Communicable diseases

• 4 Types of pathogens

  Virus, Bacteria, Fungi and Protista
• Bacteria

  Causes tuberculosis, bacterial meningitis and ring rot in potatoes/tomatoes.

  Once bacteria enters a host cell it releases toxins and prevents the nearby cells from functioning normally.
• Virus

  Causes HIV/AIDS, influenza and tobacco mosaic virus.

  Viruses are non living and cannot reproduce outside a host cell.

  They attach to the host cell, passing through the cell membrane and uses its enzyme to copy itself and reproduces within other cells in the host.
• Protoctista

  Causes malaria in mammals and potato/tomato late blight.

  They act as pathogenic parasites in humans.
• Fungi

  Causes black sigatoka in bananas, ringworm in cattle and athletes foot in humans.

  They obtain nutrients by releasing enzymes and digesting material around them where products of digestion are absorbed back into fungal cells causing damage to host cells. They release spores in the process causing it to spread.

  In plants they can reduce the rate of photosynthesis by damaging theri leaves, reducing the yield of plant crops.
• Direct transmission of communicable diseases in plants

  >pathogens in the soil infect plant by entering their roots especially if they are damaged by replanting or the weather.

  >fungi spores produced asexually and sexually are carried in the wind causing airborne transmission.

  >pathogens infect the vascular tissue so are carried to and from soil to infect other plants.

  >They can enter seeds which are distributed, so offspring is infected.
• Indirect transmission of communicable diseases in plants


  >result of an insect attack

  >spores and bacteria become attached to a burrowing insect that attacks plant, acting as a vector
• Direct transmission of communicable diseases in animals

  Social factors, overcrowding, poor ventilation, poor health and diet, homelessness, connection with people who have migrated from disease-heavy area.
• Indirect transmission of communicable diseases in animals

  Infect via a vector

  A vector - an organism used by a pathogen to gain entry to the primary host
• How does the climate affect diseases

  Diseases are found in warmer regions as they grow and reproduce more rapidly in warm, moist conditions.
• Physical defences against pathogens in plants Pt.1

  > cellulose cell wall and bark contains chemical defences

  > lignin cell walls are waterproof and indigestible

  > waxy cuticles prevent water collecting on cell surfaces reducing pathogens ability to survive

  > stomatal closure is employed when pathogens are detected
• Physical defences against pathogens in plants Pt.2

  > Callose is a large polysaccharide deposited in cell walls reinforced with lignin creating a thick barrier for pathogens.

  When pathogens are detected, callose blocks sieve tube end plates in the phloem preventing the spread of the infected area.

  It also blocks the plasmodesmata between infected and nearby cells.

  >Tylose fills the xylem vessel preventing the spread of pathogens and contains a high concentration of toxins that fight pathogens.
• Chemical defences against pathogens in plants

  Chemicals are usually produced after a plant develops an infection and requires lots of energy.

  >Tannis create a bitter taste and enzymes precipitate out, not allowing tree to get infected

  >Insect repellent like pine resin and lemongrass

  >Antibacterial compounds disrupt the cell wall and membranes of the bacteria

  >Hydrolytic enzymes like Chitinases are released to break down the chitin in the cell wall

  >Anti-oomycetes break down the cell walls on fungi like eukaryotic organisms

  Silica in grass - influences growth of organisms when eaten
• Primary non-specific defences against pathogens

  > in digestive system: hydraulic acid, mucus lining of stomach and lysosme enzymes in saliva and tears

  > in respiratory system: hair/mucus in nostrils and trachea, ciliated epithelium and goblet cells, expulsive reflexes (coughing/sneezing)

  > in the skin: skin made of keratin which is strong and waterproof only vectors can break this, clotting processes to form a scab

  >inflammation

  >mucous membranes
• Clotting process in skin

  >Endothelium is damaged and platelets in blood are exposed to proteins outside.

  >Platelets are activated, triggering a blood clotting and a plug is formed over the damaged area.

  >This releases the clotting factor chemical thromboplastin. This and Ca2+ in the blood act on the protein prothrombin and forms the active enzyme thrombin.

  >Thrombin acts on the soluble blood protein fibrogen which catalyses the formation of the insoluble fibrin, which forms a mesh trapping red blood cells, creating a clot.

  >Activated platelets then release the chemical histamine.
• Why do activated platelets release histamine during blood clotting?

  Its activation causes smooth blood vessels in the vessel wall to contract, through vasoconstriction, narrowing the blood vessel to reduce blood flow to the open area.
• Why does a clot dry to form a scab on the skins surface?

  The scab protects underlying tissue from pathogens whilst the wound healing takes place. Under this, skin cells divide and repair the damage.
• Primary defence against pathogens using inflammation

  > damaged tissue(s) activate mast cells which release histamine.

  > this causes vasodilation in nearby blood vessels increasing blood supply to infected area, causing a temperature increase / fever, which reduces the pathogens ability to reproduce and survive.

  > histamine also causes blood vessel walls to become more permeable, allowing more blood plasma to leave the blood and form tissue fluid causing nearby cells to swell.
• How does the body know to increase its temperature in primary response to pathogens

  > damaged tissues activate mast cells which release cytokines.

  > these attract phagocytes to damaged tissue to carry out phagocytosis.

  > cytokines also trigger the hypothalamus which raises the body temperature.
• How is pus enabled in response to pathogens

  Histamine allows capillaries to become more leaky, meaning there is more tissue fluid and larger windows for white blood cells to enter the tissue as pus.
• Role of mucous membranes as a primary defence against pathogens


  >The epithelial layer contains mucus secreting cells called goblet cells. In the airways, the mucus lines the passages trapping any pathogens that may be in the air.

  >The epithelial also has ciliated cells which have tiny hair-like projections that can move so waft the mucus up to the trachea where it enters the oesophagus and is killed by acid in the digestive system, as it denatures the pathogens enzymes.

  >Mucous membranes are also found in the gut, anus, ears, nose and genital areas.
• Secondary non-specific defences against pathogens that have entered the body include the response of neutrophils, antigen-presenting cells or macrophages and cytokines.
• Phagocytes

  > Phagocytes are specialised cells in the blood/tissue fluid that engulf and digest pathogens.

  > Neutrophils are the most common phagocytes with lysosomes, a multi-lobed nucleus and are short lived.
• Process of phagocytosis

  1> Neutrophil binds to the opsonin attached to the antigen of the pathogen

  2> The pathogen is then engulfed by endocytosis forming a phagosome

  3> Lysosomes fuse to the phagosome and release lytic enzymes into it

  4> After digestion the harmless products are absorbed and pathogen is dead
• Opsonins are protein molecules that bind to the antigens on the surface of a pathogen after chemotaxis so phagocytes can bind and recognise the pathogen.
• How are phagocytes specialised for their function?

  >receptors on the plasma membrane that can bind to the opsonin or specific antigen

  >a lobed nucleus that allows the cell to squeeze through narrow gaps

  >a well-developed cytoskeleton that helps the cell to change shape to engulf the pathogen and to move lysosomes and vacuoles around inside the cell

  >many lysosomes containing lysin

  >many mitochondria, to release energy from glucose

  >lots of ribosomes to synthesise enzyme involved
• Macrophages

  They are larger cells made in the bone marrow. When a macrophage engulfs a pathogen, it doesn't fully digest it. The antigen from the surface of the pathogen are saved and moved to a special protein complex on the surface of the cell, becoming an antigen-presenting cell. This exposes the antigen on its surface so other cells in the immune system can recognise it. The special protein complex prevents the cell from being identified as foreign so it isn't attacked by other phagocytes.
• Antigen-presenting cells can move around the body and comes into contact with the correct T and B lymphocytes to find one with the correct recognition site for the antigen through clonal selection. The macrophage therefore increases the chances that the antigen will come into contact with them. This is coordinated by cytokines which stimulate the differentiation and activity of macrophages, B cells and T cells.
• Observation of cells in blood smear in microscopy.

  Note they are all suspended in blood plasma.

  A) Neutrophil

  B) Lymphocyte

  C) Monocyte /wbc

  
• The specific immune response involves B cells and T cells which are white blood cells with a large nucleus and specialised receptors on their cell surface membranes. This response produces antibodies which neutralise the foreign antigens.
• T lymphocytes develop or differentiate into four types of cells

  
  

  >T helper cells: release signalling molecules, such as cytokines, that stimulate the B cells to develop and stimulate phagocytosis by the phagocytes.

  > T killer cells: attack and kill host body cells that display the foreign antigen

  > T memory cells: provide long-term immunity

  > T regulator cells: shut down immune system response after the pathogen has been successfully removed. It also helps prevent autoimmunity
• B lymphocytes develop into two types of cells

  > Plasma cells: circulate in the blood manufacturing and releasing the antibodies

  > B memory cells: remain in the body for a number of years and act as the immunological memory
• T cells are formed in the bone marrow and are produced in the thymus gland. They have unique receptors on their cell surface membrane and these proteins are complementary to the foreign antigen.
• Cell signalling in the specific immune response is vital and achieved through signalling molecules such as cytokines which are complementary to the receptor on the surface of target cells. Examples of communication using cytokines:

  >Macrophages release monokines which attract neutrophils and stimulate B cells to differentiate and release antibodies.

  >T cells and macrophages release interleukins which stimulate clonal expansion and differentiation of B and T cells.

  >Many cells release interferon which inhibits virus replication and stimulates activity of T killer cells.
• Process of the specific immune response

  Clonal selection: B and T cells detect the antigen as they have specific complementary receptors on their plasma membrane. Contact occurs through action of antigen-presenting cells or when pathogenic cells enter the lymph nodes and are in body fluids.

  Clonal expansion: correct lymphocytes are detected and undergo mitotic cell division.

  Differentiation: once selected the clones of the lymphocytes develop into useful cells.

  Note: the B and T cells do not directly make the antibodies!
• Autoimmune diseases

  Occurs when the body's immune system mistakes its own healthy tissues as foreign and attacks them. Suggested it arises when our antibodies attack our own antigens that they are not normally exposed to. Examples:

  > Arthritis: disease when antibodies attack membranes around the joints.

  > Lupus: when antibodies attack certain proteins in the nucleus of cells and affected tissues, causing swelling.
• Primary and secondary immune response

  1st response: when an infecting agent is detected the immune system starts to produce antibodies however, this takes a few days for the concentration to rise to a level that can combat the infection successfully. once combatted the concentration of antibodies in blood drops rapidly.

  2nd response: after the body is infected by the same pathogen again, antibodies will be remade. This time the antibodies reach a high concentration rapidly as there are b and t memory cells circulating in the blood which recognise the specific antigens on the pathogenic cell.
• Primary and secondary immune response

  A) primary immune response

  B) secondary immune response

  C) antibody

  
• Antigen: substance that is foreign to the body and triggers an immune response.

  Antibody: immunoglobulin secreted by plasma cells that are complementary to a non-self antigen and bind to render them harmless.
• Structure of an antibody

  A) Variable region

  B) Constant region

  C) Disulfide bridge

  D) Light chain

  E) Heavy chain

  F) Antigen-binding site

  G) Hinge region