Chapter 12: Communicable Diseases Flashcards
Define communicable disease.
- Disease that can be passed from one organism to another, of the same or different species.
Define vector.
- A living or non-living factor that transmits a pathogen from one organism to another.
How do viruses take over host cell + reproduce?
- Virus attached to host cell.
- Viral DNA inserted into host DNA.
- Viral DNA replicates.
- Synthesis of viral protein.
- Assembly of viral protein.
- Lysis of host cell.
Define parasite.
- Lives off host.
- Feeds off /gain nutrition from host at the expense of the host.
Example of plant diseases.
- Black Sigatoka (fungal).
- Tobacco Mosaic Virus (viral).
- Ring rot (bacterial)
- Potato blight (fungal).
How does reverse transcriptase in HIV lead to AIDS?
- RT in host nucleus.
- Viral DNA inserted into host DNA.
- Viral mRNA/RNA transcribed/produced.
- Codes for/translates viral proteins.
How does the Anopheles mosquito cause malaria?
- Mosquito –> vector.
- Plasmodium present in mosquito saliva/salivary gland.
- Infected mosquito feeds on human/bites skin –> creates a break in the skin.
- Plasmodium passes from saliva into blood.
Methods of direct transmission.
- Direct contact.
- Inoculation.
- Ingestion.
Methods of indirect transmission.
- Fomites.
- Vectors.
- Droplet infections.
Factors affecting transmission of communicable diseases in humans.
- Overcrowded living + working conditions.
- Poor nutrition.
- Compromised immune system.
- Poor disposal of waste.
- Culture + infrastructure –> traditional medicines.
- Socioeconomic factors –> lack of trained workers + warning when there is disease outbreak.
Methods of indirect transmission in plants?
- Soil contamination.
- Vectors –> wind, animals, humans and water.
Factors affecting spread of communicable diseases in plants.
- Plant varieties of crop that are susceptible to disease.
- Overcrowding –> increases chance of contact.
- Poor mineral nutrition –> reduces resistance.
- Damp, warm conditions –> increase spread of spores + survival of pathogen.
- Climate change.
How to prevent/reduce spread of disease in plants.
- Leave room between plants –> minimise pathogen spread.
- Rotate crops.
- Clear fields.
- Strict hygiene practices.
- Control insect vectors.
How does callose prevent spread of infection in plants?
- Callose papillae act as barriers.
- Prevent pathogens entering site around infection.
- Contain deposits of lignin –> makes barrier thicker + stronger.
- Callose blocks sieve plates –> prevents spread of pathogen + sealing off infected parts.
- Callose deposited in plasmodesmata between infected + healthy cells –> seal of infected + prevent spread.
Describe process of blood clotting.
- Blod clots rapidly to seal wound.
- Platelets in contact with collagen in skin or wall of damaged blood vessel –> adhere + secrete thromboplastin + seretonin.
- Thromboplastin –> enzyme that sets of a cascade of reactions that leads to the formation of a blood clot.
- Seretonin –> makes SM in vessel walls contract, constricting vessel –> reduce blood supply to damaged area.
- Clot dries out –> forming hard tough scab that keeps pathogen out.
- Epidermal cells below scab start to grow + seal wound permanently and damaged blood vessels regrow.
- Collagen –> deposited to give new tissue strength.
- Once epidermis reaches normal thickness –> scab sloughs off + wound healed.
List + explain features of the primary non-specific defence system.
- Skin = physical barrier to entry of pathogen.
- Mucous membrane/goblet cells = produce mucus to trap pathogen.
- Nasal hairs/cavity = trap pathogen.
- Ciliated epithelium = waft mucus.
- Sebum = inhibits growth of pathogens.
- Lysozyme/urine/tears = kills bacteria using antibacterial agent.
- Expulsive reflexes = coughing/sneezing expels pathogen from gas exchange system + vomiting/diarrhoea expels pathogen from digestive system.
- Stomach acid/gastric juices = kill pathogen –> low pH denatures enzymes + alters tertiary structure of active site.
Explain the stages of phagocytosis.
- Pathogen produce chemicals that attract phagocytes –> phagocyte receptors bind to antigens on pathogen.
- Phagocytes recognise non-human proteins on the pathogen –> response not to a specific type of pathogen but to a cell/organism that is no-self.
- Phagocyte engulfs pathogen + encloses it in a vacuole known as a phagosome.
- Lysosomes move towards + fuse with phagosome forming a phagolysosome.
- Enzymes from lysosomes digest + destroy pathogens into amino acids + glucose.
- Break down products absorbed into cytoplasm by diffusion/active transport.
- Cytoskeleton provides tracks for movement of vesicles.
What happens when macrophage has digested pathogen?
- Combines antigens from pathogen’s cell surface membrane with special glycoproteins in cytoplasm called the major histocompatibility complex.
- MHC moves pathogen antigens to macrophage’s surface membrane to form antigen presenting cell (APC).
- APC can now stimulate other cells involved in specific immune response.
How do cytokines perform their function of cell signalling?
- Cytokine/interleukin has specific shape.
- Cytokine/interleukin binds to receptors in cell surface membrane of B lymphocyte.
- Cytokine/interleukin + receptors are complementary.
- Activates clonal expansion/mitosis.
Structure of antibody.
- 2 heavy + 2 light chains held by disulfide bridges.
- Hinge region –> allows flexibility.
- Constant region –> allows binding to phagocyte.
- Variable region –> allows binding to more than one of the antigen + allows specificity to different antigens.
Describe agglutination.
- Clump together many pathogens containing antigen-antibody complex.
- Clump too large to enter host cell membrane.
- More pathogens consumed by phagocytes at once.
Describe neutralisation.
- Antibody blocks binding site on pathogen.
- Binds to toxin.
- Preventing entry to host cell.
Role of T helper cells?
- Produce interleukins + bind to B cell APC.
Role of T killer cells?
- Destroy pathogen carrying the antigen.
- Perforin –> kill pathogen by making holes in cell surface membrane –> freely permeable.
Role of T regulator cells?
- Stop immune response when pathogen eliminated.
- Prevent autoimmune response.
Role of plasma cells (type of B cell)?
- Produce antibodies to a particular antigen.
Role of T memory cell?
- Part of immunological memory.
- If pathogen met a second time –> divide rapidly to form T killer cell clones.
Role of B effector cells?
- Divide to form plasma cell clones.
Role of B memory cells?
- Provide immunological memory.
- Antigen encountered again –> form plasma cell closes –> produce antibodies –> wipe out pathogen.
Outline the steps of cell mediated immunity (response to antigens inside cell).
- In the non-specific defence system –> macrophages digest + engulf pathogens in phagocytes and process pathogen antigen’s to form APCs.
- Some receptors on T helper cells are complementary + can bind to the antigens.
- These T cells become activated + produce interleukins that:
- Stimulate more T cells to divide by mitosis.
- Produce more clones of identical T helper cells that contain the complementary antigen for a pathogen. - T cell clones may:
- Develop into memory cells –> provide rapid response if pathogen encountered again.
- Produce interleukins that stimulate phagocytosis + B cells to divide.
- Produce T killer cell clones –> specific for presented antigen + destroy infected cells.
Outline steps of humoral immunity (response to antigen outside cell).
Primary Response:
- B cell carries antibody on its surface.
- Antibody specific to one antigen.
- Clonal selection = activated T helper cell binds to B cell APC.
- Interleukins produced by activated T helper cells activate B cells.
- Clonal expansion = activated B cells divide by mitosis to differentiate into plasma cell clones + B memory cells.
- Cloned plasma cells produce antibodies –> specific to antigen.
Secondary Response:
- Memory cells remain in circulation –> form immunological memory.
- Recognise pathogen –> B memory cells divide rapidly to form plasma cell clones.
- Plasma cell clones –> produce specific antibodies to antigen + wipe out pathogen before symptoms of disease.
Role B memory cells when pathogen in body.
- Recognise pathogen/virus.
- Produce clone.
- Divide to form plasma cell clones.
- Make antibodies.
- Responsible for secondary immune response.
- Can change to form T killer cells.
Describe the actions of B lymphocytes.
Humoral response:
- B cell carries antibody on its surface
- Complementary to one antigen.
Clonal selection:
- Interleukins produced by activated T helper cells activate B cells.
Clonal expansion:
- Activated B cells divide by mitosis to form plasma cell clones + B memory cells.
- Plasma cell clones –> produce antibodies –> complementary to antigen.
- B memory cells –> immunological memory –> secondary response.
Why cannot plants obtain immunity?
- No circulatory system.
- No B or T lymphocytes.
- No antibodies.
- No memory cells.
