Module 4.1 Flashcards
Communicable diseases
Different types of pathogens
Viruses
Protoctista
Fungi
Bacteria
What type of pathogen is tuberculosis
Bacteria
What type of pathogen is ring rot
Bacteria
plants
What type of pathogen is HIV/AIDS
virus
humans
What type of pathogen is influenza
Virus
animals
What type of pathogen is tobacco mosaic virus
Virus
plants
What type of pathogen is malaria
Protoctista
What type of pathogen is potato/tomato late blight
Protoctista
What type of pathogen is black sigatoka
Fungi
Bananas
What type of pathogen is athlete’s foot
Fungi
Human
Means of direct transmission
Spores (in the air or on surfaces)
Droplets in the air
Direct contact physical contact (touching infected person, body fluids or contaminated surface)
Faecal-oral transmission (eating or drinking contaminated things)
What is a vector
Another organism that is used by a pathogen to gain entry to a primary host
What is indirect transmission
Transmission using a vector
What is direct transmission
Transmission that does not involve a vector
Primary non-specific defences against pathogens
Mucous membranes
Blood clotting
Wound repair
Inflammation
Expulsive reflexes
Skin
How mucous membranes help to prevent infection
Goblet cells secrete mucus
Pathogens get trapped in the mucus
Cilia waft the mucus with the pathogens in it upwards out of the lungs to the oesophagus to be swallowed to be killed in the acidic stomach
How blood clotting prevents infection
When blood vessels are damaged platelets release substances that via a cascade of events result in the formation of fibrin which forms a network trapping platelets and forming a clot
Creates a barrier to pathogens so they cannot enter the damaged tissue/blood and stops blood loss
How inflammation helps prevent infection
Mast cells detect the presence of pathogens and release histamine
Histamine makes capillaries more leaky so more tissue fluid can enter the infected area
Allows more WBCs mainly neutrophils to enter the area and begin to digest pathogens
Histamine also causes vasodilation of the arterioles leading to the infection site so more blood containing WBCs can enter the capillaries
How expulsive reflexes help prevent infection
Vomiting forces pathogens out of the stomach if they have been consumes
Sneezing and coughing forces pathogens out of the airways and helps to push the mucus containing pathogens out of the body/down the trachea
How skin prevents infection
Barrier to pathogens as the cells at the surface are no longer alive after being keratinised
How wound repair prevents infection
Closes the skin to create a complete barrier to infection
Scab dries and shrinks drawing sides of cut together
temporary seal created then skin is repaired
What are the types of phagocytes
Neutrophils and macrophages/antigen-presenting cells
Mode of action - neutrophils
Recognise foreign antigens on the pathogen
neutrophil binds to opsonin on the antigen of the pathogen
pseudopodia form extension of the plasma membrane around the pathogen
plasma membrane fuses around the pathogen placing it in a phagosome
Lysosomes fuse with the phagosome releasing their hydrolytic enzymes into the phagosome
Pathogen is digested
Products of digestion can be absorbed into the cell
Mode of action - macrophages/antigen presenting cells
Initiate the specific immune response
Same as neutrophil but antigens are not digested MHC/antigen complex is exposed on the surface of the cell
Antigen presenting cell is formed
Exposes the antigen so other cells of the immune system can recognise the antigen
What are opsonins
Protein molecules that attach to the antigens on the surface of a pathogen
Enhance the ability of phagocytic cells to bind to and engulf pathogens
Social factors affecting transmission
Overcrowding
poor ventilation
Poor health e.g. HIV makes it more likely to contract other diseases
Poor diet
Homelessness
Living or working with people who have migrated from an area where a disease is more common
Effect of warm climate on disease
Many bacteria, Protoctista and fungi grow and reproduce more rapidly in warm and humid condition so are more common in warmer climates
There is a greater variety of diseases found in warmer climates so plants and animals in these climates are more likely to become infected
Effect of cool climates on disease
Cooler climates may damage or kill pathogens or just reduce their ability to grow and reproduce making disease less common
Why is blood clotting needed
When the skin is not complete from lacerations and abrasion it opens the body to infection
If blood vessels are damages it could lead to excess blood loss
Why mucous membranes are needed
Exchange surfaces are very thin so are less protected
How to recognise neutrophils
Multilobed nucleus
How do macrophages travel in the body
Travel in the blood as monocytes
Settle in organs or lymph nodes then develop into macrophages and travel in lymph
How to recognise lymphocytes
Smaller with a large nucleus
how antigen presentation helps
antigen-presenting cells move around the body and can come into specific cells that activate the full immune response (T and B lymphocytes)
there may only be one T and B lymphocyte with the correct recognition site for the antigen so the more antigen presenting cells there are the more chance there is the antigen will come into contact with them
what cells are produced in the immune response
T helper cells
T killer cells
T memory cells
T regulator cells
plasma cells
B memory cells
why is cell signalling important in the immune response
specific immune response involves coordinated action of a range of cells
to work together effectively the cells need to communicate
What are interleukins
released by T cell and macrophages
stimulate clonal expansion and differentiation of B and T cells
what are autoimmune disease
the immune system attacks a part of the body
auto immune disease example
arthritis
mode of action of T-help cells
have receptors on the plasma membrane which bind to specific antigens presented by macrophages
when bound they become activated
role of T-helper cells
produce interleukins which also stimulates
activation of B cells (increase antibody production)
production of other types of T-cells
attracts and stimulates macrophage to ingest pathogens with antigen-antibody complexes
mode of action B lymphocytes
have antibodies on plasma membrane
antigens bind to antibodies to activate B-cells
role of B cells
once activated B-cells divide by mitosis to form B plasma cells
role of plasma cells
produce large amounts of antibodies which they secrete by exocytosis
have large RER for protein synthesis (antibodies)
role of T killer cells
when exposed to infected cells they release cytotoxins which enter the cytoplasm of target cells and trigger apoptosis
what is clonal selection
the activation of the specific B and T lymphocytes when the specific antigen comes into contact with the receptors on their plasma membranes
What is clonal expansion
Once the correct lymphocyte is activated they increase in number by mitotic divisions to become effective
what are antigens
proteins or glycoproteins
stimulate immune response
body recognises antigens as foreign or self
foreign antigens stimulate antibody production
how many polypeptide chains make up an antibody
4
what are the 2 region of antibodies
constant region (same in all antibodies)
variable region (specific shape to be complimentary to antigen)
role of the hinge region in antibodies
allows flexibility so molecule can grip more than one antigen
what types of poly peptide chains are in an antibody
light chain and heavy chain
what holds the polypeptides together in antibodies
disulfide bridges
what are the ways antibodies work
Opsonins
Agglutinins
Anti-toxins
how do opsonins work
bind to antigens on pathogens
then act as binding site for phagocytic cells to more easily bind and destroy the pathogen
or can neutralise pathogen by binding to antigen used to attach to host cell
how do agglutinins work
as antibodies have 2 binding sites they can join separate pathogens
clumps the pathogens together
stops pathogens from entering cells
more easily engulfed by phagocytes
how do anti-toxins work
renders toxins released by pathogens harmless
what is the primary immune response
when and infecting agent is first detected and the immune system starts to produce antibodies but it takes a few days for the number of antibodies to ride to a level that can effectively combat the infection
once the pathogen is dealt with the number of antibodies drops rapidly
what is the secondary immune response
if the body is infected a second time by the same pathogen B and T memory cells recognise the antigen and make the immune response much quicker
antibody production starts sooner and is much faster
role of T memory cells
cells that remain in the blood to provide long term immunity
role of B memory cells
cells that remain in the blood to provide long term immunity
what are vaccinations
a way of stimulating the immune response to achieve immunity to a specific pathogen
what is herd vaccination and herd immunity
using a vaccine to provide immunity to all or almost all of the population
once enough people are immune the disease can longer be spread through the population
what is ring vaccination
when a new case of a disease is reported vaccines are given to all the people in the immediate vicinity of the new case to control the spread of disease
why do vaccination programmes change
if a disease has been eradicated or reduced to very low levels that it is unlikely to spread the vaccination programme can be relaxed
why do vaccines change
some pathogens can undergo genetic mutations which change their antigens meaning the vaccine has to change
what is active immunity
the immune system is activated and produces its own antibodies
what is passive immunity
when antibodies are supplied from another source e.g. mother to baby
what is natural immunity
achieved through normal life processes
what is artificial immunity
achieved through medical intervention
what are the possible sources of new medicines
accidental discovery
traditional remedies
observation of wildlife
plants
research into disease causing mechanisms
personalised medicines
plant medicine examples
morphine (unripe poppy seeds)
willow bark pain and fever relief
microorganism medicine examples
penicillin
personalised medicine
sequencing genes from individuals with a particular condition and developing drugs for that condition
antibiotics benefits
less deaths from infection after wounds or surgery
antibiotics risks
antibiotic resistance e.g. MRSA
plant physical defences
cellulose cell wall
waxy cuticle
bark
lignin thickening of cell wall
what is callose and how does it help plants
large polysaccharide deposited in the sieve tubes at the end of growing season around the sieve plates blocking the flow in the sieve tubes
can prevent a pathogen spreading around the plant
chemical defences in plants
chemicals such as terpenoids, phenols and hydrolytic enzymes in the plant tissues have anti pathogenic properties
why are chemical defences slow in plants
production of chemical requires a lot of energy so many are not produced until the plant detects an infection
active plant defences
thickening and strengthening cell walls with additional cellulose
callose deposits near the invading pathogen
increase chemical production
