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12 - Communicable Diseases Flashcards

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1
Q

Define communicable disease

A

A disease, caused by a pathogen, that can be passed from one organism to another

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2
Q

What are bacteria cell walls made from

A

peptidoglycan

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3
Q

How to bacteria replicate

A

Binary fission

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4
Q

How are types of bacteria classified

A

Shape

Structure of cell walls (gram + or gram -)

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5
Q

Describe how different types of bacteria may appear different on staining

A

Gram-positive - walls are thicker - blue/purple colour

Gram-negative - appear red

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6
Q

How do bacteria make us feel ill

A

Production of toxins

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7
Q

How do viruses replicate?

A

Take over body cells and use their, mechanisms to replicate genetic material, cells are burst - releasing new viral particles

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8
Q

Describe the structure of a virus (4)

A

Genetic material (DNA or RNA)
surrounded by a protein coat (capsid)
surrounded by an envelope (phospholipid bilayer)
containing glycoproteins

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9
Q

Draw the structure of a virus

A

Revision number 4

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10
Q

Describe the life cycle of a virus (6)

A 
attachment to cell
penetration of cell
uncoating
gene replication and expression
assembly
release
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11
Q

Viruses that attack bacteria are called

A

bacteriophages

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12
Q

Why are the labels gram-positive and gram-negative useful?

A

The structure of the cell walls determine how they react to antibiotics so this information can inform the production of antibiotics

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13
Q

What is the cell wall of fungi made of?

A

Chitin

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14
Q

Describe the structure of protoctists and how they spread

A

eukaryotic
parasitic (use people or animals as host)
may need a vector to transfer or through polluted water

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15
Q

Describe the structure of fungi and how they spread

A

eukaryotic (multicellular or unicellular)
absorb food broken down by extracellular enzymes
parasitic
release spores to reproduce

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16
Q

Name the 4 plant diseases we study and what type of pathogen they are

A

Tobacco mosaic virus - virus
black Sigatoka - fungus
ring rot - bacterial
blight - protoctist

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17
Q

Name 5 reasons reducing infections in plants is important

A
  • yield of crops
  • quality of crop
  • waste food
  • food security
  • extinctions
  • habitats and biodiversity
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18
Q

What are the 2 ways plants can spread disease

A

Direct contact - eg. leaves touching leaves

Indirect contact - transported via vector eg. wind, water, animals, insects, contaminated soil

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19
Q

describe how ring rot affects plants and any cures or preventions

A

bacterial infection
leaves, tubers and fruit damaged
no cure - field can not be used for 2 years

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20
Q

describe how tmv affects plants and any cures or preventions

A

viral infection
leaves damaged, reduces yield and stunts growth
no cure - resistant crop strains available

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21
Q

describe how blight affects plants and any cures or preventions

A

protoctist
destroys leaves, tubers and fruit
no cure - resistant crop strains available, management and chemical treatments can reduce infection risk

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22
Q

describe how black sigatoka affects plants and any cures or preventions

A

fungal infection
destroys leaves (turn black), reduction in yield
fungicides can control spread

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23
Q

describe 4 factors that affect the transmission fo plant disease

A

monocultures
- diseases spread quickly
climate change
- more rain and higher temp. lead to higher transmission
poor farming practice
- same species in soil every year and not disinfecting tools increases indirect spread
overcrowding
- closer means more direct contact
-poor ventilation means greater humiidy, promotes growth of pathogens

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24
Q

State 5 ways to reduce the spread of plant dieases

A 
leave space between plants
remove all traces of plants after harvesting
general hygiene eg. sterilising tools
pest control eg. pesticides
removing and burning infected plants
annual crop rotation
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25
Q

State the 7 animal diseases we study

A 
TB
Bacterial meningitis 
HIV/AIDs
Influenza
Malaria
Ring Worm
Athletes foot
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26
Q

Describe TB affects animals and any cures or preventions

A

bacterial infection
damages/destroys lung tissue and suppresses immune system
curable by antibiotics
preventable by vaccination and improving living standards

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27
Q

Describe Bacterial meningitis affects animals and any cures or preventions

A

bacterial infection
infection of meninges in brain, can spread to body and cause blood poisoning
blotchy rash (does not disappear when a glass is pressed to it)
curable by antibiotics
vaccinations prevent some forms

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28
Q

Describe HIV/AIDS affects animals and any cures or preventions

A

viral infection
gradual destroys immune system
transmitted through bodily fluids
no vaccination and no cure but antiretroviral drugs can slow transmission in body

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29
Q

Describe Influenza affects animals and any cures or preventions

A

Viral infection
infection of ciliated epithelial cells in gaseous exchange system
no cure, mutates regularly, vaccination immunity only lasts for a few years max

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30
Q

Describe malaria affects animals and any cures or preventions

A

protoctist
spread through bites of infected mosquitoes
makes you weak and vulnerable to other infections
no cure and limited treatment - per cent by controlling vector eg. nets, long sleeves removing still water breeding ground

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31
Q

Describe Ring worm affects animals and any cures or preventions

A

fungal infection
grey-white crusty, infectious, circular areas of skin
antifungal creams effective cure

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32
Q

Describe athletes foot affects animals and any cures or preventions

A

fungal infection
grows on and digests warm, moist skin between toes
antifungal creams effective cure

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33
Q

State at least 5 factors that affect the transmission of animal diseases

A

overcrowded living conditions
lack of clean running water and sanitation
compromised immune system
poor nutrition
lack of vaccinations
lack of trained doctors
poor infrastructure eg. no access to health care

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34
Q

What are the 2 catagories for plant defences?

A

physical and chemical

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35
Q

Name at least 5 physical plant defences

A
  • wavy cuticle on leaves
  • callose production
  • lignified xylem
  • stomatal closure
  • meristems
  • plants can seal off and lose infected “limbs”
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36
Q

How do pathogens get into plants

A

physcial wounds eg. storm damage, cuts, animals biting off bark etc.
insect vectors eg. aphids

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37
Q

give an example fo an active defence mechanism for plants

A

callose production

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38
Q

what is callose

A

polysaccharide, polymer of b- glucose

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39
Q

how does callose production protect a plant from infection

A

callose is synthesised and deposited in
-sieve plates - prevent pathogen from spreading further
plasmodesmata - prevent pathogen from spreading between cells
-between cell walla and membrane - sealing cell off to prevent spread

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40
Q

When do cells produce callose?

A

When they detect an infection, either detect chemicals released by pathogens (eg. toxins) or products of cell wall hydrolysis (which is catalyzed by enzymes released by pathogens)

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41
Q

What are the 4 stages in the non-specific immune response in plants?

A 
RSGD
Recognise
Signaling
Gene Expression
Defend
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42
Q

In the non-specific immune response in plants, what does signaling mean?

A

Cell signaling- molecules active the defense genes

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43
Q

In the non-specific immune response in plants, what does gene expression mean?

A

defensive chemicals made (proteins) or enzymes to make the chemicals are made in the ribosomes

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44
Q

In the non-specific immune response in plants, what does defend mean?

A

directly attack pathogen/ communicate with other cells/ cause cell death

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45
Q

What is necrosis?

A

cell suicide, cells are sacrificed to prevent the spread of a pathogen

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46
Q

Name at least 5 chemical defenses in plants

A
  • insect repellents
  • insecticides
  • antibacterial compounds
  • antifungal compunds
  • anti-oomycetes
  • general toxins
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47
Q

Name at least 5 ways of limiting the spread of disease in humans

A 
Antibiotics
Vaccinations
Isolating infected individuals
avoiding contact
washing hands
covering mouth when coughing or sneezing
condoms
good food hygiene
reducing overcrowding
clean water and good sanitation
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48
Q

Name at least 5 non-specific barriers against pathogens in animals

A 
skin
mucous membranes
lysozymes (in tears and urine)
saliva
gut bacteria
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49
Q

How does skin act as a barrier against pathogens

A

physical barrier, bacteria on skin outcompete pathogens

sebum acts a an antimicrobial compund

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50
Q

How do mucous membranes act as a barrier against pathogens

A

traps microbes, contains phagocytes and lysozymes

51
Q

How do cilia act as a non-specific defense against pathogens

A

surface of gaseous exchange system

sweep mucus out of airways and to the back of the throat where it is swallowed and destroyed by stomach acid

52
Q

Name 4 expulsive réflexes and how the defend against infection

A 
Coughing
Sneezing
Vomiting
Diarrhoea
Physically expels pathogens from body
53
Q

What component of the blood causes blood clots and where are these made

A

Platelets/thrombocytes

Fragments of cells made in the bone marrow

54
Q

What are the 4 steps involved in blood clotting?

A

1 - platelets come into contact with collagen (skin/outside do blood vessels) and are activated

2 - platelets adhere to surface of damaged area and stick to each other

3 - produce serotonin - blood vessels contract

4 - produce thromboplastin enzyme - triggers reactions leading to blood clot

55
Q

How does a blood clot prevent infection from pathogens?

A

Clots dries to form a tough hard scab to keep pathogens out - physical barrier
Epidermal cells grow beneath scab, wound is healed

56
Q

What type of immune response is an inflammatory response

A

Non-specific localised response

57
Q

What are the symptoms of inflammatory response?

A

Pain
Heat
Swelling
Redness

58
Q

What starts an inflammatory responses?

A

Mast cells, type of WBC, activated

Release histamines and cytokines

59
Q

What 2 chemicals are released in inflammatory response?

A

Histamines and cytokines

60
Q

What do histamines do?

A

Cause blood vessels to dilate - increase blood supply = more WBCs, Increases temperature - unfavourable for pathogens
Increases permeability of capillaries - blood plasma forced out, causes swelling

61
Q

What do cytokines do?

A

Attract phagocytes to are to destroy pathogens by phagocytosis

  • stimulate specific immune response
  • stimulate hypothalamus to increase temp - unfavourable conditions for pathogen
62
Q

Why do your lymph nodes swell due to an inflammatory response

A

Lymphatic fluid joins back circulation at lymph nodes, more WBCs needed there to filter fluid and destroy pathogens causing swelling

63
Q

What are antigens

A

Glycolipids of the surface of cells

64
Q

What type of things can be (/have) antigens?

A

Allergens
Abnormal cells eg. Cancer cells
Non-self cells eg. Transplanted organ or blood transfusions
Pathogens

65
Q

What is phagocytosis?

A

The process by which pathogens are engulfed and destroyed (hydrolysed)

66
Q

What are the 2 types on WBCs in phagocytosis?

A

Neutrophils and macrophages

67
Q

What is the difference between neutrophils and macrophages

A

Neutrophils are quick responders

Macrophages are more slow and become antigen presenting cells

68
Q

What are the 5 stages on phagocytosis

A 
Recognition 
Attachment 
Engulfing
Digestion
Antigen Presentation
69
Q

When a pathogen is engulfed where does it go and how is it digested?

A

Vesicle-like structures called phagosomes, these are fused with a lysosomes containing hydrolytic enzymes that hydrolyse the pathogen

70
Q

After a pathogen is digested in phagocytosis, what happens to the debris?

A

Soluble debris is ejected through exocytosis

Antigens are combined with major histocompatibility complex and presented on surface

71
Q

What cells control our specific immune response?

A

WBCs- T lymphocytes and B lymphocytes

72
Q

What type of immune response do T lymphocytes control?

A

cell mediated immunity

73
Q

What type of immune response do B lymphocytes control?

A

humoral response

74
Q

What is cell-mediated immunity?

A

response to self cells that have been changed in some way eg. infection with a virus, cancerous, APCs

75
Q

What is humoral immunity?

A

Response to antigens found detached (from non-self cells or APCs)

76
Q

Describe the stages of cell-mediated immunity (up to differentiation)

A

1 - macrophage that has destroyed an antigen becomes an APC
2- complimentary receptors on the surface of a t helper cell bind to the antigen
3 - T helper cells release INTERLEUKINS that stimulate mitosis of the T-helper cell
4 - T helper cells then differentiate

77
Q

What are the 4 ways T helper cells can differentiate after the initial cell mediated response?

A
  • continue producing interleukins (attract phagocytes)
  • become t killer cells
  • become t memory cells
  • continue producing interleukins (stimulate b cells to divide)
78
Q

What do t killer cells do?

A

Produce perforin, perforates the cell membrane of pathogens to destroy them

79
Q

What do t memory cells do?

A

stay in blood long term

divide to form t killer cells on reinfection

80
Q

What are the 4 types of T lympocytes?

A

killer
helper
regulator
memory

81
Q

What the role of B lymphocytes in the humoral response?

A

B cells produce antibodies to neutralise pathogens

82
Q

Describe the process of humoral immunity

A
  • B cells are triggered when they come into contact with the antigen complementary to their antibodies
  • antigen in engulfed and presented on their surface MHCs
  • T-helper cell is attracted and selects the b-cell for cloning
  • b cells divide and mature into plasma cells (which secret antibodies and neutralise the pathogen) or memory cells (which circulate in the blood for future infection)
83
Q

Describe the secondary response to infection in terms of b cells

A

B memory cells detect the antigen (binds to antibodies)

memory cells develop into plasma cells that produce antibodies

84
Q

Compare plasma cells and memory cells

A

plasma - short-lived, immediate response, primary response

memory - long-lived, secondary, long-term immunity

85
Q

Where do T cells mature?

A

thymus gland

86
Q

Where do B cells mature?

A

bone marrow

87
Q

What type of proteins are antibodies?

A

quaternary (4 strands)

immunoglobulins

88
Q

What are the 3 ways antibodies “fight” pathogens?

A

Agglutination
Neutralise antigens
opsonisation

89
Q

What is aggultination?

A

“clumping” pathogens together

too big to enter host cells, immobilised and easier for phagocytosis

90
Q

What is neutralisation of antigens?

A

antibodies bind to toxins and block receptors on pathogens so they can’t bind to or enterr host cells

91
Q

What is opsonisation?

A

antibodies bind to antigens and “tag” them - marks them for destruction by phagocytosis
ENHANCES PHAGOCYTOSIS

92
Q

Describe the structure of an antibody

A
  • 4 polypeptide chains (2 short/light chains, 2 heavy/long chains)
  • held in Y shape by disulfide bridges
  • large area of constant region
  • 2 variable regions specific to antigens
93
Q

Draw the shape of the primary and secondary response graph, marking on the first exposure the second exposure and labelling the axes

A

revision photo 5

94
Q

What is an autoimmune diease?

A

stops recognising self cells and starts to attack and destroy healthy tissue

95
Q

How are autoimmune diseases treated?

A

Immunosuppressants

96
Q

Define antibody

A

Immunoglobulins produced by B lymphocytes in response to a specific antigen, triggering an immune response

97
Q

Define APC

A

Antigen presenting cell

a macrophage that displays foreign antigens

98
Q

Define clonal selection

A

The identification of an antibody-producing cell with complementary receptors to the shape of the specific antigen

99
Q

State the 4 types of immunitty

A

Natural active
Artificial active
Natural passive
Artificial passive

100
Q

Give an example of natural active immunity

A

Antibodies made after an exposure to an infection

101
Q

Give an example of artificial active immunity

A

Antibodies made after getting a vaccination

102
Q

Give an example of natural passive immunity

A

Antibodies transmitted from bother to baby eg. via breast milk

103
Q

Give an example of artificial passive immunity

A

Antibodies made by someone else and injected into you

104
Q

Describe when active immunity occurs and how long it lasts

A

direct contact to antigens/pathogens/spike proteins

immunological memory via B and T memory cells

105
Q

Describe when passive immunity occurs and how long it lasts

A

antibodies directly introduced into your body
you do not make antibodies yourself
immunity is immediate but does not last

106
Q

Why are booster vaccines necessary?

A
  • more memory cells produced
  • more plasma cells produced if reinfected
  • more antibodies produced so stronger fight against pathogen
107
Q

Why are vaccines given in small doses?

A

enough to trigger immune response but not overwhelm immune system

108
Q

What is herd immunity

A

a critical proportion of a population are vaccinated against a disease reduces spread and protects vulnerable people

109
Q

Why are diseases difficult to eradicate?

A
  • vaccinations might not work on some people
  • some people may be infected before vaccination and spread it
  • mutations
  • vulnerable can not be vaccinated
  • some choose not to be vaccinated
110
Q

What is antigenetic varabilty?

A

the formation of new strains of a pathogen as mutations cause changes in antigens thus antibodies and memory cells ineffective

111
Q

What are antibiotics and what do they do?

A

Inhibit growth/ destroy bacteria without affecting our cells (selective toxicity)
produced by other living organisms

112
Q

What are the 2 types of antibiotic

A

Broad spectrum/targeted

113
Q

How do antibiotics work?

A
  • inhibition of ell wall synthesis
  • disruption of cell wall
  • inhibit protein synthesis
  • inhibit RNA synthesis
  • inhibit nucleic acid synthesis

(generally enzyme inhibitors)

114
Q

Why do antibiotics not work against viruses?

A

can’t inhibit cell wall/protein synthesis as they have no cell wall and don’t use their own machinery to produce proteins

115
Q

How is antibiotic resistance caused?

A
  • –random mutation produces a gene for antibiotic resistance
  • –antibiotics are used (selection pressure) natural selection for bacteria that are resistant
  • –the number of resistant bacteria increase as they multiply, outcompete the non-resistant strain
  • –alleles for resistance passed on through conjugation
116
Q

What is conjugation?

A

cells attach to each other through pilli and genes are exchanged

117
Q

What is MRSA?

A

carried by 30% on our skin or in our nose
in blood in can cause boils, abscesses and septicaemia
treated with methicillin but now resistant

118
Q

What is C. difficile?

A

in the gut of 5%
produces toxins - damages the lining of intestines
causes diarrhoea, bleeding and death

119
Q

How can we reduce antibiotic resistance?

A
  • minimise the use of antibiotics
  • finish every course of antibiotics
  • good hygine
  • targetted antibiotics where possible
120
Q

What are medicines?

A

Drugs used to treat communicable and non-communicable diseases
treat symptoms or cures

121
Q

Where do we get medicines from?

A
    • naturally occurring compounds in plants/microorganisms that they use to defend themselves
  • – developed by complex computer programs to build 3D models and search through libraries of molecules
122
Q

Why is biodiversity important in medicines and antibiotics?

A

maintaining biodiversity is important as plants/microorganisms that could go extinct could hold the key to a life-saving drug

123
Q

What is pharmacogenetics? Give an example

A

the study of our genome and personalising medicines or treatments based on this
eg. genes alter our side effects to leukaemia treatment, blood is taken and analysed so dose can be given correctly

124
Q

Give 2 examples of synthetic biology in drugs

A

nano-technology for delivering drugs

using bacteria as factories to produce drugs

Biology (17 decks)

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