communicable diseases
pathogen
microorganisms that cause disease
for a microorganism to be considered a pathogen
• gain entry to the host
• colonise the tissues
• resist the defences
• cause damage
tuberculosis
• bacteria
• inhaling droplets from coughs and sneezes
• high temp, tiredness, weight loss
meningitis
• bacteria
• infection of the brain
• high fever, red rash that doesnt fade, stiff neck
• treated with antibiotics
ring rot (potatoes)
• bacteria
• direct contact
TMV
• virus
• contaminated tools
• damages leaves, stunts growth
HIV
• virus
• weakens ur ability to fight infections
• sharing needles, having sex without a condom
• AIDS - progressive damage to immune system
influenza
• virus
• coughs and sneezes
• high temp, cold-lile symptoms, headache
malaria
• protist
• vector
• high temp, headaches, vomiting
potato/tomato blight
• protist
• rain washes spores into soil, spores can travel in the wind
black sigatoka (bananas)
• fungus
• premature ripening, yield losses
• removing leaves, fungicides
ring worm
• fungus
• red or silvery ring-like rash
• tiny spores
athletes foot
• fungus
• scaly flaky dry skin
• antifungal medecine
direct transmission (animal)
• direct contact - kissing and body fluids, skin to skin contact
• inoculation (into blood) - animal bite, sharing needles
• ingestion - contaminated food or water
indirect transmission (animal)
• fomites - bedding, socks, cosmetics
• droplet infection - inhalation of droplets from coughs or sneezing
• vectors - mosquitoes, rat fleas
direct transmission (plant)
direct contact - of a healthy plant with a disease plant
indirect transmission (plant)
vector - soil contamination, water, spores
what increases probability of catching disease (animal)
• weakened immune system
• poor hygiene and sanitation
• overcrowding
what increases probability of disease (plant)
• overcrowding
• lack of suitable minerals
• climate change
physical plant defenses against disease
• cellulose cell wall
• callose production - blocks the flow in sieve tube
• stomatal closure
tylose formation
balloon like swelling fills xylem vessel. prevents spread through heartwood
necrosis
deliberate cell suicide, limits pathogens access to water and nutrients, prevents it spreading
chemical plant defences
insect repellent
insecticides
antifungal compounds
toxins
blood clotting
• platelets come into contact with collagen in skin and begin secreting several substances
• serotonin - makes smooth muscle in the wall of blood vessels contract - reduces supply of blood to area
inflammation
mast cells release histamine and other cytokines, this causes blood vessels to dilate, causing heat and redness, walls of the capillaries become leaky forcing WBC and anitbodies out of capillary -> swelling + pain
why is inflammation useful
brings more phagocytes and other WBC to site of infection
fever
reduces pathogen ability to reproduce quickly
two types of phagocytes
neutrophils: multi lobed (weird shape)
macrophages
process of phagocytosis
1. phagocytes respond to cytokines and chemicals released by pathogen
2. phagocytes receptors bind to the pathogen
3. pathogen gets engulfed into a phagosome
4. lysosomes move towards phagosome and fuse the form a phagolysosome
5. hydrolytic enzymes digest and destroy pathogen
macrophage
combines antigens from pathogen self-surface membrane called MHC
MHC becomes antigen presenting cell APC
opsonins
chemicals that bind to pathogens and tag them so they are more easily recognised by phagocytes
cytokines
cell signaling molecules informing phagocytes that body is under attack
antibodies
find to a specific antigen which are complementary in shape
antibody
quaternary structure
4 polypeptide chains
antibody label
antigen binding site
variable region
constant region
hinge region - allows flexibility so antibody can bind to more than one pathogen
disulfide bridge
how do antibodies defend the body
• bind to antigen -> form antibody antigen complex, act as opsonins
• immobilises pathogen -> no longer invade host cells
• act as agglutinins causing pathogen to clump together
• act as anti-toxins and bind to the toxins
T helper cells
release interleukins, stimulate B cells to develop, stimulate phagocytosis
t killer cells
attack and kill infected body cells, produce perforin - damages cell membranes of pathogen
t memory cells
recognise pathogens from previous infections
lymphocytes process
1. macrophage engulf pathogen, brcome APC
2. receptors on t helper cells fit antigens, become activated, release interleukins, stimulate more t helper cells to divide
3. cloned t helper cells may develop into memory cells
B lymphocytes
have antibodies on cell surface membrane
B cell becomes APC by binding to antigens engulfing and processing it
clonal selection
activated t helper cell binds to B cell APC
clonal expansion
interleukins are released by activated t helper cell, which activates B cell to divide by mitosis
primary and secondary immune response
B cells produce memory cells as well as plasma cells - primary
takes time due to clonal selection amd clonal expansion
response is quicker - secondary, number of antibodies increase rapidly to hire concentration and for longer
autoimmune disease
where the bodies own WBC attack and destroy their own cells as they wrongly recognize them as foreign
natural active immunity
long term
takes time
chicken pox
natural passive immunity
immediate protection
antibodies from mother
short term
breast milk or placenta
artificial active immunity
long term
takes time
vaccination
artificial passive immunity
immediate protection
short term
injection with antibodies
vaccinations
preparation of antigen
injected inhaled or given by mouth
stimulates primary immune response
herd immunity
use a vaccine to provide immunity to all of the population at risk
ring immunity
vaccinate everyone in surrounding area to prevent transmission of disease
medicines
penicillin - mould
aspirin - willow bark
digitalis - fox gloves