microorganisms that Transmission in animals Transmission in plants FACTORS AFFECTING PLANT TRANSMISSION
enter the body cause disease DIRECT-vertical (mumt child via placental, DIRECT leaves -
physically touching plants are more susceptible (clones), overcrowding
Materia prokaryotes -
horizontal (animal to animall each other causing direct contact, lack
of nutrients in soil,
reproduce rapidly drasites children INDIRECT
i
by not pathogens direct contact-skin to shin-common in dampt warm conditions, climate change
·
-
1Mm
binary fission ·
live on or in another living ·
Innoculation -
respiratory droplets from pathogens in soil enter roots
live in vascular tissues thing-take nutrition from host respiratory tract through coughing etc.
he live in vascular tissuest receptors respond to
TB(A), ringrot (P), meningitis (A) may lived unnoticed may avoid
Plant defences
↳landormucusmembranesleges,mother pathogens release signalling
seed et
nahi
·
off
+
-
Viruses -
smaller than bacteria being removed ·leaves shed once infected -
carries PHYSICAL DEFENCES * molecules to trigger response
can'treproduce without host cells head lice (external),tape worm (internall food or water, pathogens already
are
pathogens back to soil ① cell recognises pathogen and defensive molecules
to invade
Emm present or grow from improper storage fungiproduce spores by reproduction attack
cell
eventually bursts releases + INDIRECT ·
vectors -
wind, water, animals, 2
pathogenic enzymes breakdown cell wall and
viral particles inject to other cells Viral actions vectors -
an animal or insectthat carries humans
signalling molecules recognise the products + alert nucleus
HIV, shu, Herpes micro-organism that can cause disease 3
polysacharides made callose papillar acts as a
·
1. attachmentt o 2. Insertion of viral a -
host cells ⑱ nucleic acid
Fungi -may live in the skin somites hospital acquired injections from FACTORS AFFECTING ANIMAL barrier to prevent infection of surrounding cells, lignin
⑧ ⑧
-
⑧
of animals
⑧ bed linen, ste the scopes etc.not cleaned TRANSMISSION strengthens mechanical barrier, callose blocks sieve
·release sporest cause redness properly between uses -
nosocomial lack of infrastructure plates in phloem to isolate the infection callose is
of skin Ene
Imm
tissue
DNA replication of
Siral nucleic
/
4.
Synthesis of viral
protein (transcriptionFanslation)
injections
↑ ventilation:
a risk lack of sanitation/healthcare deposited plasmodesmata in
in the between infected
live in vascular airborne-droplet nucleil dust containing lack cells - reduces spread
· ·
acid
of education
⑧ ⑧
6.9
⑧ ⑧
its
hyphae mycelium .....
⑧ .. pathogens remain in defensive chemicals alert other cells to the attack
⑳
4
form the air diet
·
a ·
.
.
·
⑧
⑧
.
athletesfoot (A), black sigatoha(p) A
*
⑳ E ·
spores in animate object pathogens
-
are lack of ventilation CHEMICAL DEFENCES
ists
enkaryotic En
3mm -
5. assembly of 6. lysis of
left on - inject when touched ·
Insect repellants -
pine resintcitronella from lemon grass
Communicable disease
* ⑲ ⑨
virus particles host cell
cause harm
viruses
Insecticides- pyrethrins made
->
by entering host cells ⑨
by chrysanthemums neurotoxins
·
⑧ ⑧
-
, got infect
malaria (caused
by plasmodium), 19
⑧ ⑧ j
other
PHAGOCYTOSIS ·antibacterial compounds phenols (antiseptics), defensing
Specific
&
a sa cels -
⑨
⑧
-⑧ &
potato blight (P)
%
Idisruptbacterial fungimembranes), lysosomes
lysosomes
en
pathogen
immune
·
⑧ pathogen releases
-,
I
phagocyte antifungal compounds Saponins/disrupt fungi membranes),
·
& 0 -
chemicals that
·
T
lymphocytes -
made in bone marrow t responses attract the phagocyte chitinases (breakdown chitin in fungi cell wall)
Antibodies and mature in thymus gland .
anti-comycetes-glucanases/breakdown glucans)
Antibodies
immunity
-- attack antigens to make an APC
CELL MEDIATED RESPONSE
① antigens from virus are used to make APC
·
↳
2 phagocyte
to non-self pathogen
binds
⑧ 88
o
o
·general toxins-chemicals broken down
which is toxic to most plants
to make cyanide
produce chemicals (agglumins) causing APC's to ② Clonal selection-find T cell with correct shape for receptor
togethers easier for phagocytes
↳ phagocyte engulfs
3
·
clump to locate
③ found Tell is clonedby mitosis
↳release antitoxins detects t
④clonal expansion make more of the T cells
0 pathogen,
phagosome
making Non-specific responses
·natural immunity -
responds naturally -
E
a
The
lysosome moves towards
·
active immunity -
Bells
differentiate into -
Tregulator recognise end of injection so we don't attach our cells
-
phagosome combines forming Mucus membranes -
cover respiratory tract digestive system
plasmat memory cells which produce antibodies -
Thiller if complementary to injected cell, binds releases perforins
- + phagolysome
* ↳ have
goblet cells ciliated cells that produce mucus to trapt move
⑧
·artificial immunity medical like
-
vaccines
which make the cell membranes permeable hills the
4
go pathogens
+
cell enzymes
-
inject with weakened, dead or less harmful pathogen breakdown the
·Passive immunity -
no revention of
memory
-
Tmemory -
wait for reinjection-act quicker as lots alre
ady made
pathogen in the
·Shin-dead outer layers, stops viruses reproducing
cells inject blood plasma with antibodies) or
artificial T helper-release interleuking to stimulate cells to
T cells +B
develop blood
phagolysome clotting platelets activated
by damaged tissue release
-
-
-
natural (breastfeeding, antibodies passed in milk)
Autoimmune conditions HUMORAL RESPONSE ↳ thromboplastin that joins its cofactor cant
0
MMC by to catalyse the reaction
-
B+T cells 5
form a
-
combining antigens from
stop working healthy body attach cells B lymphocytes made mature in bone
ga of prothrombine thrombin which catalyses soluble fibrinogen to
-
t -
marrow
↳
Tregulators fail can be due to
genetics 88 a
pathogen to their
antibody to join APC
-
or an infection-cause of failure unknown
① clonal selection-choose Bell with correct glycoproteins insoluble fibrin which holds platelets together, forming a clot
⑧
-
Type diabetes (affects
1 insulin secreting cells) ② activated t helper cell attaches activates division of Bcek
E 6 M4C antigen
Inflammatory response-caused by a
pathogen entering the body,
displayed
complex 88
&
Rheumatoid arthritis (affects joints), Lupus (affects ↳ clonal cell division to a number of activated cells
·
expansion uses # on phagocyte causes redness or
swelling, release histamines (which dilate
shint joints, causing fatigue attacksorgans) E membrane -
maks APC
a
③ either plasma
-8
Sources of medicine -
plasma or
memory cells -
cells secrete antibodies blood vessels causing bigger gaps between cells for plasmat WBC
computer programmes help with design
-
-
used to destroy pathogen (primary response), memory cells circulate
·
opsonins -
attach to
pathogen bleak from) and cytokines (which attract WBC to attack
to search through chemicals
to make it
bioactive compounds in plants/microorganisms in blood forimmunity-will divide rapidly develop
long term + more recognisable pathogens)
Docetaxel in yew trees for breast cancer,
eg. into
plasmat memory cells (secondary response cytokines alertphagocytes. Fever-raises body temp. 137 which increases kinetic
·
-
in willow bark as a painkiller,
aspirin
bigoxin from foxgloves for heart failure BLOOD
WHITE
TYPES OF CELLS to presence of pathogens energy and causes pathogen enzymes to denature, WBC are
Pharmacogenetics
-
-
the study of how genes macrophages monocytes when immature -> made in
- bone marrow ·Interferons -
stimulate nearby also more
likely to attach due to MYE, a
really high fever
affect person's response to drugs
large nucleus neutrophil-multilobed nucleus-made
a
in bone cells to anti-viral defences be
drugs with efficacy
used to make stronger dangerous if our
enzymes denature
-
↳ can
tic
-
biology-DNA
sequencing + marrow with lots of lysosomes and reduce extent of infection
diseases mutation
genome editing
can reduce