OCR module 4 entire topic biology

• Communicable diseases are caused by pathogens and that includes bacteria, viruses, protoctista and fungi
• Pathogens cause harm through directly damaging the tissue or through the release of toxins
• Examples of diseases caused by different pathogens

  • Bacterial diseases
  • Viral diseases
  • Protoctista diseases
  • Fungal diseases
• Prokaryotic cells


  Classified by their shape or cell wall
• Shapes of prokaryotic cells

  • Rods
  • Spherical
  • Comma
  • Spiraled
  • Corkscrew
• Gram-positive and gram-negative bacteria

  Determined by the two types of cell walls
• Tuberculosis


  • Caused by Mycobacterium tuberculosis or Mycobacterium bovis
  • Damages lung tissue and suppresses immune system
  • Can be cured with antibiotics
  • Can be prevented through vaccination
• Bacterial meningitis


  • Caused by Streptococcus pneumoniae or Neisseria meningitidis
  • Infects the brain and meninges
  • Very serious, spreads quickly causing septicemia
  • Can be cured with antibiotics if diagnosed early
  • Some forms can be vaccinated against
• Ring rot


  • Caused by Clavibacter michiganensis
  • Infects potatoes, tomatoes and aubergines
  • Gram-positive bacteria that damages leaves, tubers and fruit
• Viruses


  • Non-living, acellular, smaller than bacteria, consist of genetic material, capsid and attachment proteins
  • Can only replicate inside host cells
• Bacteriophages


  Viruses that infect bacteria
• HIV


  • Consists of capsid, core with RNA and reverse transcriptase, envelope with lipids, and attachment proteins
  • Transported in blood, uses CD4 proteins to attach to helper T cells
  • Reverse transcriptase copies viral RNA to DNA which enters host cell nucleus
  • Destroys helper T cells, leading to AIDS when immune system is compromised
• Influenza


  • Caused by Orthomyxoviridae
  • Infects ciliated cells in gas exchange surfaces
  • Can kill these cells, leading to harmful secondary infections like pneumonia
  • Young, elderly and immunocompromised are most at risk
• Tobacco mosaic virus


  • Mainly infects tobacco plants
  • Causes damage to leaves, resulting in mosaic pattern
  • Can also damage flowers and fruits
  • Affects photosynthesis and plant growth
  • No cure, but resistant plant strains have been developed
• Protoctista


  • Eukaryotic, single-celled or colonial organisms
  • Few are pathogenic but those that are are extremely dangerous
• Malaria


  • Caused by Plasmodium protoctista
  • Transmitted by mosquitoes
  • Infects red blood cells and liver in humans
  • No vaccine or cure, but preventative medicines exist
• Potato blight


  • Caused by Phytophthora infestans protoctista
  • Fungus-like protoctista that causes damage to leaves and fruit of potatoes and tomatoes
  • No cure, but resistant plant strains have been developed
• Fungi


  • Eukaryotic, can be multicellular or single-celled
  • Pathogenic fungi are parasitic, release enzymes to digest host tissue and feed on it
• Black Sigatoka


  • Caused by Mycosphaerella fijiensis fungus
  • Infects banana leaves, causing them to turn black and preventing photosynthesis
  • Fungicides can kill the fungus, and resistant strains have been developed
• Ringworm


  • Caused by Trichophyton verrucosum fungus
  • Infects many mammals including humans, causes white crusty circles on skin
  • Not harmful but can cause itching and discomfort
• Athlete's foot


  • Caused by Tineapedis fungus
  • Only infects humans, thrives in warm damp regions like feet
  • Causes cracked, scaly skin and itchiness, but can be cured with antifungal creams
• Factors that increase disease transmission

  • Hot climates
  • Poverty and developing countries
  • Lack of infrastructure, sanitation, fresh water, medicines
• Types of disease transmission

  • Direct transmission: contact, inoculation, ingestion
  • Indirect transmission: vectors, droplets, fomites
• Plant defences

  • Physical barriers like bark and cuticles
  • Antibacterial chemicals and proteins
  • Repelling insects that are vectors
  • Physical defences to prevent spread between cells
• Animal primary defences


  Skin, blood clotting, mucus, cilia, lysozymes, inflammation, phagocytosis
• Phagocytosis


  1. Pathogens release chemicals that attract phagocytes

  2. Phagocytes have receptors to bind and engulf pathogens

  3. Lysosomes fuse with phagosomes to digest pathogens

  4. Phagocytes present pathogen antigens on their surface
• Animal secondary defences


  • Lymphocytes (B cells and T cells)
  • B cells and T cells respond to specific antigens
  • T cells mediate cell-mediated immune response
• Second line of defense

  1. Pathogen stopped from getting in or destroyed

  2. Specific response to particular shaped antigens

  3. Involves B lymphocytes and T lymphocytes

  4. B cells mature in bone marrow

  5. T cells mature in thymus
• T cells

  Responsible for cell-mediated response
• Cell-mediated response


  1. T cell receptors bind to antigen on antigen-presenting cells

  2. T cells divide rapidly by mitosis (clonal expansion)

  3. T helper cells activate B cells and macrophages

  4. T memory cells retain receptor for future infection

  5. T killer cells destroy infected/abnormal cells
• Antigen-presenting cells


  Cells that present non-self antigen on their surface, e.g. infected body cells, phagocytes that have engulfed pathogens, transplanted organ cells, cancer cells
• T killer cell action

  1. Release perforin protein

  2. Perforin embeds in cell membrane and creates pores

  3. Causes cell contents to leak out or water to enter, leading to cell death
• Humoral response


  1. T helper cells stimulate B cells

  2. B cells rapidly divide (clonal expansion)

  3. B cells differentiate into plasma cells and memory B cells

  4. Plasma cells produce antibodies
• Antibodies


  Globular quaternary structure protein with variable region that binds to antigen
• Antibody functions


  • Agglutination (clumping pathogens)
  • Opsonisation (marking pathogens for phagocytosis)
  • Antitoxin (binding to toxins)
• Primary immune response


  1. First exposure to pathogen

  2. Takes days to produce enough antibodies

  3. Causes symptoms as pathogen causes damage
• Secondary immune response


  1. Re-exposure to same pathogen

  2. Memory B cells rapidly produce antibodies

  3. Pathogen destroyed before causing symptoms
• Active immunity


  Immunity gained from being exposed to pathogen or antigen, either naturally or through vaccination
• Passive immunity


  Temporary immunity gained from direct introduction of antibodies, e.g. from placenta or breastmilk
• Cells are labeled with unique proteins to enable self/non-self recognition