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2404 > Microbiology > Flashcards

Microbiology Flashcards

(55 cards)

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1
Q

Aim of Immunisation

A
  • To produce long lasting immunity to the pathogen

- To eliminate the pathogen (smallpox)

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2
Q

Have the aims of immunisation been achieved?

A

Success story of smallpox, polio

- Less effective: TB, HIV, malaria - no vaccine

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3
Q

symbiosis

A

living together of organism

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4
Q

Commensalism

A

One partner benefits while the other partner does not get affected

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5
Q

Mutualism

A

Both organisms benefits

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6
Q

Parasitism

A

One organism benefits and the other is harmed

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7
Q

Normal Flora

A

Residents associated with healthy individuals

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8
Q

Benefits of Normal Flora

A
  • Compete with pathogens for nutrients, attachment sites
  • Aid in digestion
  • Stimulate immune response
  • Produce anti-microbial compounds which may be toxic to pathogens
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9
Q

Example of benefit of normal flora

A

Protozoa in cows. Protozoa breaks down the cellulose. Cows can’t absorb grass without the breakdown. Thus could die if no protozoa.

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10
Q

What is a pathogen?

A

Organisms invades the body and cause tissue damage

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11
Q

Factors governing symbiosis

A
  • No. of organisms (increase of no. can lead to parasitism)
  • Virulence of organism (increase leads to parasitism)
  • Host’s Resistance (if reduced then can lead to parasitism)
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12
Q

Virulence

A

intensity of pathogenicity

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13
Q

Epidemiology

A

study of disease and spread

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14
Q

Sporadic disease

A

randomly occurs, unpredictable e.g. Salmonella food poisoning

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15
Q

Outbreak

A

occurrence increases more drastically above baseline e.g. Ebola

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16
Q

Endemic disease

A

Always present in society as it is within individuals. Slow incidence of disease e.g. TB

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17
Q

Epidemic

A

A big spike or peak from the endemic - could occur due to a new different strain of the microbe. Sudden increase

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18
Q

Pandemic

A

epidemic which is more wide spread populations world wide

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19
Q

Goals of disease

A
  • control the speed of the spread

- eliminate pathogen from population

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20
Q

Common source epidemic

A

e.g. food poisoning

When the pathgoen is gone, no more individuals are affected. As it can’t be spread from human to human spread.

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21
Q

Propagated epidemic

A

e.g. chickenpox

Spread from one person to another, thus the decline after sometime is much slower.

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22
Q

Herd immunity

A

Majority of people have been vaccinated thus already have antibodies created. Thus there is a threshold of vaccinated people from infection. Thus the spread is less.

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23
Q

Influenza virus

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A

Viral factors:
- Virus has a large, enveloped viroin that is easily inactivated by dryness, acid and detergents.
-HA trimer and NA tetramer are able to change thus new strains form.
- Coinfection with animal and human strains of influenza which can combine and form new strains by genetic reassortment.
Transmission: person to person, aerosol droplets, shaking hands

24
Q

Drift

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A

Small antigenic changes, altered proteins

Not effectively recognised by the immune system

25
Shift
Drastic antigenic changes, which large scale altered proteins NOT RECOGNISED AT ALL By immune system. RESULT in major epidemics
26
Transmission
- Airborne: aerosols (sneeze or cough) or dust (nosocomial infection) - Contract: Direct skin to skin, STI - Vehicle: contaminated food/ water: cholera - Vectors: malaria or trypanosomiasis
27
Control of Disease
- Reduce or eliminate source - Stop or prevent transmission - Improve Host suceptibility
28
Transmission
stop spread one host to the next. - Change behaviour: HIV protection - Destroy insect vectors: DDT mosquitos - Control animal vectors
29
Virulence Factors
- Aid colonisation - Allow penetration of host tissue tissue - Prevent/ reduce host response - Cause direct damage
30
Aid colonisation
Capsule, pili/ Fimbriae, OMP - attachment/ adhesion - non-specific and specific (specific mechanisms to attach to cell)
31
Allow penetration of host tissue
Invasins
32
Prevent/ Reduce response
- Evade phagocytosis and immune clearance | - Encapsulation
33
Cause direct damage
- Toxic metabolic end products - proteins: cytotoxins, degradative enzymes - Endotoxins: induce inflammation
34
Colonisation: Specific Attachment vs non-specific attachment
Non-specific: - sticking polysaccharides to cell - slime, capsule, etc - The epithelium layer is protected by a slime layer, however if an unwanted pathogen enters, could disrupt the epithelium. E.g. Dental Plaque Specific: - specific mechanisms to attach to cell - E.g. Influenza Virus protein spikes (spike protrudes from the virus and attach and allows organisms to enter)
35
Pili vs Fimbriae
Protein projections which allow to bind glycoproteins in humans Fimbriae are like hair projections which have rotating mechanism
36
Host Cell Penetration and Growth
Uptake via: - Invasins: bacterial surface proteins which promotes ingestion (trigger cells to take them up via endocytosis) - Endocytosis: non-phagocytic cells e.g. influenza virus - Exocytosis: actin tail propulsion - Phagocytosis
37
Degradative enzymes
Promote: survival, penetration and damage to host e.g. coagulase - coagulates blood IgA proteases - destroys IgA antibodies (produce antibodies proteases which destroys immunoglobulins)
38
Evading the Immune response
Capsule protect and hide away antigens and prevents phagocytosis
39
Capsule
mask antigenic sites, evade detection | E.g. slime/ capsule
40
Antigenic change
shift, mimicry
41
Affect phagocytosis
- Destroy phagocyte | - Inhibit phagocytosis: prevent chemotaxis, inhibit phagosome/ lysosome fusion, resist lysosomal enzymes
42
Exotoxins
Mostly Gram + by products of growing cell, proteins and can be neutralised by antitoxin E.g. Exfoliative toxin: Scalded skin syndrome (babies have no antibodies, the body exfoliates and the tissue beneath becomes exposed).
43
3 Types of Microbial Exotoxins based on Structure and Action
1. A-B (A - active part which is part of toxin enter the cell) + (B- binding to the cell) E.g. Cholera exotoxin - causes the target proteins to become inactivate, the cells are disrupt and the water flow is disrupted. 2. Membrane-disrupting: Phosphate is snipped. Phospholipase hydrolysis of membrane: destabilises and destroy integrity. E.g. Clostridium perfringens alpha-toxin: phospholipase action causing gas gangrene. 3. Superantigens
44
Endotoxins
``` Gram - Metabolic product present in LPS of outer membrane. Lipid Not neutralised by antitoxin fever ```
45
Pathogenicity Islands
- Contribute to characteristics of pathogenicity - Large segments of DNA ~ Contain insertion-like sequences = mobile ~encode major virulence factors ~ associated with tRNA encoding genes - Pathogens may have > 1PI - maybe plasmids - acquired horizontal gene transfer E.g. alter actin microfilaments to mediate adherence + modulate host activities
46
Example PI (protein secretion)
Protein secretion: modulates host activities Yersinia pestis (Causes plague) Function: - delivers effector proteins - secretes plasmid-encoded outer membrane proteins into phagocytic cells - Action: - counteracts natural defence mechanisms - helps Y. pestis multiply and disseminate in the host
47
Physical Barriers
- Skin (sloughing outer layers of skin) - Mucous membrane - Flushing
48
Chemical Barriers
- Antimicrobial factors in body fluids: saliva, tears and mucous - Proteins - Hormones - low pH - Others: urea and bile
49
Chemical Barriers: proteins
- Enzymes - Bacteriocins: produced by microbe and inhibits other microbes from entering into their teritory --> niche env. - Complement: able to recognise non-self organisms and take to phagocytic cells - Fibronectin: difficult to breakdown, some microbes are able to. However it prevents other microbes from growing.
50
Important factors for penetration and growth
- siderophores (take iron from host and limits iron for host) - antigenic variation - alter surface proteins
51
What are the skin defences?
- dry, acidic environment: prevent growth - dead, keratinised cells: keratin is hard to degrade + discourage colonisation - slough: remove bacteria which adheres - toxic, lysosomes: reduces pH, protects hair follicles, sweat glands and sebaceous glands
52
Complement
recognises non-self organisms and then takes to phagocytosis With Ab, can cause bacterial lysis --> kill cell
53
fibronectin
proteins + polysaccharide - non-specific clearance - coats foreign cells --> clotting - blocks attachment of cell to epithelium thus reduces or limits colonisation
54
purpose of interferon
protects other cells from viral infection | antiviral proteins
55
acute inflammation
destruction of invader | localisation of infection

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