Communicable disease

Can cause communicable diseases in animals

• Viruses, Fungi, Bacteria, Protoctista

Virus - in animals

• Invades cell and takes over genetic machinery and other organelles

• Causes host cell to manufacture more copies of virus until it bursts

• Releasing viruses in body to infect healthy cells

• e.g. HIV attacks helper T cells compromising immune response

• e.g. Influenza

Viruses more detail

• Infect genetic machinery of host cell

• Combine with host cell DNA using reverse transcriptase

• Viral DNA/RNA and proteins are made using host mechanisms

How do you treat viruses?

• Must destroy own cells

• Viruses invade body cells as host cells

Fungi - in animals

• Hyphae forms mycelium - grows under skin’s surface

• specialised reproductive hyphae grow to surface and release spores - digestive enzymes

• Cause redness and irritation

• e.g. Athlete’s foot

Bacteria - in animals

• Once in host body, they can multiply rapidly

• Their presence causes disease by damaging cells by releasing waste toxins

• E.g. tuberculosis - kills cells and tissues

Protoctista - in animals

• Feeds on the contents of cells as they grow

• E.g. Plasmodium - causes malaria

Causes communicable disease in plants

Virus, fungi, bacteria, protoctista

Virus - in plants

• Virus invades cell and takes control of genetic machinery - to make more copies of virus

• Until the cell bursts - releasing viruses in plant to infect healthy cells

• e.g. Tobacco Mosaic Virus

Fungi - in plants

• Hyphae form a network and spread throughout soil

• Lives in vascular tissue release spores - with digestive enzymes e.g. cellulase

• Feeds on nutrients - xylem and phloem amino acids, sucrose

• e.g. black sigatoka - surrounding tissue decay causing shrivelled and molted leaves

Bacteria - in plants

• Live in vascular tissue cause - blackening and death

• Release infectious toxins

• e.g. Ring rot

Protoctista - in plants

• Feeds on the contents of cells as they grow

• Often use a vector

• e.g. Potato blight

Direct transmission

• From one host organism straight to another

• e.g. touch, inoculation

Indirect transmission

• Contact of a surface or object from two organisms needs a vector

Why must pathogens be able to successfully transfer from host to host?

• If pathogens are unable to find new hosts then they will go extinct

Direct contact - animals

• Touching - skin on skin contact with infected and uninfected

Inoculation - direct - animals

• There is an opening or wound

• E.g. sharing needles, blood transfusion,

Oral/ Ingestion - direct - animals

• Eating or drinking contaminated food or water

Fomite - indirect - animals

• Object an infected individual comes in contact with

• Object is then used by uninfected indidvidual

Droplet infection - indirect - animals

• Pathogen can be carried in droplets by water and air

• Sneezing/ coughing

Vector - indirect - animals

• Another organisms transfers pathogen from one to another

• e.g. female anophele transfers malaria between blood

Direct contact - plants

• Leaves of infected plant comes into contact with leaves of healthy plant

• Pathogens transferred

• E.g. Tobacco Mosaic Virus (TMV) touch the leaves of another uninfected plant, particles of the virus are transmit

Vectors - plants - indirect

• A third organisms involved in spread of pathogen

• Aphids suck sugar sap in multiple plants - transmission of pathogens

Plants - indirect

• Planting new uninfected plant in contaminated soil

Spores - indirect - plants

• Pathogens carried in wind, water

• e.g. dutch elm disease

Factors affecting transmission

Hygiene, weak immune system, overcrowding, Climate

Genetic variation

• Certain organisms have natural susceptibility

Weak immune system

• Body is less able to fight infections

Overcrowding

• Means infected people can transmit pathogens more easy

• e.g. farms

Hygiene

• Hygiene of environment

• Unhygienic environment will increase pathogen reproduction

Primary non - specific immune responses

• Skin

• Mucous membranes

• Expulsive reflexes

• Chemical secretions

Skin

• Skin possess an outer layer of dry, dead, hardened cells filled with keratin

• Dividing cel

• Water proof and germ proof

• Keratin is a tough fibrous protein

• This layer of cells acts as a physical barrier to pathogens

• There are secretions of sebum that contain fatty acids which have antimicrobial properties

Eye

• Eyelashes (protect from dust)

• Tears act as a mild antiseptic and contain antibodies and lysozymes

• Blink reflex protects against physical damage to the eye

• Scelerotic (tough outer layer)

Columnar epithelium

• Secretes mucus into stomach to

  Lubricate movement of food

• Pathogens are killed by HCL made by glands in the stomach

• Gastric Gland (secretes gastric juice contains hydrochloric acid and pepsin - digestive enzyme

How are lungs protected?

• Dust and pathogens do not usually reach the lungs. - trapped in a stream of sticky mucus made by goblet cells

• Cilia move trapped molecules up trachea - to stomach digested

Mucous membranes

• Mucous membranes line the gut, airways and reproductive system

• The mucous membrane consists of epithelial cells and mucus-secreting cells - goblet cells

• Viruses, bacteria, pollen and dust float about in the air that we breathe in - trapped

• The particles are then moved towards the back of the throat by cilia and digested in stomach

Expulsive reflexes

• When a pathogen irritates the lining of an airway it can trigger an expulsive reflex; a cough or sneeze

• Both a cough and sneeze result in a sudden expulsion of air - removing pathogens

Second line of defense

• Blood clotting

• Inflammation

• Wound repair

• Phagocytosis

Blood clotting

• After abrasions or lacerations to prevent blood loss/escape of red blood cells

• Platelets change from discs - to long thin projections - contact with collagen

• Become sticky stick to collagen stick to each other stick to escaping red blood cells - forms a clot

Why is Blood clotting useful

• Break in skin or mucous membrane - results in clotting cascade

• Blood clotting prevents excess blood loss, the entry of pathogens and provides a barrier (scab)

Clotting cascade definition

• Series of enzyme controlled reactions in blood leading to a blood clot

Clotting clascade

• When exposed to collagen platelets release thromboplastin

• Thromboplastin releases thrombokinase which changes prothrombin ——-> thrombin

• Thrombin changes soluble fibrinogen —-> insoluble fibrin

• Fibrin is insoluble so escapes blood forming long mesh - encapsulating structure

• Also traps more platelets and red blood cells

• Endothelial cells surround blood clot

Inflammation

• When microorganisms are detected histamines and cytokines are released

• Histamines cause vasodilation dilating blood vessels and making capillary walls more permeable/ leaky - to white blood cells

• Dilation - redness and localised heat - inhibits pathogen reproduction

• Cytokines - cell signalling attract phagocytes for phagocytosis

What is wound repair?

• A scab is formed as a result of blood clotting

• Underneath this scab, there are stem cells that divide by mitosis to heal the wound

Wound repair stages

• New blood vessels form

• Collagen is produced

• Granulation tissue forms to fill the wound

• Stem cells move over the new tissue and divide to produce epithelial cells

• Contractile cells cause wound contraction

• Unwanted cells die

How are neutrophils identified in blood smears?

Lobed

How are neutrophils attracted to pathogen site?

• Histamines and pathogenic chemicals attract neutrophils

• This causes them to move by chemotaxis to pathogen site - respond to stimuli

Neutrophil phagocytosis

• Receptor proteins move towards pathogens with attached antibodies

• Pathogens are engulfed by neutrophils in phagocytic vacuole

• Pathogens are trapped in phagosomes

• Fuses with lysosome to from a phagolysosome

• Digestive enzymes and destroy pathogen

Macrophage proeprties

• Antigen presenting cells - do not fulling digest pathogen - displays antigen on surface to be recognised by lymphocytes

• Major histocompatibility - complex

How do macrophages act in cell signalling?

• Release cytokines for cell signalling and opsonins which tag pathogens to be easily recognised.

• Cytokines signal cells - cause fever to enhance immune system

• Opsonins bind to antigen on surface to easier be binded to phagocytes

Why are B lymphocytes called B

• Made in the bone marrow

Why are T lymphocytes called T

• Mature in thymus

T helper cells

• T helper cells have CD4 receptors to bind to AG MHC complex on antigen -pc

• Alerting T helper cells this is an APC and immune system under attack

• Release interleukins for cell signalling

What is the role of interleukins

• Stimulate B cells to make antibodies

• Makes T cells divide

• Enhance macrophage phagocytosis

Blood plasma

• Phagocytic wbc’s leave blood enter tissue fluid

• Causing oedema/swelling

• Excess fluid drained into lymphatic system where lymphocytes have direct contact with pathogens

What do T killer cells do?

• Release perforin - makes holes in cell surface membrane of pathogens

• Destroying pathogens

How do T regulator cells prevent autoimmune disease?

• Suppress immune system with interleukins

• Ensure self antigens are not seen as foreign

• Preventing autoimmune disease

What is cell - mediated immunity

• T lymphocytes can only bind directly to antigen on a body cell using receptors

B lymphocytes

• produce antibodies

• bind with specific antigen

• freely in bodily fluids - humoral immunity

Antibodies

• Have two identical heavy chains and two identical light chains

• These chains are held together by disulfide bridges

• Two antigen binding sites - can bind to two antigens

• Flexible hinge region to vary distance between binding site

Why is secondary immune response faster

• Much more vigorous and rapid as clonal selection and expansion are not required

• Memory cells have specific binding site to antigen and will be activated on return'

• Will differentiate in:

• B plasma cells making antibodies

• T helper cells aiding differentiation

• T killer cells kill infected cells

How are pahgocytes adapted for their role

• Well developed cytoskeleton - change shape to engulf a pathogen

• Lysosomes - lysozymes - digestive enzymes

• Many mitochondria - ATP - Energy - movement + phagocytosis

• Many ribososmes - protein synthesis - lysozymes

• Lobed nucleus squeeze through narrow capillary walls

How to do opsonins aid agglutination

• Antibodies act as agglutinins causing pathogens carrying antigen-antibody complexes to clump together (agglutination).

• reduces the chance that the pathogens will spread through the body

• makes it possible for phagocytes to engulf a number of pathogens at one time - easier

Passive defence mechanisms

• Always present - before infection

• Prevent entry of pathogens

• Can be physical barriers and chemicals

Passive defence mechanisms Barriers

• Physical barriers make it harder for pathogens to gain entry into plants

• E.g. waxy cuticles, Cell wall, closed stomata, bark, casparian strip

Cellulose cell wall

• Plant cell walls contain a variety of chemical defences

Waxy cuticle

• Creates physical barrier

• Prevent water collecting on the cell surfaces - waterproof

• pathogens need water to survive, the absence of water is a passive defence

Casparian Strip

• Some fungi species can invade a plant all the way to the endodermis

• Unable to push past the Casparian strip - made of Suberin - waterproof prevents collection of water pathogens need water to survive

Bark

• External layer of dead cells which forms a physical barrier against infection

• Contain chemical defence

• Sticky resin - traps pathogens

Closed Stomata

• Stomata are possible points of entry for pathogens

• Stomatal aperture is controlled by the guard cells.

• When pathogenic organisms are detected, the guard cells will close the stomata in that part of the plant. 

Lignin

• Thickens cell walls

• Layer of dead cells which forms a physical barrier against infection

• Waterproof and indigestible - phenolic compound

Active defense mechanisms

• Active defence mechanisms in plants are activated when pathogens invade - specific, chemicals glycolipids, proteins

  • Hypersensitivity deprives pathogens of resources

  • The formation of physical barriers by callose plays a major role in limiting the spread of pathogens

  • Cell signalling plays an important role in coordinating the active defence mechanisms

Why can substances not freely move around the entire plant?

• Plant cells have cell walls

• Makes cell signalling vital

Hypersensitivity

• Hypersensitivity is the rapid death of tissue surrounding the infection site

  Deprives the pathogens of host tissue, nutrients and energy

Callose

• Deposited around the sieve plates and blocks the flow in the sieve tube.

• This can prevent a pathogen spreading around the plant. 

• Increased callose deposition, blocks flow of sieve tube  

Tylose

• Flls the xylem vessel. When a tylose is fully 

• formed, it plugs the vessel and the vessel can no longer carry water.

• Blocking the xylem vessels prevents spread of pathogens

• Tylose contains a high concentration of chemicals such as terpenes that are toxic to pathogens. 

Necrosis 

• Kills cells surrounding the infection - limiting the pathogen’s access to water and nutrients stop it spreading further around the plant

• Started by intracellular enzymes that are activated by injury

• These enzymes destroy damaged cells and produce brown spots on leaves or dieback 

Canker

• a sunken necrotic lesion in the woody tissue

• It causes death of the cambium tissue in the bark