Communicable diseases

Organisms that live in or on host and cause harm by taking nutrients and can cause damage through secondary infections

Microorganism that causes disease

Bacteria (Mycobacterium tuberculosis & M.bois)

Bacteria (Neisseria meningitolis or Streptococcus pneumonia)

Bacteria

Virus (Human immunodeficiency virus)

Virus (Orthomyxoviridae virus)

Virus (Tobacco Mosaic Virus)

Fungus (Mycosphaerella fyiensis)

Protist (Phytophtricra infestans)

Fungus (Trichphyton vernicosum)

Fungus (trichphyton rubrum)

Protist (Plasmodium falciparum, P.vivax, P.ovale, P.malariae)

Plants

Bananas

Tomatoes and Potatoes

Cattle

Kills cells and tissues, lungs most affected

Membranes surrounding brain and spinal cord swell, may cause damage

Ring of decay in vascular tissue

Wilting leaves

Attacks cells in immune system

Comprimises immune response

Attacks respiratory system

Muscle pains and headaches

Spots on leaves of plants

Reducing yields

Mottling and discolouration of leaves

Affects leaves and potato tubers

Growth of fungus in skin

Causes rash

Growth under skin on foot

Parasite in blood

Headaches and fever

May lead to death

Enter host cells and feed on contents as they grow

Has immature forms that feed on haemoglobin inside RBCs

Invade cells and take over genetic machinery & organelles

Cause cells to manufacture more copies of virus

Host cell eventually bursts, releasing viruses which invade healthy cells

Once in host, reproduce rapidly

Damages cells and releases toxins that are toxic to health

Live in vascualr tissue

Cuse balckeing and therefore death of tissue

Fungus lives in skin, its hypahe (forms a mycellium) grows under skin surface

Sends out reproductive hyphae which gows to surface of skin and releases spores - causes redness & irritation

Lives in vascualr tissue where can gain nutrients

Hyphae release extracellular enzymes e.g cellulases to digest surrounding tisses causing decay

Leaves become mottled, curl up and shrivel

Fruit and storage organs turn black and decay

Tuberculosis

Bacterial menegitis

Ring Rot

HIV/AIDS

TMV

Influenza

Black sigatoka

Ringworm

Athletes foot

Malaria

Blight

Passing a pathogen from host to new host, with no intermediary

Passing pathogen from host to new host, via a vector

Passing pathogen from infected individual to uninfected individual

Organism that carries pathogen from one host to another

Free from disease

Physically and mentally capable

Balanced diet

Happy

Social

Absence of good health

Malfunction of healthy body and mind

Symptoms

HIV/AIDS, Influenza, TMV

Tuberculosis, Bacterial menegitis, Ring Rot

Black sigatoka, Ringworm, Athletes foot

Malaria, Blight

1. Transmission

2. Entering hosts tissues

3. Reproducing

4. Leaving hosts tissues

HIV, Ringworm, Athletes foot

Cholera, Food poisoning

Flu, Tuberculosis

Anthrax, Tetanus

Touching infected person or contaminated surfaces

Eating/drinking items contaminated by pathogen

Pathogen carried in droplets in air e.g coughs and sneezes

Masks

Wash skin after contact with possible infection

Catch it, bin it, kill it

Cover mouth when cough/sneeze

Use tissues

Wash hands

Treatment of waste water and drinking water

Cooking food thoroughly

Washing fresh food

Washing hands regularly

Keep surfaces clean

Cleaning and disinfecting cuts

Using condoms

Sterilising surgical equipment

Overcrowding

Poor ventilation

Poor health

Poor diet

Homelessness

Vectors

Uninfected person is bitten

Plasmodium migrates to liver

Plasmodium migrates to blood

Person has malaria

Gametes of plasmodium in blood

Female anopheles mosquito sucks blood

Plasmodium develops and migrates to mosquitoes salivary glands

Diseases may be present in soil and infect plants by entering roots

Spores being spread in the wind

Once pathogen in plant, infects vascualr tissue

Pathogens distribute through leaves and when shed, pathogen carried to soil, grows and infects other plants

Enters fruits and seeds - offspring affected

Insect attack - spores/bacteria attach to burrowing insect which then infects plant

Insect acts as vector

Medical services

Pharmecuticals

Ill people can’t work

Protists, fungi and bacteria can reproduce more rapidly in warm and moist conditions

Warmer climates and countries as can reproduce and grow more rapidly

Pathogens may be damaged or killed or have reduced ability to grow and reproduce

Global warming is making climate more mosit and warmer so pathogens can surve more easily and grow and reproduce more rapidly

Large pollysaccharide deposit that blocks old phloem sieve tubes

Section off diseased tissue and sacrifice it

During photosynthesis

Prevent entry of pathogens

Induce response when pathogen detected

Cellulose cell wall

Lignin thickening of cell walls

Waxy cuticles

Bark

Stomatal Closure

Callose

Tylose formation

Physical barrier also contains chemical barriers which can be activated when pathogen detected

Waterproof

Almost completely indigestable

Prevents water collecting on cell surfaces - creates absence of water (pathogens collect in water and need it to survive)

Physical barrier

Possible entry point

Stomatal apeture controlled by guard cells - when pathogens detected, guard cells close stomata

Beta glucose molecules

Large polysaccharide deposited in sieve tubes, - deposited around sieve plates and blocks flow in sieve tube to prevent pathogen spreading around plant

Inflates to fill xylem vessel - when fully formed, plugs vessel so no longer carry water. Prevents spreading

Contains high conc of chemicals toxic to pathogens

Plant tissues ontaining anti-pathogenic properties

Insect repellants

Insecticides

Antibacterial compounds

Antifungal compounds

Enzymes and toxins

Pine resin

Citronella

Pyrethins act as neurotoxins to insects

Phenols

Defensins

Caffene - toxic to insects and funi

Gossypol

Saponins - found in cell membranes, interferes with fungal cell membrane

Cyanide

Chitinase - breaks down fungal cell wall

Once pathogens detected as production requires lots of energy

Thickened + strengthened cell wall with additional cellulose

Deposition of callose between wall and membrane

Increase in production of chemicals

Necrosis

Canker

Polysaccharide polymers

Impede cellular penetration at site of infection - strengthens cell wall and blocks plasmodesmata

Terpencides

Phenols

Alkaloids

Defensive proteins

Hydrolytic enzymes

Antibacterial and antifungal properties

Create scent

Antibac and antifungal properties

Tannins found in bark inhibit attack by insects - bind to salivary proteins and digestive enzymes, deacivate enzymes. Insects ingest high amount of tannins - don’t grow and die

Nitrogen-containing compounds

Give bitter taste - inhibit herbivores feeding

Act on metabolic reaction - inhibit or activate enzymes

If reduce grazing = suffer less damage = less pathogens entering

Small cyteine-rich proteins

Act in plasma membranes of pathogens - inhibit action of ion transport channels

Chitinase - breaks down chitin in fungal cell wall

Glucanase - hydrolyse glycosidic bonds in glucans

Lysozomes - degrade bacterial cell walls

Deliberate cell suicide - bought about by intracellular enzymes activated by injury

Kills cells surrounding infection - limits pathogens access to water and nutrients, stops spreading

Causes death of cambium tissue in bark, creating sunken lesion in stem

Swelling and redness of tissue caused by infection

Specialised epithelial tissue that’s covered by mucus

Those that prevent pathogens from entering body

Proteins that bind to antigen on pathogen, allowing phagocytes to bind

Hormone-like molecules used in cell-signalling to stimulate immune response

Selection of a specific T or B cell that’s specific to antigen

Type WBC that engulfs foreign matter and traps it in large vacuole (phagosome), whihc fuses with lysosomes to digest foreign matter

Cell that isolates antigen from pathogen and places it on plasma membrane so can be recognised by other cells in immune system

Specific proteins released by plasma cells that can attach to pathogenic antigens

Cells that remian in blood for long time, providing long term immunity

An increase in the number of cells by mitotic cell division

Signalling molecules used to communicate between different WBC’s

Derived from B lymphocytes, cells that manufacture antibodies

Cells that release signalling molecules to stimulate immune response

Cells that attack and destroy own body cells that are infected by pathogen

Cells that remain in blood for long time, provide long term immunity

Cells involved wiht inhibiting/ending immune response

Antibodies that cause pathogens to stick together

Antibodies that render toxins harmless

Antibodies that make it easier for pahgocytes to engulf pathogen

Initial response caused by a first infection

More rapid and vigorous response caused by second/subsequent infection by same pathogen

Where immune system is activated and manufactures its own antibodies

Immunity that’s achieved as result of medical intervention

Rapid spread od disease through high proportion of population

Immunity achieved through normal life processes

Immunity achieved when antibodies are passed to individual through breast feeding or injection

Way of stimulating immune response so immunity is achieved

Chemical which prevents the growth of microorganisms - can be antibacterial or antifungal

Development of designer medicines for individuals

The re-engeneering of biology - could be production of new molecules that mimic natural processes or use of natural molecules to produce new biological systems that don’t exist in nature

Blood clotting and skin repair

Mucus membranes

Skin

Inflammation

Coughing and Sneezing (expulsive reflexes)

Tears

Molecules that can stimulate an immune response

Specific

Antigen

In response to an infection

immunoglobulins

Complex proteins produced by plasma cells in immune system (antibodies)

Attach to antigens and render them harmless

Complementary

Antigen

Y-shaped

Region which has specifc shape to shape of antigen

Region which is same for all antibodies

Region to allow flexibility so molecule can grip more than one antigen

1. antigen binding site

2. variable region

3. constant region

4. light polypeptide chain

5. disulphide bridge

6. heavy polypeptide chain

Hinge region (where bends)

By attaching to antigens on pathogen

Opsonins

Aggulatins

Anti-toxins

Bind to antigen on pathogen than act as binding site for phagocytic cells sn can bind easily and destroy pathogen

Bind to molecules released by pathogenic cells - action of anti-toxin renders them harmless

The aggulatinated pathogens physically impeded from carry out functions e.g entering host cells

Readily engulfed by phagocytes

Have 2 identical binding sites so crosslinks pathogens by binding an antigen to one pathogen with one binding site and another on its other binding site - clump togther

Infection

When infecting agent first detected, immune system starts to produce antibodies - takes few days before level of antibodies in blood enough to combat infection

Antibodies made again - B and T memory cells in blood recognise specific antigens and immune system can kick in quicker

Conc of antibodies rises sooner and reaches higher conc

Immune system treats antigenic material as real disease and immune system activated and manufactures antibodies and memory cells for long term immunity

Toxoid

Dead pathogen

Harmless/weakened version of pathogen

Whole/live microorganism

Using vaccine to provide immunity to all/almost all of population

When new case of disease is reported

Vaccinating all in immediate vicinity of new cases

Areas to prevent spread of disease through livestock

over 65

Respiratory tract conditions

Some pathogens undergo genetic mutations which change their antigens - memory cells produced by vaccination may not recognise new antigens so pathogen may be transmitted and incidence of disease increase

Allows them to prepare for impending epidemics by stock pilling vaccines and vaccinating those at risk

Achieved through medical intervention

Achieved through normal life processes

Achieved when immune system activated and manufactures own antibodies

Achieved when antibodies supplied from another source

Immunity provided by antibodies made by immune system as result of infection - suffers from disease once and it then immune

Antibodies provided via placenta or breast milk - baby immune to which mothers immune

When baby’s immune system still developing

Immunity provided by antibodies made by immune system as result of vaccination (dead or weakened pathogen)

Immunity provided by injection of antibodies made by another individual

New diseases emerging

Some antibiotic treatments become less effective

Many diseases with no effective treatments

Accidental discovery

Traditional remedies

Observation of wildlife

Plant research

Antibiotic penicilin

Sap from unripe poppy heads

12th century - opium from poppies used as anaesthetic

Reduces nervous action in CNS. If nerves can’t carry impulse = no pain felt

Relieves pain and fever and reduces side effects of stomach bleeding

Morphine - poppy heads

Willow bark extract

Asprin and ibuprofen

Animals make use of plants with medicinal properties

Rubs citrus oils on coats as insecticides and antiseptics to prevent bites and infections

Line nest with medicinal leaves to protect chicks from blood-sucking mites

New chemical fingerprinting technology enabling scientists to screen natural chemicals more effectively for their activity as potential medicines

Sequencing genes from indi with particular condition and developing specific drugs for condition

If binding between pathogen and receptor site is blocked

Glycoprotein recceptor molecules can be isolated and sequenced. When AA sequence know, molecular modelling can be used to determine shape of receptor and can then find drug that mimics shape of receptor to bind to virus, stopping virus entering T helper cell

1. Dev of new molecules that mimic bio systems

2. Design and construction new devices and systems useful in research or healthcare

Compounds that prevent growth of fungi or bacteria

Penicillin

Enabled microorganisms to develop resistance and therefore have limited effectiveness

Macrophages and neutrophils

B and T lymphocytes

Short lived

Longer lived, immunological memory

Immediate

Delayed

Any foreign antigens

Particular antigens

Inflammatory response

Cell mediated and humoral

Hydrolytic enzymes

Immunoglobulins and perforins

Phagocytosis

Production and release of antibodies

WBC with large nucleus and specialised recceptors on plasma membrane

B and T lymphocytes

Antibodies by neutralising foreign antigens

Long term

Releases memory cells which circulate body

T helper

T killer

T memory

T regulator

Release cytokines that stimulate B cells to develop and stimulate phagocytosis by the phagocytes

Attack and kill host body cells that display foreign antigen

Provide long term immunity

Shut down immune response once pathogen removed. Involved in preventing autoimmunity

Plasma cells

Bmemory cells

Circulate in blood, manufacturing and releasing antibodies

Remain in body number years and act as immunological memory

Release of cytokines

Cell surface receptor complementary to shape of signalling molecule

Macrophages releasing monokines

T cells and macrophages releasing interleukins

Some attract neutrophils (by chemotaxis - movement of cells towards particular chemical). Others stimulate B cells to differentiate and release antibodies

Interleukines

Stimulate clonal expansion and differentiation of B and T cells

When immune system attacks part of body and antibodies start to attack own antigens

Arthritus

Lupus

Phagocytosis

Specialised cells in bloo/tissue fluid engulf and digest pathogens

Bone marrow

Large no lysosomes

Collect in area of infection and form pus

Engulf and digest pathogens

Cell mediated immunity:

Macrophage enguls antigen through phagocytosis and becomes antigen presenting cell

APC roams lymph

T-lymphocyte selected that has comp receptor on cell surface membrane to that of APC (clonal selection)

T-lymph reproduces by mitosis (clonal expansion)

T-lymphs differentiate into 4 types

Humoral immunity:

T-helper release cytokines to stimulate B cells which are comp to APC (clonal selection)

Mitosis of B cells (clonal expansion)

B cells differentiate into B memory and plasma

Plasma produces antibodies

Neutrophil binds to opsonin attached to antigen of pathogen

Pathogen engulfed by endocytosis forming a phagosome

Lysosomes fuse to phagosome and release lytic enzymes into it

After digestion, now harmless products absorbed into cell

Receptors on plasma membrane can bind to opsonin or specific antigen

Lobed nucleus - allows cell squeeze narrow gaps

Many lysosomes and mito

Lots ribosomes

Well dev cytoskeleton - helps cell change shape to engulf pathogen and move lysosomes and vacuoles inside cell

Enhance ability of phagocytic cells to bind and engulf pathoge

proteins

Cells which moive around body and come in contact with B and T lymphocytes that can activate full immune repsonse

Increase chances of antigen coming into contact with B and T lymphocyte as may only be one in whole body

Activation of specific B and T cells

Cytokines

Stimulate the differentiation and activity of macrophages, B and T cells

As monocytes

Body tissues

Lymph nodes

Mature into macrophages

Dendritic cells

Play important role initiating specific immune response to invading pathogen

Macrophage engulfs pathogen - doesn’t fully digest it. Antigen from surface of pathogen saved and moved to protein complex on surface of cell.

Cell becomes APC - exposes antigen on its surface so other cells in immune system can recognise antigen

Combat pathogens that have entered body

Chemical markers on invading pathogen so its recognised as foreign

Infected tissue

1. in tissue detected by mast cells which release histamine

2. vasodilation and makes caps walls more premeable to WBC’s and proteins

3. leave blood and enter tissue fluid which causes swelling (oedema)

4. drained into lymphatic system where lymphocytes stored

5. with lymphocytes to innitiate specific immune response

Histamine

Mucus plug in cervix and by maintaining relatively acidic conditions in vagina

Ear canal lined with wax - traps pathogens

Antibodies and enzymes in tear fluid

Sudden expulsion of air carries microorganism away

Exchange surfaces where O2 and nutrients enter blood must be thinner and less well protected from pathogens so needed to stop entrance of disease/pathogens

Epithelial

Mucus lines passages and traps pathogens from air (secreted from goblet cells in epithelium)

Epithelium has ciliated cells - waft layer of mucus along, moves to top of trachea to enter oesophagus

Mucus swallowed into digestive system - pathogens killed by acidity of stomach - denatures pathogens enzymes

Body must prevent excess blood loss by forming clot - temp seal to prevent infection

Ca 2+

Platelets

Enzyme cascade:

Damaged cells (exposed collagen) -> platelets -> clotting factors released -> Thrombokinase + Ca2+ ->

1. Prothrombine -> Thrombine

2. Fibrinogen -> Fibrin

-> Thrombus (clot) -> Scab -> stem cells undergo mitosis and differentiate to form new skin -> scab falls off

Skin

Epidermis

Layer of cells - most cells called keratinocytes

Mitosis at base epidermis then migrate skin surface

Dry out nad cytoplasm replaced by keratin - keratinisation

Waterproof top layer

Produces oil (sebum) which contains lysozyme - antibacterial

Lysosomes, eyelashes, eyebrows

Coughing

Sneezing

Vomitting