Communicable Diseases Flashcards

1
Q

What are the qualities of bacteria, and how do they cause damage?

A

Single celled
Prokaryotic
Multiply in tissues and damage cells - often vascular tissue in plants
Can also produce toxins
Reproduce rapidly

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2
Q

What are the qualities of fungi, and how do they cause damage?

A

Not major in animals, devastating in plants
Single celled (yeast) or multi cellular (mould). Most are multi.
Saprophytic (feed on dead tissue) or parasitic (feed on living tissue), parasitic are pathogenic
Reproduce by spreading millions of tiny spores, which spread huge distances

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3
Q

What are the qualities of a viruses, and how do they cause damage?

A

Invisible to humans until invention of microscope
Can only metabolise in cells of living host, not truly living
Made of genetic material with protein coat around them
Genetic material inserted into host DNA, hijacks host biochemistry
Evolve and develops adaptations to host
All natural viruses are pathogenic, can cause disease in any other type of organism
Some viruses are modified to treat diseases by killing the pathogen, gene therapy.

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4
Q

What are the qualities of protoctista, and how do they cause damage?

A

Eukaryotic
Damage living tissue
Varied, organisms that don’t fit into other groups (such as slime molds or algae)
Small number are pathogenic in plants or animals
Those that cause disease are parasitic
Often need a vector to transfer them from one organism to another
Can enter directly through polluted water

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5
Q

What are the two modes of action of the pathogen on the host?

A

Direct damage of tissues
Production of toxins

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6
Q

Tuberculosis
What type of pathogen?
How is it transmitted?
What are the symptoms?
What organisms does it effect?
How can it be prevented/treated?

A

Bacterial
Transmitted through air from one sick person to another
Symptoms are weakened immune system, so body is unable to fight other diseases, coughing
Affects humans, cows, pigs, badgers and deer
Curable with antibiotics, preventable by improving living standards, vaccines

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7
Q

Bacterial Meningitis
What type of pathogen?
How is it transmitted?
What are the symptoms?
What organisms does it effect?
How can it be prevented/treated?

A

Bacterial
Transmitted via droplets in the air
Symptoms involve red/purple rash, doesn’t go away when glass pressed. Blood poisoning, rapid death
Affects humans (very young children, teenagers from 15-19)
Treated with antibiotics if found early, vaccines can protect from some forms

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8
Q

Ring Rot
What type of pathogen?
How is it transmitted?
What are the symptoms?
What organisms does it effect?
How can it be prevented/treated?

A

Bacterial
Vascular infection caused by infected seeds
Symptoms are a ring of decay in vascular tissue, leaves wilting, damage to tuber and fruit.
Affects potatoes, tomatoes and aubergines
Prevented by avoiding growing crops in infected fields for two years

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9
Q

HIV/AIDS
What type of pathogen?
How is it transmitted?
What are the symptoms?
What organisms does it effect?
How can it be prevented/treated?

A

Viral
Passed through body fluids, unprotected sex and sharing needles
Attacks cells in immune system so people are open to other infections
Humans
No vaccine, no cure, antiretroviral drugs can slow progress. Avoid sharing needles, use contraception

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10
Q

Influenza
What type of pathogen?
How is it transmitted?
What are the symptoms?
What organisms does it effect?
How can it be prevented/treated?

A

Viral
Droplets/air
Kills ciliated epithelial cells, open to further infection
Humans, can be fatal to young children, old people, and people with chronic illnesses
Flu vaccine each year for vulnerable people, no cure

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11
Q

TMV
What type of pathogen?
How is it transmitted?
What are the symptoms?
What organisms does it effect?
How can it be prevented/treated?

A

Viral
Hands, clothing, tools
Mottling, leaf discolouration, damage to leaves, flowers and fruit, stunt growth and reduce yield
Plants, around 150 species such as peppers, tomatoes, cucumbers
Resistant crop strains but no cure available

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12
Q

Black Sigatoka
What type of pathogen?
How is it transmitted?
What are the symptoms?
What organisms does it effect?
How can it be prevented/treated?

A

Fungal
Hyphae penetrate and digest cells, turning them black
Black spots on banana, reduces yield, leaves destroyed
Bananas
Resistant strains being developed, good husbandry and fungicide treatment control it, no cure

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13
Q

Blight
What type of pathogen?
How is it transmitted?
What are the symptoms?
What organisms does it effect?
How can it be prevented/treated?

A

Protoctista
Hyphae penetrate host cells
Affects leaves and tubers, destroys them
Tomatoes, potatoes
No cure, but resistant strains, careful management and chemical treatments can help

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14
Q

Ringworm
What type of pathogen?
How is it transmitted?
What are the symptoms?
What organisms does it effect?
How can it be prevented/treated?

A

Fungal
Contact with object that is infected
Spores erupt through skin, cause rash
Cattle
Antifungal medicines

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15
Q

Athlete’s Foot
What type of pathogen?
How is it transmitted?
What are the symptoms?
What organisms does it effect?
How can it be prevented/treated?

A

Fungal
Contact with contaminated surface
Growth under skin of feet, between toes
Humans
Antifungal cream

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16
Q

Malaria
What type of pathogen?
How is it transmitted?
What are the symptoms?
What organisms does it effect?
How can it be prevented/treated?

A

Protocista
Female mosquitoes that are infected
Headache and fever, may cause coma and death
Animals
Mosquito nets, screens, long sleeves

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17
Q

Name the three types of direct transmission in humans/animals, and give some examples

A

Direct Contact
-Contagious diseases (eg, ringworm,
athletes foot)
Inoculation
-Break in the skin during sex (HIV)
-Animal bites (rabies)
-Puncture wound or sharing needles
(septicaemia, HIV)
Ingestion
-Taking in contaminated food and drink
-Transfer of pathogen from hand to
mouth (amoebic dysentery, diarrhoeal
diseases)

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18
Q

Name the three types of indirect transmission in humans/animals, and give some examples

A

Fomites
-Inanimate objects such as bedding,
clothing, cosmetics, machinery (athletes
foot, staphylococcus infections)
Droplet infection
-Droplets of saliva and mucus when
talking, sneezing and coughing
-Healthy individuals can breathe these in
and become infected
Vectors
-Transmit pathogens from one host to
another
-Often but not always animals (malaria via
mosquitoes, rat fleas transmit bubonic
plague, foxes/bats can transmit rabies)

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19
Q

What are some factors that affect the spread of pathogens, which can lead to animal diseases?

A

Overcrowding
Poor nutrition
Compromised immune system
Poor waste disposal
Climate change
Culture/infrastructure, traditional practices can increase infection
Socioeconomics, lack of health care workers, lack of education/warning when outbreak

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20
Q

Name the three modes of transmission in plants and give examples

A

Direct Transmission
-Direct contact of healthy plant with any
part of diseased plant (ringrot, TMV,
blight, black stigatoka)
Indirect Transmission
-Soil Contamination
-Infected plants can leave pathogens or
spores in the soil which can infect the
next crop (black stigatoka spores, ring
rot bacteria, TMV spores)
-Some pathogens can survive
composting, so infection can spread
through contaminated compost
Vectors
-Wind
-Black stigatoka between Carribean
Islands
-Water
- Rain droplets spraying pathogens, spores can move over water film
-Animals
-Insects and birds carry pathogens between plants
-Humans
-Can transfer pathogens via machinery, hands, clothing, crop transport

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21
Q

What are the factors affecting the transmission of pathogens which can lead to plant diseases?

A

Planting crop varieties susceptible to disease
Overcrowding increases contact
Poor mineral nutrition reduces resistance
Damp, warm conditions increase survival of pathogen and spores
-Climate change, more rainfall and wind spread disease, conditions allow animal vectors to spread to new areas, drier may reduce spread

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22
Q

Name and explain some passive plant defences

A

Waxy cuticle: prevents water from collecting on cell surfaces, as pathogens need water to survive
Cellulose cell wall: physical barrier, also contains chemicals that can be activated
Lignin: thickening of cell walls, waterproof and almost completely indigestible
Stomatal closures: can prevent entry
Bark: also contains chemicals that work against pathogenic organisms
Callose: a large polysaccharide that is deposited in the sieve tubes at the end of the growing season. Blocks flow, prevents spread
Tylose formation: a balloon like swelling that fills the xylem vessel. When fully formed it blocks the vessel, preventing water flow and spread. A tylose contains a high concentration of chemicals toxic to pathogens

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23
Q

How do plant cells recognise pathogens?

A
  1. Receptors in the plant cell wall detect toxins produced by pathogens
    -Some molecules from the pathogen are recognised directly by the plant
    -When pathogenic enzymes break down the cell wall, products recognised
  2. Signalling molecules triggered to be released as a result
    -Signalling molecules alert nucleus to attack
  3. Some defensive molecules directly attack the pathogen, polysaccharides (callose and lignin) made to strengthen cell walls, defensive chemicals give alarm to other cells before they are attacked.
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24
Q

Name and explain some active plant defences

A

Cell walls are thickened and strengthened with cellulose
Callose deposits between cell wall and cell membrane near invading pathogen
Oxidative bursts damage cells of invading organisms

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25
What are some chemicals released for plant defence, and what do they do?
Terpenoids -Essential oils, antifungal and antibacterial Phenols -antimicrobial activity -disrupt molecules in plasma membrane of pathogens, possible that inhibit action of ion transport channels Alkaloids -nitrogen containing compounds (caffine, nicotine, cocaine, morphine) -bitter in taste -interrupt metabolic reactions, inhibit enzyme activity Defensive proteins (defensins) -in spaces between cells -chitinases, glucanases and lysozymes Hydrolytic enzymes -antibiotic and antifungal properties -tanins bind to proteins in saliva and digestive enzymes, deactivated -When injested in high amounts by insects, insect has no growth, will die.
26
What is necrosis?
Deliberate cell suicide, few sacrificed to save rest of plant Limits pathogens access to water/nutrients, stops spread Brought on via intracellular ezymes Activated by injury Brown spots, dieback
27
What is canker?
A sunken necrotic lesion in the woody tissue, such as the main stem/branch
28
List some non-specific animal defenses against pathogens, and give information about them
Skin -acts as a physical barrier to prevent entry of pathogens -cells of the epidermis dry out as migrate to skin surface -sebum, lower pH Lysozomes -found in tears -tear fluid contains antibodies and enzymes Expulsive reflexes -Areas sensitive to irritation that can be caused by microorganisms or toxins -Involves coughing/sneezing/vomiting -cough/sneeze: sudden expulsion of air will carry microorganisms with it Mucous Membranes -line internal cavities exposed to external air -airways, digestive tract, genital areas, anus, ears, nose -goblet cells produce mucus, cilliated epithelial cells waft it out Stomach Acid -high acidity (1-2 pH) and so denatures enzymes of pathogen Ear wax -traps pathogens in the ear Female Reproductive System -protected by mucus plug in the cervix -relatively acidic conditions maintained
29
What is inflammation?
Localised response to pathogens or damage, resulting in inflammation at site of wound Swelling in infected tissues, heat, pain, redness Damaged mast cells release histamine and cytokines
30
What do histamines do?
Cause vasodilation, localised head and redness Make blood vessel walls more permeable, blood plasma forced out, forming more tissue fluid, causes swelling and pain, delivering more white blood cells and certain proteins Raised temperature helps prevent pathogens from reproducing
31
What do cytokines do?
Attract phagocytes, leads to phagocytosis Released by phagocytes that have engulfed a pathofen, cell signalling molecule informing other phagocytes that body is under attack, stimulated others to move to site of infection, can increase body temp and stimulate specific responses.
32
What is the process of phagocytosis?
Phagocyte is attracted to the pathogen by chemo attractants. Moves towards pathogens along concentration gradient The phagocyte binds to the pathogen Lysosomes within the phagocyte migrate towards the phagosome formed by engulfing the bacterium Lysosomes release their lytic enzymes into the phagosome, where they break down the bacterium The breakdown products of the bacterium are absorbed by the phagocyte
33
What are the qualities of neutrophils, and what do they do?
-short lived -large numbers during infections -large numbers of lysosomes -die after injecting a few pathogens -may collect in area of infection to form pus when dead -fully digest pathogens -lobed nucleus -frequently leave blood stream to patrol tissue for foreign bodies
34
What are the qualities of macrophages, and what do they do?
-larger than neutrophils -live longer than neutrophils -initiate specific responses to pathogens -does not fully digest pathogens, antigen saved and moved to protein complex on cell surface: antigen presenting cell -can be found in lymph nodes -made in bone marrow
35
What is an Antigen Presenting Cell and how is it formed? What is its role?
Macrophages that display antigens form a partially digested pathogen Antigen is moved to a special protein complex in plasma membrane Travel around body and activate specific immune system Hold out or display antigen on cell surface membrane, which allows other cells, such as T or B lymphocytes, to recognise it and to become activated as part of specific immune response
36
What do opsonins do?
Chemicals that bind to pathogens Tag them to make them more visible to phagocytes Pathogens have receptors which bind to opsonins, leading to them engulfing pathogens Immunoglobins IgG and IgM are strong opsonins
37
What is the humoral response?
Activation of B cells into plasma cells that produce and secrete antibodies to a specific antigen
38
How do B cells activate and attack pathogens?
Clonal selection -B effector cells with specific, complementary receptors, bind to the antigen on a pathogen and are activated. -Interkeukins (cell signalling molecules) secreted by Th (T helper cells) -Cells aid in activation Clonal Expansion -The B cells then divide by mitosis, producing many clones Differentiation: differentiate into two different types of cells -Plasma cells: produce antibodies that fit the antigen on the pathogen, disabling them, this is the primary immune response -B memory cells: remain in bloodstream as part of the secondary immune response
39
What is the cell mediated response?
Immune response that does not involve antibodies, involves activation of macrophages + antigen specific T lymphocytes, and release of various cytokines in response to an antigen
40
How do T cells activate and attack pathogens?
Antigen Presentation -macrophages engulf and digest pathogens, process and present antigens on the surface Clonal Selection -T helper cells with specific completmentary receptors bind to antigen and become activated, produce interleukins -Specific T cells become activated by interleukin Clonal Expansion -Selected T cells divide by mitosis, resulting in many selected T cell clones all carrying complementary receptor to the pathogen/antigen
41
What are the different types of T cells?
Killer T Cells, Helper T Cells, Regulatory T Cells and Memory T Cells
42
What are antibodies?
Specific proteins released by plasma cells that can attach to pathogenic antigens
43
What are B memory cells?
Cells that remain in the blood for a long time, providing long-term immunity
44
What is cloning expansion?
An increase in cell numbers via mitosis
45
What are cytokines?
Signalling molecules that are used to communicate between different white blood cells
46
What are plasma cells?
Derived from the B lymphocytes, these are cells that manufacture antibodies
47
What are T helper cells?
Cells that release signalling molecules to stimulate the immune response
48
What are T killer cells?
Cells that attack and destroy our own body cells that are infected by a pathogen
49
What are T memory cells?
Cells that remain in the blood stream for a long time, providing long term immunity
50
What are regulatory T cells?
Cells that are involved with inhibiting or ending the immune response
51
How does opsoisation act on pathogens?
-Antibodies act as a binding site for phagocytic cells -Easier to destroy -Can be specific and non specific -May attach to the binding site of the pathogen to the host cell rendering it neutral (neutralisation) -Macrophage has a receptor site complementary to constant region of antibody
52
How does agglutination act on pathogens?
-Causes pathogens carrying antigens/antibody complexes to clump together -Helps prevent spread through body, pathogen can't enter host cell -Easier for phagocytes to engulf more at a time
53
How do anti-toxins act on pathogens?
Some antibodies can bind to the toxin produced by the pathogen, making them harmless
54
What is the different in primary and secondary response to infection?
Secondary response is faster, produced a higher concentration of antibodies Memory cells in primary response are able to divide and differentiate into plasma cells much more rapidly Therefore more plasma cells produced = greater concentration of antibodies, more rapid No clonal expansion in secondary response as takes time
55
What is natural active immunity? Example?
Infection by pathogen, memory cells produced
56
What is natural passive immunity? Example?
Antibodies passed to baby in mothers first milk
57
What is artificial active immunity? Example?
Vaccination
58
What is artificial passive immunity? Example?
Antibodies extracted from an individual to another for short term immunity
59
What is the purpose of vaccination?
Contain antigens that cause body to manufacture antibodies and memory cells against specific pathogen. When another infection, memory cells triggered to activate immune system, destroy pathogen before symptoms develop
60
Give some examples of how antigens/pathogens may present in a vaccination
Whole, live microorganisms of less harmful form (smallpox) Attenuated (weakened) form of pathogen (TB) Dead pathogen (cholera) Harmless toxin produced by pathogen (tetanus) Isolated antigens extracted from pathogen (influenza)
61
Why are vaccines with live antigens more effective?
Stronger primary response, quicker and stronger secondary response
62
Which may individuals have side effects from vaccines?
Immunocompromised, elderly people, those on immunosupressant drugs, newborns
63
Why do some vaccination programmes have boosters?
Secondary response so more antibodies produced, ensure memory cells still produced