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Module 3 of 3 · Text

Communicable diseases

Sara Bean

Communicable diseases

  • Types of pathogen
    • bacteria
      • prokaryotes
      • classified by shape:
        • rod = bacilli
        • spherical = cocci
        • comma shaped = vibrios
        • spiralled = spirilla
        • corkscrew = spirochaetes
      • classified by cell walls and how they appear after gram staining:
        • gram positive bacteria = purple-blue under light microscope --> MRSA
        • gram negative bacteria = red under light microscope --> E.coli
        • useful because it effects how they react to antibiotics
    • viruses
      • non-living infectious agents
      • some genetic material surrounded by protein
      • they invade living cells, hijack the biochemistry and make more virsuses
      • reproduce rapidly and evolve by developing adaptations to their host
      • there are even ones that attack bacteria called bacteriophages
      • considered ultimate parasites
    • proctoctista (protista)
      • eukaryotic microorganisms with various feeding methods
      • percentage act as pathogens for both plants and animals --> parasitic
      • many need a vector to transfer them or they may enter the body through contaminated water
    • fungi
      • cause more devastation in plants
      • eukaroyitc organisms but the ones that effect humans tend to be single-celled
      • some are parasitic and feed on living plants and animals
      • normally stop plants from photosynthesising
  • Modes of action
    • damaging the host tissues directly
      • viruses take over cell metabolism --> make host cell create loads of copies of them then they burst out which destroys the cell
      • some protoctista take over cells but don't take over genetic material they just digest the cell's contents when they reproduce
      • fungi digest living cells and destroy them 
    • producing toxins
      • most bacteria produce toxins that poison or damage host cells --> breakdown the membranes, inactivate enzymes or interfere with genetic material
      • some fungi produce toxins
  • Plant diseases
    • ring rot
      • effects tomatoes, potatoes and aubergines
      • caused by gram positive bacteria
      • damages leaves, tubers and fruit
    • tobacco mosaic virus
      • effects tobacco plants, tomatoes, peppers and cucumbers
      • caused by virus
      • damages leaves, flowers and fruit 
    • potato blight
      • effects potatoes and tomatoes
      • caused by protoctist 
      • destroys leaves, tubers and fruit
      • no cure
    • black sigatoka
      • effects bananas
      • caused by fungus
      • penetrates and digests cells
      • can cause 50% reduction in yield
      • no cure
  • Animal diseases
    • tuberculosis
      • bacterial disease
      • damages lung tissue and suppresses immune system
      • both curable and preventable in humans
    • bacterial meningitis 
      • bacterial infection of meninges of the brain which can spread to the rest of the body
      • mainly effects young children and teenagers
      • antibiotics cure it if given early enough
      • vaccines prevent it
    • HIV/AIDS
      • acquired immunodeficiency syndrome caused by human immunodeficiency virus
      • HIV targets T cells in immune system
      • gradually destroys immune system so people infected are open to other diseases (TB or pneumonia) 
      • HIV = retrovirus so infects the host cell, uses reverse transcriptase to make DNA from its own RNA which interacts with the host's DNA
      • passed through bodily fluids 
      • no vaccine and no cure
      • anti-retroviral drugs slow the process
    • Influenza
      • viral infection of ciliated epithelial cells in the gas exchange system (kills them which opens the airways to secondary infection)
      • three main strains - A, B & C
      • strain A are the most virulent and classified further by proteins on their surfaces
      • mutate regularly 
      • vaccines available every year with the predicted variations
      • no cure
    • Malaria
      • protoctista spread by bites of mosquitoes
      • female mosquitoes bite for blood to get protein before she lays her eggs
      • the protoctista invades the red blood cells, liver and brain
      • the disease recurs making them weak and vulnerable
      • no vaccine and limited cures
      • need to control the vector / mosquitoes
    • Ring worm
      • fungus affecting mammals
      • not damaging, just looks unsightly and is itchy
      • antifungal creams clear it
    • Athlete's foot
      • human fungal disease
      • form of ring worm that digests the skin between the toes
      • antifungal creams cure it
  • Transmission of pathogens between animals
    • direct transmission
      • direct contact (kissing, skin-to-skin contact, microorganisms from faeces transmitted on the hands)
      • inoculation (break in the skin, bite, puncture wound)
      • ingestion (contaminated food or drink)
    • indirect transmission
      • fomites (inanimate objects like bedding, socks or cosmetics)
      • inhalation (droplets of saliva or mucus from coughing, speaking or sneezing) 
      • vectors (transfer communicable pathogens unintentionally) 
      • water acts as a vector
    • factors affecting transmission
      • overcrowded conditions
      • poor nutrition
      • compromised immune system
      • poor waste disposal
      • climate change can introduce new vectors and pathogens
      • culture and infrastructure
      • socioeconomic factors like a lack of trained health workers
  • Transmission of pathogens between plants
    • direct transmission
      • contact of healthy plant with infected one
    • indirect transmission
      • soil contamination (could leave reproductive spores in soil that infect next crop)
      • vectors (wind - may carry any pathogen, water - spores float on the surface, animals - insects and birds carry pathogens and spores as they feed, humans - transmitted by contact)
    • factors affecting transmission
      • some vareities are suceptible to diseases
      • overcrowding increases contact
      • poor nutrition reduces resistance
      • damp, warm conditions increase the survival of pathogens
      • climate change - increased rainfall and wind promote the spread of pathogens
  • Plant defences against pathogens
    • recognising an attack
      • receptors in cells respond to molecules from the pathogens or chemical produced when cell wall is attacked
      • stimulates signalling molecules which trigger responses like production of defensive chemicals, sending alarm signals to uninfected cells and physically strengthen the cell walls
    • physical defences
      • callose is synthesised and deposited in the cell walls and membranes to act as barriers around site of infection
      • large amounts of callose continue to be deposited in the cell walls and lignin is added to make the barrier thicker and stronger
      • callose blocks sieve plates of phloem to cut off infected region
      • callose is deposited in plasmodesmata to seal the cell off from healthy cells
    • chemical defences
      • insect repellents
      • insecticides
      • antibacterial compounds containing antibodies
      • antifungal compounds with chitinases which interfere with fungi membranes
      • anti-oomycetes with glucanases which breakdown glucans found in cell walls of oomycetes
      • general toxins
  • Non-specific animal defences
    • skin - produces sebum, an oily substance than inhibits the growth of pathogens
    • most body tracts are line by mucous membranes that secrete mucus to trap microorganisms (also contains lysozymes and phagocytes)
    • tears, stomach acid and urine contain lysozymes
    • expulsive reflexes (coughing and sneezing) 
    • blood clotting
      1. platelets come into contact with collagen in skin or blood vessel walls
      2. platelets adhere and secrete thromboplastin and sertonin
      3. thromoplastin catalyses the production of thrombin which catalyses the production of fibrin which forms the clot
      4. sertonin causes vasoconstriction to reduce blood flow to the area
      • scars from when to much collagen is used to stitch the wound back up
    • inflammatory response
      1. mast cells are activated by damaged tissue
      2. mast cells release cytokines and histamines
      3. cytokines attract white blood cells to the site
      4. histamines cause vasodilation to increase the temperature (stops pathogen reproduction) and increases the permeability of blood vessels so the increased tissue fluid is used to restrict the pathogen
    • fevers
      • high temperatures inhibit pathogen reproduction
      • specific immune system works faster at higher temperatures
    • phagocytosis
      1. pathogens produce chemicals that attract phagocytes
      2. they recognise the pathogen's antigens as non-self
      3. they engluf the pathogen and enclose it in a phagosome
      4. the phagosome then fuses with a lysosome to make a phagolysosome
      5. the enzymes in the lysosome digest the pathogen
      • when a macrophage englulfs a pathogen it combines the antigens with its MHCs (major histocompatibility complexes) aka special glycoproteins in its plasma membrane --> forms a APC (antigen-presenting cell) which stimulates the specific response
    • helpful chemicals
      • cytokines cell-signal other phagocytes into helping out in the infected region + increase the body temperature
      • opsonins bind to pathogens to tag them for phagocytes (bind to protein in the phagocytes membranes)
  • Specific immune response
    • antibodies
      • Y shaped glycoproteins aka immunoglobulins that bind to a specific antigen or toxin
      • two identical long heavy chains bound to two identical short light chains with disulfide bridges
      • the binding site is at the end of the light chains aka the variable region
      • rest of the atibody is the same on all of them so = constant region
      • the hinge region where the heavy binds to light chains gives it flexibility to bind to two antigens at once
      • forms antibody-antigen complexes
      • they help by:
        • complex acts as an opsonin
        • most pathogens are no longer effective when its bound to antigens
        • act as agglutinins which clump pathogens together
        • act as anti0-toxins
    • lymphocytes
      • T helper cells --> have receptors on their membranes that bind to the antigens on the APCs; they produce interleukins (type of cytokine) which stimulate the activity of B cells
      • T killer cells --> destroy pathogens with perforin which increases their membrane permeability so the pathogen cell leaks 
      • T memory cells --> part of the immunological memory (when they meet the pathogen again they quickly divide and handle it fast)
      • T regulatory cells --> suppress the immune system to control and regulate it
      • Plasma cells --> produce antibodies for the particular antigen
      • B effector cells --> divide to form plasma cell clones
      • B memory cells --> part of the immunological memory (remember specific antibody needed for that antigen)
    • cell mediated immunity
      1. phagocyte englufs pathogen to become an APC
      2. receptors on T helper cells fit the antigen
      3. T helper cell is the replicates by clonal expansion --> the clones differentiate into T helpers, T killers, T regulatory cells, and T memory cells --> also releases interleukins to stimulate more phagocytosis
    • humoral immunity
      1. APCs = B cells
      2. interleukins produced by the activated T helper cell attracts B effector cells
      3. B cells have antibodies in their membrane - when the right antibody binds to the antigen on the APC it undergoes clonal expansion
      4. clonal expansion of B cell results in plasma cells and B memory cells
      5. plasma cells release a load of antibodies into the blood to help fight the infection
  • Autoimmune diseases = when the T regulatory cells don't work properly so the immune system continues its attack but on self cells
    • type 1 diabetes, arthritis, lupus
  • Natural immunity
    • active = when the body itself acts to produce antibodies and memory cells
    • passive = breast feeding passes antibodies from mother to baby *first milk is most important aka colostrum*
  • Artificial immunity
    • active = vaccinations (prevent epidemics)
    • passive = antibody injections
  • Medicines and the management of diseases
    • sources of medicines
      • penicillin comes from a mould
      • scientists design drugs on complex comupter programmes
      • analysis of the genomes of pathogens to find vulnerabilities
  • Drug design for the future
    • pharmacogenetics
      • personalised medicine where the drugs work with your individual combination of genetics and disease (look at genome of patient and genome of pathogen)
    • synthetic biology
      • using genetic engineering we can develop populations of bacteria that produces drugs that are otherwise very rare, too expensive or not available
      • mammals also used to produce drugs in their milk (pharming)
      • nanotechnology uses tiny non-natural particles that are used for biological purposes
  • The antibiotic dilemma
    • antibiotics work through selective toxicity where bacterial cells but not body cells are affected
    • over-prescriptions of antibiotics mean that some bacteria have built up resistance to the,
    • antibiotic resistant bacteria include MRSA and C. difficile which cause real issues in hospitals and care homes
    • antibiotic resistance can be reduce long-term by:
      • minimising the use of antibiotics
      • ensuring every course is completed fully
      • good hygiene in care homes, hospitals and in general

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