thymus gland
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what are the 3 types of B lymphocytes
- B plasma cells - B effector cells - B memory cells
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what do B plasma cells do
- produce specific antibodies to particular antigens + release them into circulation - active plasma cells live only for few days but produce many when allice
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what do B effector cells do
- divide to form plasma cell clones
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what do B memory cells do
- live for very long - provide immunological memory > programmed to remember specific antigen + enable body to make very rapid response when pathogen with that specific antigen is encountered again > then is produces B plasma cells
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what are antibodies also known as
- immunoglobulins
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what are antibodies
- produced by lymphocytes in response to infection - they are globular glycoproteins that attach to antigens + make them harmless
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describe the structure of an antibody
- made of 2 long polypeptide chains called heavy chains + 2 shorter ones called light chains > chains held together by disulfide bridges + also within polypeptide chains holding them in shape - each antibody has 2 identical antigen binding sites - variable regions > order of amino acids in variable region determines shape of binding site
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how do antibodies cause agglutination
- they clump together bacteria makin it easier for pathogens to destroy + making them less likely to spread
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how do antibodies carry out neutralisation
- they block binding sites on pathogens so unable to bind to host cell
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how do antibodies work as antitoxins
- they block toxins
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how does antibodies attaching to bacteria flagella aid in phagocytosis
- makes bacteria less active + easier for phagocytes to engulf
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how do antibodies act as opsonins
- they attach to antigens forming antigen-antibody complex > this acts as an opsonin so complex is easily identified + engulfed/destroyed by phagocytes (produces a signal)
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what are the 4 main types of T lymphocytes
- T helper cells - T killer cells - T memory cells - T regulator cells
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what do T helper cells do
- bind to surface antigens on APC's because of CD4 receptors on their cell-surface membrane - produce interleukins (type of cytokine) that stimulate: > activity of B cells which increase antibody production > production of other T cells > attract + stimulate macrophages to ingest pathogens with antigen-antibody complexes
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what do T killer cells do
- produce chemical perforin which kills pathogens by making holes in cell membrane so its freely permeable > these are are specific to particular antigens
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what do T memory cells do
- live long + part of immunological memory - if they encounter antigen again they divide rapidly to form huge number of clones of T killer cells that destroy pathogen
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what do T regulator cells do
- suppress immune system, acting to control + regulate it - stop immune system once pathogen is destroyed > makes sure body recognises self antigens + doesn't set up autoimmune response > interleukins important in this control
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what are the 2 types of immunity
- cell mediated immunity - humoral immunity
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what happens in cell mediated immunity
- T lymphocytes respond to cells that have been altered e.g. by infection, mutation + cells from transplanted tissue - in non specific defence system, macrophages engulf/digest pathogens (phagocytosis) + process antigens forming APCs - receptors on some T helper cells fit antigens + they become activated + produce interleukins stimulating T cells to divide ---> form clones T helper cells - clones of T cells can develop into T memory, produce interleukins that stimulate phagocytosis / B cells division + clones of T killer cells
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what happens in humoral immunity
- B lymphocytes have antibodies on cell surface membrane that binds to complimentary antigen on pathogen > B cell engulf + process antigen to become APCs - activated T helper cell bind to B cell APC (clonal selection) - interleukins produced by T helper activate B cell - activated B cell divide mitosis + clones of plasma / B memory cells (clonal expansion) - cloned plasma cell produce antibodies that bind to antigen + disable them or act as opsonins / agglutinins - clones B cell can develop into B memory cell
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what types of cells does cell mediated immunity target
- our own cells that have been altered in some way by virus, infection, antigen processing or mutation (cancer)
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what types of cells does humoral immunity target
- foreign antigens found in pathogens not in our cells
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what is an autoimmune disease
- when the immune system starts to attack healthy body tissue as it stops to recognise self antigens
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what is natural immunity
- types of immunity that occur naturally in the body
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what is natural active immunity
- when you encounter a pathogen for the first time the immune system is activated + antibodies form + antigen destroyed - immune system produces T + B memory cells so it can recognise antigen in future
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what is natural passive immunity
- short term immunity when mother's antibodies passed to foetus via placenta + remains for several months - colostrum contains lots of antibodies that remain on surface of baby's gut wall + pass into blood
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what is artificial immunity
- immunity without requiring contact with live pathogens
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what is artificial passive immunity
- used when very rapid immune response is needed - human antibodies injected into bloodstream of another > gives temporary immunity
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what is artificial active immunity
- the immune system of body is stimulated to make its own antibodies to a safe forms of an antigen > vaccine injected into bloodstream
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what is an epidemic
- when a communicable disease spreads rapidly to a lot of people at a local or national level
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what is a pandemic
- when the same disease spreads rapidly across a number of countries + continents
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what are vaccines used for
- to give long term immunity to many diseases + prevent epidemics
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describe the steps to how a vaccine works
- pathogens made safe in a number of ways so antigens are intact but there is no risk of infection > may be a killed or weakened strain - small amounts of safe antigen injected into blood - primary immune response triggered by foreign antigens + body produces antibodies + memory cell - if you come into contact with live pathogen the secondary immune response triggered + you destroy pathogen
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what is herd immunity
- when a significant (large) number of people in population have been vaccinated so gives protection to those who haven't
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what is an example of an autoimmune disease + how does it work
- arthritis - immune system attacks smooth cartilage of joints + leads to inflammation that can affect entire body > most commonly affects hands, spine, knees + hips
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what is ring immunity
- when you vaccinate all the people around an outbreak of a disease to contain it > can be contained with quarantine
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what are some common types of medicine
- antibiotics - antifungals - antivirals - painkillers - ointment
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what are some natural sources of medicine + examples
- plants + microorganisms > penicillin (mould), aspirin (willow bark)
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what does it mean if a drug / medicine is sourced syntheitically
- it is made artificially in the lab + use computer aided design to help model the shape of the medicine to target specific areas of the pathogen
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what does it mean if a medicine is sourced semi-synthetically
- when a natural source is modified (synthetically)
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why is it important to maintain biodiversity in terms of medicine
- make sure we don't destroy a plant, animal or microorganism which could give us the key to a life-saving drug
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what is personalised medicine
- a combination of drugs that work with your individual combination of genetics + disease > you give people different medicine based on their genetics + which will be most effective
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how is personalised medicine achieved
- by analysing the human genome rapidly which gives an understanding of the genetic bases of many diseases
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what is nanotechnology
- where tiny, non-natural particles are used for biological purposes > e.g. delivering drugs to a very specific site within the cells of pathogens
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what are antibiotics used for
- treating bacterial diseases (not viruses)
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what is selective toxicity
- when antibiotics interfere with the metabolism of the bacteria without affecting the metabolism of human cells
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what are some mechanisms of action in antibiotics
- cell wall synthesis - cell membrane permeability - metabolic reactions
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what is bacteriostatic antibiotic
- doesn't kill bacteria but prevents their growth (relies on immune system to kill them)
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what is bactericidal antibiotic
- kills bacteria + doesn't rely on immune system to kill them
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what does a broad spectrum antibiotic do
- affect a large number of diff bacteria (even those that are beneficial to you)
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what does a narrow spectrum bacteria do
- affects a small number of different bacteria
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what leads to antibiotic resistance
- random mutation to an individual bacteria which is unaffected by the antibiotic - due to natural selection + rapid rate of reproduction in bacteria, this quickly leads to a large population of resistant bacteria
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what are some factors that can leads to increased antibiotic resistantce
- antibiotics added to animal feed to prevent disease - oversubscription of antibiotics > MRSA - not completing your antibiotic course
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what are some things you can do to fight antibiotic resistance
- reduce unnecessary use of antibiotics - ensure course of antibiotics goes to completion - focus on hygiene + cleaning sheets / surfaces > kill pathogens without requiring antibiotics
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