Biology Paper 2 - 4.1 Communicable Diseases

An organism that causes disease.

Bacteria, viruses, fungi and protoctista.

A disease that can spread between organisms.

Tuberculosis, bacterial meningitis and ring rot.

HIV, influenza and Tobacco mosaic virus.

Athletes foot, ringworm and Black sigatoka.

Malaria and late blight.

Indirect transmission requires an intermediate to transmit one disease from one organism to another. Direct transmission does not.

Direct – droplet infection (coughing or sneezing tiny droplets of mucus or saliva directly onto someone), sexual intercourse.
Indirect - intermediates include air, water, food or another organism (known as a vector).

Living conditions – overcrowding and poor ventilation will increase transmission rates.
Climate – wet summers increase transmission of diseases that need water to spread.
Social factors - poverty will reduce access to drugs for treatment. Poverty will also reduce access to healthcare means you will be less likely to be diagnosed. Both are factors that will increase transmission.

Does not distinguish between one type of pathogen and another.
Responds to all in the same way.
Acts immediately.
Two forms: a barrier to the entry of pathogens or phagocytosis.

Skin – physical barrier, blocking pathogens from entering; chemical barrier, producing antimicrobial chemicals and lowering pH to inhibit the growth of pathogens.
Mucus membranes – protect body openings exposed to the environment. Cells produce mucus, mucus traps pathogens, ciliated cells move the mucus.
Blood clotting – a blood clot is a mesh of (insoluble) fibrin fibres. Plug wounds to prevent entry and blood loss; formed by a series of chemical reactions that take place when platelets are exposed to damaged vessels.
Inflammation – swelling, pain, heat and redness. Triggered by tissue damage. Chemical signals (histamine) released which increase the permability of blood vessels, making them leak fluid to the surrounding area. The resulting swelling isolates any pathogens that may have entered damaged tissue. Signals also cause vasodilation, increasing the blood flow to the damaged area – making area hot and brings WBC to the area to fight off any pathogens.
Wound repair – the outer layer of skin cells divide and migrate to the edges of the wound. The tissue below the wound then contracts to bring the edges closer together. Collagen fibres aid the repair process – too many result in a scar.
Expulsive reflexes – expel foreign objects (including pathogens) from the body. Sneezing and coughing – irritation in the nasal passage or the respiratory tract.

Pathogen is recognized as foreign.
Pathogen is engulfed by the phagocyte.
Forms a phagosome.
Lysosome fuses with phagocyte and releases enzymes and lysins.
These enzymes break down the pathogen by hydrolysis.
Macrophages present antigen on surface and present to specific immune system – called antigen presenting cells (APC).

Phagocytes are able to break down many different pathogens.

Neutrophils, Monocytes and Macrophages.

Neutrophils have a lobed nucleus so can squeeze through the walls of capillaries into the tissue fluid.

Kidney-shaped.

Pathogen engulfed by phagocytes, antigen presented on its cell surface by antigen presenting cells (APC).
T-helper cells with complementary receptor bind to antigen on surface of APC.
This activates the T cell - this is called clonal selection.
Activated T-helper cell divides by mitosis (clonal expansion) into clones.
The T cell clones differentiate into: T-helper cells, T-killer cells, T-regulatory cells and T-memory cells.
T helper cells release interleukins (a type of cytokine) that bind to receptors on B cells and activates B cells.

T helper cells – release interleukins to activate other cells.
T killer cells – attach and kill cells infected with the specific pathogen.
T regulatory cells – suppress the immune response from other WBC – preventing the immune system from attacking itself.

When a B-cell meets a pathogen with a specific antigen that is complementary to its specific cell surface receptor – it binds to it.
This, together with the interleukin signal (from activated T cell) activates the B cell – B cell clonal selection.
The activated B cell divides by mitosis (clonal expansion) into B cell clones.
Some clones differentiate into plasma cells and others into B memory cells.
Plasma cells secrete many antibodies into the blood. All are specific to the antigen.

Opsonins bind to the antigen on a pathogen and aid phagocytosis.
Agglutinins – each antibody has two binding sites and so can bind to two pathogens at the same time. Agglutination clump pathogens together and immobilises them – aiding phagocytosis.
Anti-toxin antibodies bind to toxins making them harmless.

Constant region is the part that attaches to the cell-surface membrane and is the same in all antibodies.
Variable region is unique in each antibody – this region has is specific to each antigen – it is complementary shape to the antigen.
Hinge region is flexible and allows the antibody and antigen to fit together.
Disulphide bridges – hold polypeptide chains together to maintain the quaternary structure.

Memory cells are made during the primary immune response. They remain in the body for a long time.
Memory T cells remember the specific antigen and will recognise it a second time round.
Memory B cells remember the specific antibodies needed to bind to the antigen.
Memory B cells quickly divide into plasma cells and quickly produce many antibodies that are specific to the antigen.
Both memory cells quick divide and go into clonal expansion.
The secondary response is much quicker and stronger

The body does not recognise self-antigens and launches an immune response against its own tissues. Causes pain and inflammation.
Lupus – is when the immune system attacks connect tissues.
Arthritis – is when the immune system attacks cells in the joints.

Antigens are injected.

Injection of antigen or attenuated / weakened / dead form of the pathogen.
Triggers an immune response.
Injected antigens are engulfed by phagocytes and the antigens are presented to the immune system by APC.
T cell selection – activation – T cell expansion (cloning) by mitosis.
Secretion of cytokines.
Activation of B cells – B cell clone by mitosis – production of plasma cells which produce antibodies and B memory cells.
Memory cells remain in the body – upon secondary response these cells remember the specific antigen.
This results in the secondary response being quicker and greater to infection resulting in no symptoms when infected.

Vaccinate most people to stop the infection spreading within a population.

Vaccinate all people around a victim to contain the spread of infection.

Passive.
Before - Antibodies cross the placenta.
After – Antibodies present in breast milk.

Bark - physical barrier and contains tannins (chemical barrier) which inhibit digestion in insects.
Waxy cuticle – stops water collecting on the leaf, reducing indirect transmission.
Cellulose cell wall – makes it harder for pathogens to get inside the cell.
Lignin thickening of cell walls - waterproof and almost completely indigestible.
Stomatal closure - guard cells close when pathogens are detected in that part of the plant.

To block the flow of phloem to prevent a pathogen spreading around a plant.

When a plant is stressed (e.g. pathogen invasion) – callose strengthens the cell walls and blocks the plasmodesmata.

Healthy cells around an infection commit suicide to prevent the infection spreading throughout the plant.

Antimicrobial chemicals inhibit pathogen growth.

| Tannins are toxic to insects.

New drugs often originate from plants. Biodiversity is reducing - due to deforestation of the rainforest for crop growth.
Note – always name the habitat lost and state the reason for habitat destruction.

The plants used have already been identified at having potential medicinal benefits.
Reduces cost - saves time and effort and often has few side effects.

They are tailored to an individual’s DNA.

| Genetic information is used to predict individual responses to different drugs.

Uses technology for design and synthesis of new medicines.

Genetic mutations make some bacteria naturally resistant to an antibiotic.
Extensive use of antibiotics in hospitals provide a selective pressure, to which resistant bacteria have a selective advantage as they are better able to survive in a host even if treated with antibiotics.
Resistant bacteria survive and pass the resistant allele to many offspring.
Resistant allele becomes more common in a population of bacteria over time - the allele frequency increases.

Meticillin-resistant Staphylococcus aureus.

The digestive system – usually causes problems for people after antibiotic treatments. C. difficile is resistant and so flourishes in the gut at this time.