Chapter 12 - Communicable Diseases

Bacteria

-Prokaryotes

-Have no membrane-bound nucleus

-Classified by basic shapes and cell walls

-Gram positive appear purple/blue and gram negative appear red

-Damage cells

-Reproduce rapidly

-Can release toxins or waste products toxic to host

-Live in vascular tissue in plants

-Killed with antibiotics

5 basic shapes of bacteria

Bacilli - Rod shaped

Cocci - Spherical

Vibrios - Comma shaped

Spirilla - Spiralled

Spirochaetes - Corkscrew

Fungi

-Eukaryotes

-Not major problem but can be devastating in plants

-Most are multicellular (except yeast)

-Feed on dead/decaying matter

-Some are parasitic feeding on living plants and animals

-Reproduce by producing millions of spores which spread huge distances (spread rapidly through crop plants)

Viruses

-Not living so require host

-Very small 0.02-0.03 micro meters

-Basic structure, genetic material surrounded by protein coat

-Genetic material inserted into host DNA

-Can evolve and develop adaptations

-All natural viruses are pathogenic and can also cause disease in other organisms like bacteria

-Some viruses are modified to treat disease

Protocista (Protista)

-Eukaryotic

-Varied and have a variety of feeding methods

-Small number are pathogenic in plants/animals

-Protists causing disease are parasitic

-Pathogenic protists need a vector, or they can enter directly through polluted water

2 ways in which pathogens act

- Damage host tissues directly: take over cells, digest living cells and destroy them

- Produce toxins which damage host tissues

Ring rot

A bacterial disease of potatoes, tomatoes, and aubergines caused by the Gram positive bacterium Clavibacter michiganensis. It damages leaves, tubers and fruit. It can destroy up to 80% of the crop and there is no cure. Once bacterial ring rot infects a field it cannot be used to grow potatoes again for at least two years.

Tobacco mosaic virus

A virus that infects tobacco plants and around 150 other species including tomatoes, peppers, cucumbers, petunias and delphiniums. It damages leaves, flowers and fruit, stunting growth and reducing yields, and can lead to an almost total crop loss. Resistant crop strains are available but there is no cure.

Potato blight

Caused by the fungus-like protoctist oomycete Phytophthora infestans. The hyphae penetrate host cells, destroying leaves, tubers and fruit, causing millions of pounds worth of crop damage each year. There is no cure but resistant strains, careful management and chemical treatments can reduce infection risk.

Black sigatoka

A banana disease caused by the fungus Mycosphaerella fijiensis, which attacks and destroys the leaves. The hyphae penetrate and digest the cells, turning the leaves black. If plants are infected it can cause a 50% reduction in yield. Resistant strains are being developed - good husbandry and fungicide (a chemical that kills fungi) treatment can control the spread of the disease but there is no cure.

Tuberculosis

A bacterial disease of humans, cows, pigs, badgers, and deer commonly caused by Mycobacterium tuberculosis and M. bovis. TB damages and destroys lung tissue and suppresses the immune system, so the body is less able to fight off other diseases. Worldwide in 2012 around 8.6 million people had TB of which 1.3 million died. The global rise of HIV/AIDS has had a big impact on the numbers of people also suffering from diseases such as TB, because people affected by HIV/AIDS are much more likely to develop TB infections. In people TB is both curable (by antibiotics) and preventable (by improving living standards and vaccination).

Bacterial Meningitis

A bacterial infection (commonly Streptococcus pneumoniae or Neisseria meningitidis) of the meninges of the brain (protective membranes on the surface of the brain) which can spread into the rest of the body causing septicaemia (blood poisoning) and rapid death. It mainly affects very young children and teenagers aged 15-19. They have different symptoms but in both, a blotchy red/purple rash that does not disappear when a glass is pressed against it is a symptom of septicaemia and immediate medical treatment is needed. About 10% of people infected will die. Up to 25% of those who recover have some permanent damage. Antibiotics will cure the disease if delivered early. Vaccines can protect against some forms of bacterial meningitis.

HIV / AIDS

Caused by HIV (human immunodeficiency virus), which targets T helper cells in the immune system of the body (see Topic 12.6, The specific immune system). It gradually destroys the immune system so affected people are open to other infections, such as TB and pneumonia, as well as some types of cancer. HIV/AIDS can affect humans and some non-human primates. HIV is a retrovirus with RNA as its genetic material. It contains the enzyme reverse transcriptase, which transcribes the RNA to a single strand of DNA to produce a single strand of DNA in the host cell. This DNA interacts with the genetic material of the host cell. The virus is passed from one person to another in bodily fluids, most commonly through unprotected sex, shared needles, contaminated blood products and from mothers to their babies during pregnancy, birth or breast feeding. No vaccine and no cure but antiretroviral drugs can slow down the progress.

Influenza (Flu)

A viral infection (Orthomyxoviridae spp.) of the ciliated epithelial cells in the gas exchange system. It kills them, leaving the airways open to secondary infection. Flu can be fatal, especially to young children, old people and people with chronic illnesses. Many of these deaths are from severe secondary bacterial infections such as pneumonia on top of the original viral infection. Flu affects mammals, including humans and pigs, and birds, including chickens. Three strains: A, B, C, strain A is most virulent. Flu viruses mutate regularly. The change is usually quite small, so having flu one year leaves you with some immunity for the next. Every so often, however there is a major change in the surface antigens and this heralds a flu epidemic or pandemic as there are no antibodies available. Vulnerable groups are given a flu vaccine annually to protect against ever changing strains. There is no cure.

Malaria

Caused by the protoctista Plasmodium and spread by the bites of infected Anopheles mosquitoes (the vector - Topic 12.3). The Plasmodium parasite has a complex life cycle with two hosts - mosquitoes and people. They reproduce inside the female mosquito. The female needs to take two blood meals to provide her with protein before she lays her eggs - and this is when Plasmodium is passed on to people. It invades the red blood cells, liver, and even the brain. Around 200 million people are reported to have malaria each year, and over 600000 die. The disease recurs, making people weak and vulnerable to other infections. There is no vaccine against malaria and limited cures, but preventative measures can very effective. The key is to control the vector. Anopheles mosquitoes can be destroyed by insecticides and by removing the standing water where they breed. Simple measures such as mosquito nets, window and door screens and long sleeved clothing can prevent them biting people and spreading the disease.

Ring worm

A fungal disease affecting mammals including cattle, dogs, cats and humans. Different fungi infect different species - in cattle, ring worm is usually caused by Trichophyton verrucosum. It causes grey-white, crusty, infectious, circular areas of skin. It is not damaging but looks unsightly and may be itchy. Antifungal creams are an effective cure.

Athletes foot

A human fungal disease caused by Tinia pedia, a form of human ring worm that grows on and digests the warm, moist skin between the toes. It causes cracking and scaling, which is itchy and may become sore. Antifungal creams are an effective cure.

Define transmission

The way in which a parasitic microorganism travels from one host to another

Define parasites

Need a host to survive. Keep the host alive

Define parasitoids

Need a host to reproduce. Lay eggs in another organism which eventually burst out. Kill the host.

Direct transmission in animals

• Direct contact - Kissing, sexual transmission, skin to skin, faeces on hands

• Inoculation - Break in skin (e.g. sex) , animal bite, puncture wound, sharing needles

• Ingestion - Contaminated food/drink, transferring pathogen from hands to mouth

Indirect transmission in animals

• Fomites - Inanimate objects

• Droplets infection - Saliva or mucus expelled from mouth

• Vectors - Transmits communicable pathogens from one host to another

Factors affecting transmission of communicable disease in animals

• Overcrowded living/working conditions

• Poor nutrition

• Compromised immune system

• Poor disposal of waste

• Climate change

• Culture and infrastructure

• Socioeconomic factors

Direct transmission in plants

Direct contact between healthy and diseased plant

Indirect transmission in plants

• Soil contamination - Infected plants leave pathogens or reproductive spores in soil

• Vectors - Wind, water, animals humans

Factors affecting transmission of communicable disease in plants

• Planting crop varieties which are susceptible to disease

• Overcrowding

• Poor mineral nutrition reduces resistance

• Damp, warm conditions are good for spread of pathogens/spores

• Climate change

How do plants recognise an attack

• Cell signalling

• Receptors in cells respond to molecules or chemicals from pathogen

• Stimulates release of signalling molecules, trigger cellular responses, defensive chemicals, alarm signals to unaffected cells, strengthen cell walls

Plant physical defences

• Waxy cuticle - Prevent water collecting on cell surface, which pathogens need to survive

• Bark - Contains chemicals that work against pathogenic organisms

• Cell wall - Physical barrier containing chemicals which can be activated

• Lignin - Thickens cell walls, waterproof

• Stomatal closure - Prevents entry

Callose

Physical defence. Synthesised and deposited between cell wall and membrane, preventing spread of pathogen to adjacent cells. Blocks sieve plates in phloem, sealing off infected cells and preventing spread via transport system.

Tylose

Physical defence. Balloon-like swellings, filling xylem vessel. Block vessel preventing water flow and spread. Tylose contains a high concentration of chemicals toxic to pathogens.

Plant chemical defences

• Insect repellents - e.g. pine resin

• Insecticides - e.g. pyrethrins, caffeine

• Antibacterial compounds - e.g. phenols (bind to digestive enzymes), defensins (antimicrobial action)

• Antifungal compounds - e.g. phenols, caffeine, chitinases (enzymes that break down chitin)

• Anti-oomycetes - e.g. glucanases (enzymes that break down glucans)

• Terpenoids - antibacterial properties

• Alkaloids - bitter taste, deters eating, prevents damage and therefore pathogen entry

• Hydrolytic enzymes - break down cell walls of pathogens

What is necrosis

Deliberate cell suicide. Intracellular enzymes are activated during injury. A few cells are sacrificed. Brown spots. Plant kills cells surrounding infection and limits access to water/nutrients, preventing spread.

What is a canker

Necrotic lesion in woody tissue. Causes death of cambium tissue in bark preventing spread.

Define primary and secondary defences

Primary - Barriers preventing entry of pathogens

Secondary - Combat pathogens which have entered the body

Non-specific defences to keep pathogens out (primary)

• Skin acts as physical barrier

• Many body tracts are lined with mucous membranes

• Lysozymes in tears, urine and acid in stomach

• Expulsive reflexes: coughing, sneezing, vomiting, diarrhoea

• Blood clotting - Clots rapidly seal the wound, platelets come into contact with collagen and secrete thromboplastin (enzyme triggering reactions for formation of blood clotting) and serotonin (makes smooth muscle walls of blood vessels contract to reduce blood flow to wound).

• Wound repair - Clot dries out. Epidermal cells grow underneath. Blood vessels regenerate. Collagen fibres are deposited to strengthen new tissue. Scab comes off when new epidermis is thick enough

• Inflammation - Localised response to pathogens, resulting in inflammation at wound site: swelling, heat, pain, redness. Mast cells in damaged tissues release histamines (make blood vessels dilate causing redness/heat and make blood vessel walls more leaky so blood plasma forced out) and cytokines (attract white blood cells which dispose of pathogens by phagocytosis).

Non-specific defences to get rid of pathogens (secondary)

• Fevers - When pathogens invade, cytokines stimulate hypothalamus to increase body temp. This is useful because: pathogens reproduction is inhibited above 37 degrees, specific immune system works better at higher temperatures

• Phagocytosis: 1 Pathogens produce chemicals that attract phagocytes.

2 Phagocytes recognise non-human proteins on pathogen, response to non-self organism.

3 The phagocyte engulfs the pathogen and encloses it in a vacuole called a phagosome.

4 The phagosome combines with a lysosome to form a phagolysosome.

5 Enzymes from the lysosome digest and destroy the pathogen.

Macrophage

• Larger cells

• Longer-lived

• Take longer to perform phagocytosis due to more complex process

• Made in bone marrow

• Travel as monocytes until settled in tissues to become macrophages

• Found in lymph nodes, alveolar walls and liver

• Often are antigen presenting cells

Neutrophil

• More common

• Short-lived (die after ingesting bacteria)

• Takes under 10 mins to perform phagocytosis

• Lobed nucleus

• Released in large numbers

• Large lysosome

• Dead neutrophils collect and form pus

• Frequently leave blood stream to patrol tissues for foreign bodies

Describe specific immune system

• Active/acquired immunity

• Slower

• Take up to 14 days to respond effectively

• Make appropriate/specific cells and antibodies

• Complicated and involved process

Describe antibodies

• Y-shaped glycoproteins called immunoglobulins which bind to specific antigens on the pathogen

• Made of two identical long polypeptide chains called heavy chains and two shorter identical chains called light chains. Chains held together by disulphide bridges and disulphide bridges inside the polypeptide chains holding them in shape.

• Antibodies bind to antigen by lock and key mechanism.

• Antibody has a constant region, always stays the same. It also has a variable region, different for each antibody so they are complementary to the antigen.

Define antigen

A protein found in a pathogen that is specific to it found on the outside of a cell and can be used to stimulate an immune response.

Define antibody

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

How do antibodies defend the body

1. The antibody of the antigen-antibody complex acts as an opsonin so the complex is easily engulfed and digested by phagocytes.

2. Most pathogens can no longer effectively invade the host cells once they are part of an antigen-antibody complex.

3. Antibodies act as agglutinins causing pathogens carrying antigen-antibody complexes to clump together. This helps prevent them spreading through the body and makes it easier for phagocytes to engulf a number of pathogens at the same time.

4. Antibodies can act as anti-toxins, binding to the toxins produced by pathogens and making them harmless.

Difference between B-lymphocytes and T-lymphocytes

• B-lymphocytes mature in the bone marrow

• T-lymphocytes mature in the thymus gland

Main types of T lymphocytes

• T helper cells - Have CD4 receptors which bind to surface antigens. Produce interleukins (type of cell signalling molecule). Interleukins stimulate B cells which increase antibody production.

• T killer cells - Destroy pathogen carrying antigen. Produce perforin which kills pathogen by making holes in its membrane making it freely permeable.

• T memory cells - Live for long time. Part of immunological memory. If they meet an antigen a second time, they divide rapidly to produce T killer cells to defeat pathogen.

• T regulator cells - Suppress immune system. Stop immune response once pathogen has been eliminated. Ensures the body recognises self antigens and doesn’t set up an autoimmune response.

Main types of B lymphocytes

• Plasma cells - Produce antibodies to a particular antigens on the and release them into circulation. Lives for a few days. Produces around 2000 antibodies per second.

• B effector cells - Divide to form plasma cell clones

• B memory cells - Live for long time. Immunological memory. Enable body to make rapid response when specific antigen carrying pathogen is encountered again.

Cell mediated immunity

1 In the non-specific defence system, macrophages engulf and digest pathogens in phagocytosis. They process the antigens from the surface of the pathogen to form antigen-presenting cells (APCs).

2 The receptors on some of the T helper cells fit the antigens. These T helper cells become activated and produce interleukins, which stimulate more T cells to divide rapidly by mitosis.

3 The cloned T cells may:

• develop into T memory cells, which give a rapid response if this pathogen invades the body again

• produce interleukins that stimulate phagocytosis

• produce interleukins that stimulate B cells to divide

• stimulate the development of a clone of T killer cells that are specific for the presented antigen and then destroy infected cells.

Humoral immunity

1. Activated T helper cells bind to the B cell APC. This is clonal selection - the point at which the B cell with the correct antibody to overcome a particular antigen is selected for cloning.

2. Interleukins produced by the activated T helper cells activate the B cells.

3. The activated B cell divides by mitosis to give clones of plasma cells and B memory cells. This is clonal expansion.

4. Cloned plasma cells produce antibodies that fit the antigens on the surface of the pathogen, bind to the antigens and disable them, or act as opsonins or agglutinins. This is the primary immune response and it can take days or even weeks to become fully effective against a particular pathogen.

5. Some cloned B cells develop into B memory cells. If the body is infected by the same pathogen again, the B memory cells divide rapidly to form plasma cell clones. These produce the right antibody and wipe out the pathogen very quickly, before it can cause the symptoms of disease. This is the secondary immune response.

What is autoimmune disease

The immune system stops recognising 'self' cells and starts to attack healthy body tissue.

Natural Immunity (Active and Passive)

• When you meet a pathogen for the first time, your immune system is activated and antibodies are formed, which results in the destruction of the antigen. The immune system produces T and B memory cells so if you meet a pathogen for a second time, your immune system recognises the antigens and can immediately destroy the pathogen, before it causes disease symptoms. This is known as natural active immunity. It is known as active because the body has itself acted to produce antibodies and/or memory cells.

• The immune system of a new-born baby is not mature and it cannot make antibodies for the first couple of months. A system has evolved to protect the baby for those first few months of life. Some antibodies cross the placenta from the mother to her fetus while the baby is in the uterus, so it has some immunity to disease at birth. The first milk a mammalian mother makes is called colostrum, which is very high in antibodies. The infant gut allows these glycoproteins to pass into the bloodstream without being digested. So within a few days of birth, a breast-fed baby will have the same level of antibody protection against disease as the mother. This is natural passive immunity and it lasts until the immune system of the baby begins to make its own antibodies.

Artificial Immunity (Active and Passive)

• For certain potentially fatal diseases, antibodies are formed in one individual (often an animal), extracted and then injected into the bloodstream of another individual. This artificial passive immunity gives temporary immunity - it doesn't last long but it can be lifesaving.

• Vaccination - Immune system stimulated to make its own antibodies to a safe form of an antigen.

1 The pathogen is made safe in one of a number of ways so that the antigens are intact but there is no risk of infection. Vaccines may contain: killed/inactive bacteria and viruses, weakened strains, toxin molecules that have been altered or detoxified, isolated antigens, genetically engineered antigens.

2 Small amounts of the safe antigen, known as the vaccine, are injected into the blood.

3 The primary immune response is triggered by the foreign antigens and your body produces antibodies and memory cells as if you were infected with a live pathogen.

4 If you come into contact with a live pathogen, the secondary immune response is triggered and you destroy the pathogen rapidly before you suffer symptoms of the disease.

This is artificial active immunity.

What is herd immunity

When a significant number of people in the population have been vaccinated, this gives protection to those who do not have immunity.

What is antibiotic resistance

An antibiotic works because a bacterium has a binding site for the drug and a metabolic pathway that is affected by the drug. If a random mutation during bacterial reproduction produces a bacterium that is not affected by the antibiotic, that is the one which is best fitted to survive and reproduce, passing on the antibiotic resistance mutation to the daughter cells. Bacteria reproduce very quickly so it does not take long for antibiotic resistance to grow.

How can antibiotic resistance be reduced

• Minimising the use of antibiotics

• Ensuring that every course of antibiotics is completed to reduce the risk of resistant individuals surviving and developing into a resistant strain population

• Good hygiene in hospitals, care homes and in general - this has a major impact on the spread of all infections, including antibiotic-resistant strains.

Define personalised medicine

Choosing a combination of drugs based on a person’s genetic base sequence.