LECTURE - Diarrheagenic Escherichia coli (DEC) Flashcards

1
Q

1 cause of traveller’s diarrhea

A

ETEC (enterotoxigenic)

a well as serious dehydration and death in infants

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2
Q

most common pathotype of E. coli

A

ETEC

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3
Q

Pathogenesis of ETEC

A
  • attachment by different kinds of CFA (colonization factor antigen) pili (NOT the same as type 1 mannose sensitive pili found in almost all E. coli); attach to microvilli on enterocytes in small intestine
  • toxin production (plasmid encoded)
    > LT (labile toxin; can be denatured by heat; 56 degrees (pasteurization half an hour; AB5 toxin; complicated ribbon structure)
    > ST (small, stable to heat so won’t denature)
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4
Q

most common cause of diarrhea in Egypt

A

ETEC

OBS

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5
Q

How LT of ETEC deregulate enterocyte in the small intestine

A
  • toxins don’t kill enterocytes; just deregulate them (don’t absorb; secrete fluid instead)
  • LT: binds to GM1 (ganglioside; same receptor as cholera); endosome; A subunit out => ADP ribosylates Gs protein which stimulates adenylate cyclase = formation of extra cAMP = release of Cl ions and absence of absorption so fluid builds up in lumen of gut
  • voluminous diarrhea
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6
Q

these both cause bloody diarrhea in adults and potentially HUS in children

A

STEC and EHEC

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7
Q

This is implicated in Crohn’s disease

A

AIEC (adherent invasive E. coli)

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8
Q

Seven currently recognized pathotypes of E. coli

A
  1. Enteropathogenic E. coli (EPEC)
  2. Shiga toxin-producing E. coli
  3. Enteroaggregative E. coli (EAEC)
  4. Entertotoxigenic E. coli (ETEC)
  5. Diffusely-aggregative E. coli (DAEC)
  6. Adherent invasive E. coli]- Enteroinvasive E, coli (ETEC)
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9
Q

Most common of the seven pathotypes

A

ETEC

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10
Q

Another major cause of traveller’s diarrhea

A

EAEC

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11
Q

How ST of ETEC deregulate enterocyte in the small intestine

A
  • toxins don’t kill enterocytes; just deregulate them (don’t absorb; secrete fluid instead)
  • works through guanylate cyclase system; less notable but still important
  • triggers production of more GMP
  • same net effect as LT = lack of lfuid absorption and chloride secretion
  • voluminous diarrhea
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12
Q

Besides decreased absorption, what else do LT and ST lead to??

A
  • release of prostaglandins and leukotrienes
  • affects nerves of GI (motility)
  • stimulates cytokine production
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13
Q

Disease caused by EAEC

A
  • persistent diarrhea in children

- traveller’s diarrhea with mucus

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14
Q

EAEC

A

Enteroaggregative E. coli

  • aggregate on microvilli; effects on goblet cells through cytotoxins and enterotoxins ShET1, Pic, EAST1, Pet
  • do NOT invade
  • aggregation = biofilm formation
  • stick to microvilli through aggregative adherence fimbriae (AAF)
  • enteroaggregative [heat] stabile toxin
  • pore-forming toxin (hemolysin) that increases Ca2+ influx into host cells
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15
Q

Preventative drugs for EAEC and ETEC

A
  • bismuth subsalicylate (pepto bismol)
  • antimicrobials (but not really good)
  • Dukoral: oral vaccine against cholera with some ross-protection against LT (no help against ST though)
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16
Q

diseases caused by EPEC

A
  • potentially fatal diarrhea in infants (and some traveler’s diarrhea in adults); mainly in developing countries
17
Q

this is unique for EPEC

A
  • binds to microvilli which causes them to distort into a pedestal
18
Q

EPEC pathogenesis

A
  • bundle-forming pili allow non-intimate binding (EAF plasmid)
  • attaching and effacing (A/E) lesions are generated on the surface of the enterocyte by triggered by signal transduction events
  • intimate binding through intimin and Tir leads to pedestal formation
    = increased Ca2+ mobilization and phosphorylation of host proteins may cause cells to lose ability to absorb water
19
Q

in EPEC organisms = LEE

A

locus of enterocyte effacement (LEE)

- eae (E. coli attaching effacing) genes are found on a PI in one of 5 operons (LEE-15)

20
Q

STEC

A

Shiga toxin-producing E. coli; includes EHEC = enterohemorrhagic E. coli)

21
Q

diseases caused by STEC

A

bloody diarrhea in adults, life-threatening hemolytic uremic syndrome (HUS) in children

22
Q

Pathogenesis of STEC

A
  • similar to EPEC but adhesins are different and STEC also produces an A-B toxin called Stx1 (Shiga-like toxin) aka ‘verotoxin’ and/or Stx2 encoded by a bacteriophage
  • affects kidney cells
23
Q

Stx 1 and 2 of STEC

A
  • AB5 structure
  • A = N-glycosidase catalytic activity; acts by removing a specific adenine base from the 28 S rRNA of the 60 S ribosomal subunit within infected cells (adenine important for elongation factor binding)
    = stops protein synthesis
    = LETHAL in enterocytes; cytotoxic does not just deregulate
24
Q

diseases caused by DAEC

A

UTI and complications of pregnancy

- sometimes diarrhea, esp. in children >12 mos old

25
Q

pathogenesis of DAEC

A

(diffusely aggregative E. coli)

  • binding of unique “Dr” fimbrial adhesins (receptor DAF - decay-accelerating factor, CD55) promotes the formation of cell membrane extensions
  • other virulence factors cause alteration of intracellular signaling and inflammation
  • don’t form biofilms
  • coiling of microvilli when they attach but don’t typically invade
26
Q

AIEC

A

adherent invasive E. coli

27
Q

diseases caused by AIEC

A

implicated in Crohn’s disease

28
Q

pathogenesis of AIEC

A
  • colonizes the intestinal mucosa of patients with Chron’s disease and is capable of invading epithelial cells s well as replicating within macrophages
  • uses type I pili to adhere to intestinal cells ad long polar fimbriae contribute to invasion
  • can cause granulomas