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Year 2 EMS MoD > Microorganisms in Disease > Flashcards

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-outdated now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
Q

What is the host response to endotoxins?

A

Systemic inflammatory response syndrome (SIRS).

26
Q

What are possible responses involved with SIRS? (3)

A
  • Uncontrolled T-lymphocyte response (e.g. cytokine release)
  • Uncontrolled activation of clotting cascade (e.g. DIC)
  • Uncontrolled activation of complement
27
Q

How does Neisseria meningitidis cause harm?

A

Endotoxin-mediated, leads to increased vascular permeability&raquo_space; loss of protein, fluid and plasma and vasoconstriction.

28
Q

What is an exotoxin?

A

Protein secreted by living bacteria.

|&raquo_space; harm to host

29
Q

What is Clostridium botulinum?

A

Anaerobic, gram -ve bacteria.

|&raquo_space; botulism

30
Q

How does Clostridium botulinum normally cause harm to a host? (3)

A
  • Ingestion of pre-formed toxin
  • Infection of dirty wound
  • GI colonisation
31
Q

What action does the botulinum toxin have at the NMJ?

A

Botulinum toxin binds to presynaptic vesicle&raquo_space; no muscular contractions (flaccid paralysis).

32
Q

How does botulism present clinically? (5)

A
  • Diplopia
  • Dysphagia
  • Dysarthria
  • Dry mouth
  • Death (resp failure)
33
Q

What bacteria causes tetanus?

A

Clostridium tetani.

-anaerobe

34
Q

How does tetanus enter a host / cause harm? (3)

A
  • Infection of dirty wound
  • Toxin production (tetanospasmin)
  • Death by respiratory paralysis
35
Q

What is tetanospasmin, and how does it act?

A

Neurotoxin that causes tetanus.

  • produced on germination of spores
  • binds to nerve synapses
  • inhibits release of inhibitory NTs in CNS
36
Q

What are the main symptoms of tetanus?

A
  • Lockjaw
  • Muscle spasms
  • High temperature
  • Increased HR
37
Q

Give examples of other exotoxin-mediated infections. (6)

A
  • Cholera
  • Diphtheria
  • C difficile
  • E coli 0157 colitis
  • Whooping cough (pertussis)
  • Scarlet fever
38
Q

What bacteria causes scarlet fever?

A

Streptococcus pyogenes.

39
Q

How do the virulence factors produced by Strep. pyogenes act on the host?

A

Promote connective tissue breakdown and invasion.

40
Q

What syndromes does strep. pyogenes cause? (4)

A
  • Scarlet fever
  • Streptococcal sore throat
  • Necrotising fascitis
  • Erysipelas (eyes)
41
Q

What are the different virulence factors that strep pyogenes produces? (5)

A
  • Hyaluronidase and streptokinase
  • C5a peptidase
  • Streptolysins -O and -H
  • Erythrogenic toxin
  • Toxic shock syndrome toxin
42
Q

What actions do hyaluronidase and streptokinase have (S pyogenes)?

A

Break down connective tissue components.

|&raquo_space; facilitate tissue invasion

43
Q

What action does C5a peptidase have (S pyogenes)?

A

Inactivates C5a (complement component).

44
Q

What actions do streptolysins -O and -H have (S pyogenes)?

A

Lyse RBCs, WBCs and platelets.

45
Q

What action does erythogenic toxin have (S pyogenes)?

A

Causes the rash in scarlet fever.

46
Q

What actions does toxic shock syndrome toxin have (S pyogenes)?

A

Causes streptococcal toxic shock syndrome.

-similar to endotoxin release syndrome

47
Q

CASE STUDY.

  • woman scratched nose
  • tender lesion spread to cover most of face

What bacteria is responsible?

A

Streptococcal pyogenes.

-Group A beta-haemolytic streptococcus

48
Q

What are the 2 main forms of immune evasion?

A
  • Inhibition of phagocytosis

- Intracellular pathogens

49
Q

Which bacteria inhibit phagocytosis? (2)

A
  • S. pyogenes

- S. pneumoniae

50
Q

How does S. pyogenes inhibit phagocytosis?

A

M-protein binds fibrinogen and masks bacterial surface&raquo_space; blocks opsonisation.

51
Q

How does S. pneumoniae inhibit phagocytosis?

A

Polysaccharide capsule inhibits opsonisation.

52
Q

What is opsonisation?

A

Immune process where particles (e.g. bacteria) are targeted for destruction by an immune cell known as a phagocyte.

53
Q

Give 3 examples of intracellular pathogens.

A
  • Mycobacterium tuberculosis
  • Salmonella typhi
  • Listeria monocytogenes
54
Q

What are the 3 main components that make up viruses?

A

-Genome (RNA/DNA)
-Capsid (protein)
(-Envelope (lipid bilayer))

55
Q

What is a virion?

A

The complete, infective form of a virus outside a host cell, with a core of RNA and a capsid.

56
Q

What is the generic life cycle of a virus? (6)

A 
Adsorption
>>penetrance (cell)
>> uncoating (capsid)
>> synthesis
>> assembly
>> release
57
Q

What do viruses require for growth and replication?

A

Hosts.

-not capable of independent existence

Year 2 EMS MoD (20 decks)

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