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4.1.1 communicable diseases Flashcards

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1
Q

what are the different types of pathogens that cause communicable diseases?

A

bacteria
fungi
viruses
protoctista

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2
Q

bacteria

A
  • Can be classified by their cell walls – the two main types of bacterial cell walls have different structures and react differently with gram staining
    -> Gram positive bacteria – looks purple-blue under light microscope e.g. MRSA
    -> Gram negative bacteria – appears red e.g. E.coli
  • Gram staining is useful because the type of cell wall affects how bacteria reacts to different antibiotics
  • Are prokaryotes – do not have a membrane-bound nucleus or organelles
  • can be classified by their basic shape e.g. bacillus (rod), coccus (spherical) etc
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3
Q

examples of bacteria

A

tuberculosis (TB)
bacterial meningitis
ring rot (potatoes, tomatoes)

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4
Q

virus

A
  • non-living infections agents
  • 0.02-0.3um in diameter
  • 50x smaller in length than bacterium
  • basic structure: some genetic material surrounded by protein
  • Some viruses attack bacteria – these are called bacteriophages
  • They take over the bacterial cells and use them to replicate, destroying the bacteria at the same time
  • Bacteriophages are used to identify and treat diseases
  • Very important in scientific research
  • All naturally-occurring viruses are pathogenic
  • Viruses invade living cells, where the genetic material of the virus takes over the biochemistry of the host cell to make more viruses.
  • Reproduce rapidly and evolve by developing adaptations to their host, which makes them very successful pathogens
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5
Q

examples of viruses

A

HIV/AIDS (humans)
influenza (animals)
Tobacco Mosaic Virus (plants)

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6
Q

protoctista

A
  • Group of eukaryotic organisms with a wide variety of feeding methods
  • Include single-celled organisms and cells grouped into colonies
  • A small percentage of Protoctista act as pathogens, causing devastating communicable diseases in both animals and plants
  • Protists which cause disease are parasitic – use people or animals as their host organisms
    -> May need a vector to transfer them to their hosts – e.g. malaria
    -> May enter the body directly through polluted water – e.g. amoebic dysentery
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7
Q

examples of protoctista

A

malaria
potato/tomato late blight

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8
Q

fungi

A
  • Fungal diseases can cause devastation in plants
  • Fungal diseases of plants cause hardship and even starvation in many countries
  • Eukaryotic organisms that are often multicellular, although the yeasts which cause human disease e.g. thrush are single-celled
  • Cannot photosynthesis - digest their good extracellularly before absorbing the nutrients
  • Many fungi are saprophytes – they feed on dead and decaying matter
  • When fungi reproduce they produce millions of tiny spores which can spread huge distances, this adaptation means they can spread rapidly and widely through crop plants
  • Some fungi are parasitic – feeding on living plants and animals
    These are what cause communicable diseases
    -> Fungal infections often affect the leaves of plants, they stop them photosynthesizing and so kill the plant
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9
Q

examples of fungi

A

black sigatoka (bananas)
ringworm (cattle)
athlete’s foot (humans)

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10
Q

how do viruses damage the host tissue directly?

A

Viruses take over the cell metabolism
The viral genetic material gets into the host cell and is inserted into the host DNA
The virus then uses the host cell to make new viruses which burst out of the cell, destroying it and spreading to infect other cells

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11
Q

how do protoctista damage the host tissue directly?

A

Protoctista take over cells and break them open as the new generation emerge but do not take over genetic material
They digest and use cell contents as they reproduce

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12
Q

how do fungi damage the host tissue directly?

A

Fungi digest living cells and destroy them
Response of the body to the damage caused by the fungus gives the symptoms of disease

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13
Q

how does fungi produce toxins to damage the host tissue?

A

Fungi produce toxins which affect the host cells and cause disease

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14
Q

how does bacteria produce toxins to damage the host tissue?

A

Bacteria produce toxins that damage the host cell, causing disease
Some bacterial toxins damage the cell by breaking down the cell membranes, or inactivate enzymes or interfere with the host cell genetic material so the cells cannot divide
These toxins are a by-product of the normal functioning of bacteria

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15
Q

direct transmission of pathogens in animals

A

direct contact
inoculation
ingestion

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16
Q

direct transmission of pathogens in animals: direct contact

A
  • kissing or contact with bodily fluids of another person e.g. bacterial meningitis, STDs
  • direct skin-to-skin contact e.g. ringworm, athlete’s foot
  • microorganisms from faeces transmitted on the hands e.g. diarrheal diseases
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17
Q

direct transmission of pathogens in animals: inoculation

A
  • through a puncture wound or through sharing needles e.g. septicaemia
  • from an animal bite e.g. rabies
  • through a break in skin e.g. during sex (HIV/AIDS)
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18
Q

direction transmission of pathogens in animals: ingestion

A
  • taking in contaminated food or drink or transferring pathogens to the mouth from the hands e.g. amoebic dysentery, diarrhoeal diseases
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19
Q

indirect transmission of pathogens in animals

A

fomites
vectors
droplet infection (inhalation)

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20
Q

indirect transmission of pathogens in animals: fomites

A
  • inanimate objects such as bedding, socks or cosmetics can transfer pathogens e.g. athlete’s foot, gas gangrene and Staphlycoccus infections
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21
Q

indirect transmission of pathogens in animals: vectors

A
  • transmits communicable pathogens from one host to another
  • water e.g. diarrhoeal diseases
  • animals e.g. mosquitoes transmit malaria, rat fleas transmit bubonic plague, dogs transmit rabies
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22
Q

indirect transmission of pathogens in animals: droplet infection

A
  • minute droplets of saliva and mucus are expelled from mouth when talking, coughing and sneezing - may contain pathogens that can be breathed in e.g. influenza, tuberculosis
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23
Q

indirect transmission of pathogens in plants

A

soil contamination
vectors

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24
Q

indirect transmission of pathogens in plants: soil contamination

A
  • Some pathogens can survive the composting process so the infection cycle can be completed when contaminated compost is used
  • Infected plants often leave pathogens or reproductive spores from Protoctista or fungi in the soil – can infect the next crop – e.g. black sigatoka spores, ring rot bacteria, spores of P. infestans and TMV
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25
Q

indirect transmission of pathogens in plants: vectors

A
  • Wind – bacteria, viruses and fungal or oomycete spores may be carried on the wind – e.g. Black sigatoka and P. infestans
  • Water – spores swim in the surface film of water on leaves; raindrop splashes carry pathogens and spores – e.g. spores of P. infestans
  • ## Humans – pathogens and spores are transmitted by hands, clothing, fomites, farming practices and by transporting plants and crops around the world – e.g. TMV survives in tobacco products, ring rot survives on farm machinery, potato sacks etc
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26
Q

indirect transmission of pathogens in plants: vectors

A
  • Wind – bacteria, viruses and fungal or oomycete spores may be carried on the wind – e.g. Black sigatoka and P. infestans
  • Water – spores swim in the surface film of water on leaves; raindrop splashes carry pathogens and spores – e.g. spores of P. infestans
  • Humans – pathogens and spores are transmitted by hands, clothing, fomites, farming practices and by transporting plants and crops around the world – e.g. TMV survives in tobacco products, ring rot survives on farm machinery, potato sacks etc
  • Animals – insects and birds carry pathogens and spores from one plant to another as they feed e.g. insects such as aphids inoculate pathogens directly into plant tissue
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27
Q

factors affecting the transmission of communicable diseases in animals

A
  • Poor disposal of waste, providing breeding sites for vectors
  • A compromised immune system including having HIV/AIDS or needing immunosuppressant drugs after transplant surgery
  • Overcrowded living and working conditions
  • Poor nutrition
  • Climate change – can introduce new vectors and diseases e.g. increases temperatures promote the spread of malaria as the vector mosquito species is able to survive over a wider area
  • Socioeconomic factors – for example, lack of trained health workers and insufficient public warning when there is an outbreak of disease can also affect transmission rates.
  • Culture and infrastructure – in many countries traditional medical practices can increase transmission
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28
Q

factors affecting the transmission of communicable diseases in plants

A
  • Climate change – increased rainfall and wind promote the spread of diseases; changing conditions allow animal vectors to spread to new areas; drier conditions may reduce the spread of disease
  • Planting varieties of crops that are susceptible to disease
  • Damp, warm conditions increase the survival and spread of pathogens and spores
  • Poor mineral nutrition reduces resistance of plants
  • Over-crowding increases the likelihood to contact
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29
Q

what kind of disease is ringrot?

A

bacterial - caused by the gram positive bacterium Clavibacter michiganenis

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30
Q

what plants does ring rot affect?

A

potatoes, tomatoes, aubergines

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31
Q

what parts of the plant does ring rot damage?

A

leaves, tubers, fruit

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32
Q

what is the impact of ring rot?

A

Can destroy up to 80% of the crop
No cure
Once a field is infected it cannot be used to grow potatoes for at least 2 years

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33
Q

what kind of disease is TMV?

A

virus

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34
Q

what plants does TMV affect?

A

tobacco plants and 150 other species e.g. tomatoes, peppers, cucumbers, petunias and delphiniums

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35
Q

what parts of the plant does TMV damage?

A

leaves, flowers and fruit

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36
Q

what is the impact of TMV?

A

Stunts growth
Reduces yield
Leads to almost total crop loss
Resistant crop strains are available
No cure

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37
Q

what kind of disease is potato blight?

A

fungus-like protoctist oomycete
Phytophthora infestans

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38
Q

what plants does potato blight affect?

A

Hyphae penetrate host cells
potatoes, tomatoes

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39
Q

what parts of the plant does potato blight damage?

A

leaves, tubers and fruit

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40
Q

what is the impact of potato blight?

A

Crop damage
No cure
Resistant strains, careful management and chemical treatments can reduce infection risk

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41
Q

what kind of disease is black sigatoka?

A

fungus - Mycospharella fijienis

42
Q

what plants does black sigatoka affect?

A

Hyphae penetrate and digest the cells
bananas

43
Q

what parts of the plant does black sigatoka damage?

A

leaves

44
Q

what is the impact of black sigatoka?

A

Leaves turn black
Causes 50% reduction in yield
Resistant strains are being developed
Husbandry and fungicide can control the spread
No cure

45
Q

what kind of disease is tuberculosis?

A

bacterial - caused by Mycobacterium tuberculosis and M. bovis

46
Q

what animals does tuberculosis affect?

A

humans, cows, pigs, badgers and deer

47
Q

how does tuberculosis affect the animals?

A

Destroys lung tissue
Suppresses immune system – less likely to fight of disease

48
Q

is there a cure for tuberculosis?

A

Curable by antibiotics
Preventable by improving living standards and vaccination

49
Q

stats on tuberculosis

A

8.6 mil had TB
1.3 mil died
Global rise of HIV/AIDS has had a big impact because they are more likely to develop infections

50
Q

what kind of disease is bacterial meningitis?

A

bacterial - Streptoccus pneumoniae or Neisseria meningitidis

51
Q

what animals does bacterial meningitis affect?

A

humans - very young children and teens

52
Q

how does bacterial meningitis affect animals?

A

Affects the meninges of the brain which can spread to rest of the body causing blood poisoning and rapid death
Blotchy red rash
Doesn’t disappear when a glass is pressed

53
Q

is there a cure for bacterial meningitis?

A

Curable by antibiotics (delivered early)
Preventable by vaccines (some forms)

54
Q

stats for bacterial meningitis

A

10% infected will die
25% will recover with permanent damage

55
Q

what kind of disease is AIDS?

A

virus - caused by HIV

56
Q

what animals does AIDS affect?

A

Humans
Non-human primates
Passes from person to person through bodily fluids e.g. unprotected sex, shared needles, pregnancy, breast feeding

57
Q

how does AIDS affect people?

A

Targets T helper cells in the immune system
Gradually destroys immune system – likely to get other infections

58
Q

is there a cure for AIDS?

A

No vaccine
No cure
Anti-retroviral drugs slow the progress of the disease

59
Q

stats on AIDS

A

15 mil live with HIV
1.6 mil died
Women are at high risk in many countries – FGM increase infection rate

60
Q

additional info on AIDS

A

A retrovirus with RNA
Contains enzyme reverse transcriptase – transcribes the RNA to a single strand of DNA to produce a single strand of DNA in the host cell

61
Q

what kind of disease is influenza?

A

viral infection - Orthomycoviridae spp.

62
Q

what animals does influenza affect?

A

mammals - humans, pigs
birds - chickens

63
Q

how does influenza affect animals?

A

Kills the ciliated epithial cells in the gas exchange – airways open to secondary infection
Major change in the surface antigens so there are no antibodies available

64
Q

is there a cure for influenza?

A

Can be fatal to young children, old people and people with chronic illnesses
Deaths caused by secondary bacterial infection as a result of original infection
Mutate regularly
Flu vaccine annually
No cure

65
Q

strains of influenza

A

Three main strains – A, B, C
A – most virulent – classified further by proteins on surface e.g. A(H1N1) and A(H3N3)

66
Q

what kind of disease is malaria?

A

protoctista - Plasmodium

67
Q

what animals does malaria affect?

A

humans and other mammals - spread by mosquitos

68
Q

how does malaria affect the animals?

A

Parasite has a complex life cycle with 2 hosts – mosquitoes and people
Reproduce inside the female mosquito
Female needs to take 2 blood meals to provide her with protein before she lays her eggs – when malaria is passed to people
Invades the red blood cells, liver and brain

69
Q

is there a cure for malaria?

A

Disease recurs – making people weak and vulnerable to other infections
No vaccines
Limited cures
Preventative measures to control the vector
Mosquitos destroyed by insecticides and removing the standing water where they breed
Preventative by mosquito nets, window screens, long-sleeves

70
Q

stats on malaria

A

200 mil people are infected each year
Over 600,000 die

71
Q

what kind of disease is ringrot?

A

fungal disease - Trichophyton verrucosum

72
Q

what animals does ringrot affect?

A

mammals - cattle, dogs, cats, humans

73
Q

how does ringrot affect animals?

A

Causes grey-white, crusty, infectious, circular areas of skin
Not damaging but itchy

74
Q

is there a cure for ring rot?

A

Antifungal creams are effective cure

75
Q

what kind of disease is athlete’s foot?

A

fungal disease - Tinia pedia

76
Q

what animals does athlete’s foot affect?

A

humans

77
Q

how does athlete’s foot affect humans?

A

Grows on and digests the warm, moist skin between toes
Causes cracking and scaling
Itchy and score

78
Q

is there a cure for athlete’s foot?

A

Antifungal creams are effective cure

79
Q

how do plants recognise an attack?

A
  • respond rapidly to pathogen attacks
  • receptors in the cells respond to molecules from pathogens or to chemicals produced when the plant cell wall is attacked
  • stimulates the release of signalling molecules
  • triggers cellular responses
80
Q

what are some cellular responses in plant defence?

A

producing defensive chemicals
sending alarm signals to unaffected cells to trigger their defences
physically strengthening the cell walls

81
Q

explain the physical defences that plants do when under attack?

A
  • rapidly set up extra mechanical defences
  • produce high levels of callose
82
Q

structure of callose

A

polysaccharide
β-1,3 linkages and β-1,6 linkages between the glucose monomers

83
Q

function of callose

A
  • callose is deposited into the cell walls and reinforced with lignin to provide a thicker barrier for the pathogen to penetrate through
  • it blocks the sieve tube end plates in the phloem - sealing off the infected area
  • it blocks the plasmodesmata between infected cells and their neighbours
84
Q

explain the chemical defences that plants do when under attack?

A
  • plants produce powerful chemicals that either repel the insect vectors of disease or kill invading pathogens
  • used, extracted and synthesised them to help us control insects, fungi and bacteria
85
Q

examples of plant defensive chemicals

A
  • insect repellents - e.g. pine resins and citronella from lemon grass
  • insecticides - e.g. pyrethrins and caffeine
  • antibacterial compounds including antibiotics - e.g. phenols, antibacterial gossypol defensins, lysosomes
  • antifungal compounds - e.g. phenols, antifungal gossypol, caffeine, saponins, chitinases
  • anti-oomycetes - e.g. glucanases, polymers
  • general toxins - e.g. cyanide
86
Q

chemical defence examples: insecticides

A

pyrethrins - made by chrysanthemums and act as insect neurotoxins
caffeine - toxic to insects and fungi

87
Q

chemical defence examples: antibacterial compounds

A

phenols - antiseptics made in different plants
antibacterial gossypol - produced by cotton
defensins - plant proteins that disrupt bacterial and fungal cell membranes
lysosomes - organelles containing enzymes that break down bacterial cell walls

88
Q

chemical defence examples: antifungal compounds

A

phenols - antifungals made in many different plants
antifungal gossypol - produced by cotton
caffeine - toxic to fungi and insects
saponins - chemicals in many plant cell membranes that interfere with fungal cell membranes
chitinases - enzymes that break down the chitin in fungal cell walls

89
Q

chemical defence examples: anti-oomycetes

A

glucanases - enzymes made by some plants that break down glucans
polymers - found in the cell walls of oomycetes

90
Q

chemical defence examples: general toxins

A

cyanide - some plants make chemicals that can be broken down to form cyanide compounds when the plant cell is attacked which is toxic to most living things

91
Q

innate non-specific primary defences - keeping pathogens out

A
  • Skin (keratinocytes; flora; sebum)
  • Mucous membranes (mucus; lysosomes; phagocytes)
  • Expulsive reflexes (coughing, sneezing, vomiting, diarrhoea)
  • Blood clotting (platelets; thromboplastin; serotonin)
  • Inflammatory response (mast cells; histamines; cytokines)
92
Q

innate non-specific primary defences: skin

A
  • Skin covers the body and prevents the entry of pathogens.
  • The skin produces sebum, an oily substance that inhibits the growth of pathogens.
  • It has a skin flora of healthy microorganisms that outcompete pathogens for space on the body surface.
93
Q

innate non-specific primary defences: mucous membranes

A
  • Mucus contains phagocytes, which remove remaining pathogens.
  • Lysosomes in tears and urine, and the acid in the stomach, also help to prevent pathogens getting into our bodies.
  • Many of the body tracts, including the airways of the gas exchange system, are lined by mucous membranes that secrete sticky mucus. Traps microorganisms and contains lysosomes, which destroy bacterial and fungal cell walls.
94
Q

innate non-specific primary defences: inflammatory responses

A
  • Cytokines attract white blood cells to the site and dispose of pathogens by phagocytosis.
  • Mast cells are activated in damaged tissue and release chemicals called histamines and cytokines
  • Histamines make the blood vessels dilate, causing localized heat and redness. The raised temperature helps prevent pathogens reproducing
  • Histamines make blood vessel walls more leady so blood plasma is forced out, once forced out of the blood it is known as tissue fluid. Tissue fluid causes swelling and pain.
  • Inflammatory response is a localized response to pathogens resulting in inflammation at the site of a wound. Inflammation is characterized by pain, heat, redness and swelling of tissue.
95
Q

innate non-specific primary defences: blood clotting

A
  • Thromboplastin – an enzyme that triggers a cascade of reactions resulting in the formation of a blood clot
  • Serotonin – makes the smooth muscle in the walls of the blood vessels contract, so they narrow and reduce the supply of blood to the area
  • Blood clots rapidly to seal the wound. When platelets come into contact with collagen in skin or the wall of the damaged blood vessel, they adhere and begin secreting several substances.
  • The clot dries out, forming a hard, tough scab that keep pathogens out.
  • Epidermal cells below the scab start to grow, sealing the wound permanently, while damaged blood vessels regrow.
  • Collagen fibers are deposited to give the new tissue strength.
  • Once the new epidermis reaches normal thickness, the scab sloughs off and the wound is healed.
96
Q

innate non-specific secondary defences - getting rid of pathogens

A
  • Phagocytes (neutrophils and macrophages; phagocytosis; antigen presentation)
  • Neutrophils
  • 60% of all leucocytes (WBC)
  • Travel in blood: squeeze through capillary walls into tissue
  • Released in large numbers during infection
  • Short lived
  • Macrophages
  • Bigger than neutrophils
  • Found in organs
  • Leave the bone marrow as immature monocytes
  • Monocytes develop into acrophages as they settle in orgns
  • Long lived
  • Cut up and display antigens (initiate immune response)
  • Chemical messengers (cytokines; opsonins)
  • Fever
97
Q

innate non-specific secondary defences: fever

A
  • Normal temp – around 37oC – maintained by hypothalamus
  • When a pathogen invades your body, cytokines stimulate your hypothalamus to reset the thermostat and your temp goes up
  • Adaptations:
    -> Most pathogens reproduce best at or below 37oC. Higher temperatures inhibit pathogen reproduction
    -> The specific immune system works faster at higher temperatures
98
Q

innate non-specific secondary defences: phagocytes

A
  • Phagocytes build up at the site of an infection and attack pathogens. Sometimes you can see pus in a spot, cut or wound. Pus consists of dead neutrophils and pathogens.
  • Phagocytes are specialized while cells that engulf and destroy pathogens – types of phagocytes: neutrophils and macrophages
99
Q

innate non-specific secondary defences: chemical messengers

A

cytokines:
- They can increase body temperature and stimulate the specific immune system
- Phagocytes that have engulfed a pathogen produce cytokines
- They act as cell-signalling molecules, informing other phagocytes that the body is under attack and stimulating them to move to the site of infection or inflammation

opsonins:
- Different immunoglobulinopsonins but antibodies such as have the strongest effect
- They have receptors on their cell membranes that bind to common opsonins and the phagocyte then engulfs the pathogen
- They are chemicals that bind to pathogens so they are more easily recognized by phagocytes

100
Q

stages of phagocytosis

A
  1. Pathogens produce chemicals that attract phagocytes
  2. Phagocytes recognize non-human proteins on the pathogen. This is a response not to a specific type of pathogen, but simply a cell or organism that is non-self
  3. The phagocyte engulfs the pathogen and encloses it in a vacuole called a phagosome.
  4. The phagocyte combines with a lysosome to form a phagolysosome.
  5. Enzymes from the lysosome digest and destroy the pathogen

biology (10 decks)

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