Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Path > Bacteriology - pathogenesis > Flashcards

Bacteriology - pathogenesis Flashcards

1
Q

What is the name of bacterial that replicate in the host without causing disease?

A

Commensals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are virulence factors?

A

Bacterial adaptations that contribute to pathogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What features of bacteria aid colonization?

A

Pili, fimbriae and polysaccharide capsules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What do Koch’s postulates describe?

A

They are four criteria designed to establish a causative relationship between a microbe and a disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are Koch’s postulates?

A

1) The microorganisms must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms
2) The microorganism must be isolate from a diseased organism and grown in pure culture
3) The cultured microorganism should cause disease when introduced into a healthy organism
4) The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identified to the original specific causative agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is bacteraemia?

A

The presence of bacteria in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can bacteraemia lead to?

A

The immune response to the bacteria can cause sepsis and septic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which severe infections can cause bacteraemia?

A

Pneumonia or meningitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is sepsis?

A

When the body’s response to infection causes injury to its tissues and organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is septic shock?

A

Condition that occurs when sepsis leads to life-threatening low blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give basic examples of immune evasion

A
  • Host mimicry
  • Antigenic variation
  • Recruitment of immune modulators
  • Subversion of immune responses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How may gene transcription be regulated during bacterial growth?

A
  • Nutrient sensing
  • Two component signal transduction
  • Quorum sensing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is nutrient sensing?

A

Gene transcription regulated by detection of specific nutrients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is two-component signal transduction?

A

Sensor detects an environmental factor and phosphorylates a regulator that activates gene transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is quorum sensing?

A

Changes in cell-population density alter levels of diffusible autoinducers (that increase in concentration as a function of cell density) that bind to transcriptional activators inducing gene transcription - in effect, quorum sensing is a mechanism of communication between bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give an example of a bacterial cell component that mediates adhesion

A

Type 1 pili → mediate E.coli adhesion to human bladder epithelial cells → cystitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give examples of intracellular pathogens

A

Salmonella
Shigella
MTB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is speticemia?

A

The poisoning of the blood by bacteria of their toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How may bacteria invade tissues?

A
  • enzymes that degrade matrix (e.g. hyraluronidase, elastase)
  • Some IC bacteria use ligand receptor interactions to gain access to a cell → example is TB → uptake is initiated by interaction between either the macrophage mannose receptor or the complement receptors, and bacterial surface proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What types of bacteria secrete exotoxins?

A

Both G+ and G-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the composition of exotoxins?

A

They are proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are invasins?

A

Toxins that have a local activity in promoting bacterial invasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are exotoxins usually encoded on?

A

Plasmid or bacteriophage DNA, rather than on the bacterial chromosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Do endo- or exotoxins have a higher toxicity?

A

Exotoxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Do endo- or exotoxins have a higher specificity to bacterial strains?

A

Exotoxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Give examples of some mechanisms of action of exotoxins?

A 
ADP-ribosylation
Protease activity 
Cleavage of other substances 
Superantigens 
Glucosyltransferases 
Pore-forming toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are molecular Koch’s postulates?

A

A set of experimental criteria that must be satisfied to show that a gene found in a pathogenic microorganism encodes a product that contributes to the disease caused by the pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are genes that satisfy molecular Koch’s postulates known as?

A

Virulence factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the molecular Koch’s postulates?

A

1 - the disease phenotype should be associated with the pathogenic members of a genus, or strains of a species - it should be absent from pathogenic ones
2 - Specific inactivation of virulence trait genes should lead to a loss in pathogenicity
3 - Reversion or replacement of the mutated gene leads to restoration of pathogenicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Example of exotoxin acting via protease acitvity

A

Botulinum toxin released by Clostridium botulinum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What does botulinum toxin do?

A

It is a neurotoxin which functions by cleaving SNARE proteins involves in the release of ACh at the NMJ → inhibits ACh release at NMJ → muscle paralysis

32
Q

Give an example of a toxin that cleaves something other than proteins

A

Alpha toxin secreted by Clostridium perfringens

33
Q

What does alpha toxins from Clostridium perfringes do?

A

It is a phospholipase which cleaves cell membranes and kills the cell

34
Q

How do superantigens function?

A

By binding non-specifically to MHCII of APCs which then activate Th cells, without any need to undergo intracellular processing → massive release of cytokines which causes symptoms of toxic shock such as hypotension and fever

35
Q

Give example of toxin acting as glucosyltransferase

A

Toxins A and B released from Clostridium dificile

36
Q

What do toxins A and B released from C.dificile do?

A

They glycosylate GTPase which usually maintain the actin cytoskeleton → leads to apoptosis → this leads to characteristic watery diarrhoea due to compromised intercellular junctions

37
Q

Example of extracellular pathogen

A

Neiserria meningitidis

38
Q

Where does endotoxin come from?

A

outer leaflet of the outer bacterial cell membrane in Gram negative bacteria

39
Q

What does LPS consist of?

A
  • Conserved lipid A which is the endotoxin part of the molecule
  • A conserved polysaccharide core
  • A highly variable O-antigen which consists of a repeating polysaccharide chain of varying length
40
Q

What PRR does LPS eventually activate?

A

TLR4

41
Q

What are the major effects of endotoxin?

A
  • Activation of macrophages, complement, Haegman factor
  • These lead to fever, hypotension, inflammation, vascular coagulation
  • this is often called SIRS
42
Q

What is the mechanism of action of LPS?

A

Binds to lipid binding protein → transfers it to CD14 on the cell membrane → transfers it to MD2 → this associates it with TLR4 → this is coupled to NFkB

43
Q

Brief explanation of Shigella pathogenesis

A
  • By translocation through M (microfold) cells
  • M cells are specialised ECs that sample particles from gut lumen and present them to underlying mucosal lymphoid tissue
  • After this, shigella is released from the M cell to get into the cytoplasm of the intestinal epithelial cells through basolateral side
  • Once inside EC, it moves by directed polymerisation of actin to adjacent cells
  • This elicits a strong inflammatory response
44
Q

What mediates epithelial cell entry of Shigella?

A
  • Secretion of effector proteins by a type 3 secretion system at the basolateral membrane of the EC
  • This causes cytoskeletal rearrangement and lysis of vacuolar membranes for phagosome escape
45
Q

Where does Shigella invade?

A

Colon

46
Q

Where does Salmonella invade?

A

The small intestine epithelial cells in a similar manner to Shigella (translocation through M cells)

47
Q

Where in the epithelial cells does Salmonella grow and survive?

A

In the phagolysome

48
Q

Describe secretion systems of Salmonella

A

It has two T3SSs

  • SPI-1 → entry into non-phagocytic cells - induction of intestinal inflammatory responses and diarrhoea
  • SPI-1 → intracelular survival and replication (in macrophages) and induction of systemic disease
49
Q

Do G+ or G- typically have a T3SS?

A

G-

50
Q

What does the T3SS apparatus consist of?

A

Two rings that provide a continuous path across the inner and outer embranes, including the peptidoglycan layer
Also has a needle-like structure

51
Q

Give examples of some bacteria that are associated with T3SSs

A

EPEC, EHEC, Shigella, Salmonella

52
Q

Endotoxin is produced by…

A

G-

53
Q

Draw endotoxin

A

Look at essay plan

54
Q

What does LPS consist of?

A
  • Conserved lipid A
  • Conserved polysaccharide core (same within a genus of bacteria)
  • A highly variable O-antigen which consists of a repeating polysaccharide chain of varying length
55
Q

What are the effects of endotoxin?

A

Activation of macrophages → Hypothalamic temperature regulatory centre → fever
→ NO vasodilation → hypotension
Activation of complement → inflammation
Activation of Haegman factor → coagulation

56
Q

What can endotoxin ultimately lead to?

A

Endotoxic shock → severe, generalized inflammatory response induced by bloodstream infection with G- bacteria

57
Q

Give an example of an ADP-ribosylation toxin

A
  • often the mechanism by which enterotoxins cause diarrhoea (e.g cholera toxin, hexamer of 5CTB and 1CTA)
  • CTB binds enterocytes
  • CTA ribosylate GPCR, ultimately leading to Cl- efflux
58
Q

Example of toxin with protease activity

A

Botulinum

Cleaves SNARE

59
Q

Example of protein causing cleavage of other substances

A

Alpha toxin from Clostridium perfringens

Cleaves cell membranes

60
Q

Example of superantigen

A

TSST
Bind non-specifically to MHCII of APCs which then activate Th cells, without any need to undergo intracellular processing
Results in a massive release of cytokines (e.g. IL-1 and IL-2), causing symptoms of toxic shock such as hypotension and fever → cytokine storm

61
Q

Give examples of invasins

A

EC enzymes which degrade tissue allow bacterial spread (collagenase, hyaluronidase, streptokinase)

62
Q

What roles does LPS play?

A
  • acts as a protective permeability barrier
  • adhesion
  • variations of LPS allow different antigenic strains, allow species to bypass immunity
63
Q

What is the mechanism of LPS?

A
  • Binds to liid binding protein
  • LB in serum which transfers it to CD14
  • transfers it to a non-anchored protein MD2
  • this associates it with TLR4
  • TLR4 is coupled with NFkB which is the source of the symptoms of shock
64
Q

Where does BoNT primarily act?

A

NMJ → inhibits cholinergic transmission and leading to an instability of alpha motor neurons and muscles to communication and lead to contraction → flaccid paralysis

65
Q

Where does TeNT act?

A
  • retroaxonally transported from peripheral neurones to inhibitory neurons where cholinergic transmission is inhibited, leaving excitatory stimulation of motor neurons unoppsed and resulting in spastic paralysis
66
Q

What toxins mediate diarrhoea in Clostridium difficile infection? What do these do?

A

Enterotoxin (toxin A) mediates apical entry

Cytotoxin (toxin B) enters basolaterally

67
Q

What are the mechanisms of the two clostrium difficile toxins?

A

Both are glucosyltransferases which target and inactivate Rho GTPase
This impairs the cell funtions downstream from these

68
Q

Main virulence factor of N.meningitidis

A

Capsule

69
Q

What structure associted with the bacterial cell wall of certain strains of Streptococcus pneumoniae prevents phagocytosis?

A

Capsule

70
Q

Examples of encapsulated bacteria

A 
E coli (some strains)
N.menigitidis 
Salmonella typhi
Strep. pneumoniae and pyogenes
S aureus
71
Q

Capsule - more common in G+ or G-?

A

more common among G-

72
Q

What is the capsule of S.pyogenes composed of?

A

Hyaluronic acid

73
Q

What secretion system does shigella use?

A

T3SS

74
Q

Where does salmonella invade?

A

The small intestine

75
Q

Where does shigella invade?

A

colon

Path (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions