Microorganisms in Disease Flashcards

1
Q

What is pathogenicity?

A

The capacity of a microorganism to cause infection.

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2
Q

What are the requirements of a micro-organism that enable it to cause infection? (4)

A
  • Transmissibility
  • Establishment in/on a host
  • Harmful effects
  • Persistence
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3
Q

What often causes harm to the host when a pathogen invades?

A

The host response to the pathogen.

-e.g. TB

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4
Q

What is the chain of events leading to infection? (6)

A
Pathogen
>> Reservoir
>> Exit
>> Transmission
>> Entry
>> Susceptible host
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5
Q

What is a reservoir for pathogens?

A

Source that allows the organism to survive and multiply to adequate numbers.

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6
Q

What is virulence?

A

The degree to which a microorganism is able to cause diease.

-pathogenic potential

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7
Q

Which is more virulent; S. aureus or S. viridans?

A

S. aureus.

-it causes disease more readily

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8
Q

What are Koch’s postulates?

A

The requirements for an organism to cause disease.

-outdated now

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9
Q

What are the requirements in Koch’s postulates?

A

Organism should be:

  • present in disease but not health
  • isolated from diseased animal and grown in culture
  • cause same disease in inoculated animal
  • re-isolated from infected animal
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10
Q

What is the main route of transmission for Norovirus and C difficile?

A

Faecal-oral route.

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11
Q

What symptoms do norovirus and C difficile cause?

A
  • Norovirus&raquo_space; vomiting and diarrhoea.

- C difficile&raquo_space; diarrhoea.

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12
Q

What is LD50?

A

Lethal dose; the amount of a substance needed to kill 50% of a sample.

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13
Q

What is ID50?

A

Infectious dose; the amount of an organism required to produce infection in 50% of subjects.

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14
Q

What is infectivity?

A

The ability of a microorganism to become established in/on a host.

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15
Q

How does colonisation occur?

A

Ligand-receptor interactions.

-ligand on microorganism attaches to receptor on host&raquo_space; adherence.

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16
Q

What ligand-receptor interaction does E coli take part in?

A

E coli fimbriae&raquo_space; glycolipids on human uroepithelial cells.

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17
Q

What ligand-receptor interaction does S pyogenes take part in?

A

Protein F in S. pyogenes&raquo_space; fibronectin.

glycoprotein in connective tissue/cell srufaces

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18
Q

What ligand-receptor interaction does influenza take part in?

A

Haemagglutin on influenza&raquo_space; respiratory epithelial salic acid receptors.

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19
Q

What is a virulence factor?

A

Molecules produced by pathogens that enable them to colonise a host and cause harm.
-e.g. adhesins, aggressins, interferins, endotoxins

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20
Q

What encodes virulence factors?

A

Virulence genes.

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21
Q

Where are endotoxins located?

A

In the cell wall of gram -ve bacteria.

-e.g. E coli, Neisseria meningitidis

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22
Q

When are endotoxins released?

A

From damaged/dead bacteria.

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23
Q

What is the active component of endotoxins, and how does it work?

A

Lipopolysaccharide (LPS).

-binds to host cell receptors&raquo_space; host response

24
Q

What are the 3 components of lipopolysaccharide?

A
  • Lipid A (disaccharide-FA complex)
  • Oligosaccharide core
  • Polysaccharide antigen
25
What is the host response to endotoxins?
Systemic inflammatory response syndrome (SIRS).
26
What are possible responses involved with SIRS? (3)
- Uncontrolled T-lymphocyte response (e.g. cytokine release) - Uncontrolled activation of clotting cascade (e.g. DIC) - Uncontrolled activation of complement
27
How does Neisseria meningitidis cause harm?
Endotoxin-mediated, leads to increased vascular permeability >> loss of protein, fluid and plasma and vasoconstriction.
28
What is an exotoxin?
Protein secreted by living bacteria. | >> harm to host
29
What is Clostridium botulinum?
Anaerobic, gram -ve bacteria. | >> botulism
30
How does Clostridium botulinum normally cause harm to a host? (3)
- Ingestion of pre-formed toxin - Infection of dirty wound - GI colonisation
31
What action does the botulinum toxin have at the NMJ?
Botulinum toxin binds to presynaptic vesicle >> no muscular contractions (flaccid paralysis).
32
How does botulism present clinically? (5)
- Diplopia - Dysphagia - Dysarthria - Dry mouth - Death (resp failure)
33
What bacteria causes tetanus?
Clostridium tetani. | -anaerobe
34
How does tetanus enter a host / cause harm? (3)
- Infection of dirty wound - Toxin production (tetanospasmin) - Death by respiratory paralysis
35
What is tetanospasmin, and how does it act?
Neurotoxin that causes tetanus. - produced on germination of spores - binds to nerve synapses - inhibits release of inhibitory NTs in CNS
36
What are the main symptoms of tetanus?
- Lockjaw - Muscle spasms - High temperature - Increased HR
37
Give examples of other exotoxin-mediated infections. (6)
- Cholera - Diphtheria - C difficile - E coli 0157 colitis - Whooping cough (pertussis) - Scarlet fever
38
What bacteria causes scarlet fever?
Streptococcus pyogenes.
39
How do the virulence factors produced by Strep. pyogenes act on the host?
Promote connective tissue breakdown and invasion.
40
What syndromes does strep. pyogenes cause? (4)
- Scarlet fever - Streptococcal sore throat - Necrotising fascitis - Erysipelas (eyes)
41
What are the different virulence factors that strep pyogenes produces? (5)
- Hyaluronidase and streptokinase - C5a peptidase - Streptolysins -O and -H - Erythrogenic toxin - Toxic shock syndrome toxin
42
What actions do hyaluronidase and streptokinase have (S pyogenes)?
Break down connective tissue components. | >> facilitate tissue invasion
43
What action does C5a peptidase have (S pyogenes)?
Inactivates C5a (complement component).
44
What actions do streptolysins -O and -H have (S pyogenes)?
Lyse RBCs, WBCs and platelets.
45
What action does erythogenic toxin have (S pyogenes)?
Causes the rash in scarlet fever.
46
What actions does toxic shock syndrome toxin have (S pyogenes)?
Causes streptococcal toxic shock syndrome. | -similar to endotoxin release syndrome
47
CASE STUDY. - woman scratched nose - tender lesion spread to cover most of face What bacteria is responsible?
Streptococcal pyogenes. | -Group A beta-haemolytic streptococcus
48
What are the 2 main forms of immune evasion?
- Inhibition of phagocytosis | - Intracellular pathogens
49
Which bacteria inhibit phagocytosis? (2)
- S. pyogenes | - S. pneumoniae
50
How does S. pyogenes inhibit phagocytosis?
M-protein binds fibrinogen and masks bacterial surface >> blocks opsonisation.
51
How does S. pneumoniae inhibit phagocytosis?
Polysaccharide capsule inhibits opsonisation.
52
What is opsonisation?
Immune process where particles (e.g. bacteria) are targeted for destruction by an immune cell known as a phagocyte.
53
Give 3 examples of intracellular pathogens.
- Mycobacterium tuberculosis - Salmonella typhi - Listeria monocytogenes
54
What are the 3 main components that make up viruses?
-Genome (RNA/DNA) -Capsid (protein) (-Envelope (lipid bilayer))
55
What is a virion?
The complete, infective form of a virus outside a host cell, with a core of RNA and a capsid.
56
What is the generic life cycle of a virus? (6)
``` Adsorption >>penetrance (cell) >> uncoating (capsid) >> synthesis >> assembly >> release ```
57
What do viruses require for growth and replication?
Hosts. | -not capable of independent existence