Yr 12 SAC 3 (unit 4)
What is a disease
any condition that interferes w/ how an organism functions
what is an organism infected with a disease called
a host
what is an infectious agen called
the pathogen
different types of pathogens and if they are cellular or non
Bacteria - cellular
Fungi - cellular
Parasites - cellular
protozoans - cellular
virus - noncellular
viroids - noncellular
prions - noncellular
characteristics of bacteria
cellular
prokaryotic
intra or extracellular
have cell wall
treated with antibiotics
characteristics of fungi
cellular
eukaryotic
reproduce w/ spores (on broken skin)
opportunistic pathogens
external usually
cell wall of chitia
characteristics of protozoans
cellular
unicellular eukaryote
sexual/asexual reproduction
characteristics of virus
noncellular
obligate parasites (need host to replicate)
called a VIRION when out of cell
DNA or RNA
has protein coat (capsid)
Steps for the Lytic life style (virus thing)
First 4 steps are incubation period:
1. virus attaches to host
2. virus injects nucleid acid into host cell
3. directs host cell to make copies of viral protein coat/nucleic acid (capsid)
4. assembled into new viruses
5. cell undergoed lysis (bursting of cell) or budding (exocytosis)
6. infects other cells
Steps for the Lytic life style (virus thing)
First 4 steps are incubation period:
1. virus attaches to host
2. virus injects nucleid acid into host cell
3. directs host cell to make copies of viral protein coat/nucleic acid (capsid)
4. assembled into new viruses
5. cell undergoed lysis (bursting of cell) or budding (exocytosis)
6. infects other cells
why do viruses stimulate an immune response
they are recognised as non-self
characteristics of viroids
noncellular
simpler form of virus (no capsid)
ussually only infects plants
need host cell to replicate
Characteristics of prions
noncellular
small, infectious proteins
lack nucleid acids
has two forms:
harmless or harmful, infectious
triggers cascading effect (known for effect on brain)
What are antigens
antibody generators
molecules that stimulate immune response
What are the two types of antigen
self antigens
recognised as self and thus usually doesnt amount immune response
non self antigens
do nto belong to bodys own cells
What are MHC Markers and what do they do
receptor protons on surface of body cells
allow immune system to distingui self from non
What are the two diff types of MHC markers and what they do
MHC-I
on all nucleated cells
MHC-II
present on antigen presenting cells
such as macrophage, dendritic etc
What are allergens
antigen that causes an abnormal/innaporpriate immune response (and allergic response)
What is an allergy
when a person immune system reacts ABNORMALLY to substances in enviro that are harmless to most ppl
traits of the non-specific (innate) barrier
same response for all infections
no memory of infections
same level of response for each successive infection
fast
genetically determined
Examples of the physical innate barrier
in tact skin
mucous
cillia (hair)
coughing/sneezing
tears (both)
Examples of the chemical innate barrier
skin producing chemicals that inhibit growth of microorganisms
sweat/oil
stomach acid
tears (both), saliva and mucous (which contain lysozomes)
where are lysozomes and what do they do
tears, salive, mucous
lyse cells (cut)
Plant defence strategies
all physical:
thick bark/stems
hairs/thorns which deter vectors of pathogens and animals
closed stomata
hairs around stomata
cell wall
traits of the innate response (second line of defence)
lacks memory
lacks specificity
distinguishes non self from self
done through:
pathogen associated molecular patterns
and pattern recognition receptors
what is phagocytosis
engulfing/digesting of pathogens
preformed by neutrophils, macrophages and dendritic cells
steps to phagocytosis (5)
1. phagocyte engulfs pathogen
2. pathogen engulfed in vescicle, then called phagosome
3. lysozomes fuse w/phagosome (produces phagolysozome)
4. toxic chem in lysozome (lysozymes + protease) digests an ddestroys pathogen
5. indugestible material discharged from phagocytic cells (exocytosis)
steps to phagocytosis (5)
1. phagocyte engulfs pathogen
2. pathogen engulfed in vescicle, then called phagosome
3. lysozomes fuse w/phagosome (produces phagolysozome)
4. toxic chem in lysozome (lysozymes + protease) digests an ddestroys pathogen
5. indugestible material discharged from phagocytic cells (exocytosis)
Types of phagocytes
Macrohpage (APC)
Nuetrophils
Dendritic cells (APC)
traits of macrophage
in innate and adaptive immunity
phagocytes
APC
Nuetorphils traits
abundant
phagocytes
die after phagocytosis
attracted to non self by chem signals
traits of dendritic cells
phagocytes
APCs
increased SA:V ratio
types of granulocytes
eusinophils
mast cells
traits of eusinophils
granulocytes
have granules w/ histamine/toxic chem
also have granukles of ribonuclease (RNases) that help fight infection
fight parasites
what is degranulation
when the granulocytes release the contents of their granules
traits of natural killer cells
lymphocytes that realese toxins (degranulation)
kill virus infected/cancerous cells
induce apoptosis in said cells
granules contain proteases (granzyme(digest proteins)) and perforin (puts lots of holes in)
prevent spread of virus
traits of mast cells
has granules with cytokines, histamine and heparin
releases these
what does histamine do
causes blood vessels to dilate and become more permeable (inflammation)
causes smooth muscle contractions
what do cytokines do
attract other immune cells to site of infection
thus they are signalling molecules
steps to an allergic response (from pre first exposure )
steps 1-3 are sensitisation
1. initial exposure to allergen
2. B cells recognise as non self and make IgE antibodies for allergies
3. antibodies bind to mast cells
4. second exposure to allergen
5. antigens cross link antibodies (stimulus)
6. mast cells release histamine (response to stimulus)
steps to an allergic response (from pre first exposure )
steps 1-3 are sensitisation
1. initial exposure to allergen
2. B cells recognise as non self and make IgE antibodies for allergies
3. antibodies bind to mast cells
4. second exposure to allergen
5. antigens cross link antibodies (stimulus)
6. mast cells release histamine (response to stimulus)
what is humoral innate immunity
soluble proteins in extracellular body fluids (blood/lymph)
types of cytokines
interferons
chemokines
complement proteins
charactistics of interferons
cytokine type
cellular warning signal
prep/protect cells from vrial infections
how do interferons protect/prep cells
activating production of enzymes that break down viral proteins
decrease fluidity of plasma membrane
cause virally infected cells to undergo apoptosis
activate NK cells
traits of the complement system
small proteins inactive that are important in inflammatory system
activation occurs when in direct contact w/ molecules on surface of pathogen
cascade effect occurs, activating other proteins
what activities are performed by the complement system
stimulates phagocytosis
stim mast cells to produce histamine
membran attach complex (forms pores)
opsonisation (sticks out to become more visible (marker))
chemotaxis (attracts other cells)
What is the antibody for Allergies
IgE
what are symptoms of inflammation
swelling
redness
heat
pus
pain
What are the stages of inflammation in order
Vascular
Cellular
Resolution
Traits of the vascular stage of inflammation
initiation of inflammation
damaged cells release cytokines
these attract neutrophil (thru chemotaxis)
mast cells release histamine
dilates and increases permeability of blood vessels
blood clotting (isolating infection)
traits of cellular stage of inflammation
immune cells migrate into tissue
neutrophils arrive (first bc of cytokines)
macrophages etc release cytokines + histamines
phagocytosis occurs
pus produced (dead cells/living debris cleaned)
Traits of resolution stage of inflammation
once pathogen eliminated
normal stage restored
all processes reversed
asisted by anti inflammatory cytokines + other molecules
if fails then chronic inflammation occurs
traits of the lymphatic system (conists of what)
lymphoid organs
-primary
-bone marrow
-thymus
-scondary
-lymph nodes
-spleen
transport vessels
-carry lymph between these and back to blood
traits of the primary lymphoid organs
location of maturaiton of lymphocytes (both B and T) and development of self tolerance
Bone marrow
Thymus
traits of the Bone marrow
source of all blood cells (B and T)
site of maturation of B cells (B for B)
traits of Thymus
site of maturation of T cells ( T for T)
traits of secondary lymphoid organs
sites where T/B cells activated
done by meeting complimentary antigens
thus develop into effector cells (clonal selection/expansion)
spleen
lymph nodes
traits of the spleen
filters blood
clears pathogens/ worn out blood cells
contains T/B cells, macrophage, dendritic cells
traits of lymph nodes
main site of adaptive immune response
swells when infected
How is the adaptive immune response initiated
APC's (dendrites/macrophage) link the innate/adaptive immune system
Steps of Antigen presentation (7 steps)
1. Phagocytosis occurs
(pathogen digested in lysosome)
2. some fragments released by exocytosis
(thus displayed on MHC 2 mrkers on APCs)
3. Phagocyte APCs move to lymph node
(present antigens to naive (not mature) helper T cells specific to antigen)
4. clonal expansion occurs
5. T cells release cytokines
6. clonal selection occurs
7. clonal expansion of B and T cells occurs
Steps of Antigen presentation (7 steps)
1. Phagocytosis occurs
(pathogen digested in lysosome)
2. some fragments released by exocytosis
(thus displayed on MHC 2 mrkers on APCs)
3. Phagocyte APCs move to lymph node
(present antigens to naive (not mature) helper T cells specific to antigen)
4. clonal expansion occurs
5. T cells release cytokines
6. clonal selection occurs
7. clonal expansion of B and T cells occurs
traits of helper T cells (TH cells)
do not kill pathogens directly
instead activate cytoxic T cells and normal B cells
result in proliferation and stium (of B/T cells) of immune response secondary lymphoid organs
activate macrophages
functions of helper T cells
activate cytotoxic T cells
activate B cells -> plasma cells
activate macrophages
Traits of the adaptive immune response
acquired by exposure to pathogens
slower than innate
specific to pathogen
immunological memory created
humoral/ cell mediated immunity
components of adaptive immune response
T/B lymphocytes
antibodies
lymph nodes
traits of T cells
slime the opps
deliver cell mediated immune defences
include direct elimination of pathogen infected and cancer cells
traits of B cells
produce what assists in sliming the opps (plasma cells producing antibodies)
deliver humoral immune defences
done by
secreting antibodies which bind to pathogen (opsonisation) (MHC1 markers)
Where are humoral and cell mediated
Humoral (B cells) is extracellular (outside the cell)
cell mediated (T cells) is intracellular (inside the cell)
traits of humoral immunity
B lymphocytes fight extracellular infections
formed in bone marrow
plasma cells secrete antibodies specific to plasma cells)
memory B cells remain in lymphatic tisue with memory to prep for faster/greater magnitude next time
What occurs once humorl response activated
B cells clonaly selected
produces antibodies
circulate in bloodstream and defend against extracellular antigens
Steps to activation of humoral response (6 steps)
1. antigen enters body
reach lymph nodes via APCs
come in contact with naive (not activated) B cells
2. antigen meets B cells that recognise (specific)
binds to it (clonal selection)
3. Helper T cells release cytokines
activate B cells
4. B cells differentiate/proliferate -> plasma cells/ mem B cells
done through clonal expansion
5. Plasma cells secrete antibodies against specific antigen
6. mem B cells remain in lymphoid tissue
Steps to activation of humoral response (6 steps)
1. antigen enters body
reach lymph nodes via APCs
come in contact with naive (not activated) B cells
2. antigen meets B cells that recognise (specific)
binds to it (clonal selection)
3. Helper T cells release cytokines
activate B cells
4. B cells differentiate/proliferate -> plasma cells/ mem B cells
done through clonal expansion
5. Plasma cells secrete antibodies against specific antigen
6. mem B cells remain in lymphoid tissue
Antibody structure traits
NEED TO BE ABLE TO DRAW SO PLEASE SEARCH NOW
antigen binding proteins produced by plasma cells
four polypeptide chains
amino acid sequence at variable region differs
gives specificity for diff antigens
Functions of antibodies using the acronym
P(precipitation, soluble antigens -> insoluble, more visible to cells, thus easier to locate to destruct)
I(inflammation, release of histamine)
A(agglutination, pathogens trapped w/antibodies (glued tgther), prone to distruction)
N(nuetralisation (block antigens from binding))
O(opsonisation, antibodies 'tag' pathogens, easier to locate to destruct )
C(complement activation, activate cascade of compliment proteins)
Functions of antibodies using the acronym
P(precipitation, soluble antigens -> insoluble, more visible to cells, thus easier to locate to destruct)
I(inflammation, release of histamine)
A(agglutination, pathogens trapped w/antibodies (glued tgther), prone to distruction)
N(nuetralisation (block antigens from binding))
O(opsonisation, antibodies 'tag' pathogens, easier to locate to destruct )
C(complement activation, activate cascade of compliment proteins)
Humoral immunity summary steps (8 steps kinda)
1. immature B lymphocyte carries specific antibody
2. encounters specific antigen
3. antigen + antibody bond (after MHC recognised)
4. series of reactions occur
5. B lymphocyte proliferates
6. some activated B lymphocyte clones become plasma cells
7. Produce/secrete increased number of antibody cells
8. destroys pathogen
what occurs with a secondary/subsequential response
KNOW THE GRAPH
the secondary/subsequential response is faster and greater in magnitude
traits of cell mediated immunity
targets/eliminates intracellular infected/cancerous cells
T cells activated -> effector T cells
cytotoxic T cells involved
dont bind directly w/antigens
bind w/ antigens on MHC-1 markers
release perforin/granzyme (like NK cells, but specific)
cells involves in cell mediated immunity
-dendritic
antigen presentation
-helper T cells
antigen recognition
activation of T cells
-cytotic T cells
kill virus infected/cencerous cells
-mem T cells
remain in body for future exposure
traits of apoptosis by T cells
TC release perforin
created pores in plasma membrane
TC release granules of granzyme B
enters infected cells via pores
initiates apoptosis
TC repeats
Activation of cell-mediated responses (6 steps)
1. APC's displaying antigens on MHC-2
bind to specific helper T cells
2. Helper T cells undergo clonal selection/expansion
produces more effectors helper T cells + T mem cells
3. Helper T cells secrete cytokines (interluekin)
stimulate immature T cells
4. Immature T cells bind to self-cell w/foreign MHC markers (MHC 2)
or to APC's
5. Cytokines stim T cells proliferation
activated T cells + memory T cells through clonal selection/expansion
6. T cells destory infected/cancerous cells
Traits of active immunity
active development of immunity
thus body produces antibodies/memory cells
two types
natural (from infection)
artificial (vaccination)
Natural active immunity
develops from infection
immunological memory created by this
artificial active immunity
introduction of antigen via vaccination
activated immune system to produce antibodies/memory cells
vaccine types
-live attenuated (changed to be harmless)
produces more, longer lasting level of antibodies
-killed bacteria/ inactivated viruses
-subunits of pathogen stimulate antibody formations
-bacteria/toxins created
traits of passive immunity
no production of memory cells/antibodies
transfer of antibodies from external source
immediate protection
short lasting
two types:
natural (antibodies from source)
aritificial (infection of antibodies)
natural passive immunity
antibodies received from natural source
examples are breastfeeding/placenta
artificial passive immunity
infection of antibodies
eg. antivenoms
anti-toxins
tenus shot
emerging disease meaning
newly identified/previously known agent that causes increase in human infection in past 2 decades
what is a disease
condition that impairs normal functioning
what is an epidemic
widespread occurance disease in community
what is a pandemic
widespread occurance of disease across multiple countries/communities
why do diseases spread
lack of previous exposure to pathogens
increase in population density
health status of people (poor)
what may cause a pandemic
new strain/pathogen in new area
pathogen spread by animals
pathogen easily transmissible
uncontrolled spread occurs across wide geographic area
what is a resovoir
habitat in which pathogen lives/grows/multiplies
not the symptoms
what is transmission
when pathogen leaves resovoir/host
then enters susceptible host
what is susceptibility dtermined by
genetics
specific immunity (vaccines)
sex
age
nutrition
what is an index case
patient 0
allows tracking of disease spread
long incubation period means more difficult to detect