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4.1)Communicable Diseases Flashcards

1
Q

what is a communicable disease?

A

disease that can be passed from person to person

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2
Q

what causes communicable diseases?

A

pathogens

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3
Q

what are the types pathogens?

A

bacteria
fungi
protists
virus

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4
Q

what is a vector?

A

something that carries pathogens from organism to organism

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5
Q

how do bacteria cause disease?

A

reproduce rapidly inside the host cell—>release waste products/toxins that are toxic to host—>disease

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6
Q

where do bacteria live in plants nd why?

A

vascular tissue (phloem + xylem where nutrients are transported)

able to gain the nutrients from the plant

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7
Q

what kingdom does bacteria belong to?

A

prokaryotes

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8
Q

what are viruses?

A

non-living infectious agents
50x smaller than average bacterium

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9
Q

how do viruses cause disease?

A

invade host cell
takes over hosts genetics to produce more viruses
virus adapts to host + evolves
=
disease

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10
Q

what is bacteriophage nd used for what?

A

virus that infects nd replicates inside of bacteria
used to identify nd treat diseases

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11
Q

what is fungi?

A

(pathogen)
multicellular eukaryotes
heterophic (intake food from surroundings)
saprophytic (lives off dead material) & parasitic (lives off host)

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12
Q

how can fungi live of skin of animals?

A

hyphae of fungi form a mycelium that grow under skin surface = sends ot specialised reproductive hyphae that grow to surface of skin = releases spores

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13
Q

what molecules do fungi release?

A

cellulase (digestive enzyme) to digest cellulose cell wall of plant = infiltrates vascular system = takes nutrients from phloem nd xylem

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14
Q

what are protists?

A

unicellular/multicellular
eukaryotes
often need vector to transfer

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15
Q

what are the vectors of protista?

A

animal (e.g mosquito insect)
OR
pollutes water

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16
Q

what is the malarial parasite nd what does it feed off?

A

plasmodium
feeds on haemoglobin inside red blood cells

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17
Q

diff between the way that virus nd protists cause disease?

A

virus = takes over hosts DNA nd uses host to make new virus
protists = DO NOT take over hosts DNA nd jst uses it

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18
Q

animal diseases caused by bacteria?

A

TB
Bacterial meningitis

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19
Q

plant disease caused by bacterium?

A

Ring rot

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20
Q

animal diseases caused by virus?

A

HIV/AIDS
Influenza

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21
Q

plant disease caused by virus?

A

tobacco mosaic virus (TBV)

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22
Q

plant disease caused by fungi?

A

Black sigatoka (in banana)

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23
Q

animal diseases caused by fungi?

A

ringworm (cattle)
athlete’s foot (human)

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24
Q

animal disease caused by protoctista?

A

malaria

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25
Q

plant disease caused by protoctista?

A

blight (tomatoes nd potatoes)

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26
Q

what does HIV virus contain nd why?

A

RNA & Reverse Transcriptase Enzyme (RTE)

RTE coverts RNA—>DNA so that the DNA can be replicated

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27
Q

What are the 2 types of transmission nd which is more common?

A

Direct - more common
Indirect

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28
Q

What is the means of transmission of:
HIV
Bacterial meningitis
STI’s
Ringworm
Athlete’s foot

&

How to reduce transmission route?

A

Direct physical contact w someone’s bodily fluids 👥
-wash hands regularly 🖐️
-sterilise equipment ✂︎
-sterilise surfaces 🧽
-use condoms

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29
Q

What is the means of transmission of:
Rabies
Septicemia (blood infection)

&

How to reduce transmission route?

A

Breaks in skin (e.g Animal bites, wounds/cuts, needle puncture)
-cleaning & covering wounds🩹

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30
Q

what is the means of transmission of:
Dysentery
Cholera
Diarrhoeal diseases

&

How to reduce means of transmission?

A

(faecal-oral route) Ingesting contaminated food or transferring pathogens to mouth (e.g. eating w unwashed hands after using toilet)
-treating waste/drinking water 💧
-washing food 🫑
-cooking food thoroughly 🥩

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31
Q

what is the means of transmission of:
Anthrax (caused by bacteria found in soil)
Tetanus

&

How to reduce means of transmission?

A

Transmission by SPORES (resistant stage of pathogen) carried in air(wind), residue on surfaces or in soil
-use mask 😷
-wash skin after contact w soil 🧼

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32
Q

what is the means of transmission of:
Herpes
Athlete’s foot

&

How to reduce means of transmission?

A

Inanimate objects (e.g. bed sheets, surfaces, socks, cosmetics, brushes)
-wash clothes/bedding regularly 🧺
-clean surfaces 🧼

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33
Q

What is the means of transmission of:
Influenza
Tuberculosis

&

How to reduce means of transmission?

A

Pathogen carried in water droplets through air (e.g talking, coughing, sneezing)
-cover mouth when sneezing/coughing
-dispose of tissues correctly🧻

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34
Q

What is the means of transmission of:
Bubonic plague
Malaria
Rabies
Diarrhoeal diseases

&

How to reduce means of transmission?

A

Vectors (e.g. rat fleas, mosquito, raccoons, dogs, water) that transmit the pathogen from one organism to another
-wash animal🦝🛁
-insect repellant🦗
-ensure water is clean💧

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35
Q

What causes someone to be infected w malaria?

A

Plasmodium parasite transmitted by female Anopheles mosquito vector🦟🦟🦟🦟🦟🦟🦟🦟🦟🦟🦟🦟🦟🦟🦟🦟🦟🦟 🦟🦟🦟 🦟🦟🦟 🩸

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36
Q

What are the ways to control spread of malaria?

A

-reduce stagnant water 🏊(mosquitos favour stagnant water & reproduce here)
-malarial tablets (6 weeks before going to 🦟 environment)
-mosquito nets
-insect repellant🦗

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37
Q

Describe cycle of transmission of malaria

A

Female Anopheles 🦟 sucks blood w Plasmodium gamete
↓
Plasmodium gamete migrate to salivary glands of 🦟
↓
🦟 bites uninfected person 👤
↓
plasmodium parasite moves to liver of person
↓
plasmodium parasite moves to blood🩸
＝
👤person is infected

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38
Q

what are some factors affecting pathogen transmissions in animals?

A

OVERCROWDING (close proximity = easy spread)
POOR VENTILATION (no dispersion of airbourne particles that carry pathogens)
POOR HEALTH (weak immune system unable to fight pathogens)
MIGRATION FROM INFECTED AREAS (higher risk of transmission)
CULTURE/INFRASTRUCTURE (traditional medicinal practices/way food is cooked may increase risk of transmission)
POOR WASTE DISPOSAL (build up of pathogens creating unsanitary conditions)
SOCIOECONOMIC FACTORS (lack of trained health workers/insufficient public warning during outbreak of disease=less prepared=increase outbreak/rate of transmissions)

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39
Q

what are examples of direct transmission of plant pathogens?

A

direct contact of healthy plant w infected plant
RINGROT
TOBACCO MOSAIC VIRUS
TOMATO/POTATO BLIGHT
BLACK SIGATOKA

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40
Q

what are the means of indirect transmission in plants?

A

SOIL CONTAMINATION (pathogens in soil enetr via roots when roots damaged by replanting, burrowing animals, uprooting)
SPORES (carried in wind)
LEAVES (leaves carrying pathogens are shed and carried to soil where it can grow/infect another plant)
FRUITS/SEEDS (pathogens enter fruit/seed which are distributed within the plant=infect offspring)
VECTORS (animals, humans, water, wind)

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41
Q

what are other factors that affect pathogen transmission in plants?

A

PLANTING VARIETIES OF CROPS THAT R SUSPECTIBLE TO DISEASE
OVERCROWDING
POOR MINERAL NUTRITION
DAMP, WARM CONDITIONS
CLIMATE CHANGE

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42
Q

what are the means of reducing plant transmissions?

A

1)leave room between plants so pathogens can’t spread easily
2)clear fields thoroughly to remove all traces of plants from the soil
3)rotate crops so spores/bacteria will dies as they don’t have access to host plant
4)strict hygiene practices to prevent bacteria coming into contact w plants
5)control insects - that could act as vectors that transport pathogens

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43
Q

why do people suffer from food poisoning when travelling to tropical regions?

A

-pathogens thrive in damper/warmer conditions
-there are diff pathogens that we don’t have immunity to
-diff countries cook food in diff ways

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44
Q

why do diseases such as malaria nd dutch elm disease not ham the vector that is involved in transmitting the pathogen?

A

the specific cell surface receptors are absent in the vector

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45
Q

why do some large trees die years after a major storm?

A

strong winds may cause uprooting which exposes roots and allows pathogen-infected soil to penetrate nd infect the tree

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46
Q

why can’t pathogens living in the soil infect plants unless the roots are damaged/exposed?

A

outer tissues of roots act as physical barriers nd some pathogens mau not have the enzymes to penetrate nd break through the cell wall

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47
Q

where are meristems founds?

A

in the tips of roots/shoots

48
Q

what are passive defences?

A

-defences present b4 infection that prevent the entry nd spread of the pathogen
-both pyshical nd chemical

49
Q

what are examples of physical plant defences?

A

CELLULOSE CELL WALLS - contain lignin that make wall waterproof nd completely indigestible
WAXY CUTICLE - prevents water collecting on leaves as pathogens often collect in water nd require water to survive
BARK - contains range of chemicals that protect against pathogens
STOMATAL CLOSURE - guard cells close the stomata in the part of the plant where the pathogen is detected
TYLOSE FORMATIONS - balloon like swelling that fills the xylem nd blocks xylem so it cannot transport pathogen infected water
TYLOSE FORMATION 2 -conatins high conc of terpenes = toxic to many pathogens
CALLOSE POLYSACCHARIDES deposited in sieve tubes at end of growing season to seal off the infected area and prevent pathogen spreading

50
Q

what are examples of chemical plant defense?

A

INSECT REPELLANTS
INSECTICIDES that are toxic to insect/fungi
ANTIBACTERIAL COMPOUNDS (e.g. lysosome organelles containing lysozyme enzymes that break down bacterial cell walls)
ANTIFUNGAL COMPOUNDS (e.g saponin chemicals in plant cell membranes that break down fungal cell walls)
GENERAL TOXINS chemicals made in some plants that break down to form cyanide when the plant cell is attacked

51
Q

how is the plant’s response to a pathogen triggered?

A

1)receptors attach to molecules from pathogen/chemicals produced by the plant when attacked
2)signalling molecules are stimulated
3)gene in nucleus is switched on
this triggers a cellular response

52
Q

what are examples of active defences in plants🌱
?

A

CELL WALLS THICKEN/STRENGTHEN w extra cellulose
CALLOSE deposited between plant cell wall and membrane to impede penetration, strengthens cells wall and block plasmodesmata (channels) to prevent spread of pathogens
OXIDATIVE BURSTS that produce highly reactive oxygen molecules capable of damaging cells of invading organisms
NECROSIS (cell suicide) cells surrounding the infection killed to limit the pathogen’s access to water/nutrients which prevents further spread around the plant
CANKER sunken necrotic lesion in woody tissue causing death of cambium tissue which means water/nutrients can’t be transported which prevents further spread of pathogens

53
Q

what are some commonly used chemicals?

A

TERPENOIDS essential oils w antibacterial/fungal properties (e.g menthol form mints)
PHENOLS bind nd deactivate enzymes (e.g insects ingest TANNINS nd their enzymes become deactivated causing them to stop growing nd die = pathogens aren’t able to be transmitted)
ALKANOIDS nitrogen-containing compounds inhibiting protein synthesis nd having bitter taste to inhibit herbivore feeding (e.g caffeine, nicotine, morphine, solanine)
DEFENSINS cysteine-rich proteins that kill lots of types of bacteria by inhibiting ion transport channels
HYDROLYTIC ENZYMES found in spaces between cells (e.g CHITINASES that breaks down chitin found in cell walls

54
Q

when do secondary defences come into action?

A

when pathogens have entered body

55
Q

what are the 2 main phagocytes?

A

NEUTROPHILS
MACROPHAGES

56
Q

where r neutrophil phagocytes manufactured?

A

bone marrow nd are releases in large amounts as result of an infection

57
Q

what do neutrophils contain lots of?

A

lysosome organelles containing lysozyme enzyme that digest pathogens

58
Q

what are the first line of defences of humans?

A

skin
mucous membranes
expulsive reflexes
chemical secretions

59
Q

how does skin help to protect against pathogens?

A

has outer layer of dead hardened cells w keratin which act as a physical barrier

sebum on surface containing fatty acid w antimicrobial properties

evaporation of sweat leaves behind salt residue

low moisture, low pH, high salinity creates inhospitable env for pathogens

60
Q

how does mucous membrane help to protect against pathogens?

A

mucus in the airways trap the virus, bacteria nd pollen particles

cilia wafts the mucous to the back of the throat so it can be swallowed nd destroyed by HCL in stomach or coughed out

61
Q

how do expulsive reflexes help to protect against pathogens?

A

pathogen lining the airway triggers cough/sneeze which results in sudden expulsion of air containing the pathogens

62
Q

how do chemical secretions help to protect against pathogens?

A

lysozyme (digestive enzyme) that breaks down the bacterial cell wall

HCl produced by the cells that line the stomach create low pH that kill bacteria

63
Q

why does the gut not get damaged even though lots of HCL is produced there?

A

gut cells secrete mucus that acts as protective lining against the HCL

64
Q

how do commensal organisms protect us against pathogens?

A

Candida albicans nd E.coli bacteria growing on skin, mouth nd intestines compete w pathogens nd prevent them from invading host cells

65
Q

what is the 2nd line of defence for humans?

A

blood clotting
inflammation
wound repair
phagocytosis

66
Q

how does blood clotting prevent pathogens from spreading?

A

the scab formed for wound healing acts as a physical barrier against pathogens

67
Q

how does inflammation happen?

A

tissue is damaged and cell-signalling molecule HISTAMINE is secreted which causes:
1)vasodilation increases blood flow through capillaries
2)leaky capillaries allow fluid to enter tissue nd create swelling
3)phagocytes to enter blood nd engulf pathogens
4)cells to release cytokines that trigger an immune response to infected area

68
Q

what are cytokines?

A

cell-signalling compounds made of small protein molecules that trigger an immune response

69
Q

how does wound repair happen?

A

1)scab is formed as a result of blood clotting
2)
-new blood vessels form
-collagen is produced
-granulation tissue produced to fill the wound
-stem cells divide to produce epithelial cells
-contractile cells cause wound to contract
-unwanted cells die

70
Q

what are macrophages?

A

type of phagocyte that travel in blood as monocytes before settling in body tissue
monocytes mature into macrophages i n the lymph nodes

71
Q

where are dendritic macrophages found?

A

peripheral tissue

72
Q

how do macrophages initiate a specific immune response?

A

1)macrophage engulfs the pathogen and combines antigen (on pathogen cell surface) w MHC(glycoproteins in macrophages cytoplasm)
2)MHC moves antigen to macrophage’s surface nd the macrophage becomes APC
3)APC moves around body where it comes into contact w T-lymphocytes nd B-lymphocytes to activate specific immune response

73
Q

what is the role of the APC?

A

increase the chances of antigen coming into contact w pathogen as there may only be 1 T-cell and B-cell w the correct recognition site for the antigen

74
Q

why can neutrophils be identified in blood smears?

A

lobed nucleus

75
Q

what is the 3rd line of defence against pathogens?

A

production of lymphocytes nd antibodies that are specific to the pathogen

(slower but more effective than non-specific response)

76
Q

where are lymphocytes produced?

A

bone marrow

77
Q

what are the 2 types of lymphocytes and where are they found?

A

T-cells = Thymus gland
B-cells = bone marrow

78
Q

why is there a large number of T-cell receptors?

A

diff T-cells have diff T-cell-Receptors (TCR) which allows the T-cell to recognise a wide range of foreign antigens (on surface of foreign bodies/pathogens)

79
Q

Describe the maturation of T-cells…

A

Immature T-cells originate in the bone marrow and move to the Thymus gland where they become mature

80
Q

When do T-cells become activated?

A

When they encounter their specific antigens

81
Q

What happens to T-cells in the bone marrow?

A

Divide by mitosis into 3 types of T-cells:
1)T-helper
2)T-killer
3)T-regulator

82
Q

How do T-cells work in an immune response?

A

1) are activated by macrophages engulfing the pathogen and presenting the pathogen’s antigens on their own cell surface to become an APC and binding w T-cells w receptors that are complementary to the specific pathogen
2)activated T-cells divide by mitosis to produce clones
3)・T-helper = release interleukins (cytokine) which activate B cells & cause phagocyte activity to increase
　・T-killer attach to foreign antigens on cell surface of infected cells and secrete Perforins which punch hole in surface membrane of infected cells so toxins (which are also secreted) can enter and Kill pathogen
　・T-regulator = regulate the immune response by shutting down the immune system once body is clear of pathogens & preventing T-cells from attacking and killing uninfected host cells

83
Q

Describe the maturation of B-cells…

A

・B-cells remain in the bone marrow until they are mature nd then spread throughout the body in lymph nodes
・gain special B-Cell-Receptors (BCR) aka antibodies
・each antibody forms Glycoprotein receptor that combines w 1 type of antigen

84
Q

What are B-cells w the same type of BCR’s called?

A

Clones

85
Q

How are B-cells activated?

A

・B-cells w complementary antibody receptors bind to antigens on APC (phagocytes, infected cells, pathogens) & release interleukins
・activated B-cells divide by mistosis & some B-cells differentiate into plasma cells

86
Q

What is the role of plasma cells?

A

Secrete lots of antibody molecules (that are complementary to the antigen) into the blood, lymph or linings of lungs nd gut

87
Q

What is the role of memory cells?

A

Remain in blood for long time (sometimes life time) so that they are able to initiate a immune response when the pathogen enters the body again

88
Q

What are primary immune responses activated by?

A

Newly encountered antigen

89
Q

What are secondary immune responses activated by?

A

Previously encountered antigen

90
Q

How do B-cells initiate a secondary immune response?

A

1)B-memory cells recognise the same antigen (from a previously encountered pathogen)
2)the memory cells quickly divide and differentiate into plasma cells to produce antibodies and more memory cells

91
Q

Why are secondary immune responses quicker?

A

there are more memory cells present which can be selected, so there are more antibodies produced within a short time period

92
Q

Describe the structure of antibodies…

A

・globular glycoproteins called immunoglobulins
・Y-shaped w 2 heavy chains bonded by disulfide bonds to 2 light chains
・each chain has constant & variable region
・constant region determines the mechanism used to destroy the antigens

93
Q

What is diff in the variable region of antibodies?

A

・AA sequence where the antibody attaches to antigen to form ANTIGEN-ANTIBODY COMPLEX
・（end of variable region) is ANTIGEN-BINDING SITE composed of 110〜130 diff AA = variation = specific to epitope

94
Q

Where is the epitope?

A

The part of the antigen that binds to the antibody

95
Q

Where and what is the role of the hinge region?

A

・where the disulfide bonds join the heavy chains together
・provide flexibility to antibody molecule so that the antigen-binding-Site can be placed at diff angles when binding to the antigens

96
Q

How many antibodies do each antigens have?

A

1

97
Q

What is the role of antibodies?

A

To destroy pathogens within the body by acting as:
1)Anti-toxins 2)Opsonins 3) Agglutinins

98
Q

Describe how Anti-toxins work…

A

Antibodies bind to toxins produced by the pathogens and neutralises them to make them ahrmless

99
Q

Describe how opsonins work…

A

・Antibodies attach to bacteria making them readily identifiable to phagocytes.
Once identified, phagocyte has receptor proteins for the heavy chain on the antibodies, enabling phagocytosis to occur

・Antibodies attach to flagella of bacteria, making the bacteria less active and making it easier for phagocytosis to occur

100
Q

Describe how Agglutinins work…

A

Causes pathogens carrying antigen-antibody complexes to clump together. This reduces chance that pathogens spread through the body and allows phagocytes to engulf many pathogens at a time.

101
Q

Describe Active immunity…

A

・occurs when an antigen enters the body and triggers a specific immune response
・Naturally acquired by exposure to pathogens
・Artificially acquired by pathogens in vaccinations💉
・takes 1/2 weeks for antibody concentration to increase during PRIMARY response
・takes shorter time for antibody concentration to increase when same pathogen invades body during SECONDARY response

102
Q

Describe passive immunity…

A

・acquired without an immune response (antibodies aren’t produced by the infected person) as there are no memory cells that can produce antibodies
・Artificially acquired through injection/transfusion of antibodies that were collected from other people (who’s immune system had been triggered by a vaccination)
・Naturally acquired by fetus from mother’s placenta
・Naturally acquired by babies from mother’s breastmilk

103
Q

What is colostrum?

A

The initial breast milk from mother’s (to their babies)

104
Q

How do autoimmune diseases occur?

A

When Antibodies, T cells (helper cells & cytotoxic cells) attack 1 or more self-antigens and damages body cells as a result

105
Q

Describe 2 types of Autoimmune diseases…

A

LUPUS
・butterfly rash across the face
・connectives tissue of body is attacked by immune system and affects joints, kidney, heart, lungs nd skin
・causes long term destruction

RHEUMATOID ARTHRITIS
・muscle spasms
・inflamed tendons
・lethargy
・joint pain
・begins in fingers and hands, spreads to shoulders nd elsewhere〜

106
Q

what is the cause of autoimmune disease?

A

1)likelihood of developing the disease when exposed to a particular pathogen is due to inheritance of genes

2)environment-moving to areas of high autoimmune disease from areas of low autoimmune disease increased likeliness of developing the disease

107
Q

What is a vaccine?

A

A suspension of antigens that are intentionally put into the body to induce artificial active immunity

108
Q

How are vaccines administered?

A

-injection (into vein or muscle)
-orally

109
Q

How do vaccinations produce long-term immunity?

A

Cause memory cells to be created so the immune system remembers the antigen when reencountered (w the same pathogen) and produces stronger antibodies to it at a faster rate

110
Q

How are epidemics/pandemics prevented?

A

Vaccination programmes that are offered to citizens (e.g babies vaccinated against measles, mumps nd rubella)

111
Q

What are problems w vaccines?

A

-body having poor response (weak/defective immune system)
-variations in antigens of pathogens cause vaccines to not trigger an immune response (e.g malaria has too many antigens so vaccines could be ineffective)
-pathogens could be in parts of body that are difficult to reach by vaccine (e.g cholera that remains in the small intestine)
-cross breeding between diff strains of the virus, making the vaccine ineffective

112
Q

When does herd immunity occur?

A

when a large proportion of a population has been vaccinated (and is therefore immune) which makes it difficult for the pathogen to spread within that population

113
Q

Why is herd immunity important?

A

Allows for individuals who aren’t able to be vaccinated (e.g children & those who have weak immune systems) to be protected from the disease

114
Q

What is Ring immunity?

A

When all the people living/working near a vulnerable/infected people are vaccinated to prevent them from catching and transmitting the disease.

Vaccinated individuals don’t spread the pathogen onto others so the ‘vulnerable individuals’ within the ring are protected as the people they interact with will not have the disease

115
Q

How do live attenuated vaccines work?

A

-Contain whole pathogens that have been weakened
-weakened pathogens slowly multiply and allow for the body to recognise the antigens which trigger the immune response (plasma cells producing antibodies)
-produce stronger + longer immune response
-e.g MMR vaccine

116
Q

How do inactivated pathogens work?

A

-Contain whole pathogens that have been killed
-can’t cause diseases as the pathogens are dead nd inactivated
-immune response is not strong/long-lasting so booster doses often required
-e.g Polio vaccine

117
Q

Describe the diff sources of medicines…

A

1)Bacteria nd Fungi providing antibiotics
2)Plants
・Artemisinin drug (found in sweet wormwood) treats Malaria by killing the pathogen while it is in the rbc
・Quindine drug (found in Quinine tree) treats Fast Heart Rate by blocking channel proteins in cardiac muscle to reduce impulse condunction

Biology🧬🪼 (9 decks)

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