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Infectious diseases pathophysiology > Escherichia coli > Flashcards

Escherichia coli Flashcards

1
Q

What is the most common facultative anaerobe in the human gastrointestinal tract?

A

E. coli

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2
Q

T/F. E. coli is always pathogenic.

A

False

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3
Q

What are two key characteristics of E. coli related to motility and metabolism?

A
  • Motile
  • Lactose fermenters
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4
Q

How do E. coli acquire virulence factors?

A

Horizontal gene transfer

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5
Q

What are the main pathotypes of diarrheagenic E. coli (DEC)?

A
  • Enterotoxigenic E. coli (ETEC)
  • Enteropathogenic E. coli (EPEC)
  • Shiga toxin-producing E. coli (STEC/EHEC)
  • Enteroaggregative E. coli (EAEC)
  • Enteroinvasive E. coli (EIEC)
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6
Q

What are the two additional enteric pathotypes of E. coli?

A
  • Diffusely adherent E. coli (DAEC)
  • Adherent-invasive E. coli (AIEC)
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7
Q

ETEC

How is Enterotoxigenic E. coli (ETEC) transmitted?

A

Ingestion of contaminated water or food

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8
Q

ETEC

Who is most affected by ETEC infections?

A
  • Children in developing countries
  • Returning travelers
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9
Q

ETEC

How do foodborne outbreaks of ETEC occur in developed countries?

A

Improper sanitation

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10
Q

ETEC

What is the first step in ETEC pathogenesis?

A

Adherence and colonization of small intestine mucosa, mediated by adhesins or colonization factors

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11
Q

ETEC

What are the types of colonization factors (CFs) in ETEC?

A
  • Chaperone-usher type pili
  • Type IV pili
  • Thinner fibrillae
  • Afimbrial factor
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12
Q

ETEC

What are examples of nonpilus adhesins involved in ETEC adherence?

A

Tia, TibA, and EtpA

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13
Q

ETEC

What toxin produced by ETEC shares a nearly identical structure and mechanism with cholera toxin?

A

Heat-labile enterotoxin (LT)

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14
Q

ETEC

What is the result of LT-mediated GαS activation?

A
  • Increased cAMP
  • Activation of protein kinase A (PKA)
  • Stimulation of CFTR
  • Chloride secretion and sodium and water loss
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15
Q

ETEC

This toxin is produced by 75%-80% of ETEC isolates and is associated with more severe disease than LT-only producing strains.

A

Heat-stable enterotoxin (ST)

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16
Q

ETEC

What is the traditional mechanism of ST-mediated pathogenesis?

A
  • Increased cGMP
  • Activates protein kinase G (PKG)
  • Stimulates CFTR
  • Chloride secretion and sodium and water loss
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17
Q

ETEC

What diagnostic methods can confirm ETEC diarrhea?

A
  • Immunoassays
  • PCR assays
  • DNA probe assays (for toxins)
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18
Q

ETEC

What antibiotic therapies are effective in shortening the duration of traveler’s diarrhea caused by ETEC?

A
  • Azithromycin
  • Levofloxacin
  • Rifaximin
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19
Q

EPEC

How is EPEC classified?

A
  • Typical EPEC (tEPEC): contains type IV bundle-forming pili (BFP)
  • Atypical EPEC (aEPEC): Lacks BFP
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20
Q

EPEC

How soon after ingestion can EPEC diarrhea start?

A

As early as 3 hours

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21
Q

EPEC

Which age group is most affected by tEPEC?

A

Infants aged 0-11 months

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22
Q

EPEC

How is EPEC transmitted?

A

Person-to-person contact

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23
Q

EPEC

Where are EPEC outbreaks commonly seen?

A
  • Nosocomial settings
  • Childcare centers
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24
Q

EPEC

What are the primary symptoms of EPEC infection?

A
  • Watery, nonbloody diarrhea
  • Vomiting
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25
Q

EPEC

What role does BFP play in tEPEC adherence?

A

Aids in biofilm formation and retraction

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26
Q

EPEC

Where are attaching and effacing (A/E) lesions formed?

A

On the apical surface of intestinal epithelial cells

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27
Q

EPEC

What genetic locus regulates A/E lesion formation in EPEC?

A

The locus of enterocyte effacement (LEE).

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28
Q

EPEC

What key virulence factors are encoded by the LEE?

A
  • T3SS
  • Intimin
  • Translocated intimin receptor (Tir)
  • EPEC-secreted proteins (Esp)
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29
Q

EPEC

What is the role of EspA in EPEC adhesion?

A

Forms filamentous extension of T3SS, sonnecting it to the host cell

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30
Q

EPEC

Leads to microvilli loss and actin pedestal formation.

A

Tir

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31
Q

EPEC

What proteins form pores in the host cell membrane for Tir insertion?

A

EspB and EspD

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32
Q

EPEC

How does EPEC disrupt the host immune response?

A

By inhibiting the NK-κB pathway.

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33
Q

EPEC

It participates in protein-protein interactions affecting intestinal barrier function.

A

EspF

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34
Q

EPEC

They inhibit luminal chloride transport.

A

EspG and EspG2

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35
Q

EPEC

How does EPEC contribute to malnutrition in prolonged disease?

A

It inhibits thiamine uptake

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36
Q

EPEC

What rapid diagnostic test is available for EPEC in low-income countries?

A

Rapid agglutination test specific to EspB

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37
Q

EPEC

Whats a measure that helps prevent EPEC infection?

A

Human breast milk

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38
Q

EPEC

How does human breast milk help prevent EPEC infection?

A

It contains antibodies against BFP, intimin, EspA, EspB, and O antigens

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39
Q

STEC/EHEC

What are the main symptoms of STEC infection?

A

Watery, often bloody diarrhea, which can lead to hemolytic-uremic syndrome

40
Q

STEC/EHEC

What is the leading cause of renal failure in children?

A

Hemolytic-uremic syndrome (HUS)

41
Q

STEC/EHEC

What are the three key features of HUS?

A
  • Anemia
  • Thrombocytopenia
  • Renal failure
42
Q

STEC/EHEC

What complications can arise from thrombosis in HUS?

A
  • Ischemic bowel
  • Peripheral necrosis
  • Neurologic complications
43
Q

STEC/EHEC

What are the potential long-term sequelae of HUS?

A
  • Cardiac
  • Renal
  • Gastrointestinal
  • Neurologic
  • Endocrine
44
Q

STEC/EHEC

What is the primary natural reservoir for STEC?

45
Q

STEC/EHEC

What are common sources of STEC infection?

A
  • Undercooked beef
  • Contaminated water
  • Contaminated beverages
46
Q

STEC/EHEC

How can fecal-oral transmission of STEC occur?

A
  • Farm animal exposure
  • Petting zoos
  • Person-to-person contact
47
Q

STEC/EHEC

When does bloody diarrhea typically develop in STEC infection?

A

Around 2 days after infection

48
Q

STEC/EHEC

What are the two types of Shiga toxins produced by STEC?

A

Stx1 and Stx2

49
Q

STEC/EHEC

What organelle is inhibited by shiga toxin?

50
Q

STEC/EHEC

Besides inhibiting ribosomal function, how else does Shiga toxin affect host cells?

A

Affects cell signaling, promoting inflammation and apoptosis

51
Q

STEC/EHEC

How does Shiga toxin spread through the bloodstream?

A

Binding to leukocytes

52
Q

STEC/EHEC

What type of lesions does EHEC produce on intestinal cells similar to EPEC?

A

Attaching and effacing (A/E) lesions

53
Q

STEC/EHEC

What key virulence factors are encoded by the LEE in EHEC?

A
  • T3SSS
  • Intimin
  • Tir
  • Esp
54
Q

STEC/EHEC

What molecular techniques can be used to detect STEC?

A

PCR assays and immunoassays

55
Q

STEC/EHEC

Why is antibiotic therapy not recommended for STEC infections?

A

It may increase the risk of HUS

56
Q

EAEC

In which regions is EAEC a major cause of diarrhea?

A

Both developed and developing countries

57
Q

EAEC

How is EAEC primarily transmitted?

A

Fecal-oral route

58
Q

EAEC

What conditions are associated with EAEC infection?

A
  • Foodborne outbreaks
  • Traveler’s diarrhea
  • Postinfectious irritable bowel syndrome
59
Q

EAEC

What populations are at higher risk for chronic diarrhea due to EAEC?

A

Children and HIV patients

60
Q

EAEC

What type of mucosal damage does EAEC infection cause?

A

Microvilli loss and cell death

61
Q

EAEC

What inflammatory marker is elevated in EAEC diarrhea?

62
Q

EAEC

What type of adhesion mechanism is linked to EAEC?

A

Aggregative adherence, mediated by fimbriae (AAF)

63
Q

EAEC

T/F. EAEC strains form thick biofilms on both intestinal mucosa and abiotic surfaces.

64
Q

EAEC

Biofilms can harbor bacteria in dense aggregates, interfering with…

A

Host nutrient absorption

65
Q

EAEC

What are the key toxins produced by EAEC?

A
  • EAST-1
  • Plasmid-encoded enterotoxin (Pet)
66
Q

EAEC

Protein structurally similar to ETEC toxins, increasing cGMP levels.

A

Enteroaggregative heat-stable enterotoxin 1 (EAST-1)

67
Q

EAEC

SPATE family toxin that causes intestinal crypt dilation and cell damage.

A

Plasmid-encoded enterotoxin (Pet)

68
Q

EAEC

What laboratory tests are commonly used to detect EAEC?

A
  • Clump-formation tests
  • Tissue culture adhesion assays
69
Q

EAEC

What molecular methods can help diagnose EAEC?

A

PCR and DNA probes

70
Q

EIEC

What bacterial pathogen shares a similar pathogenesis with EIEC?

71
Q

EIEC

What are the key biochemical characteristics of EIEC, making it similar to Shigella?

A
  • Non-motile
  • Lactose non-fermenting
  • Lysine descarboxylase negative
72
Q

EIEC

How does EIEC infection compare clinically to shigellosis?

A

Indistinguishable

73
Q

EIEC

How does the infectious dose of EIEC compare to Shigella?

A

The inoculum required is higher

74
Q

EIEC

What are the initial symptoms of EIEC infection?

A

Watery stools, which may progress to dysentery

75
Q

EIEC

Who is most commonly affected by EIEC dysentery?

A

Children in developing world

76
Q

EIEC

How do EIEC outbreaks occur in developed countries?

A
  • Person-toperson transmission
  • Foodborne outbreaks
77
Q

EIEC

What foods are commonly associated with EIEC outbreaks?

A

Contaminated cheese, milk products, and beef

78
Q

EIEC

What plasmid mediates EIEC invasion?

79
Q

EIEC

What virulence mechanism does pInv encode?

80
Q

EIEC

What are the two key functions of the T3SS in EIEC?

A
  • Escape phagocytosis
  • Invasion of intestinal epithelial cells
  • Cell-to-cell spread
81
Q

EIEC

T/F. EIEC causes cell-to-cell spread using the host actin-filament machinery.

82
Q

EIEC

What historical test was used to identify Shigella and EIEC?

A

The Sereny test, which observed keratoconjunctivitis in guinea pigs.

83
Q

EIEC

What modern methods are used to diagnose EIEC?

A
  • PCR
  • Biochemical assays
  • Multilocus sequence typing (MLST) analysis
84
Q

DAEC

What type of diarrhea is caused by DAEC infection?

A

Watery diarrhea

85
Q

DAEC

Which age group is primarily affected by DAEC?

A

Older children

86
Q

DAEC

What adherence pattern is characteristic of DAEC?

A

Diffuse adherence (DA), associated with fimbrial and afimbrial adhesins from the Afa/Dr family.

87
Q

DAEC

What does Afa/Dr+ adhesins bind to on epithelial cells?

A

Human decay-accelerating factor (DAF) on the brush border.

88
Q

DAEC

What cellular effects result from DAEC binding to DAF?

A
  • Increased permeability
  • Cytoskeletal changes
  • Defective brush border proteins
  • Microvilli loss
89
Q

DAEC

What potential role does DAEC play in Crohn’s disease (CD)?

A

DAEC has been found in CD patients, where increased DAF expression is observed.

90
Q

DAEC

What toxins are expressed by diarrheal DAEC strains?

A
  • EAST-1 (Enteroaggregative heat-stable enterotoxin 1)
  • ShET1 (Shigella enterotoxin 1)
  • Hemolysin
91
Q

DAEC

How does DAEC flagellar stimulation contribute to inflammation?

A
  • TLR5 activation induces IL-8 secretion.
  • Leads to neutrophil migration and inflammation.
  • Further promotes DAF expression.
92
Q

AIEC

T/F. AIEC expresses traditional DEC virulence factors

93
Q

AIEC

What fimbriae facilitate AIEC adherence?

A
  • Type I fimbriae
  • Long polar fimbriae (LPF)
94
Q

AIEC

What host structures do AIEC fimbriae target?

A
  • M cells on Peyer patches
  • CEACAM6 on intestinal epithelial cells
95
Q

AIEC

This is a membrane-bound protein, promotes fusion of outer membrane vesicles (OMVs) with Gp96, a host ER stress response chaperone.

96
Q

AIEC

Where is Gp96 overexpressed?

A

In the ileum of Crohn’s disease patients.

97
Q

AIEC

What happens after AIEC invades the lamina propria?

A
  • It replicates in macrophages
  • Induces TNF-α production
  • Does not provoke macrophage death

Infectious diseases pathophysiology (13 decks)

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