module 4-communicable diseases Flashcards
communicable diseases
caused by bacteria
viruses
protists
fungi
bacteria
has cell walls.
gram positive=purple blue
gram negative=red
pathogens
damage host cells.
viruses-take over cell metabolism.
fungi-damage cell.
produces toxins, and provide damage to host cells.
plant diseases
ringrot, toabic moasic virus, potato blight, black sigatoka,
ring rot
bacterial disease of potatoes, tomatoes, and caused by bacterium,
damages leaves, fruits.
tobaic moasic virus
infects plants and other species.
no cure.
potato blight
fungus like proticist.
no cure.
black sigatoka
banana disease caused by fungus.
cause reduction in yield.
animal diseases
TB, bacterial meningitis, HIV, influenza, malaria, ringworm, atheles foot.
TB
bacterial diseases
damages lung tissue
suppresses immune system
bacterial megingitis
bacterial infection affecting membrane of brain. if spread to rest of body, can cause blood poisoning and sudden death.
CURED-if antibiotics given in good time
HIV/aids
target T helper cells in immume system, by destroying it,
passed through body fluids.
no vaacine and cure.
influenza
viral infection of cells in gas exhcange, by killing cells, can lead to secondary infection.
can be vetal.
has 3 streps.
malaria
caused by protcista, has complex life cycle
invades red blood cells, liver and brain.
ringworm
fungal disease affecting mammals, dogs, causes circular areas of skin
direct transmission-animals
direct contact
inoculation-breaking in skin
indigestion
indirect transmission-animals
bedding, socking
droplets
vectors-transmit via hosts
factors affecting transmission
overcrowding
poor nutrition
poor disposal of waste.
direct transmission-plants
direct contact
indirect transmission-plants
soil contamination
vectors, wind water animalsp
plants defence against pathogens-recongising an attack
1)receptors in cells respond to molecules.
2)releases signalling molecules, which switch genes in nucleus.
3)starts producing defensive chemicals, sneding signalling and physically strengthen cell wall
physical defences of plants
produce high levels of callose, goes between cell walls, and acts as barriers.
lignin added, as mechanical barrier to invasion,
block sieve plates, seal of infected part.
callose-seals of healthy/prevent spreading.
non specific animal defences.
keeping pathogen out. skin covers body, so no entrance of pathogens.
lined by mucous membranes, secrete sticky mucus, which traps organisms.
also has lysozymes which destroys fungal and bacteiral cell walls.
lysozyme-acid in stomach
blood clotting
enzyme triggering cascade of reactions resulting in blood clots.
make smooth muscle contract, reduces blood.
clot dries, forms tough, hard scab, so epidermal cell grows, which forms a scab slough.
inflammory response
mast cells activated, releases histamines and cytokines.
histamines
more blood vessels dilate, make red. high yemp=prevents pathogens reproducing, so more blood plasma goes out
cytokines
attracts phagocytes, as can get removed by phagocytosis.
getting rid of pathogens
fever
phagocytosis
fever
pathogen invades body cytokines, stimulate hypothalamus. pathogens reproduce best at lower than 37. specific immune system works better at higher temperatures.
phagocytosis
phagocytes are specialised white blood cells, they enfulf and destroy pathogens. two types=macrophages, and neutohpills
steps of phagocytosis
produce chemical atrracting phagocytes.
these recongise non human proteins, and enulfs it to vacuole.
FORMS PHAGOSOME. this combines with lysozyme=PHAGOLYSOZYME.
Cytokine
cell signalling molecules
to inform body if body is under attack.
opsonins
chemicals binding to pathogen, so easily recognised by phagocytes.
antibodies
y shaped glycoprotein,
bind to specific antigen.
2 identical long polypepticide chain, held by disulfide bridges
hinge region
2 binding sites.
antigen antibody complex
antibody binding to antigen.
hinge region
flexability in antibiotics.
how antibodies defend body
antibodies act as opsonin, complex is englufed and digested.
most pathogens no longer invade.
act as aggulutins,
aggulutins
pathogens clumping together, so easily engulfed.
helper cell
produces interleukins (cytokine),
stimulate activty of b cells,
more antibiotics,
killer cell
destroy pathogen carrying antigen
memory cell
live for long life, if meet again, rapidly formed
regulator cell
suppress immune system, when pathogen is killed.
b lympocytes
plasma=antibodies to antigen
effector-divide to form clones of plasma
memeoryc
cell mediated immunity
cells changing in a way, mutation or inside cell ext.
1)macrophage engulf/digest pathogens
2)receptors in t helper cell fit antigen, produce interlukins, more cells produced by mitsosi, these van develop to t cell memory, or interleukins for phagocytisis.
humoral immunity
outside cell
1)activated t cell bind to cell. clonal selection meetx correct t cell
2)interleukins activates b cell, divided by mitosis to give clones-CLONAL EXPANSION
3)produce antibodies
=disable them
=act as opsonins/aggulations
some b cells become memory=secondary immume
autoimmume disease
immume system attacking healthy tissue
type 1 diabetes
arthisis
lupus
natural active
infection with pathogen
natural passive
antibodies from mum
artificial active
vaacination
artificial passive
injecting antibodies.
