!!! OCR AS Level Biology: Communicable Diseases, Disease Prevention and the Immune System單詞卡 | Quizlet

Different types of pathogen

Bacteria, virus, protoctista, fungi

Diseases caused by bacteria

Tuberculosis, bacterial meningitis, ring rot

Diseases caused by viruses

HIV/AIDS, influenza, tobacco mosaic virus

Diseases caused by protoctista

Malaria, potato/tomato late blight

Diseases caused by fungi

Black sigatoka, ring worm, athlete's foot

Organisms affected by ring rot

Potatoes, tomatoes

Organisms affected by black sigatoka

Bananas

Organisms affected by ring worm

Cattle

Types of transmission of communicable pathogens

Direct, indirect

Direct transmission

The transfer of a pathogen directly from one individual to another

Methods of direct transmission in humans

Direct contact, inoculation, ingestion

Types of direct contact

Kissing, contact with bodily fluids, direct skin-to-skin, microorganisms from faeces

Things kissing and contact with bodily fluids can pass on

Bacterial meningitis, STDs

Things direct skin-to-skin contact can pass on

Ring worm, athlete's foot

Things microorganisms from faeces can pass on

Diarrhoeal diseases

Types of inoculation

Break in the skin, animal bite, puncture wound, sharing needles

Things breaks in the skin can pass on

HIV/AIDS

Things animal bites can pass on

Rabies

Things puncture wound/sharing needles can pass on

Septicaemia

Things ingestion can pass on

Amoebic dysentery, diarrhoea diseases

Methods of indirect transmission in animals

Fomites, droplet infection, vectors

Examples of fomites

Bedding, socks, cosmetics

Things fomites can pass on

Athlete's foot, gas gangrene, Staphylococcus infections

Examples of droplet infection

Expulsion of saliva and mucus

Things droplet infections can pass on

Influenza, tuberculosis

What do vectors do?

Transmit communicable pathogens from one host to another

Things vectors can pass on

Malaria, bubonic plague, rabies

Examples of vectors

Mosquitoes, rat fleas, dogs, foxes, bats, water

Factors affecting the transmission of communicable diseases in animals

Overcrowding living and working conditions, poor nutrition, compromised immune system, poor disposal of waste, climate change, culture, infrastructure, socioeconomic factors

How can climate change affect transmission of communicable diseases?

Introduce new vectors and new diseases

Example of direct transmission in plants

Direct contact of a healthy plant with any part of a diseased plant

Things that direct contact in plants can pass on

Ring rot, tobacco mosaic virus, tomato/potato blight, black sigatoka

Examples of indirect transmission in plants

Soil contamination, vectors

Things that soil contamination can pass on

Black sigatoka spores, ring rot bacteria, spores of P. infestans and TMV

Examples of vectors for plants

Wind, water, animals, humans

Things that wind as a vector in plants can pass on

Black sigatoka, P. infestans sporangia

Things that water as a vector in plants can pass on

Potato blight

Examples of animal vectors in plants

Insects, birds, aphids

Examples of things humans do as vectors for plants

Hands, clothing, fomites, farming practices, transporting plants and crops around the world

Things humans as vectors can pass on for plants

TMV, ring rot

Factors affecting the transmission of communicable diseases in plants

Varieties of crops that are susceptible to disease, over crowding, poor mineral nutrition which reduces the resistance of plants, damp and warm conditions, climate change

How does climate change affect the transmission of communicable diseases in plants?

Increased rainfall and wind promote the spread of diseases, animal vectors can spread to new areas, drier conditions reduce the spread of the disease

General pattern of defence in plants

Receptors in cells respond to molecules from the pathogen or chemicals produced when the cell wall is attacked, signalling molecules released which switch on genes in the nucleus, triggers cellular responses such as producing defensive chemicals and sending alarm signal to unaffected cells to trigger their defences

Structure of callose

Beta 1,3 and 1,6 linkages

Roles of callose in plant defences

Deposited between cell walls to act as barriers to prevent pathogens entering cell walls around the site of infection, lignin can be added to the callose deposits, blocks sieve tubes in the phloem to sell off the infected part, blocks plasmodesmata between infected cells

Why can plants react by sealing off and sacrificing?

They are continually growing at the meristems so can replace damaged parts

Examples of chemicals produced by plants in defence

Insect repellents, insecticides, antibacterial compounds, anti fungal compounds, anti-oomycetes, toxins

Examples of insect repellents produced by plants

Pine resin and citronella from lemon grass

Examples of insecticides produced by plants

Pyrethrins from chrysanthemums, caffeine

Examples of antibacterial compounds produced by plants

Phenols, gossypol from cotton, defensins, lysosomes

Examples of anti fungal compounds produced by plants

Phenols, gossypol from cotton, caffeine, saponins, chitinases

Examples of anti-oomycetes

Glucanases

Glucanases

Enzymes made by some plants that break down glucans

Glucans

Polymers found in cell walls of oomycetes

Non-specific animal defences against disease

Skin, blood clotting, wound repair, inflammation, expulsive refluxes, mucous membranes

How does the skin defend against disease?

Prevents entry, healthy microorganisms that outcompete pathogens, production of sebum that inhibits the growth of pathogens

How do mucuous membranes defend against disease?

Secrete mucus that traps microorganisms and contains lysozymes and phagocytes

Blood clotting cascade

The tissue is damaged, platelets are activated by damaged tissues, thromboplastin is released which catalyses the production of thrombin, Ca2+ and prothrombin will affect the production of thrombin, thrombin catalyses the production of fibrin, fibrinogen will affect the production of the fibrin, fibrin forms the clot

What does serotonin do in blood clotting and wound repair?

Makes the smooth muscle in the walls of the blood vessel contract so they narrow and reduce the supply of blood to the area

What happens after clotting in wound repair?

Clot dries out, scab formed to keep pathogens out, epidermal cells below the scab start to grow which leads to permanent sealing and damaged blood vessels regrow, collagen fibres are deposited, new epidermis reaches normal thickness, scab sloughs off

Inflammatory Response

The localised response to pathogens, resulting in inflammation at the site of a wound

Characteristics of the inflammatory response

Pain, heat, rednesss, swelling of tissue

What happens in the inflammatory response?

Mast cells are activated in damaged tissue to release histamines and cytokines

What do histamines do?

Makes the blood vessels dilate to cause localised heat and redness, raised temperature prevents pathogens reproducing, make blood vessel walls more leaky so blood plasma is forced out in the form of tissue fluid which causes swelling and pain

Oedema

Swelling

What do cytokines do in the inflammatory response?

Attract white blood cells

Phagocytes

Specialised white blood cells that engulf and destroy pathogens

Types of phagocytes

Neutrophils, macrophages

What is in pus?

Dead neutrophils and pathogens

Stages of phagocytosis

Phagocytes recognise non-human proteins on the pathogen, phagocyte engulfs the pathogen, puts it in a phagosome, phagosome fuses with lysosome to form a phagolysosome, lysins from the lysosome digest and destroy the pathogen by hydrolysis, parts of the pathogen absorbed into the cytoplasm

How do macrophages work? (This is the antigen presenting cell stuff)

Macrophage digests a pathogen, combines antigens from the pathogen surface membrane with glycoproteins in the cytoplasm called the major histocompatibility complex, MHC complex moves the pathogen antigens to the macrophage's own surface membrane to become an antigen presenting cell

General use of cytokines

Act as cell-signalling molecules to inform phagocytes that they need to move to the site of infection or inflammation, increase body temperature

General use of opsonins

Chemicals that bind to pathogens and tag them so they can be recognised by phagocytes. Phagocytes have receptors in cell membranes that bid to opsonins so the phagocyte then engulfs the pathogen

Role of plasma cells

Produce antibodies for a particular antigen and release them into circulation

Role of T helper cells

CD4 receptors on the cell surface membrane will bind to surface antigens on antigen presenting cells, producing interleukins. Interleukins then stimulate the activity of B cells, increase antibody and T cell production and stimulate macrophages to ingest pathogens

Role of T killer cells

To destroy the pathogen containing the antigen by producing perforin which kills the pathogen by making holes in the cell membrane

Role of T regulator cells

To suppress the immune system and regulate it, to stop the immune response once the pathogen has been eliminated, to make sure the body recognises self antigens and does not set up autoimmune response

When are interleukins particularly important?

In preventing the set up of autoimmune responses

Role of T memory cells

To provide immunological memory, to rapidly divide to form a large number of clones of T killer cells during the second exposure to the pathogen

Role of B memory cells

To provide immunological memory, to remember specific antigens and to enable the body to make a rapid response when a pathogen is encountered again

Process of cell mediated immunity

Macrophages engulf and digest pathogens in phagocytosis, process the antigens from the surface of the pathogen to make APCs, receptors on T helper cells fit some of the antigens in clonal selection, T helper cells become activated and produce interleukins to stimulate more T cell to divide by mitosis in clonal expansion

What can the cloned T cells do in the cell mediated response?

Develop into T memory cells, produce interleukins to stimulate phagocytosis or the division of B cells, stimulate the development of a clone of T killer cells that are specific for the antigen

Process of humoral immunity

Activated T helper cells bind to the B cell APC in clonal selection, interleukins are produced by the activated T helper cells, activate the B cells, activated B cells divide by mitosis to give clones in clonal expansion, cloned plasma cells produce antibodies that act as opsonins or agglutinins in the primary immune response, cloned B cells develop into B memory cells which will divide rapidly to form plasma cell clones if infected again in the secondary immune response

Humoral immunity

When the body responds to antigens found outside the cells and APCs.

What does the humoral immune system do?

To produce antibodies that are soluble in blood and tissue fluid but aren't attached to cells

General structure of antibodies

Made of two polypeptide chains called the heavy chains and two other chains called light chains, chains held together by disulfide bridges, the binding site is an area on both the heavy and light chains called the variable region, the variable region is a different shape on each antibody

How antibodies defend the body

Antibodies in the antigen-antibody complex can act as an opsonin so the complex is more easily engulfed, act as agglutinins to clump antigen-antibody complexes together, antitoxins

How do agglutinins help?

They cause antigen-antibody complexes to clump together so they don't spread through the body which makes it easier for the phagocytes to engulf a number of pathogens at the same time

How do anti-toxins help?

They bind to the toxins produced by pathogens which makes them harmless

How do opsonins help?

They bind to pathogens and tag them so they can be recognised by phagocytes as phagocytes have receptors on their cell membranes that bind to opsonins so they can engulf stuff

Important opsonins

Immunoglobulin G, immunoglobulin M

Natural active immunity

The body has acted to produce its own antibodies and memory cells, making it active, and exposure to the antigen occurred in a not medical intervention way

How does natural active immunity develop?

Meet a pathogen for the first time, activation of the immune system, antibodies are formed, T and B memory cells produced, meets pathogen for a second time, immune system recognises the antigen, destroys it before causing any symptoms

Active immunity

Body has acted to produce new antibodies and memory cells

Example of natural passive immunity

Breastfeeding, placenta

How does natural passive immunity develop?

First milk a mother makes is called colostrum which is high in antibodies, glycoproteins pass into the baby's bloodstream

When does natural passive immunity last until?

Until the baby starts to make its own antibodies

How does artificial passive immunity develop (In the broadest sense of the word)?

Injecting antibodies into the bloodstream

Examples of diseases that need artificial passive immunity to fight

Tetanus, rabies

How does artificial active immunity develop?

Immune system of the body stimulated to make its own antibodies by a safe form of the antigen