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Module 4
Communicable diseases
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Cards (93)
host
- the organism the pathogen infects
Types of pathogens
virus
bacteria
fungi
protista
Virus
HIV
/
AIDS
,
influenza
,
tobacco
mosaic
virus
non living
cause host cell to manufacture copies of the virsus causing it to bust
Bacteria
Tuberculosis
,
ring rot
( potatoes/tomatoes ) ,
bacterial
meningitis
release toxins inhibiting host cells functions
Fungi
black
sigatoka
(bananna) ,
athletes
foot
,
ring
worm
uni cellular / multicellular
release enzymes and digest material around them,
products of digestion are absorbed back into fungal cells- causing
damage
to host cells/tissues
Protista
malaria
, potato / tomato
late blight
Direct transmission of pathogens in plants
pathogens in
soil
infect plant by entering
roots
(easier if damaged by
weather
, replanting or
burrowing
)
fungi
spores
produced sexually/asexually are carried in the
wind
-
airborne
transmission
pathogens infect
vascular
tissue, carry to and from soil to infect other plants can enter
seeds
and be distributed so
offspring
are infected
Indirect transmission of pathogens in plants
spores/
bacteria
become attached to a
burrowing insect
which acts as a
vector
while attacking plants
Diseases grow and
reproduce
more rapidly in
warm
,
moist
climates
Indirect transmission between animals can occur via a
vector
Vector
- organism used by
pathogen
to gain entry to the
primary
host
Direct transmission of pathogens between animals - social factors
overcrowding
poor
ventilation
poor
health
/ diet
homelessness
contact with people who have
migrated
from areas where a disease is more common
drinking contaminated
water
contact with infected
faeces
or animals
Physical plant defences:
cellulose
wall / bark - contains
chemical
defences
lignin
cell wall - waterproof /
indigestible
thick
barrier
waxy
cuticles
- prevents water collecting on cell surfaces
stomatal closure - close when pathogens are detected
callose
tylose
Role of Callose in physical plant defences -
large
polysaccharide
deposited in cell walls reinforced with
lignin
blocks
sieve
tube
end plates in
phloem
preventing
spread
of infected area
blocks
plasmodesmata
between infected and nearby cells
Role of Tylose in physical plant defences -
fills
xylem
vessel preventing spread of pathogens
contains high conc. of
toxins
Chemical
plant defences are produced after plant develops an
infection
requiring lots of
energy
Chemical plant defences -
Tannins
- bitter taste from enzymes
Hydrolytic enzymes - break down the
chitin
in the cell wall (
Chitinases
)
insect
repellent
(pine resin / lemongrass)
insecticides
(
caffeine
- neurotoxin )
antibacterial
compounds - disrupt the cell wall of
bacteria
Anti-oomycetes
- break down the cell walls on fungi
Primary non-specific defences:
>
digestive
system
>
respiratory
system
>
skin
>
inflammation
>
ear
wax
Primary defence in digestive system
hydraulic
acid
mucus
lining of stomach
lysosome
enzymes in
saliva
/ tears
Primary defence in respiratory system
hair
/
mucus
in nostrils and
trachea
ciliated
epithelium
and
goblet
cells
expulsive
reflexes (coughing and sneezing)
Primary defence in skin
skin made of
keratin
-strong and
waterproof
vector
organisms can break this skin
infection triggers
clotting
Clotting process in skin
endothelium
is damaged
platelets
exposed to outside
proteins
and are activated, triggering blood clotting
plug
is formed over damaged area
releases clotting factor chemical
thromboplastin
thromboplastin
+
Ca2+
in blood act on protein
prothrombin
-> enzyme
thrombin
thrombin
acts on soluble
fibrogen
forming insoluble
fibrin
forms
mesh
, trapping RBCs ->clot
activated platelets release chemical
histamine
causing
smooth
muscle cells in blood vessel wall to contract,
narrowing
blood vessel
reducing
blood flow to area
Blood clots form
scabs
on skin surfaces
protects
underlying tissue from pathogens whilst
healing
occurs
skin cells under scab
divide
and
repair
tissue damage
Inflammation
damaged tissue activates
mast
cells, releasing
histamine
causes nearby blood vessels to
vasodilate-
increasing blood supply to infected area
causes a
temperature
increase, reducing pathogens ability to
reproduce
blood vessel walls become more
permeable
, more blood
plasma
and
WBCs
leave blood forming
tissue
fluid causing nearby cells to
swell
Damaged tissues release
Mast
cells which release
cytokines
:
attract
phagocytes
to damaged tissue for
phagocytosis
trigger the
hypothalamus
, raising
body
temperature, reducing pathogens ability to
reproduce
-
fever
First line of secondary defence is
phagocytosis
- specialised cells engulf pathogens and destroy them:
phagocytes
neutrophils
macrophages
Antigen
-
glycoprotein
on
plasma membrane
of pathogen that
triggers
and
immune response
Opsonins
- bind to
antigen
on surface of
pathogen
allowing
phagocytes
to bind
Phagocytes
-specialised cells in blood/tissue fluid that engulf and digest pathogens
neutrophils
(phagocyte)-
WBC
that engulf foreign matter and traps it in a
phagosome
which fuse with
lysosomes
to digest
Macrophages
are
antigen
presenting cells and travel as
monocytes
Macrophages -
engulf pathogen via
endocytosis
antigens
are saved and moved to special
protein
complex on macrophage surface
becomes an
antigen-presenting
cell
exposes antigen to
immune
system for recognition
protein
complex prevents the cell from being identified as
foreign
Cytokines
stimulate the
differentiation
of macrophages,
B
and
T
lymphocytes
Phagocytosis process by neutrophils
opsonins
bind to antigens
phagocytes recognise and bind to
opsonin
by
chemotaxis
phagocyte
engulfs
pathogen by
endocytosis
, forming a
phagosome
lysosomes
fuse with
phagocytic
vacuole
releasing
hydrolytic
enzymes into it
digestion and killing of pathogen
Phagocytes specialisations:
receptors on plasma membrane that bind to
opsonin
or
antigen
lobed
nucleus that allows that allows cell to squeeze through
narrow
gaps
well developed
cytoskeleton
- cells changes
shape
to engulf pathogen and
move
lysosomes/ vacuoles in the cell
many lysosomes
many
mitochondria
to release energy from glucose
many ribosomes to synthesise
enzymes
needed
Blood smear
A)
Platelet
B)
RBC
C)
neutrophil
D)
neutrophil
E)
monocyte
F)
lymphocyte
6
B
lymphocytes form and
mature
in the
bone marrow
T
lymphocytes form and
mature
in the
thymus
gland
T cells have complementary
receptors
on their surface that bind to specific
antigens
Differentiation of T cells:
T
helper
cells
T
killer
cells
T
memory
cells
T
regulator
cells
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