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BMED2404 > Introductory Content > Flashcards

Introductory Content Flashcards

1
Q
  1. Order the following in most morbid to least:
  • Malaria
  • Diarrhoeal diseases
  • Acute respiratory infections
  • STIs
  • Pertussis
  • Tropical diseases
  • HIV/AIDS
  • Tuberculosis
  • Measles
A 
Acute respiratory infections
Diarrhoeal diseases
HIV/AIDS
Malaria
Measles
Tuberculosis
STIs
Pertussis
Tropical Diseases
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2
Q
  1. What are 3 examples contributing to the spread of epidemics?
A

Mass travel
Modern high density living
Animal husbandry: close proximity with pigs, birds

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3
Q
  1. Infectious diseases whose incidence in humans has increased in the past 2 decades or threatens to increase in the near future, include:

a) New infections resulting from changes or evolution of existing organisms
b) Known infections spreading to new geographic areas/populations
c) Previously unrecognised infections appearing in areas undergoing ecologic transformation
d) Old infections re-emerging as a result of antimicrobial resistance in known agents or breakdowns in public health measures
e) all of the above

A

e) all of the above

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4
Q
  1. Which is NOT a major factor contributing to the emergence of infectious diseases?

a) human demographics & behaviour
b) economic development & land use
c) breakdown of public health measures
d) regular sanitary measures
e) international travel & commerce

A

d) regular sanitary measures, although, extreme sanitary measures can prevent the development of the human immune system…

other major factors include:

  • technology & industry
  • microbial adaptation & change
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5
Q
  1. What are the two most common diseases affecting tourists?

a) respiratory infections & gonorrhoea
b) diarrhoeal diseases & fever (cause unknown)
c) diarrhoeal diseases and gonorrhoea
d) respiratory infections & diarrhoeal diseases
e) fever & malaria

A

d) respiratory infections (8%) & diarrhoeal diseases (64%).

Other major tourists diseases (to a lesser extent) are gonorrhoea, hepatitis, fever (cause unknown) and malaria.

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6
Q
  1. What are 3 major microbial species exhibiting extensive antimicrobial resistance?
A

Malaria, Tuberculosis and Staphylococcus.

For example, Malaria already exhibits complete resistance to some antibiotics in Thailand.

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7
Q
  1. What are the AIMS of ACTIVE IMMUNISATION? Have they been achieved?
A
  • to produce long-lasting immunity to pathogens in individuals & the community
  • to eliminate the pathogen (where possible)
  • successes: smallpox, polio
  • less effective: BCG vaccine for TB, whooping cough vaccine
  • major deficiencies - no vaccine for: HIV, malaria
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8
Q
  1. Which is correct regarding COMMENSALISM, MUTUALISM and PARASITISM?

a) commensalism is where one partner benefits and the other is harmed
b) parasitism can exist when the host is unaffected
c) mutualism is where one partner benefits and the other is harmed
d) none of the above

A

d) none of the above:

  • ‘commensal’ = lives in / on another, i.e. interaction bw normal flora & host: one partner benefits, other partner not affected
  • ‘mutualist’ / ‘symbiont’: both partners benefit (often obligatory eg ruminants, GIT flora)
  • ‘parasitic organisms’: one partner benefits, other harmed (pathogen = parasitic organism causing specific disease)
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9
Q
  1. SYMBIOSIS SPECTRUM
A

Mutualism-Commensalism-ParasitismShift right: initiate disease Shift left: re-establish a healthy host.

The spectrum is DYNAMIC. (see #10 & 11)

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10
Q
  1. Describe VIRULENCE.
A

Degree or intensity of pathogenicity, i.e. increase virulence –> likely to cause harm; a shift towards Parasitism. A standard strain of an organism may change, acquiring new virulence factors and mechanisms for damaging the host. Can lead to epidemics.

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11
Q
  1. What are 3 factors governing symbiosis?
A
  1. No. organisms: increase numbers = shift to parasitism, e.g. poor hygiene.
  2. Virulence of organisms: increase virulence = shift to parasitism
  3. Host’s defence / resistance: healthy = high resistance, decreases resistance = shift to parasitism.
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12
Q
  1. When is a disease an infectious disease?
A

Koche’s Postulates:

  1. The same pathogen must: be PRESENT IN EVERY CASE of the disease
  2. The pathogen must: be ISOLATED FROM THE DISEASED HOST and grown in pure culture
  3. The pathogen from the pure culture must: CAUSE THE DISEASE when inoculated into a healthy, susceptible laboratory animal
  4. The pathogen must: again be ISOLATED FROM THE INOCULATED ANIMAL and must be shown to be the original organism
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13
Q
  1. Give examples diseases of the following:

a) Outbreak
b) Endemic
c) Epidemic
d) Pandemic
e) Sporadic

A

a) Sudden, unexpected occurrences: Hendra virus Qld 2012 & 2013, Ebola in West Africa
b) Usually within a population; steady, at fairly low levels without any peaks: common cold, TB, malaria
c) Sudden occurrence; sudden increase above a baseline: influenza
d) Disease increases within large widespread populations usually worldwide: SARS
e) Random & irregular: Salmonella food poisoning outbreak

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14
Q
  1. Explain the concept of “Herd Immunity”
A

Scenario when people immunised or have recovered from the disease and developed natural immunity block susceptible individuals from the index case or spread of disease. If an infected individual however comes into contact with the susceptible individual they will become sick. In an unprotected population, herd immunity does not (yet) exist, and a disease will spread rapidly.

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15
Q
  1. Explain the differing functions of the HA & NA proteins of the Influenza Virus, and how they contribute to endemics.
A

Haemagglutinin protein - for attaching the virus to epithelial cells in our respiratory tract.

Neuraminidase - punches a hole in the outer surface of epithelial cells & allows the cells to enter & thus replicate.

These 2 proteins can change & give way to different versions of the virus, which can allow it to overcome immune response (host cells no longer immune).

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16
Q
  1. Explain the differences between antigenic SHIFT and DRIFT.
A

Drift = SMALL antigenic changes, e.g. altered protein which leads to ineffective recognition by the immune system (mutation)

Shift = DRASTIC antigenic changes e.g. large scale altered proteins, leading to complete non-recognition by the immune system. Coinfection with animal & human strains of influenza can generate very different virus strains by genetic reassortment (sharing/incorporation of virulence-causing DNA). Can lead to major epidemics/pandemics.

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17
Q
  1. Which of the following is not an example of vector-borne transmission?

a) malaria
b) flu
c) trypanosomiasis
d) none of the above

A

b) flu is air-borne transmission, on aerosols or ‘fomites’ (air-borne particles which carry infectious organisms). The flu can transmit via coughing, talking or sneezing, as examples. Other air-borne examples include chicken pox, mumps & measles. (even dust can be a factor, e.g. in hospitals, can lead to nosocomial infections).

NB trypanosomiasis = any tropical disease caused by trypanosomes and typically transmitted by biting insects, especially sleeping sickness and Chagas’ disease. Other examples include dengue fever & zika virus, transmitted via mosquitos.

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18
Q
  1. How do CONTACT & VEHICLE modes of transmission differ?
A

Contact: direct, usually skin to skin, or utensils; includes STIs.

Vehicle: contaminated food/water; e.g. cholera & food poisoning

19
Q
  1. What is the most important step in Control of Disease?

a) The pathogen
b) Source of the pathogen
c) Transmission to host
d) Host susceptibility
e) Exit from the host

A

c) Controlling TRANSMISSION: stopping the spread from one host to the next:
- change behaviour: HIV protection
- destroy insect vectors: DDT mosquitos
- control animal vectors: cattle: brucellosis, TB

20
Q
  1. How are VIRULENCE and MODE OF TRANSMISSION related?
A

Virulence = intensity of pathogenicity OR degree of ability to cause disease. It is affected by the ability to live outside a host. If virulence is low e.g. in the common cold, the host is still active, moves around, and can spread the virus. If the virulence is increased to the point the host is bed-ridden, the transmission drops.

Conversely, vector transmission eg African sleeping sickness: the host can’t transmit as the pathogen is reliant on a vector. I.e. the virulence is not connected with transmission.

21
Q
  1. How do Virulence Factors assist pathogenic microbial survival?
A
  1. Aid colonisation (eg capsule, pili/fimbriae)
  2. Allow penetration of host tissue
  3. Prevent/reduce host response
  4. Cause direct damage eg toxicity
22
Q
  1. What is the difference between specific and non-specific attachment/adhesion?
A

Specific - between particular proteins (e.g. flu virus protein spikes receptors)

Non-specific - just ‘sticking on a membrane’, eg slime/capsule/glycocalyx; dental plaque

23
Q
  1. How might an organism penetrate a host cell for further growth?
A

Uptake via:

  • Invasins: bacterial surface proteins (promote ingestion)
  • Endocytosis: non-phagocytic cells (exocytosis: actin tail propulsion)
  • Phagocytosis

e. g. Flu virus: endocytic uptake
e. g. Measles virus: membrane fusion uptake

24
Q
  1. What are some of the microbial enzymes that promote survival, penetration & damage to the host?
A

Coagulase: Coagulates blood
Kinases: Digests fibrin clots
Hyaluronidase: Hydrolyses hyaluronic acid
Collagenase: Hydrolyses collagen
IgA proteases: Destroys IgA antibodies = survival

Other important factors for penetration & growth:

  • Siderophores: Take iron from host (iron-binding proteins)
  • Antigenic variation: Alter surface proteins
25
Q
  1. What is one of the most significant microbial defences against immunological clearance that contributes to high virulence capacities?
A

CAPSULES. They are PROTECTIVE and ANTI-PHAGOCYTIC. They mask antigenic sites & evade detection.

E.g. glycocalyx layer around E. coli, a protection & important attachment mechanism on intestinal tissue.

E.g. polysaccharide coat around pathogenic yeast (Cryptococcus neoformans), appears as a ‘shiny halo’ under microscopy; very thick & protective, a hydrophilic capsule that inhibits phagocytosis & evades immune response.

26
Q
  1. Other than capsules, what are other microbial defences against immunological clearance?
A

Antigenic change: shift, mimicry (mimicry = coat themselves in host protein so not seen as ‘non-self’)
Produce antibody proteases: destroy immunoglobulins
Intracellular survival
Affect phagocytosis: destroy phagocyte, or inhibit phagocytosis (prevent chemotaxis / inhibit phagosome/lysosome fusion / resist lysosomal enzymes)

27
Q
  1. Describe the following characteristics of exotoxins:

a) source
b) metabolic product
c) chemistry
d) fever
e) neutralised by antitoxin

A

a) mostly G+
b) by-products of growing cell (diffuse / actively transported out)
c) protein
d) none
e) yes

28
Q
  1. What are the 3 types of microbial exotoxins based on structure & action?
A
  1. A-B
  2. Membrane-disrupting
  3. Superantigens
29
Q
  1. How do membrane-disrupting exotoxins lead to cell death?
A

If exotoxin is pore/channel-forming: cytoplasmic contents will leak out and water will enter the cell (osmotic effects), leading to swelling, host cell lysis and death.
If exotoxin is Phospholipase: will hydrolyse the membrane, and destabilise the lipid bilayer. Destroyed integrity will lead to cell lysis & death.

30
Q
  1. Describe the following characteristics of endotoxins:

a) source
b) metabolic product
c) chemistry
d) fever
e) neutralised by antitoxin

A

a) G- (mostly*) - LPS
b) present in LPS of outer membrane (part of the cell wall)
c) lipid (lipopolysaccharide)
d) occurs (inflammatory mediators)
e) no (not proteins, so can’t use Ab’s)

*G+ sources exist, but far less virulent - peptidoglycan, LTA, TA

31
Q
  1. Why are endotoxin releasing organisms difficult to treat?
A

The SHOCK (septic) of breaking up bacteria with antibiotics, and the resultant release of the membrane blebs in the blood stream, can be in some cases considered worse than an individual’s current infection with the organism.

32
Q
  1. Provide an example of how Pathogenicity Islands contribute to characteristics of pathogenicity.
A

PI’s are large segments of DNA that contain insertion-like sequences (mobile), encoding major virulence factors and associated with tRNA encoding genes. They are acquired by horizontal gene transfer and thus can be spread from cell to cell.

E.g. Protein secretion by Yersinia pestis (plague) modulates host activities. Through a ‘needle-like’ structure, it delivers effector proteins, secreting plasmid-encoded outer membrane proteins into phagocytic host cells. This damages & counteracts natural defence mechanisms, helping Y. pestis multiply & disseminate in the host.

33
Q
  1. Discuss COMPLEMENT and its roles in the innate immune system.
A

A component of blood, complement is always present in serum. Involves:

  • a series of 9 serum enzymes, act in cascade
  • activated when Ag/Ab rxn’s occur
  • in association with Ab, causes bacterial lysis (kills cells)
  • aids phagocytosis

Ultimate outcome is opsonisation/destruction of bacteria by a phagocytic cell. (opsonisation = molecular mechanisms where microbes/cells (etc.) are chemically modified to have stronger interactions with and “appear more delicious” to surface receptors on phagocytes and NKCs.

34
Q
  1. What are GLYCOPROTEINS and how do they contribute to the innate immune system?
A

= proteins + polysaccharide moieties.

e. g. Fibronectin:
- mediates non-specific clearance (of foreign cells)
- Coats foreign cells -> clotting
- Blocks attachment of foreign organisms to epithelial cells

RESULT: limits colonisation (maintains CT integrity)

35
Q
  1. What are CYTOKINES and how do they contribute to the innate immune system?
A
  • Intercellular signals
  • Bind to receptors on cells
  • Triggers cellular behaviours:
    • Initiate signal transduction pathway
      ○ Regulates specific transcription, translation events
  • Soluble small protein/glycoprotein
  • Can induce production of other cytokines
  • Produced in response to non-specific stimulus from:
    • Microbes: bacteria, viruses, parasites
    • Cancer
    • Inflammation
      • Action of specific immune cells
36
Q
  1. Discuss COMPLEMENT and its roles in the innate immune system.
A

A component of blood, complement is always present in serum. Involves:

  • a series of 9 serum enzymes, act in cascade
  • activated when Ag/Ab rxn’s occur
  • in association with Ab, causes bacterial lysis (kills cells)
  • aids phagocytosis

Ultimate outcome is opsonisation/destruction of bacteria by a phagocytic cell. (opsonisation = molecular mechanisms where microbes/cells (etc.) are chemically modified to have stronger interactions with and “appear more delicious” to surface receptors on phagocytes and NKCs.

37
Q
  1. What are GLYCOPROTEINS and how do they contribute to the innate immune system?
A

= proteins + polysaccharide moieties.

e. g. Fibronectin:
- mediates non-specific clearance (of foreign cells)
- Coats foreign cells -> clotting
- Blocks attachment of foreign organisms to epithelial cells

RESULT: limits colonisation (maintains CT integrity)

38
Q
  1. What are INTERFERONS and how do they contribute to the innate immune system?
A
  • Antiviral proteins
  • Formed in response to viral infection
  • Excreted by infected cell; can be taken up by neighbouring cells, trigger them to not stimulate virus replication
  • Species-specific, not virus-specific (i.e. more general)
  • Interesting as anti-viral drug:
    • Expensive; genetic engineering

RESULT: Protects other cells from viral infection.

39
Q
  1. List the steps in Anti-viral Actions of Interferons.
A
  1. Viral RNA enters the cell.
  2. Infecting virus replicates.
  3. The infecting virus induces RNA to produce alpha & beta interferon.
  4. Interferons released by virus-infected cell bind to plasma membrane of neighbouring uninfected cells inducing them to produce anti-viral proteins (AVPs).
  5. New viruses infect neighbouring cells.
  6. AVPs degrade new viral mRNA, inhibiting protein synthesis & replication.
40
Q
  1. What are BACTERIOCINS and how do they contribute to the innate immune system?
A

Proteinaceous/peptidic toxins produced by bacteria to inhibit the growth of similar or closely related bacterial strain(s). Normal flora as part of our Biological Barrier to infection provides competition with other organisms for nutrients & sites of colonisation. These antimicrobial compounds (bacteriocins) in combination to metabolic end products toxic to foreign/invading bacteria thus contribute to the innate immune system.

41
Q
  1. Briefly describe the process of ACUTE INFLAMMATION and the end result.
A
  • Results from tissue injury & infection
  • See redness, swelling, warmth, pain
  • 4 steps:
    1. Increased blood flow & dilation
    2. Rise in temperature
    3. Formation of fibrin clot
      1. Phagocytic action

RESULTS: destruction of invader, localisation of infection.

42
Q
  1. How does Capillary penetration by immune cells lead to the onset of acute inflammation?
A

Damaged tissue -> Inflammatory signals -> Dilation/permeability -> Chemotaxis -> Attraction of phagocytes to site -> Destruction of foreign microbe.

43
Q
  1. The outcome of phagocytosis of SALMONELLA TYPHI would MOST LIKELY be:

a) No uptake/endocytosis into the phagocyte
b) Engulfed & pathogen is destroyed by lysosomal enzymes
c) Engulfed & pathogen reproduce within phagocyte
d) Engulfed but produce anti-phagocytic compounds that destroy the phagocyte

A

c) Engulfed & pathogen reproduce within phagocyte; some microbes can survive the lysosomal fusion and disseminate through the phagocyte (a severe virulence factor). Another example is Mycobacterium tuberculosis.

Re (a): eg’s include Streptococcus pneumoniae/pyogenes
Re (b): eg’s include most non-encapsulated bacteria
Re (d): pathogens produce leukocidin and destroy the phagocyte, eg’s include Staphylococcus aureus and Streptococcus pyogenes.

44
Q
  1. What are NATURAL KILLER CELLS (NKCs) and how do they contribute to the innate immune system?
A
  • Non-phagocytic lymphocytes
  • Recognise cells with defective MHC-I protein on cell surface
  • Result in production of pore-forming perforin proteins & granzymes = lyse target cells = apoptosis
  • Attack and destroy cells:
    • Malignant
    • Containing microbes
    • Opsonised with Antibody

BMED2404 (6 decks)

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