Module 4

• Bacteria

  • Prokaryotic cells that multiply rapidly, often causing harm by releasing toxins or waste products into host tissues. 
  • For example: Tuberculosis, Bacterial meningitis and ring rot. Bacteria have a variety of shapes: Rod (bacilli), spherical (cocci), comma (vibrio), spiralled (spirilla) and corkscrew (spirochaetes). 
  • The two types of cell walls determine whether a bacterium is classified as Gram-positive or Gram-negative.
• Tuberculosis 

  • Caused by Mycobacterium tuberculosis and M.bovis.
  • Infects - humans, deer, cows, pigs and badgers.
  • Causes harm by - damaging lung tissue and suppressing the immune system.
  • Cured using - antibiotics and prevented through vaccination
• Bacterial Meningitis 

  • Caused by Streptococcus pneumoniae or Neisseria meningitidis and infects the brain (the meninges protective layer). 
  • Spreads through the body quickly causing septicaemia and death. 
  • Antibiotics can cure if detected early and some can be vaccinated against.
• Ring rot  

  • Caused by Calvibacter michiganensis. 
  • Infects potatoes, tomatoes and aubergines. 
  • It is a gram-positive bacteria that damages leaves, tubers and fruit.
• Fungi (Eukaryotes)

  • Are multicellular or single-celled and pathogenic ones parasitic as they release enzymes to digest the host's tissue.
  • Often grow projections called hyphae under skin, which can release spores. 
  • In plants, it can invade the vascular tissue for nutrients.  
  • For example: Black sigatoka, ringworm and athlete’s foot.
• Black sigatoka

  • Caused by Mycosphaerella fijiensis fungus.
  • Infects Bananas.
  • The fungal hyphae cause damage to the leaves, causing them to turn black preventing plant growth.
  • Fungicides can kill fungus and resistant strains have been developed.
• Ringworm

  • Caused by Trichophyton verrucosum and infects many mammals, including humans.
  • Causes white, crusty circles on the skin. It is not harmful, but it can cause itching and discomfort.
• Athlete’s Foot

  • Caused by Tinea Pedia
  • Only infects humans
  • A type of ring worm that thrives, damp regions between the toes.
  • Causes the skin to crack and to become scaly, causing itchiness and soreness.
  • Cure using antifungal creams.
• Viruses

  • Invade cell machinery for replication and burst cells to spread.  
  • For example: HIV/AIDS, influenza and tobacco mosaic virus. 
  • They are non-living and acellular and are smaller than bacteria. 
  • Consists of genetic material (DNA or RNA), a capsid and attachment proteins. 
  • Replication occurs inside the host cells and involves the injection of nucleic acid into the cell. Bacteriophages are viruses that infect bacteria.
• Structure of HIV - Capsid (outer protein coat), Core (RNA and the enzyme reverse transcriptase which are needed for viral replication), an envelope (an extra outer later, made out of lipids taken from the host’s cell membrane) and protein attachments (on the exterior of the envelope to enable the virus to attach to the host’s helper T cell).
• • How HIV infects: 
  • HIV is transported in the blood until it attaches to a CD4 protein on the helper T cells. 
  • The HIV protein capsule then fuses with the helper T cell membrane, enabling the RNA and enzymes from HIV to enter. 
  • The HIV enzyme reverse transcriptase copies the viral RNA into a DNA copy and moves to the helper T cell nucleus, this is why it is called a retrovirus. 
  • Here, mRNA is transcribed and the helper T cell starts to create viral proteins to make new viral particles. 
• • IV positive is when a person is infected with HIV. 
  • AIDS is when the replicating viruses in the helper T cells interfere with the normal functioning of the immune system. 
  • With the helper T cells being destroyed by the virus, the host is unable to produce an adequate immune response to other pathogens and is left vulnerable to infections and cancer. The destruction of the immune system causes death. 
• Influenza

  • Orthomyxoviridae infects the ciliated cells lining gas exchange surfaces.
  • The infection can kill these cells, and cause harmful secondary infections.
  • Pneumonia is caused by a bacterium that infects the airways, and if sufferers develop this as a secondary infection it can result in death.
  • Those with a lowered immune system are at risk of having severe symptoms or dying if they get the flu.
• Tobacco mosaic virus

  • Infects plants, mainly tobacco plants.
  • Causes damage to the leaves, resulting in a mosaic pattern on them.
  • Damages flowers and fruits preventing the plant from growing.
  • No cure but resistant strains have been developed.
• Protoctist

  Protoctista (protista) are eukaryotes that are single-celled organisms or cells grouped into colonies and very few are pathogenic. They are parasites feeding off the host cell and are usually transmitted via a vector. For example: Malaria and potato/tomato late blight.
• Malaria

  • Caused by Plasmodium and is spread to humans through mosquitos (vectors and only female Anopheles mosquitoes). 
  • Plasmodium reproduces both sexually and asexually, within mosquitos and within human hosts. 
  • Passed from mosquitoes to humans when mosquitoes bite and take blood from humans. 
  • In humans, the Plasmodium infects red blood cells, the liver and the brain. 
  • There are some preventative medicines, but no vaccine or cure. 
• Potato Blight

  • Caused by Phytophthora infestans, a fungus-like Protoctista.
  • Causes potato blight and tomato late blight.
  • Has hyphae which enter the plant and cause damage to the leaves and fruit.
  • No cure, but resistant strains have been developed.
• • The life cycle of a pathogen involves invading a host, reproducing and spreading to new hosts in transmission. 
  • Direct transmission involves physical contact, the faecal-oral route, droplet infection, transmission as spores, inoculation, ingestion,
  • Indirect transmission uses a living vector to transmit the pathogen, such as malaria, droplets, fomites, contaminated soil (plants only).
  • Plants can be infected directly by the soil or spores in the air, or indirectly via insects.
• Modes of Transmission

  Certain living conditions can make transmission more likely.

  • Hot climates - increased heat provides more kinetic energy for chemical reactions and reproduction.
  • Social factors (poverty/ developing countries) - could result in poorer sewage infrastructure, a lack of fresh water and food, poorer sanitation and overcrowded living quarters. Medicine and vaccines being less readily available to prevent the spread.
• Plants defend against pathogens using passive and active mechanisms:

  • Passive physical - Cell wall, Lignin, Waxy cuticle, Bark, callose blocking sieve tubes at the end of growing season, tylose blocking old xylem vessels. All prevent entry.
  • Passive chemical - Phenols, alkaloids and enzymes with anti-pathogenic properties to kill pathogens and repel insects.
  • Active - Thickening of cell wall with the phenolic compound lignin, callose production, toxic oxidative species increased chemical production. This prevents pathogens from spreading.
• Primary defences against pathogens are non-specific and rapid:

  • Skin - Physical barrier. Helpful microflora compete with pathogens. Blood clots shut off wounds.
  • Tears and mucus - Tears contain lysozyme enzymes, mucus traps, pathogens and dust to be excreted.
  • Inflammation - Mast cells release histamine and cytokines for inflammation and sensitivity.
  • Phagocytosis - White cells engulfing and containing pathogens.
  • Histamine
  • Lysozymes - Hydrolytic enzymes which digest pathogens.
  • Expulsive reflexes (sneezing, coughing, vomiting) - force pathogens out.
  • Blood clots - Forms a new barrier.
• Histamine - causes the blood vessels to dilate, increasing blood flow to the area of damaged tissue. It also increases capillary permeability, enabling the leak of plasma fluid, white blood cells and antibodies to the damaged tissue causing swelling. Causes increased temperature of blood, killing pathogens.
• Blood Clotting

  Following a break-in the skin there is a cascade of events that leads to blood clotting:

  1. Platelets release the enzyme thromboplastin.
  2. Thromboplastin converts prothrombin into thrombin (enzyme).
  3. Thromboplastin and thrombin are both enzymes.
  4. Thrombin converts fibrinogen into fibrin.
  5. Fibrin fibres from a mesh. This traps erythrocytes and platelets to form a blood clot.
  6. Process requires CO2 to achieve thromboplastin. 
• Phagocytes can detect foreign antigens and engulf pathogens in phagocytosis, presenting their antigens to the specific immune system:

  1. Damaged cells and pathogens release cell-signalling chemicals (cytokines) that attract the phagocytes to the site of infection. 
  2. An opsonin protein can attach to pathogens to mark them and make it easier for neutrophils and macrophages to engulf them. 
  3. Phagocytes have receptors which can attach onto chemicals on the surface of pathogens. 
  4. The phagocyte that engulfs the pathogen into a vesicle to create a phagosome. 
• Secondary non-specific defences

  5.Within the phagocytes, there are lysosomes which contain hydrolytic lysozyme enzymes. 

  6. The lysosome fuses with the phagosome to expose the pathogen to the lysozyme. The lysozyme hydrolyses the pathogen and any soluble useful molecules are absorbed into the cytoplasm of the phagocyte. 

  7.The phagocytes will present the antigen of the digested pathogen on their surface -_they are then called antigen-presenting cells. 
• Neutrophils are the most common phagocyte. Monocytes are white blood cells that leave blood and enter tissues to mature into a macrophage.

  Opsonins are molecules that can bind antigens and flag them for phagocytosis.
• Antigen-presenting cells recruit specific T and B cells in clonal selection and expansion for specific immune responses. They are both created by the bone marrow stem cells but B cells mature in the bone marrow whereas the T cells mature in the thymus.
• There are 4 types of T - cells:

  • T killer cell - Attack and Kill infected body cells displaying antigens by releasing a protein (perforin) which embeds in the cell surface membrane and makes a pore so that any substances can or leaves the cell and this causes cell death which is most common in viral infections.
  • T helper cell - Release cytokines to stimulate B cells.
  • T memory cells - Long term immunity.
  • T regulatory cell - Shuts down immune response when finished.
• B cells form plasma cells, which release antibodies, and B memory cells for long term immunity. Clonal selection involves selecting the correct cell, and its subsequent division by mitosis is clonal expansion.
• Cell-mediated response (T-cells)

  Receptors on the T cells bind to antigens on antigen-presenting cells (APCs) causes the T cell to divide rapidly by mitosis. 

  1. APC
  2. T helper cells have receptors on their surface which can attach to the antigens on APC.
  3. Once attached, interleukins are produced which activates the T helper cells to divide by mitosis to replicate and make large numbers of clones.
  4. Cloned T helper cells differentiate into different T cells.
• Antigen-presenting (APC) are cells that present a non-self antigen on their surface. These include:

  • Infected body cells presenting viral antigens on their surface.
  • A macrophage which has engulfed and destroyed a pathogen presenting the antigens on their surface.
  • Cells of a transplanted organ will have different shaped antigens on their surface compared to your self-cell antigens. 
  • Cancer cells will have abnormal-shaped self-antigens.
• Autoimmune disorders

  Autoimmune diseases occur when our T and B cells attack our antigens and cells. Normally autoimmune cells are killed off in early development, but genetic and environmental factors may cause them to remain present. For example, Arthritis causing painful inflammation of membranes around joints and Lupus - causes antibodies to cell nuclei causing swelling and pain.
• T helper cells stimulate the B cells by producing interleukins, initiating the humoral response. Antigens are proteins found in the membrane of pathogens that trigger immune responses via their tertiary structure, whereas antibodies are proteins produced by plasma cells in the specific response.
• Antibodies

  • Globular, quaternary proteins that have binding sites complementary in shape to antigens.
  • Made up of 4 polypeptide chains, two heavy polypeptide chains and two light polypeptide chains.
  • The binding site is the variable region, where the antibody binds to a complementary-shaped antigen.
  • The rest of the antibody is the constant region.
  • When an antigen binds to the antibody it is described as an antigen-antibody complex.
• Humoral Response

  • Opsonin - Binds antigens when an antibody-antigen complex is formed making them more susceptible to phagocytosis or to neutralise.
  • Agglutinins - 2 variable regions allow pathogens to be cross-linked and clumped together. This inhibits their function and makes them easily engulfed by phagocytes. 

  Antitoxins - Neutralise toxins rendering them harmless.
• Process of Humoral Response

  1. Activated T helper cells bind to B cells with the complementary antibody to the antigen.
  2. Interleukins from T-cell activate B cell.
  3. The B cells rapidly divide by mitosis to make clones which differentiate into either memory B cells or plasma cells.
  4. The plasma cells produce antibodies. The antibodies attach to the antigens on the pathogen to help destroy them by agglutination and marking them for phagocytes. 
  5. The B memory cells remain in the blood.
• The B memory cells remain in the blood after infection and can rapidly produce large amounts of antibodies if there is reinfection with the same pathogen.
• Primary and Secondary Responses

  • The first time a host is infected, it takes days for clonal selection and expansion to form the correct antibodies i.e. the primary response which causes the infected person to suffer symptoms before the pathogen is destroyed. 
  • The secondary response is much faster and releases more antibodies. This is due to circuiting memory T and B cells, which can recognise the antigen and produce antibodies quickly before causing any symptoms (active immunity).
• Vaccines

  • Vaccinations introduce a weakened disease antigen to stimulate an immune response. 
  • They are used to tackle epidemics (when a disease spreads rapidly on a national level) and pandemics (when a disease spreads rapidly on a global level). 
  • They are not always effective for a long time. 
• Antigen Variability - Pathogen’s genetic material can mutate, resulting in a pathogen producing a different shaped antigen.