Communicable diseases, disease prevention & the immune system Flashcards
(114 cards)
1
Q
Define pathogen
A
- Microorganism that causes disease
- e.g. virus, bacteria
2
Q
What are 4 types of pathogen?
A
- Bacteria
- Virus
- Protista
- Fungi
3
Q
How do pathogens cause disease?
A
Damage host tissue directly
- e.g. viruses cause cell lysis as particles leave host cell
- e.g. some protists digest host cells as they reproduce
- e.g. fungi digest living cells and destroy them
Produce toxins
- e.g. bacteria produce toxins that damage host cells
- Break down membranes or inactivate enzymes
- e.g. some fungi also produce toxins
4
Q
Define parasite
A
- Lives in and gains nutrition from host
- At the expense of host
5
Q
Define vector
A
- Something that carries pathogens from one organism to another
- e.g. water, mosquitoes
6
Q
Describe how ring rot is caused in plants
A
- Bacterial disease
- Damages leaves, tubers and fruit
- No cure
7
Q
What are the economic effects of ring rot?
A
- Can destroy crops
- Causes loss of income for farmer
8
Q
Describe the effects of tobacco mosaic virus (TMV) on plants
A
- Virus infects tobacco plants and other common fruits and flowers
- Stunts growth, damages leaves
- Can lead to almost total crop loss
- No cure
9
Q
Describe the effects of potato blight
A
- Caused by protist
- Penetrates host cells, destroying leaves, tubes and fruit
- No cure
- Resistant plant strains available
10
Q
What are the effects of TB?
A
- Destroys lung tissue
- Suppresses immune system
11
Q
Describe how the bacteria that causes TB is transmitted from one individual to another
A
- Droplets containing pathogen released by coughing / sneezing
- Inhaled by uninfected individual
12
Q
Give the factors that increase the likelihood of contracting TB
A
- Not vaccinated against TB
- Weakened immune system (e.g. HIV)
- Overcrowding
- Consumption of milk or beef from infected cattle
13
Q
How is TB treated?
A
Using antibiotics
14
Q
How is the spread of TB prevented?
A
- Improving living conditions
- Vaccinations
15
Q
What are the effects of bacterial meningitis?
A
- Infects membrane on surface of brain
- Can spread around body causing septicaemia
16
Q
How is bacterial meningitis treated?
A
- Antibiotics can cure disease
- Vaccines can protect against disease
17
Q
What does AIDS stand for?
A
Acquired Immunodeficiency Syndrome
18
Q
Describe the structure of HIV
A
- Retrovirus
- Contains RNA and reverse transcriptase enzyme
- Protein coat (capsid)
- Surrounded by phospholipid bilayer formed from cell-surface membrane of host
- Glycoproteins in bilayer allow virus to re-infect new host cells
19
Q
Describe the action of HIV
A
- Infects T-lymphocytes
- Reverse transcriptase converts viral RNA to DNA in host nucleus
- Viral DNA inserted into host DNA
- Viral mRNA produced to code for viral proteins
20
Q
How does HIV develop into AIDS?
A
- HIV infects T lymphocytes
- Causes reduction of active lymphocytes
- Loss of ability to make antibodies (AIDS) results in lower immunity
- Infections that would usually be destroyed by body no longer are and can be fatal
21
Q
How can HIV be spread?
A
- Blood on hypodermic needles shared by intravenous drug users
- Across the placenta during pregnancy
- Breast feeding
- Infected blood transfusions
- Small cuts in the penis, vagina, mouth, intestine during sex
22
Q
What type of infective agency causes influenza (flu)?
A
Virus
23
Q
Suggest why the influenza vaccine has to be changed each year
A
- Flu virus mutates regularly
- Different strains of the virus arise due to mutation
- New strains have different antigens
24
Q
Name the parasite that causes malaria
A
Plasmodium
25
Name the vector for the malarial parasite
Female Anopheles mosquito
26
Which human cells do malarial parasites reproduce in?
- Hepatocytes (liver cells)
- Erythrocytes
27
Describe how the female Anopheles mosquito transmits the malarial parasite to a humans
- Mosquito is vector
- Plasmodium present in mosquito saliva
- Infected mosquito bites human
- Plasmodium passes from saliva to blood
28
How is the spread of Plasmodium controlled?
- Insecticides used to kill Anopheles mosquitoes
- Removing breeding sites (standing water)
- Use mosquito nets
- Wear long-sleeved clothing
29
Identify the infective agent that causes ring worm
A fungus
30
Identify the infective agent that causes athlete’s foot
- A fungus
31
How is ring worm and athlete’s foot treated?
Antifungal creams
32
Define direct transmission
Pathogen transferred from one individual to another - host to host
33
Give examples of direct transmission
Direct contact
- e.g. sexual intercourse, faecal-oral transmission, skin-to-skin contact
- e.g. direct contact of healthy plant with diseased plant
Inoculation
- Enters blood stream
- e.g. through break in skin, animal bite, sharing needles
Ingestion
- Consuming contaminated food or drink
34
Define indirect transmission
Pathogen travels from one individual to another via an intermediate
35
Give examples of indirect transmission
Fomites
- Objects such as clothing, bedding etc.
- e.g. athlete’s foot
Droplet infection
- Inhalation of droplets of saliva from sneezing/coughing
- e.g. TB, influenza
Vectors
- Transmit pathogens from one host to another
- e.g. female Anopheles mosquito transmits
Soil contamination (plants)
- Pathogens or spores left in soil by infected plants
- Can infect new crops
- e.g. black sigatoka, ring rot
36
Explain the difference between direct and indirect transmission
Direct
- Pathogen spread directly from one organism to another
Indirect
- Pathogen spread from one organism to another through another medium
- e.g. the air, water, a vector
37
Why is direct transmission more common in animals than plants?
- Animals can move around
- Means direct contact more likely
38
Give factors that increase the transmission of communicable diseases in humans
- Weakened immune system (e.g. caused by HIV)
- Poor diet / lack of protein
- Homelessness / overcrowding increases likelihood of close contact
- Poor ventilation in housing increases likelihood of indirect transmission
- Climate change can introduce new vectors and diseases
- Socioeconomic factors, e.g. lack of trained health workers
39
Give factors that increase the transmission of communicable diseases in plants
- Planting varieties of crops that are susceptible to diseases
- Over-crowding of plants increases likelihood of contact
- Poor mineral nutrition reduces resistance of plants
- Damp, warm conditions increase pathogen survival
- Climate change
- Increased rainfall and wind promote the spread of disease
40
Describe how a plant’s response to a pathogen is triggered
- Receptors in plant respond to antigens from pathogens
- Or to chemicals produced by plant cell wall when attacked
- This stimulates release of signalling molecules
- Switch on genes in the nucleus, triggering cellular response
41
What is callose?
- Polysaccharide of β-glucose
- 1,3 and 1,6 linkages
- Produced by plants when attacked by pathogens
42
Describe the use of callose as a physical defence in plants
- Callose barriers immediately synthesised upon infection
- Deposited between cell walls and cell membranes in cells next to infection
- Callose and lignin deposited in cell walls longer term
- Callose blocks sieve plates to prevent spreading through the phloem
- Callose deposited in plasmodesmata to prevent spread of pathogens from one cell to
another
43
Describe the chemical defences that plants employ against pathogens
- Insect repellents (e.g. pine resin, citronella)
- Insecticides (e.g. caffeine is toxic to fungi and insects)
- Antibacterial compounds (e.g. phenols act as antibiotics)
- Antifungal compounds (e.g. chitinase enzymes break down chitin in fungal cell walls)
- General toxins (e.g. cyanide is toxic to most living things)
44
Define non-specific defence
Able to break down or prevent entry from a range of different pathogens
45
What are non-specific defences used by animals?
- Physical barriers
- Production of enzymes and acids
- Blood clotting at wounds
- Inflammatory responses
- Phagocytosis
46
Describe how entry of pathogens is prevented in animals
- Tough skin acts as a physical barrier
- Sebaceous glands secrete lactic acid and fatty acids preventing growth of pathogens
- Mucous membranes (nose, trachea, vagina) trap pathogens
- Lysozymes in tears and urine kill bacteria
- Stomach acid destroys pathogens
- Expulsive reflexes (e.g. sneezing) ejects pathogens from gas exchange system
47
What is the role of cilia?
- Waft mucus ladened with bacteria up to the mouth
- Mucus swallowed
- Bacteria destroyed by hydrochloric acid in the stomach
48
Describe the role of platelets
- Secrete clotting factors
- Clot the blood at the site of a wound
49
Explain how cuts in the skin are sealed by blood clotting
- Thromboplastin and serotonin released from platelets
- Thromboplastin triggers clotting process involving a cascade of reactions
- Results in thrombin causing rapid conversion of fibrinogen into fibrin
- Fibrin makes a mesh to seal the wound
- Serotonin makes smooth muscle in blood vessels contract
- Vessels narrow to reduce blood supple to area
50
What is an inflammatory response?
- Localised response to pathogens or damage
- Results in inflammation at the site
51
What is the role of mast cells in the inflammatory response?
- Activated in damaged tissue
- Secrete histamines and cytokines
52
What are the physical signs of inflammation?
- Pain
- Heat
- Redness
- Swelling of tissue
53
What is the role of histamine in the inflammatory response?
**Makes blood vessels dilate**
- Causes localised heat and redness
- Raised temperature helps prevent pathogen reproduction
**Makes blood vessel walls ‘leaky’**
- More blood plasma containing phagocytes forced out to become tissue fluid
- Causes swelling and pain
54
Define allergy
Reactions by the immune system to usually harmless substances
- e.g. bee stings, pollen, nuts
55
Describe what happens in an allergic reaction
- Over-activation of mast cells
- Over-secretion of histamine
- Leads to inflammation of tissues, itching, sneezing, mucus secretion
- Serious effect: anaphylaxis, swelling of throat and mouth, death
56
What is the role of cytokines in the inflammatory response?
Attract phagocytes to site of infection/damage (cell signalling)
57
What are the two types of phagocyte?
- Neutrophils
- Macrophages
58
Describe the role of phagocytes
- Destroy pathogens by ingesting them
- Can squeeze out of the walls of capillaries
- Engulf pathogens by endocytosis
- Enzymes digest pathogens
- Non-specific immune response
59
Outline how phagocytes ingest pathogens
- Phagocytes attracted to foreign pathogen (chemotaxis)
- Foreign matter engulfed by phagocyte (phagocytosis)
- Pathogen enclosed in phagosome
- Phagosome fuses with lysosome to form phagolysosome
- Lysosome contains lysozyme enzymes
- Pathogen digested
- Products absorbed into cytoplasm by diffusion
60
What is the major histocompatibility complex (MHC)?
- Glycoproteins found in cytoplasm of macrophage
- Can combine with antigens from pathogen
61
What happens once a macrophage digests a pathogen?
- Antigens from pathogen combined with MHC in cytoplasm
- MHC displayed on macrophage cell surface membrane
- Macrophage become antigen presenting cell (APC)
62
What are opsonins?
Chemicals that bind to pathogens
- Make pathogens easier to recognise by phagocytes
- e.g. IgG and IgM antibodies
63
What are the two types of white blood cells?
- Lymphocytes
- Phagocytes
64
What is the role of macrophages in the specific immune response?
- Engulf and digest pathogens
- Display antigens
- Activate T lymphocytes
65
Where do T lymphocytes mature?
Thymus gland
66
Where do B lymphocytes mature?
Bone marrow
67
What is the role of T killer cells?
Destroy pathogens by producing perforin
68
What is the role of T memory cells?
Provide immunity - circulate in blood and recognise specific antigens
69
What is the role of T regulator cells?
Control immune response once pathogen eliminated
70
What is the role of plasma cells?
Produce and release antibodies specific to an antigen
71
What is the role of B memory cells?
Provide immunity - circulate in blood and rapidly produce antibodies
upon reinfection
72
Describe cell-mediated immunity
T lymphocytes respond to changes in an organism’s own cells
- e.g. viral infection, antigen processing (macrophage), cancer cells, transplanted
tissue
73
Describe humoral immunity
- Body responds to antigens found outside of cells
- e.g. bacteria and fungi
- B plasma cells produce antibodies
74
Define clonal selection
Lymphocyte with correct antibody complementary to a specific antigen is selected for cloning
75
Define clonal expansion
Activated lymphocyte divides by mitosis
- Produces clones
76
Describe the cell-mediated immune response
- Macrophages engulf and digest pathogen
- Display antigen from pathogen (become APC)
- T helper cells bind to specific antigens and are activated (clonal selection)
- Activated T helper cells produce interleukins
- Interleukins stimulate more T cells to divide rapidly by mitosis (clonal expansion)
- Example of cell signalling
- Cloned T cells all carry receptor for particular antigen
- Cloned T cells can:
- Develop into T memory cells
- Provide rapid response to reinfection
- Develop into T killer cells
- Destroy infected cells
- Produce interleukins
- Stimulate phagocytes
- Stimulate B cells to divide
77
Describe the humoral immune response
- B lymphocytes have IgM antibodies on cell-surface membrane
- Antibody on B lymphocyte binds to one complementary antigen on pathogen
- B lymphocyte engulfs pathogen, digests it and presents antigens to become APC
- Activated T helper cell binds to B cell APC (clonal selection)
- Interleukins produced by activated T helper cell activates specific B cells
- Activated B cells divide by mitosis (clonal expansion)
- Clones differentiate into plasma cells and B memory cells
- Plasma cells produce antibodies specific for the antigen
- B memory cells provide faster response to reinfection
78
Describe how cytokine molecules (interleukins) can stimulate specific B lymphocytes to divide
- Cytokine / interleukin receptor has specific shape
- Cytokine / interleukin binds to receptor on cell surface membrane of B lymphocyte
- Receptor and cytokine have complementary shapes
- Activates clonal expansion of B cells
79
Describe the structure of an antibody
- Protein
- Variable region - contains antigen binding sites
- Constant region - aids recognition and binding to host phagocytes
80
How do antibodies help fight infection?
- Act as antitoxins - combine with and neutralise toxins produced by pathogens
- Prevent viruses attaching to host cells (neutralisation)
- Cause agglutination - stick pathogens together - more easily engulfed by phagocytes
- Help lyse the pathogen
- Act as opsonins - make pathogens easier for phagocytes to recognise
81
Describe the processes of neutralisation
- Antibodies block binding sites on pathogen
- Bind to toxins
- Prevent entry of pathogen to host cell
82
Describe the processes of agglutination
- Bind together many pathogens
- Clumps too large to enter host cell
- Increase likelihood of being consumed by phagocyte
83
Describe how the structure of an antibody molecule is related to its function
- Y-shaped molecule made from light and heavy chains
- Disulfide bonds hold light and heavy chains together
- Constant region
- Binds to phagocytes
- Variable region
- Has complementary shape to antigen
- Gives specificity
- Hinge region
- Allows flexibility
- More than one variable region
- Allows agglutination and blocking of pathogen’s binding sites
84
Describe the role of memory cells when a pathogen re-enters the body
- Recognise pathogen
- Produce clones
- B cell clones can form plasma cells to make antibodies
- T cell clones can form T helper cells and T killer cells
- Responsible for secondary response
85
What is the difference between the primary and secondary immune response?
- Primary response produces antibodies slower and at a lower level
- Secondary response produces antibodies faster and in greater amounts
86
Outline the principle of immunity
- Immunity is the ability of an organism to resist infection
- Due to presence of antibodies
- Pathogen invades body
- Leads to clonal selection of B memory cells
- B-cells produce specific antibodies
- If same pathogen enters body again, memory cells activated
- Antibodies produced faster and in greater amounts
87
Define passive immunity
Receiving antibodies from external sources
- e.g. across placenta, from breast milk, injection of antibodies
88
Define active immunity
Body produces own antibodies
- e.g. from facing an infection directly or through vaccination
89
Define natural immunity
Immunity occurs naturally in the body
90
Define artificial immunity
Immunity provided by intentional exposure to small quantities of pathogen
91
Explain the difference between the body’s response in active and passive immunity
- Active immunity leads to creation of B and T memory cells
- Leads to long lasting immunity
- Passive immunity does not produce immune response
- No memory cells made
- Does not lead to faster secondary immune response
92
Define autoimmune disease
- Immune system stops recognising ‘self’ cells
- Starts to attack healthy body tissue
- e.g. type 1 diabetes, lupus, rheumatoid arthritis
93
Discuss the problems that could arise from treating an autoimmune disease with
immunosuppressant drugs
- Immunosuppressant drugs reduce activity of immune system
- Prevent destruction of healthy tissue
- But susceptibility to infection increases
- Immune system less effective at recognising pathogens
94
Explain how vaccinations work
- Artificial active immunity
- Inject dead, weakened or attenuated form of pathogen
- Antigens stimulate specific immune response
- T-cells activated
- T-cells stimulate clonal expansion of B-cells
- Memory cells are made
- Specific antibodies produced by B-cells
- Result is specific immunity
- Vaccination causes slow production of antibodies and lower level of antibodies
- Upon re-entry of pathogen, antibodies are produced sooner, faster, and in greater number
- Second/booster shot may be given to stimulate memory cells
95
Benefits of vaccines
- Can eradicate diseases e.g. smallpox
- Reduces deaths due to disease
96
Risks of vaccines
- Individual may react badly to vaccine
- Immunity may not be life-long (booster required)
97
Define epidemic
When a communicable disease spreads rapidly at a local/national level
98
Define pandemic
When a communicable disease spreads rapidly on a global scale
99
How can vaccination programmes help prevent epidemics?
- Mass vaccination can prevent spread of pathogen into wider population
- When a significant number of people have been vaccinated, it gives protection to those who do not have immunity (herd immunity)
100
Why do vaccines have to be changed regularly?
- Mutations in antigens on pathogens
- Produces different strains with different antigens
- New vaccine needed for most new strains
101
State the biological reasons why it has not been possible to produce an effective vaccine for malaria
- Different species of Plasmodium cause malaria
- Different antigens due to mutation
- More than one stage in the life cycle is within the human
- Different stages have different antigens
- Different vaccine for each stage required
- Parasite hidden in cells
102
State the biological reasons why it has not been possible to produce an effective vaccine for HIV
- HIV hidden in cells
- Infects and destroys immune system
103
What are antibiotics?
- Chemicals produced by microorganisms
- Used to kill bacteria
104
Explain how antibiotics work
- Relies on differences between eukaryotes and prokaryotes
- Only harmful to bacteria and not the host organism (usually humans)
- Interrupts usual prokaryotic cell process, e.g.:
- Prevents cross-linking of bacterial cell walls
- Inhibition of protein synthesis
- Inhibition of nucleic acid synthesis
105
Explain why antibiotics cannot be used to treat viral diseases
- Viruses are not living
- Viruses lack metabolism
- Antibiotics target cell wall production
106
What is antibiotic resistance?
- Some strains of bacteria have evolved genes that confer resistance to antibiotics
- Some strains of bacteria have evolved resistance to multiple antibiotics
- e.g. MRSA (methicillin-resistant Staphylococcus aureus)
- e.g. Clostridium difficile
107
What are the potential causes of antibiotic resistance?
- Mutations leading to antibiotic-resistant strains
- Prescription misuse of antibiotics for viral infections
- Patient misuse by halting treatment too early
- Overuse of antibiotics
- Use of antibiotics in farming
108
How can antibiotic-resistant infections be reduced?
- Minimise use of antibiotics
- Ensure every course of antibiotics is completed
- Good hygiene in hospitals and care homes
109
Why is antibiotic resistance a concern?
- Bacterial infections harder to treat
- Potential for large disease outbreak
- Developing new antibiotics is long and expensive process
110
How is penicillin used?
- Extracted from mould growing on
melons
- Antibiotic - prevents cross-linking of
bacterial cell walls
111
How is aspirin used?
- Extracted from compounds found in willow bark
- Painkiller and anti-inflammatory
112
Describe the different ways that medicines can be identified and developed
- Compounds produced by fungi and other plants and animals isolated
- Possible genes that may produce suitable drugs identified
- Develop molecules that will fit into receptor proteins on membranes e.g. for hormones or
neurotransmitters
- Modification of existing drugs
- Traditional plant remedies that offer potential medicines
113
Define pharmacogenetics
- Personalising medicines for the individual
- Drug treatment based on individual’s genome
114
Define synthetic biology
- Using genetic engineering to produce drugs that are rare or expensive
- Nanotechnology used to deliver drugs to specific targets
