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Bio Infectious Diseases > Exam 4: Intestinal Bacteria > Flashcards

Exam 4: Intestinal Bacteria Flashcards

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1
Q
  • lives in stomach
  • wants to live in neutral area
  • live in epithelia because mucus makes it less acidic
A

hylobacter pylori

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2
Q

what are koch’s postulates?

A
  1. infectious agent must be found in the diseased individuals and not in healthy individuals
  2. grow infectious agent in pure culture
  3. recapitulate disease in model host with pure culture
  4. needed to recapture pathogen
  5. if you can remove infectious agent, you should be able to get rid of disease
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3
Q

does H. pylori follow Koch’s first postulate?

A

no because it is found in both sick and healthy individuals

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4
Q

what are non-invasive ways to look for H. pylori?

A
  • serology test
  • ELISA (enzyme linked immunosorbent assay)
  • urea breath test
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5
Q
  • looks for antibody that responds to pathogens in patients

- if antibodies are there, pathogen must be there

A

serology test

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6
Q
  • type of serology test

- if there are more antibodies present, there is greater color intensity of the assay

A

ELISA

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7
Q
  • breaks down urea into CO2 and NH3

- H. pylori has it

A

urease

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8
Q

how does the urea breath tes work?

A

give 13C-urea or 14C-urea to patient and look for 13C-CO2 or 14C-CO2 in breath

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9
Q

what are invasive methods of looking for H. pylori?

A
  • biopsy
  • microscopy
  • gram staining (H. pylori Gram -, spiral shape, motile)
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10
Q

how can H. pylori be grown in pure culture?

A
  • it is microaerophilic
  • prefers 2-5% oxygen and 5-10% CO2
  • takes 5-10% of blood (sheep, horse)
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11
Q

how do you recapitulate a disease in a model host with pure culture?

A
  • multiple cell lines

- primary cells

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12
Q

-usually immortalized by viruses or derived from cancer cells
~in gastric epithelium

A

multiple cells lines

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13
Q

have a limited life span

A

primary cells

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14
Q

what poses a threat for H. pylori?

A
  • acid
  • peristalsis
  • muscosal barrier
  • immune detection
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15
Q

how does H. pylori deal with acid?

A
  • urease

- proton driven pump that transports urea into cells to neutralize acid

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16
Q

how does H. pylori deal with peristalsis?

A
  • gets to epithelium with chemotaxis (flagella)

- rotates, corkscrew motion to penetrate mucus

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17
Q

during chemotaxis, what does H. pylori move toward and away from?

A
  • moves away from acid (H+)

- moves toward amino acids

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18
Q

when is H.pylori able to penetrate the mucus the fastest?

A

when the environment is viscous

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19
Q

how does H. pylori deal with the mucosal barrier?

A
  • BabA

- SabA

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20
Q
  • attach to our blood group antigens

- binds to fucose

A

BabA

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21
Q
  • attach to our blood group antigens

- binds to things with sialic acid

A

SabA

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22
Q

what is the gene protein of non-secretor people?

A

Le

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23
Q

what is the gene protein of secretor poeple?/

A

Le + Se

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24
Q

what is the antigen of non-secretor people?

A

substrate + fucrose

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25
Q

what is the antigen of secretor people?

A

Le^a + fucrose

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26
Q
  • gram -
  • microaerophilic
  • spiral and polar flagella
  • H+ gated urea channel and urease
  • chemotaxis + swimming
  • BabA and SabA bind to blood group antigens
  • upper intestinal tract
A

H. pylori

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27
Q

how does H. pylori evade our immune system?

A
  • LPS

- flagella

28
Q

what does H. pylori add to its LPS so its not recognized by the host receptor TLR4?

A

sialic acid

29
Q

how does H. pylori prevent its flagella from being recognized by TLR5?

A

-flagella is sheathed/covered by outer membrane

30
Q

how does H. pylori compete with gastric epithelium for nutrients?

A
  • H. pylori neutrophil activating protein (HP-NAP)
  • vacuolating cytotoxin A (VacA)
  • cytotoxin associated gene A (CagA)
31
Q

-recruit and activate neutrophils–>secrete ROS–> damage epithelium and release nutrients

A

HP-NAP

32
Q
  • a secreted protein

- insert itself into epithelial membrane

A

VacA

33
Q

what does VacA cause once its inserted into the epithelial membrane?

A

-cause endocytosis
~disruption of endosomal membrane
-no antigen presentation
-release nutrients

34
Q
  • oncogene
  • changes the transcription activity of host
  • de-differentiation–> proliferation & move & anti-apoptotic
A

cytotoxin associated gene A (CagA)

35
Q
  • aquatic organism (wide range of salinity)
  • does not want to be in human body
  • causes watery diarrhea
  • not much inflammation
  • gram -
  • comma shaped
  • single polar flagella (sheathed), motile
  • 3 types of pili that are all type 4
A

vibrio cholerae

36
Q

what are the 3 types of pili of vibrio cholerae?

A
  • mannose sensitive hemagglutinin pili (MSHA)
  • toxin co-regulated pili (TCP)
  • chitin regulated pili
37
Q

eukaryotic microbe and macrobe attachments

A

chitin regulated pili

38
Q

what are the 2 chromosomes of vibrio choleae?

A

-chromosome 1 (3mbp)
-chromosome 2 (1mbp)
~both have essential genes

39
Q

the box on chromosome 1 is a….?

A

prophage

40
Q

what does the box on chromosome 1 contain?

A
  • toxin co-regulated pili (TCP)

- cholera toxin (CTX)~ makes it human pathogen

41
Q

can infect other cholera pathogen that dont have TCP or CTX

-lysogenic conversion

A

filamentous phage

42
Q

what is the environment of vibrio cholerae (outside of human)?

A

-biofilm (biotic or abiotic surface)
-viable but not culturable state (VBNC)
~alive, active

43
Q

how does vibrio cholerae resist stomach acid?

A
  • acid tolerance responses (get rid of H+)

- infectious dose

44
Q

how does Vibrio cholerae penetrate mucosa in GI tract and then infect the small intestine?

A
  • protease and mucinases (degrade mucus)

- flagella and MSHA (attach to epithleium)

45
Q
  • closely related
  • 16s sequence ~ 96% similarity
  • gram - rods
  • peritrichous flagella
  • metabolic and serotype differences
A

shigella, e. coli, salmonella

46
Q

what are types of shigella?

A

-flexneri
-dysentariae (bloody)
~both cause diarrhea

47
Q

what is a type of salmonella enterica?

A

serovar Typhi Typhimurium

48
Q

intracellular pathogen

A

shigella

49
Q

secretes shiga toxin and AB toxin

A

dysentariae

50
Q

host receptor for AB toxin of dysentariae?

A

Gb3 (globotriaosylceramide)

51
Q

when is E. coli bad?

A

when it has virulence factors

-infections in intestine, extraintestinal, urinary tract

52
Q

what are the pathovars of bad E.coli?

A
  • EPEC (enteropathogenic E.coli)
  • ETEC (enterotoxigenic E.coli)
  • EHEC (enterohemorrhagic E. coli)
53
Q

-locus of enterocyte effacement pathogenicity island (LEE)
~more than 1 gene
-long range attachment by type 3 secretion system
-secretes its own receptor (Tir)
~intimin binds to it (short range)

A

EPEC

54
Q

what happens when Tir and intimin bind?

A
  • actin pedestal formation
  • actin polymerization
  • causes effacement ~ cells slough off
55
Q

-has heat labile toxin
-heat stable toxin
~both AB toxin
-plasmid encoded

A

ETEC

56
Q

-LEE +—> attachment/effacement lesion
-shiga like toxin –> bloody diarhhea
- O157: H7
~O antigen on LPS
~H antigen on flagella

A

EHEC

57
Q

foodborne illnesses

A

S. enterica

58
Q
  • serovar
  • dependent on H antigen
  • local gastroenteritis
  • strong inflammation in intestines
A

Typhimurium

59
Q
  • serovar
  • systemic infection (typhoid fever)
  • good at hiding~polysaccharide capsule
  • no inflammation
  • evade immune system
  • invasive ~ cross epithelium and spread to peripheral organs
  • bactermia —> fever
A

typhi

60
Q

host receptor is GM1

A

cholera toxin

61
Q

causes watery diarrhea

A

cholera

62
Q

host receptor is GB3 (endothelium)

A

shiga toxin

63
Q
  • inhibits protein synthesis

- cellular apoptosis

A

shiga toxin

64
Q
  • causes hemolytic uremic syndrome (HUS)
    • lysis of RBC
    • lysis of platelets
    • renal failure
A

shiga toxin

65
Q

-ETEC
-increase camp
increase Cl- eflux
-watery diarrhea (travellers)

A

heat labile toxin

66
Q
  • ETEC
  • increase cGMP
  • increase Cl- efflux
  • watery diarrhea (travellers)
A

heat stable toxin

67
Q

shigella dysenteriae and EHEC

A

shiga toxin

Bio Infectious Diseases (10 decks)

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