4.3 - Communicable Diseases

Types of pathogens

• Bacteria

  • Produce toxins that damage body cells

• Viruses

  • Use host cells to replicate before bursting out and destroying cells

• Protists

  • Take over cells and break them open

• Fungi

  • Digest living cells to destroy them

  • Can produce toxins

Modes of transmission

• Direct transmission

  • Airborne droplets

    • Sneezing or coughing mucus or saliva onto someone

  • Direct contact

    • Skin-to-skin, kissing

• Indirect transmission

  • Food and drinking water

  • Vectors

  • Contaminated objects

Risk factors that worsen transmission

• Living conditions - overcrowded areas

• Climate - warmer temperatures allow mosquitoes to breed and transmit malaria

• Social factors - lack of health education

Bacterial diseases

• TB

  • Affects: humans, cows, pigs and badgers

  • Effects: damages lungs and suppresses immune system

  • Transmission: airborne droplets, contaminated food

• Ring rot

  • Affects: potatoes

  • Effects: cheese-like ooze and internal hollowing, necrosis

  • Transmission: direct contact, contaminated equipment of surfaces

Viral

• HIV/AIDS

  • Affects: humans and primates

  • Effects: destroys immune system

  • Transmission: exchange of bodily fluids

• Influenza

  • Affects: mammals

  • Effects: kills ciliated epithelial cells in the gas exchange system

  • Transmission: airborne droplets, contamination

• Tobacco mosaic virus

  • Affects: tobacco, tomatoes, peppers

  • Effects: discolouration, stunted growth

  • Transmission: direct contact, contamination

Protists

• Malaria

  • Affects: humans, mammals, reptiles and birds

  • Effects: damages the RBC, liver and brain

  • Transmission: vector (anopheles mosquito)

• Blight - fungus like microorganism

  • Affects: plants (potatoes)

  • Effects: wilting and death of plant tissue

  • Transmission: airborne, contamination

Fungi

• Black sigatoka

  • Affects: bananas

  • Effects: yellow streaks, necrosis

  • Transmission: airborne

• Athlete's foot

  • Affects: humans

  • Effects: causes the cracking and scaling of skin between the toes

  • Transmission: contamination

Modes of transmission 2

• Direct

  • Healthy plant touches unhealthy plant

• Indirect

  • Soil contamination

• Vectors

  • Wind, water, animals, humans

Risk factor

• Crop variety - some crops are more susceptible to disease

• Overcrowding - likelihood of direct contact

• Mineral nutrition - poor nutrition reduces resistance of plants

• Climate change - increased rainfall and wind increase spread of disease

Plant physical defences

• Waxy cuticle

  • Provides a physical barrier against pathogens

• Cell walls

  • Plant cells are surrounded by cell wall that forms a physical barrier

• Callose production

  • When plants are attacked they produce polysaccharide callose

  • Is deposited between the cell wall and membrane to make it harder for pathogens to enter cell

Chemical plant defences

• Insect repellents

  • Reduce number of insects feeding on plants to prevent pathogen transmission

• Insecticides

  • Kill insects to prevent transmission

• Antibacterial substances

  • Chemicals such as antibiotics are produced to kill bacteria or inhibit growth

• Toxins

  • Some plants produce chemicals that break down into cyanide when plant cells are attacked

Animal defences

• Non-specific

  • Act quickly to defend the body, but respond in the same way for all pathogens

• Specific

  • Slower to defend the body but produce a specific response for each pathogen

Physical and chemical animal defences (skin, mucous membranes, expulsive reflexes)

• Skin

  • Physical barrier to block pathogens from entering

  • Acts a chemical barrier by producing sebum

    • Oily, antimicrobial substance that lowers pH to inhibit the growth of pathogens

• Mucous membranes

  • Parts of ear, nose, throat and digestive tract are lined by mucous membrane

  • Secrete mucus to trap pathogens and use lysozymes to destroy them

• Expulsive reflexes

  • Coughing and sneezing are methods for expelling foreign objects from gas exchange system

  • Vomiting and diarrhoea expel the contents of the gut along with any pathogens present

Physical and chemical animal defences (blood clotting, inflammation)

• Blood clotting and wound repair

  • A cut to the skin provides a possible entry for pathogens

  • Blood clots act to seal any wounds

  • Clot dries out to form a scab that blocks entry to the body

    • After it forms the skin is capable of repairing itself to reform its physical barrier

  • Epidermal cells underneath the scab divide while damaged blood vessels regrow

    • Collagen fibres are used to provide strength

  • Once epidermis is thick enough, scab breaks off

• Inflammation

  • Consists of

    • Swelling and heat

    • Redness and pain

  • Triggers by damaged tissues that release chemicals

    • Affect the blood vessels by:

      • Causing blood vessels to dilate which increases blood flow to the area making it hotter

        • Prevents pathogens from reproducing

      • Blood vessel walls become more permeable so they leak tissue fluid

        • Causes swelling and isolates any pathogens in the damaged tissues

Antigens

• Allow immune system to distinguish between body cells and foreign cells

• Identification

  • Pathogens

    • Immune system recognises antigens as being foreign and activates cells to destroy the pathogens

  • Abnormal body cells

    • Cancerous or infected cells display abnormal antigens and trigger an immune response

  • Toxins

    • Antigen molecules themselves and can be recognised by immune system

  • Cells from other organisms of the same species

    • Can cause rejection of transplanted organs

Non-specific: phagocytes

• White blood cells that engulf and destroy pathogens

• Neutrophils

  • Engulf and destroy pathogens at the site of infection

• Macrophages

  • Engulf and digest pathogens but also present the pathogen's antigens on the cell surface to active lymphocytes

Phagocytosis

• Pathogens releases chemicals that attract a phagocyte

• Phagocyte recognises pathogen's antigens as non-self

• Phagocyte binds to pathogen

• Engulfs the pathogen

• Pathogen is now contained within a vesicle (phagosome)

• Lysosome, containing hydrolytic enzymes called lysozymes, fuse with the phagosomes to form a phagolysosome

• Lysozymes digest and destroy the pathogens

• Phagocyte presents the pathogen's antigens on its surface to activate other cells in immune system

  • Is now referred as APC

Cytokines

• Chemicals released by phagocytes after pathogen engulfed

• Act as cell-signalling molecules to trigger the movement of other phagocytes to infection

• Also trigger an increase in body temperature

  • Inhibits pathogen reproduction

Opsonins

• Chemicals that bind to pathogens

  • Make them easily recognisable by phagocytes

• Contain receptors on cell-surface which bind to common opsonin

  • Make it easier for phagocyte to bind to pathogens and destroy it

Lymphocytes

• T cells

  • Mature in the thymus gland

  • Cellular response where they respond to antigens

• B cells

  • Mature in bone marrow

  • Involved in humoral response

T helper cells

• Cells have receptors on their cell-surface that bind to complementary antigens on antigen-presenting cells

• Produce interleukin (a type of cytokine) which stimulates B cells

• Can also transform into memory cells or T killer cells

T Killer cells

• Kill abnormal and foreign cells using perforin (protein)

• Protein makes holes in the cell-surface membrane which makes it become freely permeable and causes cell death

T regulator cells

• Suppress the immune system after pathogens have been destroyed

• Helps prevent IS from attacking body cells

T memory cells

• Long-term immunity against specific pathogens

• Provide a rapid response if body is re-infected

Cellular respiration

• Macrophage engulf pathogens and display their antigens on the cell-surface

  • Now antigen-presenting

• T helper cells with complementary receptors bind to these antigens

• On binding, the T helper cell is activated to divide by mitosis to form clones

• Cloned T cells then

  • Develop into memory cells

  • Develop into T cells

  • Stimulate phagocytosis (produce interleukins)

  • Stimulates divisions of B cells (interleukins)

How do antibiotics work

• Drugs that kill or inhibit growth of bacteria

• Target bacterial enzymes and ribosomes in metabolic reactions

  • Do not damage human cells

• Affect bacteria by

  • Preventing synthesis of bacterial cell walls

  • Disrupting protein activity in cell membrane

  • Disrupting enzyme action

  • Preventing DNA and protein synthesis

• Do not work on viruses

  • Do not have cell structures

  • Cannot be disrupted by antibiotics

Antibiotic resistance

• Genetic mutations occur which make some bacteria resistance to antibiotics

• Resistant bacteria can survive antibiotics

• Pass this on to their offspring

  • Often occurs on plasmids, meaning that they can also be transferred

Impact of antibiotic resistance

• Bacteria with many resistances

  • MRSA

    • Cause wound infections and are resistance to multiple antibiotics

  • C difficile

    • Infects digestive system and can reproduce in presence of many antibiotics

• How to prevent

  • Choosing appropriate antibiotics

  • Using antibiotics when needed

  • Avoiding wide-spectrum antibiotics

  • Ensuring patients complete their course

  • Avoiding use of antibiotics in farming

Source of medicines

• Examples

  • Penicillin - mould

  • Aspirin - willow bark

  • Prialt - pain-killing drug derived from venom of cone snail

• Future medicines

  • Personalised medicines

    • Tailored to individual's DNA

    • Analysis of genome so can see what would be more effective and less likely to cause side effects

  • Synthetic biology

    • Genetic engineering to develop artificial proteins, cells and microorganisms

Humoral response cells

• B cells

  • Cells have antibodies on their cell-surface membrane

    • Bind to complimentary antigens

  • Engulf the antigens and display them on their surface to become antigen-presenting cells

  • Once activated, B cells can divide into plasma and memory cells

• Plasma cells

  • These are types of B cells that can produce and secrete antibodies against a specific antigen

  • Short lifespan of only a few day

• Memory cells

  • Type of B cell that provides long-term immunity against specific pathogens

  • Longer lifespan than plasma

  • Divide rapidly into plasma cells if re-infected

• Helper T cells

  • Bind to antigen presenting cells to activate the division of B cells

Humoral response

• B cell with a complementary antibody binds to antigen on pathogen

• B cell engulfs pathogen

  • Presents antigens on cell surface to become APC

• Clonal selection

  • Activated T helper cells bind to B cell causing activation of this B cell

• Clonal expansion

  • Activated B cell divides by mitosis to form plasma and memory cell clones

• Cloned plasma cells produce and secrete the specific antibody which is complementary to antigen

  • Antibodies attach to antigens on pathogens and destroy them

• Memory cells circulate the blood and tissue fluid, ready to divide if the body is re-infected by the same pathogen

Primary and secondary immune response

• Depends on whether the specific pathogen has been encountered before or not

• Primary

  • Takes place when the body is exposed to a pathogen for the first time

  • Response is slow

  • Infected individual experiences symptoms of the disease

• Secondary

  • Takes place when the body has been exposed to the same pathogen before

  • Faster and stronger and no symptoms

Primary response

• Production of antibodies si slow after exposure to the pathogen (longer lag phase)

• Concentration of antibodies increases slowly

  • Very few B cells that are specific to the pathogen's antigens

• Takes time for the B cells to divide into plasma cells to produce the correct antibody

  • Symptoms occur

• B cells divide into memory cells to make the individual immune to this disease

Secondary response

• Production of antibodies is much quicker after exposure to the pathogen

• Concentration of antibodies increases quickly

• Because memory B cells recognise the pathogen's antigens

  • Divide quickly into plasma cells

• They secrete more antibodies to quickly destroy the pathogen

  • No symptoms

• Memory T cells activated to divide into T killer cells to destroy pathogen

Comparison

Autoimmune diseases

• Immune system cannot recognise self antigens and attacks them

• Examples

  • Type 1 diabetes

  • Lupus

    • Connective tissues

  • Rheumatoid arthritis

    • Attacks cells in the joints

Antibodies structure

• Y shaped glycoproteins

  • Made of four polypeptide chains

  • 2 heavy and 2 light chains

  • Held together via disulphide bridges

• Made up of various regions

  • Constant region

    • Same for all antibodies and binds to receptors on cells such as B cells

  • Variable region

    • Different for each antibody

    • Complimentary to specific antigen

  • Hinger region

    • Flexible so can bind to multiple antigens at once

Agglutination of pathogen

• Clumping pathogens together to enable easier phagocytosis

• Can engulf a number of pathogens at once

• Antibodies also act as opsonins which makes pathogens easily recognisable by phagocytes

Neutralisation of toxins

• Antibodies bind to inactivate toxins

• Neutralises the toxins to prevent them damaging body cells

Preventing the pathogen from binding

• To stop them from infecting body cells

• Block cell-surface receptors needed to bind to host cells

Types of immunity

• Active immunity

  • Develops when the immune system makes its own antibodies after exposure to antigens

  • Takes a while but its long term protection (memory cells)

• Passive

  • An individual gets antibodies made by a different organism

  • Provides immediate immunity

  • Short-term as the antibodies are broken down and memory cells are not produced

Vaccinations

• Involves introduction of antigens into body

• Stimulates immune response - artificial active immunity

• May contain

  • Dead/inactivated pathogens

  • Weakened pathogen strains

  • Harmless version of toxin

  • Isolated antigens from pathogen

  • Genetically engineered antigens

How is immunity provided

• The vaccine, containing antigens, is injected into the blood. 

• This stimulates the primary immune response to produce antibodies against the pathogen. 

• Memory cells, capable of recognising these antigens, are produced. 

• On second exposure to this pathogen, memory cells rapidly divide into plasma cells. 

• Plasma cells rapidly produce antibodies against the pathogen. 

• The pathogen is destroyed before any symptoms are experienced.

Criteria for successful vaccination

• Availability

  • Affordable and available in large amounts for mass immunisation

• Minimal side effects

• Infrastructure

  • Necessary storing, transporting and production

• Herd immunity

  • Vaccinate the majority of the population

  • Can provide protection to those not vaccinated

  • Most of population is immune and cannot transmit pathogen

  • Reduces likelihood of non-vaccinated individuals coming into contact with the pathogen

Why might vaccines not work

• Individual immunity failures

  • People with weak immunity may not be able to withstand vaccines

• Pre-immunity infection

  • Some individuals may contract disease post vaccination before immunity occurs

• Pathogen mutation

  • Rapid antigenic changes due to frequent mutations can make vaccines ineffective

• Pathogen variety

  • Variants can make universally effective vaccines nearly impossible

• Pathogen hidings

  • Some pathogens can evade immune system by 'hiding inside cells or inhabiting hard-to-reach body regions

• Vaccine objections

  • Misinformation, religion, ethics

• Antigenic variety

  • Relies on introducing a pathogen's antigens into the body to stimulate an immune response

  • Some pathogens can change their antigens

  • Means its hard to develop vaccines against some pathogens