Module 4: Communicable diseases Flashcards
Examples of bacteria
Tuberculosis
Bacterial meningitis
Ring rot (potato and tomato)
Examples of Virus
HIV/AIDS
influenza
Tobacco Mosaic Virus (plants)
Examples of protoctista
Malaria
potato blight
Examples of fungi
athletes foot
ring worm
black Sigatoka
Direct transmission examples
Droplet-sneezing
Physical contact- infected animal brushing against an uninfected animal
Faecal-oral- consumption of food or water with traces of faeces from infected animal
Spores- can resist extremes of temperature, pH, and even strong disinfectants
Indirect transmission
Vector transmission mosquito is vector parasite present in mosquito saliva infected mosquito bites human parasite passes from saliva to blood
Effect of climate and environment
Climate
Some vectors only live in hot climates and many viruses, protoctists and bacteria survive better in warm climates
Very cold climates can kill pathogens
Environment
Cramped and crowded environments are conducive to spread of disease-droplet infection and contact infection rate likely to be higher
Dirty environments harbour pathogens-this is likely to cause the spread of faecal-oral pathogen spread
Physical defences
Cellulose cell wall
Stomatal closure
Callose – large polysaccharide that is deposited in the sieve tubes which blocks the flow in the tube. This can prevent a pathogen spreading around the plant
Tylose formation – balloon like swelling that fills the xylem vessel, when fully formed it can completely block off that part of the xylem vessel.
Chemical defences
terpenoids phenols alkaloids hydrolytic enzymes. some of these chemicals are present before infection. However, because the production of chemicals requires a lot of energy, many chemicals are not produced until after an infection is discovered.
Primary defences against pathogens in animals
Skin:
Epidermis secretes sebum to waterproof skin and keratin secreted, toughening skin
Blood clotting and skin repair:
Abrasions damage the skin and open the body to infection
The body prevents excess blood loss by forming a clot and making a temporary seal to prevent infection
As the skin grows and the scab shrinks the edges of the abrasions are pulled together.
Inflamation: the tissue may be hot and painful as the presence of harmful microorganisms has been detected by mast cells which release histamine which causes vasodilation to make the capillary walls more permeable to white blood cells and proteins.
Coughing and sneezing:
Reflexes that expel pathogen trapped in mucous
Mucous membranes:
Present at most interfaces between body and external environment and secrete sticky mucus and lysosomes enzymes
Structure and mode of action of phagocytes
Two types:
Neutrophils- Multi-lobed nucleus which enhances flexibility of cell released in large quantities
Macrophage
Phagocyte mode of action:
Phagocyte envelopes and engulfs the pathogen and membrane folds inwards
Pathogen is trapped inside in phagosome
Lysosome fuse with the phagosome forming phagolysosome
Release enzymes-lysins which digest the bacterium
Products of the digestion are entirely harmless
Nutrients can then be absorbed into the cytoplasm or exocytosed into extracellular fluid
B and T Lymphocytes
White blood cells with specialised receptors which produce antibodies
B Cells can be:
Plasma cells- Circulate in blood and produce and secrete antibodies into circulation
B memory cells- Remain in the body for many years after the initial infection and serve to ‘remember’ the antigen
T Cells can be:
T helper cells- Release cytokines, stimulate B cell maturation and promote phagocytosis
T killer cells- Identify and kill infected host cells
T regulator cells- Recognise when the pathogen has been removed and is no longer a threat and alerts the rest of the immune system that it no longer needs to be active
Structure of antibodies
4 polypeptide chains held together by disulphide bridges
Constant regions, which remains the same
Variable region which changes
Hinge regions, which allow for flexibility
Function of antibodies
Attach to antigen on pathogen
Blocks binding site, preventing pathogen from binding to host cells
3 types:
Agglutinins- large antibody can bind many pathogens together
Antitoxins-antibodies can also bind to toxins released by the pathogens, rendering them harmless
Opsonins-antibodies can label the pathogens as foreign to phagocytes which speeds up the process of phagocytes identifying antigens
Active immunity
Artificial
Immunity provided by antibodies made as result of injection
Person injected with weakened virus, activating the immune system
Natural
Immunity provided by antibodies made in immune system as a result of infection
Person suffer from diseases only once, then is immune
