Lec12 EColi Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What is the micro of enterobacteriacea? shape, gram, lac? where are they normally found?

A
  • gram negative rods
  • lactose fermenting
  • found in GI of humans/animals or in environment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What infections are caused E. coli

A
  • UTI
  • diarrhea
  • neonatal sepsi
  • intra-abdominal infections
  • nosocomial infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What diseases associated with klebsiella?

A

pneumonia, UTI, nosocomial [hospital acquired] infections

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

What diseases associated with salmonella

A

diarrhea, typhoid fever

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

What disease associated with shingella?

A

diarrhea

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

What diseases associated with yersinia?

A

diarrhea, the plague

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

What type of disease associated with enterobacter, serratia, and citrobacter?

A

nosocomial [aka hospital acquired] infections

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

What disease associated with proteus?

A

UTI

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

What is pathogenesis of E coli infection?

A
  • E coli is part of normal GI flora –> makes it hard to diagnose diarrheal disease cause by E coli
  • infection causes by virulence factors [diarrhea, uti] or disruption of host barriers [intraabdominal infection following intestinal perforation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is MacConkey agar?

A
  • grows gram negative bacteria
  • differentiated between them based on who is a lactose fermenter
  • lactose fermenting bacteria turn red/pink
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 3 important surface antigens of E coli used to serotype strains?

A

O antigen = LPS [lipopolisaccharide]
H antigen = flagella
K antigen = capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are clinical signs of a lower UTI [cystitis urethritis]?

A
  • dysuria, frequency of urination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are clinical signs of an upper UTI [pyelonephritis]

A
  • fever, flank pain, dysuria, frequency of urination, costo-vertebral angle tenderness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the most common cause of UTI? what are the other causes?

A
E coli most common by far
then
- coagulase negative staph
- proteus mirabilis
- other gram negatives
- other gram positives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is function of P-Pilli in E Coli?

A
  • type of pili that is present in some uropathogenic strains
  • allow e coli to adhere to urinary epithelium
  • specific for urinary tract epithelium and nowhere else
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are type 1 pili?

A

the common type of pili

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

How do you treat lower UTI?

A
  • oral medication
  • fluoroquinolone [ex cipro]
  • or 3rd gen cephalosporin [ex ceftriaxone]
  • or trimethoprim-sulfamethoxazole
18
Q

How do you treat upper UTI?

A
  • by IV drug
  • fluoroquinolone [ex cipro]
  • or 3rd gen cephalosporin [ex ceftriaxone]
19
Q

What is enterotoxigenic E Coli [ETEC]? How transmitted, what diseases?

A
  • transmitted through food/water contaminated by infected individual
  • travelers diarrhea
  • watery diarrhea in infants in developing country
20
Q

What is the pathogenesis of ETEC [enterotoxigenic]?

A
  • Adheres to intestinal epithelial cell via CF pili
  • does not invade cell
  • releases heat labile and heat stable exotoxins that go into cell and cause diarrhea
21
Q

What is treatment for ETEC?

A

supportive treatment

22
Q

What is heat labile toxin [LT]?

A
  • similar to cholera toxin
  • type of AB exotoxin
  • stimulates adenylate cyclase and leads to secretion of Na, K, and water
23
Q

What is heat stable toxin [ST]?

A
  • exotoxin

- stimulates guanylate cyclase and leads to secretion Cl, HCO3, and water

24
Q

How does commensal E Coli bcome ETEC?

A
  • gains single pENT plasmid

- LT, ST, and CF genes all contained on single plasmid

25
Q

What is enteropathogenic E Coli [EPEC]? How transmitted, what diseases?

A
  • produces water diarrhea in infants in developing world

- transmitted by fecal-oral route from carrier to infant

26
Q

What is the characteristic finding of enteropathogenic E Coli?

A

attachment/effacement [A/E] lesion

27
Q

what is pathogenesis of EPEC infection?

A
  • bundle-forming pili mediate attachment
  • assemble type III secretion system injects proteins in epithelial cell that act as virulence factors and trigger rearrangement of cytoskeleton leads to loss of normal structure
28
Q

How does normal commensual E Coli become EPEC?

A

introduction of virulence genes on a pathogenicity island [PAI]

29
Q

What are enteroaggregative E Coli? Disease?

A
  • cause prolonged watery diarrhea [weeks] in children in developing world
  • organisms pile up on top of cell and form thick mucous-bacterial biofilm
  • stacked brick appearance
30
Q

What is a pathogenicity island?

A

segment of DNA with multiple virulence factors back to back

31
Q

What disease does enterohemorrhagic E Coli [EHEC or STEC] cause? symptoms?

A
  • bloody diarrhea without fever
  • hemolytic-uremic syndrome [HUS] triad of:
  • —— microangiopathic anemia [RBCs destroyed in small vessels]
  • ——- thrombocytopenia [absence of platelets]
  • ——- renal failure
32
Q

What is the triad of hemolytic uremic syndrome

A
  • —— microangiopathic anemia [RBCs destroyed in small vessels]
  • ——- thrombocytopenia [absence of platelets]
  • ——- renal failure
33
Q

How is EHEC [enterohemorrhagic] acquired?

A
  • consumption of not fully cooked beef
  • direct contact with animals
  • food contaminated by animal feces
34
Q

What is pathogenesis of EHEC? What is its primary exotoxin?

A
  • EColi 0157:H7 and others
  • releases Shigatoxin [Stx]
  • Shigatoxin is AB exotoxin that interferes with protein synthesis at level of ribosome
  • causes injury to enterocytes –> get blood diarrhea
  • if gets into blood stream causes injury to renal endothelium –> get renal failure, thrombocytopenia, enemia
35
Q

What is treatment of EHEC?

A

supportive treatment

antibiotics don’t help

36
Q

How is EHEC diagnosed?

A
  • test for shigatoxin in stool
  • sorbitol agar: 0157:H7 will show up as clear as opposed to normal E coli will have pink [but this will not distinguish other EHEC strains]
37
Q

How does commensal E coli become EHEC?

A

gets shigatoxin gene from a phage

38
Q

What is enteroinvasic E coli [EIEC]? What diseases? Who gets it? What is site of infection?

A
  • causes dysentary: small volume bloody diarrhea, crampy abdominal pain, fever
  • stool smear will have many WBCs
  • seen in children in developing world
  • site of infection is colon [other E Colis mostly small intestine]
39
Q

What is pathogenesis of EIEC?

A
  • e coli gets into enterocyte
  • spreads from one cell to the next causes cell death
  • little or no systemic disemination
40
Q

When do you get intra-abdominal infection? what is treatment?

A
  • occurs following rupture of intestine [appendicitis, diverticulitis, trauma]
  • requires surgical and medical management with broad spectrum antibiotics
41
Q

What are signs of neonatal sepsis and meningitis? what are top bacterial etiologies? treatment?

A
  • fever, hypothermia, abnormal vital signs often only clue
  • top causes: E Coli [particularly those wtih K1 capsular antigen], Group B streptococcus, Listeria
  • treat: cefotaxamine + ampicillin [for listeria]
42
Q

What are signs of nosocomial E coli infection? What are two types of resistant enzymes they can contain?

A

can cause:

  • bacteremia
  • urinary tract infections
  • ventilator associated pneumonia
  • can be very resistant
  • – extended spectrum betalacamases [ESBLs] –> inactivate 1st-3rd gen cephalosporins
    • klebsiella pneumoniae carbapenamase [KPCs]