4.1 COMMUNICABLE DISEASE Flashcards
(75 cards)
1
Q
State the four types of pathogens
A
1) Bacteria (prokaryotes)
2) Virus
3) Fungi (eukaryotes)
4) Protoctista
2
Q
State and describe the communicable diseases caused by bacteria
A
1) Tuberculosis
- Kills the cells and tissues of host
2) Bacterial meningitis
- Causes infection of nervous system membranes
3) Ring rot in plants
- Causes leaf wilting
- Causes decay in vascular tissue
3
Q
State and describe the communicable diseases caused by viruses
A
1) HIV/AIDS
- Attacks cells of immune system
2) Influenza
- Attacks respiratory system and causes muscle pain
3) Tobacco mosaic virus in plants
- Causes discolouration of leafs
4
Q
State and describe the communicable diseases caused by fungi
A
1) Athletes foot
- Fungal growth between toes
2) Ringworm in cattle
- Growth of spores in skin causing rash by erupting
3) Black sigatoka in bananas
- Causes leaf spots which reduces yeild
5
Q
State and describe the communicable diseases caused by protoctista
A
1) Malaria
- Parasite in the blood transmitted by mosquito causes fever/coma/death
2) Blight in tomatoes/potatoes
- Affects leaves and potatoes
6
Q
Describe the general action of bacteria
A
- Reproduce rapidly to damage by releasing toxins into host cell
7
Q
Describe the general action of viruses
A
- Take over genetic machinery by copying viral cells in the nucleus of host
- Host cell eventually bursts/dies
8
Q
Describe the general action of fungi
A
- Contain hyphae that release spores
9
Q
Describe the general action of protoctista
A
- Feed on host cells contents
10
Q
Define primary non-specific defence
A
- Defence that prevents pathogens from entering the body
11
Q
State the five primary non-specific defences in animals
A
1) The skin
2) Blood clotting for wound repair
3) Mucous membranes
4) Coughing/sneezing
5) Inflammation
12
Q
Explain the role of the skin in primary non-specific response
A
- Is a tough physical barrier made of the protein keratin
- Keratin replaces the cytoplasm of dead cells on the skin surface
13
Q
Explain the role of blood clotting in primary non-specific response
A
- Clotting factors are released from platelets which activate enzyme cascades
- This then clots the cut so a scab can form, creating a temporary seal
14
Q
Define and explain the role of mucous membranes in primary non-specific response
A
- They are specialised epithelial cells that are covered in mucus
- Contain golblet cells which secrete mucus to trap any pathogens
- Their cilia then wafts away the pathogens trapped in mucus down to the acidic stomach
15
Q
Explain the role of the coughing/sneezing in primary non-specific response
A
- When pathogens irrittate or secrete toxins sudden expulsions of air will carry out the microorganisms
16
Q
Define and explain the role of inflammation in primary non-specific response
A
- When tissues swell and go red due to infection
- Histamine is released when p, raasathogens are in tissue
- Histamine causes vasodilation which results in the capillary walls to be more permeable to phagocytes/lymphocytes
- Blood plasma and phagocytes leave the blood and enter tissue fluid which causes swelling
- Excess tissue fluid drains into lymphatic system where lymphs are so that pathogens are in contact with lymphocytes
- This then initiates an immune response
17
Q
Define antigen-presenting cell
A
- A cell that isolates the antigen of a pathogen and places it on its plasma membrane to increase the chance of being recognised by T or B lymphocytes in the immune system
18
Q
Define and describe clonal selection
A
- Activation of a specific B or T cell that is specific to the antigen on an antigen presenting cell
- Causes a specific immune response
- Results in long-term immunity
19
Q
Define antigen
A
- Chemical markers on the outer membrane of a cell that causes an immune response
- Glycoproteins on the plasma membrane that are specific to that cell
20
Q
Define cytokines
A
- Hormone-like molecules used in cell signalling to stimulate an immune response
21
Q
Define neutrophil
A
- A type of white blood cell that engulfs foreign matter and traps it in a large vacuole (phagosome) which fuses with lysosomes to digest the foreign matter
22
Q
Define opsonin
A
- Proteins that bind to the antigens on a pathogen and then enhance phagocytes (neutrophils) ability to bind
23
Q
Define secondary non-specific defence
A
- Used to combat pathogens already in the body, detected by their antigens
24
Q
Draw and describe neutrophils
A
- Multilobed nucleus
- Manufactured in bone marrow
- Travel in blood and pop out into tissue fluid
- Short-lived
- Released in large numbers at site of infection
- Contain lysosome/digestive enzymes
25
Explain how **neutrophils** are adapted to their function
- Have **receptors** on **plasma membrane** that can **bind** to **specific opsonin** or **antigen**
- The **multi-lobed nucleus** allows it to **squeeze** through **narrow gaps**
- A **well developed cytoskeleton** allows it to **change shape** to **engulf pathogens ** and to move **lysosome vacuoles** around the **cell**
- Many **lysosomes** containing **lysin** for **digestion**
- Many **mitochondria** to release **energy** from **glucose**
- Many **ribosomes** to produce the **enzymes** involved
26
Draw the process of **phagocytosis**
27
Define **macrophage**
- Are **monocytes**
- **Large phagocytes** also produced in **bone marrow** that become **antigen-presenting cells** when they **engulf pathogens**
28
Define **active immunity**
- **Immunity** obtained from the production of **antibodies** in response to **infection** or **vaccination** (exposure to **antigens**)
29
Define **auto-immune disease**
- When **anitbodies** **attack** our own **antigens** by mistake
30
State how **auto-immune diseases** arise
- When **B** or **T lymphocytes** that are **specific** to our **antigens** are **NOT KILLED** when they should be at **early stages**
31
State **two auto-immune diseases**
1) **Arthirits**
2) **Lupus**
32
Define **lymphocytes**
- **White blood cells** with **large nuclei** and **specialised receptors** on their **plasma membranes**
33
State which **lymphocytes** are involved in the **specific immune response**
- **T lymphocytes**
- **B lymphocytes**
34
What type of **immunity** does **specific immune response** provide
- **Long-term immunity**
35
Describe **T-lymphocytes**
- **Produced** in the **bone marrow**
- **Mature** in the **thymus gland**
- Are **smaller** than **phagocytes**
- Have a **large nucleus**
- Travel in the **blood**
36
State the **four T cells**
1) **T-helper cells**
2) **T-killer cells**
3) **T-memory cells**
4) **T-regulatory cells**
37
Describe the role of **T-helper cells**
- **Release chemical messangers** (**cytokines**) that stimulate **B-lymphocytes** to **develop** and stimulates **phagocytes** to **develop**
38
Describe the role of **T-killer cells**
- **Attack** and **kill infected host-body cells** that display the **foreign antigen**
39
Describe the role of **T-memory cells**
- Remain in the **blood** for a **long-time** after, to produce a **secondary, longterm immune response**
40
Describe the role of **T-regulatory cells**
- **Inhibit** the **immune response** after **pathogen** is removed to **prevent** **auto-immunity**
41
Describe **B-lymphocytes**
- **Produced** and **mature** in the **bone marrow**
- Are **smaller** than **phagocytes**
- Have a **large nucleus**
- Travel in the **blood**
42
State the **two** types of **B-cells**
1) **B-memory cells**
2) **Plasma cells**
43
Describe the **role** of **B-memory cells**
- **Remain** in the **body** after to produce a **longterm immune response**
44
Describe the role of **plasma cells**
- **Manufacture** and **release antibodies**
45
State the **chemical** that allows for **cell signalling** in the **immune system**
- **Cytokines**
46
How can a **target cell** be **detected** via **cell signalling**
- Must have a **cell surface receptor** that is **specific** to **cytokines shape**
47
State **two** ways in which **cell signalling** is used in the **immune system**
1) **Macrophages** release **specific cytokines** which attract **neutrophils** and **stimulate B cells** to **differenciate** and **release antibodies**
2) **T-cells** and **macrophages** release **specific cytokines** which stimulate the **clonal expansion** and **differenciation** of **T** and **B lymphocytes**
48
Define **immunoglobulin**
- **Complex proteins** produced by **plasma cells** (**B**) in the **immune response** to an **infection**
49
Give an example of an **immunoglobulin**
- **Antibodies**
50
Draw a detailed structure of **antibodies**
51
State the **three** ways that **antibodies** work in
1) As **opsonins**
2) As **agglutinins**
3) As **antitoxins**
52
Describe **antibodies** as **opsonins**
- Antibodies can **bind** to **antigens** of a **pathogen** then act as a **binding site** for **neutrophils/phagocytes**
53
Describe **antibodies** as **agglutinins**
- Because each **antibody** molecule has **two identicle binding sites** for **antigens**, it can **crosslink pathogens**
- When many **antibodies crosslink pathogens** togther, they **clump** together many **pathogens** (agglutination)
- This **physically impaires** them and means they are more **easily detected** by **phagocytes/neutrophils**
54
Describe **antibodies** as **antitoxins**
- Some **antibodies** bind to **molecules** that are **released** by **pathogens** which may be **toxic** so **antibodies neutralise/untoxicate** them
55
Describe ,with a graph, the **primary** and **secondary specific immune response**
- **Antibodies** are produced in **response** to **infection**
- It takes a **few days** for the **antibody level** to **rise** in the **blood** that can **efficiently** combat **pathogens** (**PRIMARY immune response**)
- Once **pathogens** are dealt with, **antibody levels drop rapidly**
- The **second** time the **pathogen** enters the body, **T-memory** and **B-memory** cells **recognise** the **specific antigens**
- Thus **antibodies** are produced much more **rapidly** and at **higher concentrations** (**SECONDARY immune response**)
- No **symptoms produced** for the **host**
56
Compare the different types of **immunity**
57
Define **active immunity**
- Where the **immune system** is **activated** and **manufactures** its **own antibodies**
58
Define **passive immunity**
- Where **immunity** is achieved when **antibodies** are **passed** to an individual through **breast feeding** or **injection**
59
Define **artificial immunity**
- **Immunity** that is achieved as a result of **medical intervention**
60
Define **natural immunity**
- **Immunity** achieved through **normal life processes**
61
Define **vaccination**
- **Stimulating** an **immune response** via **harmless antigenic material** to provide **immunity**
- Releases **antibodies** and **T-memory**/**B-memory cells**
62
Define **epidemic**
- A **rapid** spread of **disease** through a **high proportion** of the **population**
63
State the **four** forms of **antigenic material** that can be used in **vaccines**
1) A **dead pathogen**
2) A **toxoid** (harmless version of toxin)
3) An **attenuated pathogen**
4) A **preperation** of **antigens** from the **pathogen**
64
Define **herd vaccination**
- **Vaccine** that provides **immunity** to **all/almost all** of the **population**
- **Disease** can no longer **spread** once enough people are **vaccinated**
65
Define **ring vaccination**
- **Vaccinating** the **people** in **immediate vicinity** of the **reported case**
66
State how **epidemics** arise
- When the **pathogen** undergoes **genetic mutation** so the **antigens** are **not recognised** by **memory cells** during the **second exposure**
67
State **three** reasons **drugs** are needed
1) **New diseases** are **emerging**
2) Some **antibiotics** are becoming **less effective**
3) There is still **no medicine** for some **current diseases**
68
State how **wildlife** use **natural medicines**
1) **Animals** rub **citrus oils** on their **octas** as **insecticides**/**antiseptics** to prevent **insect bites**/**infection**
2) **Birds** line their **nests** with **medicinal leaves** to protect **chicks** from **blood-sucking mites**
69
State how **medicines** can be made via **pathogen plamsa membrane antigens**
- The **binding site** between **pathogen antigens** and **body cell receptors** needs to be **blocked**
- The **glycoprotein receptor molecule** needs to be **isolated**, **sequenced**
- This is to determine a **drug** that **mimics** the **shape** of the **receptor** so that the **antigen** can be **binded** to and **blocked**
70
State the effect of the **overuse** of **antibiotic**
- Causes **pathogenic micro-organisms** to become **resistant**
71
State **two bacteria** that have **resistance** to **multiple antibiotics**
1) **MRSA**
2) **Clostridium *difficile*** (**C. *diff***)
72
State the use of **synthetic biology** in **medicine**
- Can produce **new molecules** (particularlly **enzymes**) that can **mimic biological systems**
73
Describe **personalised medicine**
- **Medicinal compounds** can be produced from **DNA sequences** via **sequencing**/**molecular modelling** an organisms **genome**
74
State a widely used **antibiotic**
- **Penicillin**
75
