disease and immunity Flashcards
what causes communicable disease
pathogens
what are pathogens
infective organisms
what are the 4 types of pathogens
bacteria, virus, fungi, Protoctista
are bacteria prokaryotes or eukaryotes
prokaryotes
bacteria being prokaryotes means that they have - cell structure to -
very different, the eukaryotic cells they infect
how do we classify bacteria
by their shape or cell wall
what shape is a bacilli bacteria
rod
what shape is a cocci bacteria
spherical
what shape is a vibrios bacteria
comma shaped
what shape is a spirilla bacteria
spiral
what shape is a spirochaetes bacteria
corkscrew
what do we use to see the cell wall of bacteria
gram staining
gram positive bacteria look
purple
gram negative bacteria look
red
why is gram staining useful
it can allow us to tell how the bacteria would react to antibiotics
are viruses living
no
viruses are bigger/smaller than bacteria
smaller
once viruses invade living cells, what do they do?
take over the biochemistry of the host cell to make more viruses
how are viruses successful pathogens
they reproduce rapidly and adapt to the environment of their host
what are bacteriophages
viruses that attack bacteria
all natural viruses are…
pathogens
Protoctista are prokaryotic/eukaryotic
eukaryotic
are all Protoctista pathogens
no
many protoctista move between hosts through
vectors
fungal diseases are typically worse in
plants
fungi are prokaryotic/eukaryotic
eukaryotic
many fungi are saprophytes meaning that
they feed off of dead and decaying matter
what is produced when fungi reproduce
spores
which pathogens directly damage their host cells
viruses, Protoctista, fungi
which pathogens produce damaging toxins
bacteria, fungi
how do viruses damage their host cells
they insert their DNA into the host cell’s DNA, then burst out of the cell and destroy it
how do Protoctista damage their host cells
they take over cells and break them open, using the cell contents for reproduction
how do fungi directly damage their host cells
they digest living cells and break them down for food
how do bacteria damage their host cells
they produce poisonous toxins, which either break down cell surface membranes, inactivate enzymes or interfere with genetic material to prevent mitosis
how do fungi indirectly damage their host cells
they produce toxins which affect the host cells
direct transmission of pathogens occurs as pathogens
move directly from one host to another
the 3 methods of direct transmission of pathogens are
- direct contact
- inoculation
- ingestion
what is direct contact (examples)
kissing, exchange of bodily fluids, skin to skin contact and microorganisms
what is inoculation (examples)
sex, animal bites, shared needles, puncture wounds
what is ingestion (examples)
contaminated food or drink, pathogens on the hands
what re the 3 modes of indirect pathogen transmission
- fomites
- inhalation
- vectors
what are fomites
where the pathogen travels through inanimate objects such as bedding
what is inhalation
small droplets of saliva or mucus containing pathogens may be breathed in
what are vectors
things which carry pathogens from host to host, such as insects or water
direct transmission of pathogens in plants is where
leaves or other plant parts touch
indirect transmission of pathogens in plants is
soil contamination or vectors
animal bacteria disease-
tuberculosis
what does tuberculosis do
destroys lung tissue and suppresses the immune system
how can we prevent tuberculosis
vaccines
how can we cure tuberculosis
antibiotics
plant bacteria disease-
ringrot
what does ringrot do
destroys leaves, tubers and fruit of potatoes, tomatoes and aubergines
animal virus disease-
HIV
what does HIV do
targets t helper cells and destroys the immune system
can we prevent or cure HIV
no
plant virus disease-
tobacco mosaic virus
what does tobacco mosaic virus do
damages leaves, flowers, fruits and stunts growth of plants
plant fungus disease-
black sigatoka
what plants get black sigatoka
bananas
what does black sigatoka do
destroys banana leaves and turns them black
plant protoctista disease-
late blight
what cause late blight
the protoctista oomycete
what does late blight do
destroys leaves, tubers and fruit
animal fungus disease-
athlete’s foot
what does athlete’s foot do
fungi grow on the moist, warm skin between toes
how can we cure athlete’s foot
anti-fungal creams
animal protoctista disease-
malaria
what causes malaria
a Protoctista called plasmodium
how is malaria spread
through the vector of mosquitoes
what does malaria do
Protoctista invade the liver, red blood cells and brain
how can we cure malaria
we can’t
how do we control malaria
by controlling mosquito populations
what are the 2 ways which plants recognise pathogens
chemicals are released when the cell wall is attacked, receptors in the cells respond to molecules from the pathogens
what happens when plant cells recognise pathogens
genes on the nucleus are switched on, sending alarm signals to unaffected cells and triggering responses
what is a plants physical defence
- callose is synthesised and deposited between cell walls and surface membranes in cells next to the infected ones, and in phloem sieve plates and plasmodesmata; the callose papillae act as barrier to prevent the spread of the infection.
- Lignin is added to the cell wall, making the barrier thicker
what are the plants chemical defences
- insect repellents
- insecticides
- antibitotics, antiseptics, lysosomes
- antifungal compounds
- anti-oomycetes
- general toxins
what are all the human non-specific primary defences
- skin
- mucous membranes
- lysozymes in tears and urine and stomach acid
- expulsive refluxes
- blood clotting and wound repair
- inflammatory response
how does our skin protect us
it is impermeable to most pathogens, and has a flora of healthy microorganisms to outcompete pathogens, and sebum to inhibit pathogen growth
how do mucous membranes act as a primary defence
they line body tracts, and secrete sticky mucus to trap microorganisms, contains phagocytes and lysozymes to destroy bacterial and fungal cell walls
how do lysozymes in tears and urine act as a primary defence
destroy bacterial and fungal cell walls
how do expulsive reflexes protect us
they expel pathogens
why is blood clotting used as a primary defence
it creates a scab so that pathogens can’t enter through wounds
when is blood clotting triggered
when platelets come into contact with a broken vessel wall, they adhere to it and secrete substances
platelets secrete
thromboplastin
what does thromboplastin work with
ca 2+ ions
thromboplastin and ca2+ ions catalyse the
conversion of prothrombin into thrombin
thrombin catalyses the
conversion of fibrinogen into fibrin
fibrin forms a
mesh over a wound, creating a clot
serotonin is secreted by plasma, which has the effect of
smooth muscle walls of the blood vessel contracting, so narrowing and reducing blood supply to a cut area
what characterises inflammation
pain, swelling, redness, heat
what is activated in damaged tissue
mast cells
what is secreted when mast cells are damaged
histamines and cytokines
what do histamines do in the inflammatory response
- make blood vessels dilate, increasing heat and redness so pathogens can’t reproduce
- make blood vessels leakier to create more tissue fluid
what do cytokines do in the inflammatory response
attract phagocytes
what is the animal secondary non-specific response
phagocytosis, cytokines being released
what do cytokines do in the secondary non-specific response
the stimulate the hypothalamus to raise body temperature so pathogens can’t reproduce
what are the steps of phagocytosis:
- pathogen produces chemicals which attract phagocytes
- phagocytes recognise non-human proteins on the pathogen
- the phagocyte engulfs the pathogen and encloses it in a vacuole called the phagosome
- the phagosome combines with a lysosome to form a phagolysosome
- enzymes from the lysosome digest the pathogen
what attracts phagocytes to pathogens
the chemicals pathogens produce
how do phagocytes identify pathogens
they recognise non human proteins on the pathogen
what does a phagocyte do after identifying a pathogen
engulf it and encloses it into the phagosome
what is a phagaosome
a vacuole in the phagocyte which encloses pathogens
what happens after a phagosome engulfs a pathogen
it combines with a lysosome to form a phagolysosome
what is a phagolysosome
a phagosome combined with a lysosome
what happens after a phagolysosome has formed
enzymes from the lysosome digest the pathogen
what are phagocytes
specialised cells in the blood and tissue which carry out phagocytosis
where are phagocytes produced
the bone marrow
what organelles do phagocytes contain lots of
lysosomes, ribosomes and RER
phagocytes migrate around the body towards
signals from cytokines
what are the 3 types of phagocytes
- neutrophils
- macrophages
- dendritic cells
which types of phagocytes are APCs
macrophages, dendritic cells
which type of phagocyte is most common
neutrophils
when do neutrophils join tissue fluid
during infections
a large number of neutrophils are made during infection, then
they die and make up pus
what do neutrophils do
engulf and digest pathogens
what do macrophages do
engulf and digest pathogens
are neutrophils or macrophages larger
macrophages
where do we find macrophages
in the organs and lymph
macrophages are long/ short lived
long
macrophages can become
APCs
after digesting a pathogen, macrophages and dendritic cells can combine with
antigens from the pathogen surface membrane
macrophages and dendritic cells take antigens from the pathogen surface membrane and combine them with
special glycoproteins in the cytoplasm called major histocompatibility complex (MHC)
what is a major histocompatibility complex
special glycoproteins in the cytoplasm which combine with antigens from the pathogen surface membrane
what does the MHC do
moves the pathogen antigens to the surface membrane of dendritic cells and macrophages to create APCs
what do APCs do
stimulate other cells from the specific immune response
dendritic cells have long processes- what are these
arm like structures
why do dendritic cells have processes
to increase surface area to interact with pathogens
where are dendritic cells found
entry points such as skin, digestive tract and mucous membranes
are dendritic cells APCs
yes
where do dendritic cells go after phagocytosis
lymph nodes
phagocytes release cytokines, which here act as
cell signalling molecules to attract other phagocytes and trigger the specific immune response
what do opsonins do
bind to pathogens and tag them to make identifying them easier
what is an antigen
a molecule on the cell surface membrane which is usually a protein or a glycoprotein
which cells have antigens
all of them
what is another name for antibodies
immunoglobulins
what shape are antibodies
y shaped
what molecules are antibodies
globular glycoproteins
what hold light chains together
disulfide bridges
which mechanism allows antibodies to bind to antigens
lock and key
what is the binding site
an area of 110 amino acids on the heavy and light chains
what do amino acids in the binding site do
give antibodies their shape and specificity
what is the binding site part of
the variable region
purpose of the hinge region
provide the molecule with flexibility and allow it to bind to 2 separate pathogens
an antibody in an antibody-antigen complex acts as
an opsonin
can pathogens invade host cells when part of an antibody-antigen complex
no
antibodies act as -, clumping pathogens together
agglutinins
antibodies act as antitoxins, meaning that
they neutralise toxins produced by pathogens
why are secondary responses so much fastere
T memory cells
in humoral immunity, the body responds to pathogens found
outside of cells
humoral immunity step 1
a pathogen enters the body and multiplies
humoral immunity step 2
lymphocytes come into contact with the pathogen in one of 3 ways
- encountering the pathogen
- encountering APCs
- encountering infected cells displaying the antigen of the pathogen
3 ways lymphocytes can come into contact with pathigens
- encountering the pathogen
- encountering APCs
- encountering infected cells displaying the antigen of the pathogen
humoral immunity step 3
clonal selection, where correct T and B cells bind with pathogenic antigens
humoral immunity step 4
clonal expansion or proliferation, when the correct lymphocytes divide rapidly by mitosis
humoral immunity step 5
the cells differentiate into particular types of B or T cells
4 types of T cells
- killer
- memory
- helper
- regulator
T killer cells function
attack infected host cells
T memory cells function
stay in the blood for future infections
T helper cells function
release cytokines to stimulate B cells to divide and stimulate phagocytosis
T regulator cells function
stop immune response after pathogen is removed and prevent T cells from attacking own tissue
what do b cells differentiate into
- plasma cells
- B memory cells
plasma cells function
blood clotting, make antibodies
B memory cells function
stay in the blood for future infections
in cell-mediated immunity, what respond
T lymphocytes
in cell-mediated immunity what do T lymphocytes respond to
cells of organisms changed in some way
examples of in cell-mediated immunity
viruses and cancers
what do macrophages release
monokines
what do monokines do
attract neutrophils by chemotaxis, stimulate b cells to differentiate and release antibodies
what to T cells, B cells and macrophages release
interleukins
why do T cells, B cells and macrophages release interleukins
to stimulate proliferation and differentiation of T and B cells
many cells release interferon, which
inhibits virus replication and stimulates T killer cells
in cell-mediated immunity, macrophages
engulf and digest pathogens, then become APCs
in cell-mediated immunity, interleukins are released, causing
T cells to divide rapidly
in cell-mediated immunity, cloned T cells may
- develop into memory cells
- stimulate phagocytosis
- stimulate B cells to divide
- stimulate development of specific T killer cells
active natural immunity example
being infected
passive natural immunity example
breastfeeding, antibodies passing across placenta
active artificial immunity example
vaccination
passive artificial immunity example
injecting antibodies or antitoxins
name 4 autoimmune diseases
multiple sclerosis, type 1 diabetes, arthritis, lupus
multiple sclerosis tissues affected
myelin sheath
multiple sclerosis symptoms
fatigue, limited mobility, numbness and tingling, muscle spasms
multiple sclerosis treatments
- disease-modifying therapies
- stem cell transplant
- physiotherapy
type 1 diabetes tissue affceted
insulin-secreting cells in the pancreas
type 1 diabetes symptoms
feeling thirsty, sweet-smelling breath, weight loss, cuts don’t heal
type 1 diabetes treatments
insulin injections, pancreas transplants, immunosuppressant drugs
arthritis tissue affected
joints
arthritis symptoms
joint pain, inflammation, restricted movement
arthritis treatments
anti-inflammatory drugs, steroids, immunosuppressant drugs
lupus tissue affected
skin and joints, all organs
lupus symptoms
fatigue, fever, joint pain, butterfly rash
lupus treatments
anti-inflammatory drugs, steroids, immunosuppressant drugs
what are autoimmune diseases
where the T regulator cells don’t function well, so white blood cells attack human tissue
where do we source medicine (3)
computer programmes, plants, microorganisms
where is penicillin from
mould
where is aspirin from
willow bark
people have different genes, and therefore different
enzymes
people having different enzymes means
they react differently to different medicines
by testing someone’s genome, we can see
which drugs will be most effective for them
what is personalised medicine
testing someone’s genome and using it to prescribe them to most effective medicine possible
example of personalised medicine
Herceptin
Herceptin use
treat breast cancer
why do we use synthetic biology
some drugs are too expensive or difficult to mass produce
how do we create synthetic drugs
genetic engineering to develop bacteria to produce drugs
example of microorganism synthetic drugs
E.coli can be used to produce a precursor for an antimalarial drug
how can mammals be used in synthetic drugs
they can be genetically modified to produce drugs in their milk
example of mammal synthetic drugs
goats can produce human antithrombin used in blood clotting
nanotechnology uses
tiny synthetic particles to deliver drugs to specific cells
when do we use nanotechnology
to deliver drugs to kill cancer cells without harming healthy cells
