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Biology ๐Ÿ„๐Ÿ๐Ÿ›๐Ÿคฐ๐Ÿป๐Ÿงฌ > M7 > Flashcards

M7 Flashcards

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1
Q

7.2 path types

how could we define health? when would we use this def?

how could we define disease? what are the issues surrounding this def?

A
  • WHO: โ€œa state of complete mental physical and social wellbeing, and not merely the absence of disease or infirmityโ€ (at the beginning of long responses!)
  • Any condition that adversely affects the function of any part of a living thing (key issue is for eg braces could also be a โ€œdiseaseโ€ with this def = broad + imprecise)
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2
Q

7.2 path types

what are the diff pathogen types? (6)

can you give an example of each pathgn?

A

Prion - BSE prion
Virus - HPV (human polio virus)
Bacteria - Mycobacterium tuberculosis
Protozoa - Plasmodium sp.
Fungi - Tinea pedis
Macro-parasite - tapeworms

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3
Q

7.2 path types

what disease is associated with each of these pathogens?

1) A prion
2) HPV
3) Mycobacterium tuberculosis
4) Plasmodium sp.
5) Tinea pedis
6) Tapeworms

A

1) CJD (Creutzfeldt-Jakob disease), or aka BSE, or aka mad cow disease
2) Polio
3) Tuberculosis
4) Malaria
5) Tinea (athleteโ€™s ๐Ÿฆถ)
6) Tapeworm disease

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4
Q

7.2 path types

prions - living/non-living, characteristics, relative size, explain the example

A

eg

Incurable disease transmitted by eating nerve tissue from infected animals - prion proteins are not digested in the gut and can enter the bloodstream, eventually reaching the brain. (holes in the brain?)

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5
Q

7.2 path types

viruses - living/non-living, characteristics, relative size, explain the example

A

Highly contagious via the โ€œfaecal-oralโ€ route - virus normally attacks cells in the digestive tract โ†’ billions of viral particles present in faeces of infected people. Poor personal hygiene + sub-standard sewerage system = contaminated water + food supply = disease becomes endemic.

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6
Q

7.2 path types

bac - living/non-living, characteristics, relative size, explain the example

A

characteristics - unicellular, prokaryotic, microscopic pathogens with a single loop of double stranded DNA

size
up to 100 um

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7
Q

7.2 path types

protozoa - living/non-living, characteristics, relative size, explain the example

A

size: 50-150 um

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8
Q

7.2 path types

fungi - living/non-living, characteristics, relative size, explain the example

A

size: 4 ฮผm (unicellular)

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9
Q

7.2 path types

macroparasites - living/non-living, characteristics, relative size, explain the example

A
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10
Q

7.2 path types

  • size of a prion?
  • description? (super brief)
  • transmitted by eating ____ tissue of an infected animal
  • how to describe mad cow disease?
A

10nm

defective form of proteinโ€ฆ

nerve

fatal neurological disease

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11
Q

7.2 path types

  • size of a virus?
  • ___-cellular
A

<500 nm

non-cellular (NOT LIVING)

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12
Q

7.2 path types

HOW PATH TYPES ARE ALL AN UPGRADED AND MORE COMPLEX VERSION further down the list?

A
  • prions: non-living, no DNA or RNA
  • viruses: non-living, but do have DNA, RNA, protective coating of protein
  • bacteria: unicellular, prokary, single loop of double stranded DNA
  • protozoa: unicellular but EUKARY
  • fungi: unicellular or MULTICELLULAR, eukary
  • macro: multicellular, eukary, seen with naked eye
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13
Q

7.2 path types

how does malaria (a protozoan) infect ๐Ÿคต๐Ÿป?

A

travels to humanโ€™s LIVER to grow + multiply, then travels to BLOODSTREAM to infect + DESTROY RBCs

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14
Q

7.3 named epid trans

what is the structure of the Zaire ebolavirus?

A

most fatal (contains 7 distinct proteins of large molecules arranged in a long, braided strand of negative RNA)

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15
Q

7.3 named epid trans

what are the key symptoms of EVD?

A
  • incub period 2-21 days
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16
Q

7.3 named epid trans

what are some adaptations EV has had to assist entry + transmission?

A

RNA virus -> high mutation rate

  • early 2014, Ebola virus picked up a mutation called A82V, which made it worse at infecting bat cells, but 2x better at infecting human ones
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17
Q

7.3 named epid trans

is there a treatment for ebola?

A

no cure, patients supported w/ oral + intravenous fluids

  • 2016: successful highly protective rVSV-ZEBOV vaccine
  • mAbs (monoclonal antibodies) bind to a portion of the Ebola virusโ€™s surface called the glycoprotein, which prevents the virus from entering a personโ€™s cells
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18
Q

7.3 named epid trans

what is the mortality rate?

A

Killed 11,300 out of 28,600 infections

fatality rate 50%

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19
Q

7.3 named epid trans

Are there any strategies to prevent this disease from becoming an epidemic again in the future? (2)

A
  1. Targeted programmes for behaviour change (ie convince people to stop eating wild primates)
  2. Vaccine development (ie vaccinating health care workers as a preventative measure)
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20
Q

7.4 micr ๐Ÿฆ  test exp

risk 1

how would you mitigate it?

A

microbes from ๐Ÿ’ฆ samples ingested in body, causing illness
(breathing in microbes, microbes getting into cuts in skin)

PPE (๐Ÿงค, ๐Ÿ˜ท, ๐Ÿฅฝs) + NOT OPENING the agar plate once it has been sealed

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21
Q

7.4 micr ๐Ÿฆ  test exp

risk 2

how would you mitigate it?

A

Burns on hands (or other parts of the body, eg hair) caused by placing hands into spirit lamp or overflowing boiled water

  • Use test tube tongs and angle the test tube opening away from the body, continuously moving through the flame
  • Tie ๐Ÿ‘ฑ๐Ÿปโ€โ™€๏ธ back
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22
Q

7.5 types of transmission

what is a vector?

A

a living organism that carries a disease causing agent from one host to another in the life cycle of a pathogen

  • mech trans = vect. not infected themselves
  • biolog trans = when the pathogen reproduces within the vect. (animal)
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23
Q

7.6 koch + pasteur

when talking about Kโ€™s postulates, word to use is?

A

microbes

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24
Q

7.6 koch + pasteur

what are Pโ€™s contributions? (3)

A
  1. Disproved spontaneous generation
  2. Developed worldโ€™s first attenuated vaccine (anthrax, ๐Ÿ” cholera, rabies) + est. principle of immunity
  3. Invented pasteurisation (heating -> KILL THEM MICROBES)
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25
Q

7.7 ๐ŸŒ๐ŸŽ๐Ÿ๐Ÿ + ๐Ÿ„๐Ÿ” diseases

what are some key facts about panama disease?

assess the threat?

A

High rates of transmission, no cure, no resistant ๐ŸŒ varieties

80% of global production is under threat from Panama disease

SIGNIFICANT THREAT to banana industry/production

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26
Q

7.7 ๐ŸŒ๐ŸŽ๐Ÿ๐Ÿ + ๐Ÿ„๐Ÿ” diseases
general causes of infectious diseases in plants + animals (4)

A
  1. Increased movement of human populations
  2. Loss of genetic diversity - monoculture, cloning practices, selective breeding
  3. Increase in โ€˜hobby farmsโ€™
  4. Pesticide resistance
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27
Q

7.7 ๐ŸŒ๐ŸŽ๐Ÿ๐Ÿ + ๐Ÿ„๐Ÿ” diseases
NDV effect?

A
  • can typically kill 80% of unprotected poultry in rural areas, thus constraining large-scale expansions of the poultry industry in these regions
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28
Q

7.7 ๐ŸŒ๐ŸŽ๐Ÿ๐Ÿ + ๐Ÿ„๐Ÿ” diseases
FMD effect?

A
  • entire herds destroyed to contain outbreak
  • projected that a 12 month outbreak of FMD in Australia would result in a loss totalling $16bil -> bc trigger export bans, reduce meat quality, reduce financial return to producers
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29
Q

7.8 path adaptns

what are the pathogens youโ€™ll be focusing on for this dp? what groups are they in?

A
  1. Yersinia pestis (bacteria)
  2. Measles virus
  3. Giardia (protozoa)
  4. Tapeworms (macro)
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30
Q

7.8 path adaptns

YersP, entry adap?

A

Pili and fimbriae - extensions on the bacteria which bind to the host cellโ€™s receptor proteins that are matching

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31
Q

7.8 path adaptns

YersP, transm adap? (2)

A
  1. Use of a vector (flea) to transmit pathogen to host
  2. When Yersinia pestis infects a flea, production of biofilm inside the fleaโ€™s foregut starves the flea which makes it bite repeatedly - helps bacteria be spread via regurgitation into the wound at next feeding on host
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32
Q

7.8 path adaptns

Measles adaps?

A

Entry

Has 2 important proteins on its surface

  • H protein - able to attach to receptors found on human cells
  • F protein - gives virus ability to fuse with host cellโ€™s plasma membrane, allowing viral DNA to enter host cell
    โ†’ increased ability of virus to enter human cells
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33
Q

7.8 path adaptns

GiardDuo adaps?

A

Transmission

  • When in the external environment, Giardia can switch to a cyst form that is more durable
  • Cyst form allows them to survive outside the intestines for months
  • Once inside a host, the cysts dissolve and the parasites are released
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34
Q

7.8 path adaptns

apart from its โ€˜entryโ€™ adaptation, what is the tapewormโ€™s โ€˜transmissionโ€™ adaptation?

A

Tapeworms made up of many sections, each of which contain reproductive organs

These sections can release lots of eggs that end up in the hostโ€™s faeces

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35
Q

7.9 plant resp: fungal, viral

P.cinnamomic symptoms/imp

A
  • damages ALL parts of plant: wilted/yellowing leaves, stunted growth, coloured cankers
  • 1970s destroyed >282,000 ha of E.marginate in WA
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36
Q

7.9 plant resp: fungal, viral

what is the significance of ^ lignin prod. for E.cal? like, how does it actually help instead of โ€œkeeps the plant aliveโ€?

A
  • Lignin plays a role in protecting the cellulose cell wall of plant cells from damage by pathogens

forming a physical barrier that is impervious to the pathogen

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37
Q

7.9 plant resp: fungal, viral

Bush ๐Ÿ… resp to TSWV?

A

SAR response, presence of Sw-5 resistance breaking genes = resistance to TSWV

38
Q

7.9 plant resp: fungal, viral

could you explain g4g resistance?

A
  • plants possess Resistance genes (R) with path. specific proteins
  • R protein interacts directly with Antivirulence gene (Avr) protein produced by pathogen
  • Pathogen is then inhibited from infecting new cells
  • If a plant does not possess relevant R gene, it is at great risk of infection
39
Q

7.9 plant resp: fungal, viral

could you explain how basal resistance (Br) works?

A
  • Pathogen-associated molecular patterns (PAMPs) are conserved molecules common to different groups of pathogens
  • Plants recognise these elicitor molecules as โ€˜non-selfโ€™ and activate basal resistance โ†’ results in fortification of plant tissues where cellular junctions are tightened + cell walls become impenetrable to the invading pathogen
40
Q

7.9 plant resp: fungal, viral

how does hypersensitive response work?

A
  • If Br fails, the HR (a localised response) is activated to prevent further spread of pathogen to other plant parts
  • Plant cells in the region produce oxidative agents that alter the cell wall chemistry, trapping pathogen inside the host which die with the cell during apoptosis
  • HR more effective if the R gene-Avr gene complex is present
41
Q

7.9 plant resp: fungal, viral

what is SAR?

A

Non-specific, whole plant response that occurs after an earlier localised exposure to a pathogen

42
Q

7.11 second/third def

_______ increases permeability of nearby blood vessels

A

histamines (released by mast cells) + other inflammatory chemicals

43
Q

7.11 second/third def

what happens if there are too many pathogens for the phagocytes to fight off?

A

phagocytes let loose pyrogen chemicals which tap the hypothalamus + raise the bodyโ€™s temperature โ†’ fever = burn everything

44
Q

7.11 second/third def

after phagocytosis, what do the macrophages to? (ie after pathogen has been gobbled up)

A

Macrophages release cytokines to call up other immune cells such as neutrophils and natural killer cells

45
Q

7.11 second/third def

how lymph syst works in 2nd LoD?

A
  1. Bacteria + other microbes picked up in lymphatic fluid and trapped inside lymph nodes
  2. In LN: pathogen attacked + destroyed by macrophages (swollen lymph nodes glands are a good indicator of infection)
46
Q

7.11 second/third def

what is the role of the thymus + spleen in the lymph syst?

A

THYMUS

  • lymphocytes mature and become specialised T-cells in your thymus

SPLEEN

  • stores and filters blood for pathogens/debris/worn out cells and makes WBCs that protect you from infection
47
Q

7.11 second/third def

what are mechanisms for cell death (aPAOPtosis - amoeba sisters hehehe) in the 2nd LoD?

A
  • All nucleated cells have MHC I molecules on their surface
  • If cells become infected with virus, the expression of MHC I molecules diminishes
  • Presence of MHC I molecules prevents the NK cell from attacking it
48
Q

7.11 second/third def

types of WBCs (6)

A
  • mast cell
  • monocyte (differentiates into macrophage or neutrophil)
  • dendritic cell (messenger btwn 2nd + 3rd LoD)
  • NK cell (destroyed entire INFECTED cell)
  • basophil
  • eosinophil
49
Q

7.11 second/third def
(brief)

basophil, eosinophil

A

both: defence against parasites

b: releases histamines that cause inflammation + may be responsible for allergic reactions

e: releases toxins that kill bacteria & parasites

50
Q

7.11 second/third def

โœ๐Ÿป humoral response, cell-mediated response

A

:)

51
Q

7.11 second/third def

explain this diagram

A

acquired immunity diagram

52
Q

7.14 loc, reg, glob factors limit

a VERY IMPORTANT local + regional factor limiting spread of an infectious disease eg ebola

A

Active contact tracing

53
Q

7.15 first LoD

how is skin part of 1st LoD?

A

skin

  • keratin in epidermis cells (helps bind cellular matrix)
  • dead cells of upp epider continually being shed, replaced from below -> pathog off
  • sebaceous & sweat glands (found in dermis) -> salty acidic environ -> inhibit path growth
54
Q

7.15 first LoD

what are the chemical barriers in 1st LoD?

A
  1. Lysozymes in saliva + stomach acids (able to denature proteins within various pathogens)
  2. Alkali pH of the small intestine (duod, bile, neutralises pH)
  3. Tears contain lysozymes + lactoferrin which inhibit or kill microbes, earwax lowers pH to 4
55
Q

7.16 ๐Ÿ’Š antibiotics, antivirals

2 types of antibiotics, name + what they do

A
  • bacteriostatic: inhibit bacteria growth
  • bactericidal: kill bacteria
56
Q

7.16 ๐Ÿ’Š antibiotics, antivirals

why do people need to take a FULL course of antibiotics? not just stopping when symptoms subside?

A

within first few months, rapid reduc in # of bac, so inflamm at SOI reduces -> ppl feel better quickly

BUT there are persisting bac, if you stop early, they can grow + cause reinfection

they have experienced sub-lethal exposure to your first antibiotic and IF itโ€™s because they are genetically or physically better suited to dealing with that antibiotic (they could be resistant to those antibiotics) -> those antibiotics become useless against your infection

57
Q

7.16 ๐Ÿ’Š antibiotics, antivirals

how can bac develop antib resis?

A
  • intercepting antibiotics, changing the molecule so it becomes harmless
  • invest energy in pumps that remove antibiot BEFORE they harm
  • spread immunity via exchanging plasmids or transformation from environ
58
Q

7.16 ๐Ÿ’Š antibiotics, antivirals

antib benefits?

A
  • bac diff cell structure (eg cell wall) easily targeted
  • saved countless lives
59
Q

7.16 ๐Ÿ’Š antibiotics, antivirals

what do viruses do when they get inside cells?

ie stages in the replication of a virus in a host cell

A

so the viral genome, once it enters the cell, either goes to do the replication thing OR protein synthesis (gotta make viral proteins)

60
Q

what type of pathogen is herpes?

A

virus

61
Q

the mite varroa destructor causes the collapse of honeybee colonies by spreading viruses and feeding on the fat reserve of adults and larvae.

which of the following terms is NOT applicable to the varroa destructor in this example?

                   (a) pathogen
                   (b) vector
                   (c) host
                   (d) macroparasite
A

(a) PATHOGEN, YOU DINGBAT!!!

  • vector bc itโ€™s literary carrying viruses and giving viruses to the honeybees
  • host bc itโ€™s infected by the virus
    macro bc itโ€™s a parasite - feeds on adults and larvae
  • THE VIRUS IS THE PATHOGEN
62
Q

7.21 Aboriginal protocols

what are the past and contemporary uses of tea tree?

A
63
Q

7.21 Aboriginal protocols

what were the ethical implications of smoke bush use in contemp?

A

1 of 4 plants / 7000 smoke bush plants contained anti-HIV agents

US National Cancer Institute
Amrad

  • there are concerns that Indigenous Australians wonโ€™t be given credit or financial compensation for the development of drugs with this traditional medicinal plant
64
Q

7.15 infectious disease prevention

how specifically do hygiene practices prevent spread?

A

hygiene practices KILL the pathogens which reduces the risk of transfer

65
Q

7.15 infectious disease prevention

โœ๐Ÿป EVALUATE the effectiveness of quarantine (LOTS)

A
66
Q

7.15 infectious disease prevention

natural passive immunity includes?

(in terms of antibodies)

A

IgA breastfeeding, IgG crossing placenta

67
Q

7.15 infectious disease prevention

PLEASE correctly define immunisation

A

the process of getting the vaccine AND becoming immune to the disease following vaccination

68
Q

7.15 infectious disease prevention

what are real-life egs of PHCs?

โœ๐Ÿป in detail

A

COVIDSafe App Campaign

HPV Vaccination

69
Q

7.15 infectious disease prevention

what is an eg of pesticide use to prevent infectious diseases?

A
  • DDT insecticide was used to kill Anopheles Mosquito, which is a vector for malaria disease as it carries the plasmodium pathogen
  • but as expected, resistance developed
70
Q

7.15 infectious disease prevention

how does gen engineering work to prevent infectious disease spread? please refer to a specific eg

A

edits the genome of animal vectors to alter the production of certain proteins -> making path less able to survive inside it and thus spread

eg CRISPR for mosquitoes

71
Q

7.17 quar + environ manage of an epidemic

evaluate the above for ebola

A

enhancing surveillance + active contract tracing + quarantine/screening -> prevent intl ๐ŸŒ๐ŸŒŽ๐ŸŒ outbreak

BUT ^ pop densities + cultural trad + lack of ๐Ÿ‘ฉ๐Ÿปโ€๐Ÿซ + widespread pov -> optimised greater spread within West Africa

72
Q

7.18 imm + imm

what is the correct formula for incidence?

A
73
Q

7.18 imm + imm

what is the correct formula for prevalence?

A
74
Q

7.19 Dengue

What is the incidence and prevalence of Dengue fever? (in case theyโ€™re like WRITE WRITE WRITE with no stimulus, but I doubt it, BUT just in case)

A

INCREASING incidence - once limited to south-east asia (9 countries) but now common worldwide with estimated 390 million people infected annually (500,000 cases developed into severe) with 25,000 deaths worldwide annually

75
Q

7.20 histor, cultural, contemp predict / control

yr of John Snowโ€™s epidemiological study?

A

1854

76
Q

7.20 histor, cultural, contemp predict / control

what is an example of a NOT EFFECTIVE historical prediction of infectious disease method?

A
77
Q

7.20 histor, cultural, contemp predict / control

how did Indigenous Australians use tea tree traditionally?

A

Leaves and bark crushed; vapour inhaled -> treat headache

Brewed as tea -> throat ailment + relieve cold

Applied externally to wounds / superficial injuries

78
Q

7.21 Aboriginal protocols

justify importance of Indigenous IP?

A
  • not only connected to physical wellbeing
  • social, cultural, emotional wellbeing
  • so their expertise is neither disregarded nor exploited
  • must work together, benefits all people
79
Q

7.17 envir manage + quar

what are some reasons/processes for Australia being disease-free or pesticide-free for many infectious diseases?

A
  1. Biosecurity - rejecting/removing articles that may have come in contact withโ€ฆ strict import guidelines AND quarantine practices
  2. Actively tracking and informing the general public of overseas areas with [disease/pest] ie public education
80
Q

7.9 plant resp to path

compare and contrast physical resp of plants and animals to path

A
  • ๐ŸŒณ thick cuticle, stomatal openings vs ๐Ÿ‘ฑ๐Ÿปโ€โ™‚๏ธ skin (keratin, dead skin shedding)
  • ๐Ÿ‘ฑ๐Ÿปโ€โ™‚๏ธ more active phys resp, eg cilia, mucous membranes, peristalsis, coughing, sneezing, vomiting, diarrhoea
81
Q

7.9 plant resp to path

what are (extra) chemical responses that plants use to defeat pathogens once they have passed into the plantโ€™s tissues?

A
  • When plant cells are damaged by a pathogen they can secrete chemicals such as hydrogen peroxide which can kill microbes
  • Stored oils in the leaves have antibacterial and antifungal properties
82
Q

7.11, second + third LoD

in the inflammatory response for second LoD, what does the leaked protein do?

A

SWELLING, helps clot blood + form scabs (clotting elements)

83
Q

7.11, second + third LoD

what in the phagocyte breaks down and destroys path?

A

lysosomes

84
Q

7.11, second + third LoD

what do cytokines do in the body?

A
  • promote inflammation as part of the bodyโ€™s defense against infection and injury
  • facilitate communication between immune cells
85
Q

7.11, second + third LoD

what do CD4+ cells do?

A

provide protection against infections and cancers

86
Q

7.11, second + third LoD

compare monocytes and lymphocytes

A

BOTH are WBCs

  • monocyte (innate), lymphocytes (adaptive)
  • monocytes fight antigens by directly killing them, while lymphocytes target them with antibodies, or special proteins that neutralize antigens
  • monocytes larger in size than lymphocytes
87
Q

if thereโ€™s a higher number of a particular group of cells than usual, what might this indicate?

A

could indicate uncontrolled cell division which is (usually) cancer

88
Q

where are B and T cells made?

A

in the bone marrow ๐Ÿฆด

89
Q

vaccination reduces theโ€ฆwhich in turn reducesโ€ฆ

A

number of hosts in a population

the viability of the pathogen

90
Q

7.16 antibiot and antivir

what are the types of virus mutations?

A

antigenic shift and antigenic drift

91
Q

what antivirals do?

A

Rather than killing a virus directly, antivirals usually suppress the ability for a virus to infect and multiply in the cells

Biology ๐Ÿ„๐Ÿ๐Ÿ›๐Ÿคฐ๐Ÿป๐Ÿงฌ (6 decks)

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