Communicable Diseases

• Prokaryotes
• 2 classification systems:
• Basic shapes: rod, spherical, comma, spiralled and corkscrew.
• Cell walls: Gram staining i.e. purple = positive, red = negative.

• Non-living.
• 0.02-0.3um.
• Basic structure is genetic material surrounded by protein.
• Take over biochemistry of host cells.
• Pathogenic.
• Bacteriophages can be used as a treatment (attack bacteria).

• Eukaryotic.
• Single-celled + colonies.
• Small % are pathogens -> parasitic.
• Vector neeses e.g. malaria.

• Eukaryotic.
• Digest food extracellularly + absorb nutrients.
• Saprophytes i.e. live off dead matter (some parasitic).
• Spread and reprosuce rapidly.

Direct Damage

• Viruses take over cell metabolism.
• Fungi digest and destroy.
• Protoctista digest cell contents and burst out.

Producing toxins

• Damage inactive enzymes.
• Break down cell membranes.
• Interfere with DNA.
• Toxins are by-products of normal bacterial functions.

• Bacterial disease - cavibacter michiganensis
• Leaves, tubers + fruit.
• Destroys 80% of the plant.
• NO CURE.
• Infected ground needs to be left for 2 years.

• Virus.
• 150 species infected.
• Leaves, fruit + flowers.
• Stunts growth + reduces yields.
• NO CURE,

• Fungus-like protoctist omycete - phytophthora infestans.
• Penetrate host cells.
• Leaves, tubers and fruit.
• NO CURE but risk can be reduced.

• Fungal disease - Mycosphaerella fijiensis.
• Leaves.
• Hyphae penetrate + digest cells.
• 50% yield reduction.
• Prevented by good husbandry + fungicide.
• NO CURE.

• Bacteria.
• Humans, cows, pigs, badgers + deer.
• Mycobacterium tuberculosis.
• Destroys lung tissue + suppresses immune system.
• 2012 = 1.3 million people died from TB.
• HIV/AIDS = more likely to get infected.
• Treatable by antibiotics + preventable.

• Bacteria.
• Meninges of the brain (protective membranes).
• Can cause septicaemia + rapid death.
• Very young children and teenagers 15-19.
• Blotchy rash that does not disappear when glass is pressed = septacaemia.
• 10% infected die.
• 25% recoveries have permanent damage.
• Antibiotics work if caught early.
• Vaccines may work against some strands.

• Acquired immunodefficiency syndrome.
• Human immunodefficiency virus.
• Targets T helper cells.
• Destroys immune system.
• HIV is a retrovirus with RNA as genetic material.
• Contains reverse transcriptase so is able to interact with the DNA of host cell.
• Bodily fluids is the vector.
• 2012 = 35 million living with it + 1.6 million died.
• No vaccine and NO CURE but anti-retroviral deugs available to slow process.
• Female genital mutilation = higher risk.

• Virus.
• Ciliated epithelial cells in the gas exchange system - kills them.
• Open to secondary infection.
• Can be fatal.
• Secondary infections include pneumonia.
• Affects mammals.
• 3 main strains - A, B + C.
• Strain A are the most virulent and classified further by proteins (A(H1N1) and A(H3N3) mutate regularly).
• Vulnerable groups given vaccines annually.
• NO CURE.

• Protoctista - plasmodium.
• Anopheles mosquitoes.
• Plasmodium parasite has complex lifecycle with 2 hosts - mosquitoes and people.
• Reproduce inside female mosquito.
• Female has 2 blood meals then lays eggs passing on plasmodium to people.
• It invades red blood cells, liver + brain.
• 200 million infected each year.
• 600,000 die annually.
• Recurring disease = weak and vulnerable to infection.
• No vaccines and limited cures.
• Control vector with insecticides + removing breeding sites (standing water).
• Screens + long sleeves.

• Fungi.
• Mammals - cattle, humans, dogs + cats.
• Different fungi infect different species.
• In cattle = grey-white crusty, infectious, circular areas of skin.
• Antifungal creams effective cure.

• Fungi.
• Tinia pedia.
• Form of human ring worm that grows on and digests warm, moist skin between the toes.
• Cracking and scaling.
• Itchy and sore.
• Antifungal creams.

Direct Transmission

• Direct contact - bodily fluids, skin-to-skin, faeces.
• Inoculation - break in the skin, animal bite, puncture wound.
• Ingestion - food and drink.

Indirect Transmission

• Fomites - inanimate objects.
• Droplet infection - coughing, sneezing, talking.
• Vectors - usually animals e.g. malaria in mosquitoes and rabies in bats.
• Water - e.g. diarrhoeal diseases.

• Overcrowding.
• Poor nutrition.
• Compromised immune system.
• Poor waste disposal.
• Climate change - new vectors, species, etc. E.g. malaria increases in warm, wet conditions.
• Culture and infrastructure - medical practices.
• Socioeconomic factors - lack of trained health workers.

Direct transmission

• Direct contact.

Indirect transmission

• Reproductive spores in soil from protoctista or fungi.
• E.g. black sigatoka + ring rot.
• Some pathogens survive composting.
• Vectors:
• Wind, water, animals and humans.

• Planting susceptible crops.
• Overcrowding.
• Poor mineral nutrition = less resistance.
• Damp, warm conditions increases disease survival.
• Climage change - wind and rainfall spreads vectors.

Physical defences:

• Produce high levels of callose (polysaccharide) - contains β-1,3 and β-1,6 linkages between glucose monomers.
• Roles of callose include; deposited between cell walls and membrane around infected cells, lignin is added too for strength and thickness, callose blocks sieve tube plates in phloem to prevent spread of pathogen, also deposited in pladmodesmata to seal off healthy cells.

Chemical defences:

• Insect repellants, e.g. pine resin.
• Insecticides, e.g. pyrethins and caffeine.
• Antibiotics, e.g. phenols and lysosomes.
• Antifungals, e.g. phenols and caffiene.
• Anti-oomycetes, e.g. glucanases (enzymes that break down glucans).
• General toxins, e.g. cyanide.

Keeping pathogens out:

• Skin - healthy flora outcompete space with pathogens + sebum inhibits pathogen growth.
• Tracts lined with mucous membranes - contains lysosomes and phagocytes.
• Lysosomes in tears, urine and stomach acid.
• Impulsive reflexes, e.g. coughs and sneezes.

Blood clotting:

• Thromboplastin - enzyme for formation of blood clot or thrombus.
• Serotonin - smooth muscle walls blood vessels contract, reducing blood supply.
• Scab - epidermal cell repair - damaged blood vessels regrow - collagen fibres for strength - healed.

Inflammatory response:

• Histamines and cytokines.
• Histamines make blood vessels dilate = heat and redness. Prevents pathogens reproducing.
• Histamines make blood vessels leakier = blood plasma forced out = tissue fluid = swelling and pain.
• Cytokines attract phagocytes to the sitte for phagocytosis.

Fevers:

• Cytokines stimulate hypothalamus to reset and temperature goes up because:
• Higher temperatures inhibit pathogen reproduction.
• The specific immune system works faster at higher temperatures.

Phagocytosis:

1) Pathogens produce chemicals that attract phagocytes.

2) Phagocytes recognise non-self proteins on the pathogen.

3) Phagocyte engulfs pathogen and encloses in vacuole called a phagosome.

4) Phagosome combines with a lysosome to form phagolysosome.

5) Enzymes from the lysosome digest and destroy the pathogen.

• Neutrophil - 10 minutes to engulf and destroy.
• Macrophages take longer: -digests pathogen, - combines antigens from pathogen surface membrane with glycoproteins from cytoplasm called the major histocompatability complex (MHC), - MHC moves antigens to macrophages surface membrane, - antigen-presenting cell (APC), - stimulates other cells in the immune response.

Helpful chemicals:

• Cytokines act as cell-signalling molecules for phagocytes.
• Cytokines also increase body temp + stimulate specific immune response.
• Opsonins bind to pathogens for recognition by phagocytes.
• Phagocytes have receptors to bind to common opsonins on pathogens.
• Antibodies such as immunoglobin G (IgM) and immunoglobin M (IgM) hve the strongest effect.

• Y-shaped glycoproteins - immunoglobins.
• Bind to specific antigens.
• 2 heavy polypeptide chains + 2 light chains (identical).
• Disulfide bridges.
• Binding site = 110 amino acids (variable region).
• Rest of antibody is constant region.

How antibodies defend the body:

• Antigen-antibody complex - antibody is opsonin.
• Pathogens cannot invade if part of antigen-antibody complex.
• Antibodies act as agglutinins causing clumping = prevents spreading + easier to engulf.
• Act as anti-toxins making toxins harmless.

• T helper cells - CD4 receptors on surface membrane which bind to antigens on APCs. Produce interleukins (cytokine) -> Stimulate B cells to produce antibodies and attracts macrophages.
• T killer cells - destroy the pathogen carrying the antigen. Produce perforin -> makes holes in membrane so freely permeable.
• T memory cells - Immunological memory. Divide rapidly upon secondary invasion.
• T regulator cells - suppress the immune system to prevent autoimmune diseases - interleukins are important in this control.

• Plasma cells - produce antibodies. Active plasma cell only lives a few days but produces 2000 antbodies/second while alive.
• B effector cells - divide rapidly to form plasma clones.
• B memory cells - immunological memory. Remember specific antigen to produce antibodies rapidly upon secondary invasion.

1) Non-specific defence system, macrophages = phagocytosis = Antigen presenting cells (APC).

2) Receptors on T helper cells fit antigens = activated + produce interleukins. Clones of T helper cells are formed by mitosis.

3)The cloned T cells may:

• Develop into T memory cells.
• Produce interleukins that stimulate phagocytosis.
• Produce interleukins that stimulate B cells to divide.
• Develop into T killer cells and destroy infected cells.

1) Activated T helper cells bind to B cell APC - clonal selection i.e. the B cell with the correct antibody to overcome a particular antigen is selected for cloning.

2) Interleukins activate B cells.

3) B cells divide by mitosis for clones of plasma and B memory cells - clonal expansion.

4) Cloned plasma cels produce antibodies for pathogen - bind to antigens and disable/ act as agglutinins/opsonins.

5) Some B cells turn into B memory cells. They divide rapidly to form plasma cell clones. SECONDARY IMMUNE RESPONSE.

• Type 1 Diabetes: 

- Insulin-secreting cells of pancreas.

- Insulin injections, pancreas transplants, immunosuppressant drugs.

• Rheumatoid Arthritis:

- Joints.

- No cure, Anti-inflammatory drugs, speroids, pain relief, immonosuppressants.

• Lupus:

- Skin, joints, fatigue, organs.

- No cure, anti-inflammatory drugs, speroids, immunosuppressants.

Primary response:

• Plasma cells.
• Antibodies produced.
• Few days for number of antibodies in blood to rise.

Secondary response:

• B memory cells.
• Rapidly reproduce plasma cells.
• Antibodies rapidly.
• Rapid response.

• Meet pathogen for first time = antibodies produced. T + B memory cells.

- Natural active immunity.

• Baby immune system cannot make antibodies for first couple of months.
  
• Some antibdies from placenta, some from colostrum (breast milk).
• Infant gut allows these glycoproteins to pass into bloodstream without being digested.

- Natural passive immunity.

• Antibodies formed in one individual and transplnted into another.
• Temporary immunity.
• Life saving.
• Example: people at risk of tetanus will be injected with tetanus antibodies from horse blood.
• This is not long-term immunity.

1) Pathogen made safe by:

• Killed/inactive bacteria or virus,
• Attenuated strains of live bacteria or virus (taken orally),
• Detoxified toxin molecules,
• Isolated antigens extracted from pathogen,
• Genetically engineered antigens.

2) Small amounts of safe pathogen injected into blood.

3) Primary immune response triggered.

4) Second contact with pathogen = secondary immune response = rapid pathogen destruction.

Boosters are sometimes needed.

• Living attenuated microorganisms that cannot cause symptoms or multiply.
• Dead microorganisms - harmless but induce immunity.
• Preparation of antigens.
• Harmless toxins (detoxified).

• Herd immunity - all population at risk vaccinated.
• Ring immunity - all population in surrounding area vaccinated to prevent spreading.
• Epidemic = local or national scale.
• Pandemic = many countries/continents.
• Mass vaccinations during epidemics.
• Vaccines for common diseases have to be changed often because of mutations.

• Penicillin first widely used antibiotic.
• Alexander Fleming 1928.
• Howard Florey and Ernst Chain developed industrial process for making the drug.
• Now computer programmes for drug design.
• 3-D models for potential drugs to be built and designed specifically to particulat parts of pathogens.
• Penicillin - originally from mould on melons, antibiotic against common bacterial diseases.
• Docetaxel/paclitaxel - yew trees, breast cancer.
• Asprin - sallow bark, painkiller.
• Prialt - venom of cone snail, new pain killing drug 1000x more effective than morphine.
• Vancomycin - soil fungus, one of the most powerful antibiotics.
• Digoxin - foxgloves, atrial fibrilation and heart failure.

Pharmacogenetics:

• Personalised medicine that works with your individual combination of genetics and disease.
• E.g. 30% breast cancers have mutation HER2 gene. Can be shut down by Herceptin and Lapatinib.
• Deaths can be reduced by up to 50%.

Synthetic biology:

• Develop populations of bacteria to produce drugs that would otherwise be rare or expensive.
• E.g. mammals have been genetically modified to produce therapeutic proteins in their milk.
• Nanotechnology can be used to deliver drugs to very specific dites withn the cells of pathogens or tumours.

• Random mutation = not affected by antibiotic = survives + reproduces =  passing on resistant genes to saughter cells.
• Some countries farmers feed animals antibiotics regularly BUT means more likely for bacteria to develop resistance because they're exposed to the same antibiotics regularly. (ILLEGAL IN THE UK).

• MRSA (methicillin-resistant Staphylococcus aureus) and Clostridium difficile (C.difficile) have been high profile examples of antibiotic resistant bacteria.
• MRSA - 30% population on skin or in nose. Causes boils, abscesses + septicemia.
• C.difficile - guts of 5% population. Produces toxins that damage lining of intestines, causes bleeding + diarrhoea and eventualy death. When commonly used antibiotics kill off much of the helpful gut bacteria it survives, reproduces and takes effect rapidly.
• Infections reduced by:

- Minimising use of antibiotics and making sure courses are completed fully.

- Practice good hygiene.

New antibiotics are being developed from coil microorganisms, crocodile blood, fish slime, honey and the deepest abysses of the oceans.