Module 4:Communicable Diseases Flashcards

(90 cards)

1
Q

What is a communicable disease?

A

A communicable disease is passed from one organism to another.

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2
Q

Can I delete cards?

A

Apparently not

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3
Q

Why are pathogenic bacteria harmful?

A

Most produce toxins that poison or damage host cells. They do this by: interrupting cell membranes, inactivate enzymes or interfere with genetic material.

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4
Q

What are the different shapes of bacteria?

A

Rod shaped, spherical, comma shaped, spiralled and corkscrew.

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5
Q

What are the two types of bacteria?

A

Gram +ve (Appear purple-blue after staining)

Gram -ve (Appear red after staining)

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6
Q

What is an antibiotic?

A

A compound that kills or inhibits the growth of bacteria.

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7
Q

What is the name of a rod-shaped bacteria?

A

Bacilli

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8
Q

What is the name of a spherical bacteria?

A

cocci

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9
Q

What is the name of a comma-shaped bacteria?

A

vibrio

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10
Q

What is the name of a spiral-shaped bacteria?

A

sprilla

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11
Q

What is the name of a corkscrew-shaped bacteria?

A

spirochaete

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12
Q

What is the name of a virus that infects bacteria?

A

Bacteriophage

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13
Q

What does different type of cell wall change about it’s treatment?

A

Different antibiotics are useful.

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14
Q

What are protocista (protista)?

A

Eukaryotic organisms with a wide variety of feeding methods. They tend to either be single-cellular or a large colony of cells.

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15
Q

What are Fungi?

A

Fungi are eukaryotic organisms that are often multi-cellular. Although thrush is single celled. They cannot photosynthesize and-so digest their food extracellularly and then absorb the nutrients. Some are saprophytic (feeding off dead matter). Some are parasytic.

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16
Q

Why are fungi lethal to plants?

A

Fungal infections tend to effect the leaves of a plant, preventing photosynthesis, which then prevents aerobic respiration, killing the plant quickly.

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17
Q

How do fungi reproduce?

A

They produce lots of spores, which allows for the rapid spread of the fungi.

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18
Q

What 3 types of pathogen directly damage host tissue?

A

Viruses, protoctista and fungi.

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19
Q

How do protoctista directly damage host tissues?

A

Take over cells and break them open as a new generation emerge. They don’t take over the genetic material, they digest and use the cell contents as they reproduce.

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20
Q

How do fungi directly damage host tissues?

A

Fungi digest living cells and destroy them. The bodies response to this causes the symptoms of the disease.

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21
Q

Why do plant diseases threaten humans?

A

They can cause famine and lead to the economy struggling, leading to loss of jobs. Further destruction of an ecosystem can occur.

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22
Q

What is Ring Rot?

A

A bacterial disease of potatoes, tomatoes and aubergines. Caused by a gram +ve bacteria. It damages the leaves, tubers and fruit. No cure. Can destroy up to 80% of crops. To prevent spread don’t grow crops in infected field for two years. (Ring of rot in tubers)

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23
Q

What is the tobacco mosaic virus?

A

A virus that infects tobacco plants and 150 other species. e.g tomatoes and peppers
It damages the leaves, flowers and fruit. Stunts growth and reduces yields, can lead to almost total crop loss. No cure but resistant crop strains available. (Causes mosaic pattern)

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24
Q

What is potato blight?

A

Fungus-like protoctista. Their hyphae penetrate host cells, destroy leaves, tubers and fruit. No cure. Resistant strains and careful management, chemical treatment can reduce infection risk. (Discolouration and becomes brown)

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25
What is Black sigatoka?
pathogenic fungus. Attacks and destroys leaves. Hyphae penetrate and digest host cells, causing the leaves to turn black. If plants infected 50% reduction of crop yield. Resistant strains, good husbandry and fungicide control are used to control the spread. There is no cure.
26
What are the 3 types of Direct Transmission?
Direct Contact, Inoculation, ingestion
27
Direct Contact:
Direct skin to skin contact. Microorganisms from faeces transmitted onto hands.
28
Inoculation:
Direct transmission through a break in the skin. e.g from animal bites. Or through a puncture wound.
29
Ingestion:
Contaminated food or drink directly transferring pathogens to the mouth and digestive system.
30
What are the 3 types of indirect transmission?
Fomites, Droplet Infection, Vectors
31
Fomites:
Inanimate objects that can transfer pathogens
32
Droplet Infection:
Miniature droplets of saliva and mucus expelled from the mouth or nose containing pathogens.
33
Vectors:
A vector transmits communicable pathogens between organisms. Can be biotic and abiotic.
34
How to limit interspecies transmission?
Minimising close contact can reduce infection rates. Washing hands thoroughly.
35
What are the factors affecting the transmission of communicable diseases in animals:
overcrowding, poor nutrition, poor disposal of waste, climate change affecting vector populations, culture (traditional medicine), Socioeconomic factors (lack of trained medical staff)
36
What are the factors affecting the transmission of communicable diseases in plants:
Susceptible varieties, over-crowding (increases likelihood of direct contact), malnutrition, damp and warm conditions, climate change (increased rainfall and wind promote spread of disease) .
37
What are the two types of indirect transmission between plants?
Soil contamination and Vectors
38
How does soil contamination spread disease between plants?
Infected plants leave pathogens or reproductive spores in the soil. These remain and can infect the next crop.
39
What are the different vectors that can spread disease between plants?
Wind, Water, Animals, and Humans (or their fomites e.g contaminated equipment)
40
What is tuberculosis?
A bacterial disease that damages lung tissue and suppresses the immune system. TB is curable with anti-biotics and preventable with vaccinations.
41
What is Bacterial Meningitis?
A bacterial infection of the meninges in the brain. It can spread to the rest of the body and cause septicemia. Mainly affects young people. Can be cured with antibiotics if found early. Can be vaccinated against.
42
What is HIV/AIDS
(Human Immunodeficiency virus) targets T-helper cells. The immune system is destroyed and so the infected are susceptible to other diseases. Retrovirus with RNA genetic material. uses reverse transcriptase to produce a strand of DNA in the host cell. DNA interacts with the host cell DNA.
43
What is influenza
Viral infection of ciliated epithelial cells. Leaves airways open to secondary infection. Secondary infections tend to be lethal.
44
What is Malaria
Caused by a protoctista. spread through the bites of mosquitoes. Reproduce in female mosquito. No vaccine and limited cures. Main method is to kill vectors with insecticides.
45
What is Ring worm.
A fungal disease the affects mammals. Grey-white, crusty, infectious circular areas of skin. Not damaging. Can be cured with anti-fungal cream.
46
What is Athlete's foot?
Fungal disease- form of ring worm- digests warm moist skin between toes - causes cracking and scaling. Anti-fungal creams used as cure.
47
What do opsonins do?
Opsonins mark antigens on pathogens to signal the phagocytes and aid the phagocyte binding to the pathogen
48
What is an antigen?
An antigen is a molecular tracer on the outside of a cell or virus that is used for cell signaling. And will illicit an immune response.
49
What are antibodies?
Y-shaped glycoproteins (immunoglobulins) on the surface of lymphocytes that bind to the antigens on a pathogen to stop it from functioning.
50
Agglutination:
one antibody binds to two pathogens - clumping the pathogens together - facilitating phagocytosis.
51
Antibodies in neutralisation:
Antibodies act as anti-toxins and are complimentary to the toxin, binding and causing the toxin to be less harmful.
52
Blood clotting cascade
Platelets contact collagen or cell walls - Secrete thromboplastin and serotonin. serotonin contracts smooth muscle in arteries and reduces blood supply. thromboplastin catalyses with a calcium ion and prothrombin to form thrombin. thrombin catalyses firbinogen into fibrin- forms fibres for a blood clot.
53
6 stages of viral life cycle
``` Attach to cell surface membrane inserts viral nucleic acid replicate nucleic acid synthesis of viral protein assembly of virus lysis of host cell. ```
54
Active immunity
Specific production of antibodies/ anti-toxins | Either through natural/ vacination
55
What do cytokines do?
Signal lymphocytes to an area.
56
Passive immunity
Maternal or artificial} antibodies provided from externally
57
Primary response:
1st pathogen entry - triggers phagocytes and t-effector cells Symptoms include fever and swelling - histamines released to reduce pathogen replication through more extreme temperatures.
58
T helper cells
produce interleukins (cytokine) - stimulate B cell to secrete antibodies - attracts other t cells and antibodies
59
T killer cells
Kill pathogens by producing perforin that forms a hole in the infected/pathogenic plasma membrane.
60
T memory cells
Immunological memory - remain in the blood for a long period of time - divide rapidly in second infection - forms many t-killer cells
61
T regulator cells
Prevent autoimmune response by repressing immune system after all the pathogens have been destroyed.
62
What is the role of phagocytes?
TO consume the invader and recognise the antigens.
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B effector cells
Divide to form plasma cell drones
64
B plasma cells
Secrete antibodies/antitoxins
65
Secondary response
2nd pathogen entry B-memory cells stimulate the creation of specific monoclonal antibodies no symptoms
66
Neutrophils
multi-lobed nucleus granular phagocytes that release antimicrobial factors in specialized granules - extruded by nucleic acids - for neutrophil extracellular traps.
67
Lymphocytes
B & T little to no cytoplasm Large nucleus
68
Eosinophils
Bilobed nucleus - contains enzymes and proteins - granular (200 granules)
69
Basophil
Bilobed nucleus - cytoplasmic granules - glycogen storage - release cytokines, histamines, and leukotrienes.
70
Monocyte
Secrete chemokines - recognise 'danger signals'
71
Outline phagocytosis
phagocyte signaled to invader by cytokines. phagocyte makes contact with invaded. phagocyte engulfs the invader. the phagosome fuses with the lysosomes to form a phagolysosome. the invader is broken down with perforin contents spill out and useful material used. Waste products packaged into vesicles and leaves through exocytosis.
72
Plant physical defences to disease:
Callose is synthesised and deposited between cell walls and membrane. Callose papillae act as barriers, preventing pathogens from entering the plant cells. Lignin makes the mechanical barrier to the invasion thicker. Callose blocks sieve plates in the phloem, sealing off the infected part of the plant. Callose deposited in plasmodesmata between infected cells and their neighbours to seal off infected cells.
73
Outline the physical defence process in plants.
Entry into the cells triggers detector molecules. When the pathogen's enzymes breakdown the cell wall the products are recognised. This stimulates signal molecules to alert the nucleus. Polysaccharides and defensive chemicals synthesised. Defensive molecules stimulate neighboring cells and some attack the pathogen and cellulose blocks pathways.
74
Plant chemical defences.
- insect repellent (citronella) - insecticides (Pyrethrins) - antibacterial compounds (Saponins and caffeine) - toxins - anti-oomycetes (glucanase)
75
Human non-specific defences:
Skin - physical barrier - produces sebum which inhibits pathogen growth Mucous membranes - trap microorganisms and contain lysosomes that break down cell walls( also contain phagocytes) Expulsive reflexes. Inflammation
76
Macrophage phagocytosis difference:
When the pathogen has been digested, the macrophage combines antigens from the pathogen surface membrane with glycoproteins called the major histocompatibility complex. The MHC complex moves the pathogen antigens across the macrophage's surface, becoming an antigen-presenting cell. These stimulate other cells to produce antibodies.
77
Inflammmation:
Mast cells stimulated by damaged tissue release cytokines and histamines. Histamines dilate blood vessels, causing a localised heat and redness. Histamines increase the water potential of the blood, causing blood plasma to transfer into tissue fluid. This causes increased temp and swelling. Cytokines attract white blood cells to the site.
78
Where are B lymphs produced?
Bone marrow
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Where are T lymphs produced?
Thymus gland
80
Cell-mediated immunity:
Macrophages do their thing after detecting abnormal cell antigens. Used to treat cancer and viruses. Macrophage -> APC -> stimulates T helper cells -> cloning (into t memory cell, produce interleukins that stimulate phagocytosis or B cell division, into T-killer cells)
81
Humoral immunity:
A B cell with complimentary antibodies bind to the pathogen and engulf pathogen. Becomes APC. T helper cells binds to B cell APC. (This was clonal selection) Interleukins produced stimulate B cell mitosis. (clonal expansion.) Cloned cells produce antibodies to disable the pathogen. (KEY FACTOR IS THE ACTION OF ANTIBODIES IN THE LYSIS AND DEATH OF PATHOGENIC ORGANISMS)
82
What is an autoimmune disease?
The immune system begins to attack healthy body tissue. Treated with immunosuppressant drugs. - but make patient susceptible to other diseases. e.g Lupus
83
Principles of vaccination:
Pathogen is made safe by maintaining antigens but eliminating the risk of infection. Small amounts injected into the blood. Primary immune response triggered. Contact with pathogen will now trigger secondary response, destroying pathogen rapidly.
84
In what ways can antigens be put into a vaccine safely?
Killed or inactivated pathogen Weakened (attenuated) pathogen Genetically engineered antigens produced antigens isolated
85
What are the sources of medicine?
Plants Microorganisms Personalised medicine (Pharmacogenetics) Synthetic Biology
86
Examples of drugs extracted from plants?
Penicillin -> mould on melons -> antibiotic | Aspirin -> willow bark -> Pain Killer
87
Synthetic biology:
Using genetic engineering, colonies of bacteria can be produced to produce antibodies.
88
Anti-biotic resistance
Bacteria culture reproduce. Genetic variation due to mutation. Exposure to antibiotics. More resistant bacteria survive. Less competition. Higher population of more resistant bacteria.
89
MRSA:
Bacteria 30% population have it on their skin Can cause boils, abscesses, and potentially septicemia. Treated with methicilin and penicillin-like antibiotics, however some strains are resistant.
90
C. difficile:
Bacteria In guts of 5% of pop Produces toxins that could damage the lining of the intestines. Dangerous when overused antibiotics kill healthy gut bacteria.