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Communicable Diseases & the Immune System

Communicable Diseases

 

  • Pathogen is a microorganism which can cause disease

    • Bacteria - Prokaryotes and ince in an organism multiply rapidly and damage cells or release waste products or toxins that are toxic to the host  

      • Tuberculosis (humans & animals affects many parts of the body and kills the cells and tissues with lungs being the most frequently affected) 

      • Bacterial meningitis (Humans, affects the meninges which is the membrane which surrounds the brain and spinal cord as membranes become swollen) 

      • Ring rot (Potatoes and Tomatoes, ring of decay in the vascular tissue of a potato tuber or tomato accompanied by the leaf wilting) 

    • Virus - Invade a cell and cause the cell to manufacture more of the virus infecting numerous healthy cells

      • HIV/AIDS (humans, attack cells in the immune system and compromise the immune response)

      • Influenza (animals & humans, attacks respiratory system and cause muscle pains) 

      • Tobacco Mosaic Virus (plants, mottling and leaf discoloration) 

    • Fungus - Release spores from hyphae which grow to the skin surface and send spores 

      • Black Sigatoka (banana, leaf spots and reduces yield) 

      • Ringworm (Cattle, growth of fungus in skin and causing rash)

      • Athletes foot (humans, growth between toes and under skin of feet) 

    • Protoctista - enter host cell and feed on the contents 

      • Malaria (animals and humans, parasite in the blood causes headache and fever and can progress to coma and death)

      • Blight (tomatoes and potatoes, affects leaves and potato tubers)

  • Transmission: Direct 

    • Direct physical contact: risk increased through bad hygiene, close living quarters, not disinfecting, not using condoms or protection during interourse etc.

    • Faecal/Oral Transmission: Human sewage is often used to fertilise crops and not treating waste often occurs, food must also be washed 

    • Droplet Infection: Cover mouth or nose when coughing sneezing etc. 

    • Spores: masks etc should be worn and general hygiene 

      • Factors: 

        • Crowded living 

        • Poor ventilation 

        • Poor health/diet 

        • Homelessness 

        • Living or working with individuals from where the disease is more common

  • Transmission: Indirect 

    • Vectors may transmit a pathogen 

    • An example is malaria where the anopheles female mosquito is a carrier and vector 

  • Plant pathogens 

    • Also can be indirect or direct through insect attack for example or through pathogens present in the soil 

 

Defences: Plant

  • Physical: 

    • Cellulose cell wall which may be lignified to provide further protection 

    • Waxy cuticle to prevent potentially pathogen carrying water accumulating on the leaf

    • Bark containing a variety of chemicals that work against pathogens 

    • Stomatal Closure as this is a possible point of entry 

    • CALLOSE FORMATION: Can be deposited at the ends of sieve tubes to stop flow and prevent spread of a pathogen 

    • TYLOSE FORMATION: swelling that fills the xylem to prevent spread of a pathogen in the water and contains high chemical conc to kill the pathogen 

    • (THINK: CSK - Callose Sieve tubes) 

  • Chemical: 

    • Terpenes in tyloses are harmful to pathogens

    • Tannins in the bark make them taste bad 

    • Terpenoids - essential oils with antibacterial and antifungal properties and can have a scent 

    • Phenols - antibiotic and antifungal. Basis of tannins which inhibit attack as the bind to salivary proteins and digestive enzymes and deactivate them which lead to a lack of growth and eventual death in insects if ingested in high amounts 

    • Alkaloids - Nitrogen containing and give a bitter taste to inhibit herbivores and act on a variety of metabolic reactions to inhibit enzyme action 

    • Defensive proteins - broad antimicrobial properties 

    • Hydrolytic enzymes  can break down parts fo a pathogen such as chitinase which breaks down the chitin cell wall of a fungus 

 

Defenences: Animals 

  • Primary:

    • Skin - cells migrate to position and are keratinocytes so in doing so dry out cytoplasm and it biomes replaced with keratin which is a barrier for pathogen (they undergo keratinization) 

    • Blood Clotting: Involves many clotting factors such as calcium ions (link to bio mols) which activate an enzyme cascade. Clot forms due to platelets and this dries and forms a scab which draws the cut sides together making a seal under which the skin can be repaired. First stage would be deposition of collagen under the scab and then mitosis to form new cells while tissues contract to bind the cut ends closer together this is how the barrier of the skin is repaired 

    • Mucous membranes - epithelial layer has goblet cells and mucous secreting membranes. Mucous traps the pathogens and then cilia move back and forth to woft the mucous up the trachea and then it can be passed into the stomach down the oesophagus where the bacteria or pathogen is then killed. 

    • Coughing and Sneezing - as well as vomiting etc may be caused as a reaction to chemicals etc but expel pathogens 

    • Inflammation - cells release histamine from mast cells which acts to combat infection by causing vasodilation and making capillary walls more permeable to white blood cells and further production of tissues fluid so there is a greater chance of the pathogen contacting lymphocytes and initiating a specific immune response 

  • Secondary: 

    • Pathogen invades and is recognised as foreign due to having non-self antigens 

    • Opsonins bind to the antigens on the pathogen to enhance the ability of the phagocyte to engulf the pathogen 

      • Opsonins not too specific to assure that they can bind to many antigens 

    • Most common phagocytes are neutrophils (MULTILOBED NUCLEUS) 

      • Neutrophils are manufactured in the bone marrow and can be in the blood or tissue fluid and will likely die soon after ingesting the pathogen. They have many lysosomes to digest the pathogen 

    • Neutrophil binds to the opsonin attached to the antigen of the pathogen 

    • Endocytosis occurs and the pathogen is engulfed, this forms a phagosome 

    • Lysosomes fuse to the phagosome and release lytic enzymes which digest the pathogen 

    • The harmless products are then absorbed into the cell 

    • OR 

    • Macrophage travels in the blood as a monocyte (kidney shaped nucleus) when the macrophage engulf the pathogen it is not fully digested 

    • Phagocyte attracted by chemicals produced by the pathogen → Chemotaxis

    • Phagocyte recognises the pathogen as a non-self cell and binds to it 

    • Phagocyte engulf the pathogen in endocytosis to form a phagosome 

    • Lysosomes move to phagosome and combine to form phagolysosome 

    • Enzymes break down the pathogen within the phagolysosome 

    • Digestion of the pathogen is complete and phagocyte-antigens will absorb the pathogen with major histocompatibility complex (MHC)

    • MHC complex is displayed on the phagocyte membrane making the antigen presenting cell 

    • This is called a processed antigen 

 

Antibodies: 

  • Specific to an antigen

  • They are immunoglobulins which are complex proteins produces by plasma cells \

  • Structure: 

    • 4 polypeptide chains, 2 heavy two light chains and the two heavy are the two on the inner part of the Y that make the stem and the inner part of each branch 

    • Variable region and a constant region 

    • Variable regions the part that is complementary to the antigen 

    • Overall has a Y shape 

    • Held together by disulfide linkages/bridges 

    • Has a hinge region which allows flexibility so a molecule can grip more than more 

  • How they work: 

    • Work by attaching to the antigens but divide into 3 groups 

    • Opsonins: Bind to the antigen and act as a binding site for the phagocyte so they can bind more easily and destroy the pathogen 

      • Can be non specific or specific if created in the specific immune response and bind to specific antigens some cna partake in neutralisation whereby if the virus uses the antigen to bind to host cells the binding of the antibody renders the antigen useless 

    • Agglutinins: As there are two binding sites on an antibody the agglutinins enable the crosslinking of pathogenic molecules by binding an antigen to one pathogen and then the other to a separate pathogen this makes it easier to engulf by phagocytes and prevents the pathogen from carrying out functions such as invading host cells 

    • Antitoxins: Bind to the molecules released by pathogenic cells which can be toxic and renders the toxic substance useless 

 

Specific Immune Response: 

  • Involves T & B lymphocytes which are both white blood cells with a large nucleus and specialised receptors on the plasma membranes 

  • Leads to antibody production which then neutralise the foreign antigen 

  • Leads to immunological memory 

  • 4 types of T cell: 

    • T helper cell: release cytokines which stimulate B cells to develop and sustain phagocytosis by phagocytes (THINK: helpers help to continue phagocytosis)

    • T killer cells: attack and kill host body cells that display the foreign antigen (THINK killers kill)

    • T memory cells: provide long term immunity (Memory remembers) 

    • T regulator cells: shut down the immune response and prevent autoimmune attack 

  • 2 types of B lymphocyte: 

    • Plasma Cell: circulate the blood an manufacture and release antibodies  

    • B memory cells: provide immunological memory 

  • Requires communication which occurs using cytokines or other singalling compounds such as monokines (macrophages - causing B cell differentiation), interleukins (T cells and macrophages to cause clonal expansion which is an increase in the number of cells by mitotic division) or interferon (inhibits virus replication + activates T killer)

  • Overview:

    • Foreign antigen detected by T and B lymphocytes either through the antigen presenting cell or when the pathogen enters the lymph system where the majority of the T & B cells are 

    • The first step us thus the presentation of antigens through either an antigen presenting macrophage, an infected cell or the pathogen itself 

    • There is then clonal expansion, Once the correct lymphocytes with complementary antibodies on its surface have been selected as they are complementary to the antigen their numbers must be increases 

    • This increase in numbers is proliferation and is stimulated by interleukins and the interleukins cause the B plasma cell to make more antibodies of the correct nature in a process aided by T helper cells. (the plasma cell does not create the antibodies directly but differentiates into a variety of cells required to synthesise antibodies) 

    • Thus differentiation is the next step to form a large quantity of the required antibody 

    • The last stage is action 

      • T killer cells attack infected cells to remove kill them (this may be using perforin to pierce the membrane and render the cell useles sor other method) 

      • T memory cells remain in the blood to provide long term immunity 

      • T helper cells continue to cause the differentiation of plasma cells and synthesis of antibodies which act in the ways outlines above 

      • Plasma cells continue to divide and enable the response 

      • B memory cells also remain in the blood to provide immunological memory 

    • The response is finally ended by the T regulator cells

 

Autoimmune diseases occur when the immune system attacks a part of the body, typically T or B cells that are specific to self cells are apoptosed and killed during development but sometimes this may be missed. This leads to antigens that are not normally exposed being exposed 

  • Arthritis - inflammation as antibodies attack the membranes around the joint 

  • Lupus - causes swelling and pain and is associated with antibodies which attack certain proteins in the nucleus 

 

Primary and Secondary Response Size:

  • 1st response: Primary - takes a few days and the response can be somewhat slow as there need to be adequate antibodies to combat the disease successfully and after the pathogen is delt with the number of antibodies drops rapidly 

  • 2nd/subsequent response: Secondary - B memory and T memory cells in the blood which recognise the specific antigen and immune system comes into action more quickly so antibody production starts sooner and is more rapid and the amount of antibodies produced is far greater. The levels of antibodies also decreases more slowly 

 

Vaccination: 

  • Typically an attenuated version but can be a whole live microorganism if not too harmful or a dead pathogen or a toxoid or even a preparation of only the antigens

  • Can be used with the aim of herd vaccination to provide immunity to the majority of the population (at risk) as then the disease can no longer spread as easily (needs 80-95% of population) 

  • Can be used in ring vaccination: when a new case is reported the individuals in the immediate vicinity of the case can be vaccinated and thus the disease cannot spread 

  • Often used to control epidemics and pandemics (COVID)

  • Different types of immunity: 

    • Active Natural: Immunity provided by antibodies made by the immune system as a result of infection which they contracted naturally 

    • Active Artificial: Immunity provided by antibodies made by the immune system as a result of vaccination 

    • Passive Natural: Placenta or Breast milk to assure a babies immune to the diseases the mother is immune to prior to when the baby has developed a strong enough immune system 

    • Passive Artificial: Injection of antiBODIES from another individual. The individual themselves does not synthesise any antibodies they are given the 

  • The passive or active refers to whether the individual synthesised the antibodies themselves while the natural or artificial refers to whether the individual had the disease through a natural method or not 

 

Medicine & Antibiotics: 

  • Medication can be developed 

    • Accidentally such as penicillin 

    • Through adaptation of traditional remedies such as morphine which was used traditionally and then adapted 

    • Observation of wildlife such as how monkeys and bears rub citrus on their coats to prevent insect bites which lead to insecticide development 

  • Now there is an emphasis on

    • Further research into disease causing mechanisms to find ways to prevent these such as in HIV and AIDS to understand which receptor the virus binds to and the shape of the binding site on the virus to synthesise a medication which can be used to block this site 

    • Personalised medicine: DNA sequencing to develop specific drugs away from any side effects or adverse effects that a drug may have if a general medication is used

    • Synthetic Biology: biology synthetically developed that mimics natural processes

  • MRSA and Antibiotic resistance

    • The overuse of antibiotics can lead to an increased chance of new strains of bacteria which are resistant to a given antibiotic

    • This is problematic as it renders the antibiotic useless 

    • As a result it is important that antibiotics are not overused 

    • Surfaces are kept clean to prevent spread of resistant bacteria

    • Patients who are infected with resistant bacteria are treated separately 

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