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HHAD: Microbiology > Pathogenicity: Colonisation & evasion of host defence > Flashcards

Pathogenicity: Colonisation & evasion of host defence Flashcards

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Biology 101 flashcards
1
Q

What does pathogenicity mean?

A

It refers to a microbes ability to be able to cause disease

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2
Q

What is the definition of virulence?

A

It refers to the degree of pathogenicity - can be a spectrum and have varying degrees

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3
Q

If a bacteria can usually cause disease but only when they infect - what would this be called?

A

Virulent bacteria

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4
Q

What is a virulence factor/gene?

A

Bacterial/component only involved in pathogenesis

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5
Q

What is a house keeping gene?

A

gene involved in all aspects of a bacterium’s life, so is more heavily associated with DNA replication, metabolism etc

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6
Q

When was Koch’s postulates defined?

A

1877

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7
Q

Outline Koch’s postulates (3)

A
  1. Pathogen occurs in every case of the disease and distribution corresponds to that of lesions observed.
  2. Pathogen does not occur in healthy subjects
  3. After isolation and repeated growth of microbe in pure culture, pathogen can induce disease in susceptible animals
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8
Q

Name 3 diseases where Koch’s postulates may not be relevant and why

A

HIV - can’t grow in culture, poor animal model
H Pylori - carriage doesn’t necessarily = disease (naturally found in healthy subjects), no good animal model
S. Mutans - not only cause, can be present without disease
Chlamydia - cannot grow in separate culture - only grows in host

Cholera - poor animal models

Diphtheria - disease expressed throughout body, but bacteria is found in the throat
TB- asymptomatic carriage

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9
Q

What are the 3 MOLECULAR Koch’s postulates?

A
  1. Disease phenotype should be associated significantly more often with the pathogenic organism than with a non-pathogenic member or strain
  2. Specific inactivation of the gene(s) associated with the suspected virulence trait should lead to a measurable decrease in virulence
  3. Restoration of full pathogenicity should accompany replacement of the mutated gene with the wild type original

Still need good animal model to test these postulates.

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10
Q

What is a mobile genetic element?

A

They can move around within a genome or that can be transferred from one species to another

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11
Q

Where are virulence genes often encoded?

A

Often encoded on mobile genetic elements

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12
Q

Give 3 examples of where you could find virulence genes encoded

A

Plasmids, transposons, bacteriophages

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13
Q

What are pathogenicity (genomic) islands?

A

They are distinct genetic elements (/DNA segments) on the chromosome that carry genes encoding for one or more virulence factors (including adhesins, toxins, invasins)

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14
Q

what do adhesin genes do?

A

They allow bacteria to attach to host cells

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14
Q

How many genes does a pathogenicity island contain?

A

From 20 - 50 genes (all linked to pathogenicity and virulence)

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15
Q

Which virulence genes/factors can be found on plasmids? (3)

A

Adhesin genes
Antibiotic resistance genes
Toxin genes

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16
Q

What virulence gene do bacteriophages often code for?

A

Toxin genes

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17
Q

What virulence gene system is often encoded for by pathogenicity islands?

A

Toxin gene systems - rather than an individual gene a whole system of genes convey pathogenicity/virulence to an organism

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18
Q

What are 4 conditions of bacterial pathogenicity?

A

Transmission
Adherence
Invasiveness (sometimes)
Ability to cause damage

19
Q

In what ways could pathogens be transmitted? (3)

A

Inhalation
Ingestion (faecal contamination)
Inoculation (needles, skin contact, insects, sexual contact)

20
Q

What is meant by fomite transmission?

A

It is the transmission of infectious diseases by objects/surfaces

21
Q

What is meant by fomite transmission?

A

It is the transmission of infectious diseases by objects/surfaces

22
Q

What could be found on the surface of microbes that can help them adhere?

A

Fimbriae (pili) - protein structures
Flagellae (usually talked about re motility but can be used in adhesion also)
Specialised surface proteins within these structures that can directly attach to host cell and can also signal to cell to further adhere.

23
Q

Is adhesion always directly linked to virulence?

A

No - commensal cells can adhere too.

24
Q

What is colonisation?

A

Presence of microbes without accompanying disease

25
Q

What is infection?

A

Presence of microbes resulting in disease

26
Q

What is the benefit of both colonisation and infection to bacteria?

A

Obtaining nutrients

27
Q

What do infecting microbes have to do to survive in a host?

A

May need to evade the immune system (antigenic shift).

May need to oppose immune function (e.g superoxide dismutase that prevent phagocytes from working effectively, i.e. the inactivate immune cells)

28
Q

What can a microbe do that can help aid it’s invasion of a host? (3)

A 
Secrete bacterial enzymes (e.g. coagulase)
Antiphagocytic factors (e.g. capsule preventing being phagocytosed)
Toxins that control uptake mechanism or kill macrophages (e.g. leukotoxins)
29
Q

What does transcytosis mean?

A

Movement through tissues or through a cell - it is transient so passes through rather than living within the cell for any amount of time

30
Q

How does intracellular bacteria invade host cells?

A

Phagocytosis.

Induce uptake by micropinocytosis or endocytosis - can be by interaction of invasins (bacterial surface proteins) with host receptors or injection of bacterial proteins int the cell.

31
Q

How do bacteria survive the inhospitable conditions once taken up by a host cell?

A
  1. Modify phagosomal compartment
  2. Escape the phagosome into the cytosol
  3. Nullify host response
32
Q

What type of microbe can be called a genuine obligate intracellular pathogen?

A

Viruses.

Because they cannot replicate outside of host cells

33
Q

What are facultative intracellular pathogens?

A

They are capable of living and reproducing either inside or outside host cells

34
Q

Name the 3 most common obligate intracellular bacterial pathogens

A 
Mycobacterium leprae (leprosy) 
Chamydiaceae (common STD) 
Rickettsia prowazekii (typhus)
35
Q

Which disease could you describe as having a ‘dimorphic life cycle’?

A

Chlamydia

36
Q

Which intracellular obligate bacteria replicates in the cytosol of endothelial cells?

A

Rickettsiae (that causes typhus)

37
Q

What are the properties of obligate intracellular bacteria?

A
  1. Long generation time (doesn’t have same environmental pressures as extracellular bacteria)
  2. Small size with small genome
  3. Require exogenous energy supply
  4. May infect non-phagocytic cells
  5. Protected from lysosomal degradation
  6. Use own expression and replication mechanisms (unlike viruses that need this from their host)
  7. No environmental reservoir (acquired from other hosts)
  8. Cannot be grown by standard bacterial culture techniques (so they are difficult to study)
38
Q

What are the advantages of intracellular infection? (4)

A
  1. Immune evasion
  2. Carriage around the body
  3. Obtain nutrients from host
  4. Smaller genome size (reductive evolution, e.g. dont need all the metabolic pathways, just need more niche, selective genes due to the environment)
39
Q

What happens with pyogenic inflammation (fever, acute)? (3)

Give 1 example of a bacteria that may cause this response

A

Cytokine induction
Recruitment of neutrophils and macrophages
Opsonisation and bacterial killing

Staph aureus, S pneumoniae

40
Q

What happens in granulomatous inflammation (chronic)?

Name a bacteria which causes this response

A

Macrophage and T cell response- formation of granuloma to sequester the pathogen.

Mycobacterium tuberculosis

41
Q

What is the most common event that occurs when an immune system is over-activated?

A

Cytokine storm

42
Q

What is a cytokine storm?

A

Over-activation of a healthy immune system that can lead to massive production of cytokines, in particular, pro inflammatory cytokines.

43
Q

What suppresses the pro-inflammatory cytokines?

A

Anti-inflammatory cytokines

44
Q

Name the 2 main cytokine participants involved in a cytokine storm

A

TNF-a (tumour necrosis factor alpha)

IL-6 (interleukin-6)

45
Q

What are the main effects of a cytokine storm? (4)

A

Tissue damage
Multiple organ failure
Shock
Death

46
Q

Outline the 3 types of specific damage that may be caused by an immune response

A
  1. Mimicry (microbes can induce a harmful antibody response)
  2. Cytokine induction (e.g. cytokine storm)
  3. Toxins that inhibit immune function

HHAD: Microbiology (6 decks)

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