Enterobacteriaceae Flashcards

1
Q

List the four unvarying characteristics of the family Enterobacteriaceae:

  1. Are they gram neg or pos (+ what shape)?
  2. Do they ferment glucose?
  3. Do they reduce nitrate to nitrite?
  4. Are they oxidase pos or neg?
A
  1. Facultative Gram-Neg rods
  2. Ferment glucose
  3. Reduce nitrate to nitrite
  4. Oxidase negative
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2
Q

Where are Enterobacteriaceae found in the wild?

A

Indigenous flora of GI tract

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3
Q

Name 3 important antigens of Enterobacteriaceae and where they are located.

A
  • H-antigen (located in peritrichous flagella)
  • K-antigen (located in capsule (important in causing extraintestinal colonization, UTI, and invasive disease))
  • O-antigen (of LPS)
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4
Q

What Enterobacteriaceae ferment lactose and which don’t? (just read)

A
- Non-lactose fermenters:
Salmonella
Shigella
Proteus
Yersinia
- Ferment lactose:
E. coli
Klebsiella
Enterobacter
Citrobacter
Serratia
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5
Q

What is the habitat of Enterobacteriaceae Genus Escherichia (main e.g. E coli)

A

Intestines of humans and animals

- We get it at birth

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6
Q

What does the presence of E coli in water indicate?

A

Fecal contamination

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7
Q

Is E coli gram neg or pos?

A

Gram-neg

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8
Q

What clinical syndromes are a/w E. coli?

A
  • Gram negative sepsis
  • UTIs (80% of community acquired UTIs)
  • Wound infections
  • PNA in IC hospitalized patients
  • Meningitis in neonates
  • Gastroenteritis
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9
Q

*Name the 5 types (+ 1 important subtype) of E coli that cause gastroenteritis.

A
  1. Enterotoxigenic E. coli (ETEC)
  2. Enteropathogenic E. coli (EPEC)
  3. Enteroinvasive E. coli (EIEC)
  4. Enterohemorrhagic E. coli (EHEC)
    - Shiga Toxin producing E. coli (STEC)
  5. Enteroaggregative E. coli (EAggEC)
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10
Q

Main signs/sx of Enterotoxigenic E. coli (ETEC)?

A

Profuse watery diarrhea

e.g. in Mexico

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11
Q

Main signs/sx of Enteropathogenic

E. coli (EPEC)?

A
  • Occurs in infants

- Diarrhea w/o gross blood

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12
Q

Main signs/sx of Enteroinvasive E. coli (EIEC)

A

Blood, mucus, and many leukocytes in stool

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13
Q

Main signs/sx of Enterohemorrhagic E. coli (EHEC)?

A

Bloody diarrhea without WBCs.

- In STEC, may progress to hemolytic uremic syndrome (HUS).

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14
Q

Main signs/sx of Enteroaggregative E. coli (EAggEC).

A

Watery diarrhea with blood and mucus.

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15
Q

What is the commonly ID’d serotype of shiga toxin E coli?

How is it transmitted?

A
  • E. coli 0157
  • Undercooked meat, veggies
  • Also thru person-to-person contact
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16
Q

What demo’s are at increased risk for hemolytic uremic syndrome (HUS) a/w E coli 0157?

A

Young children and elderly

- Retarded people

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17
Q

What’s another name for hemolytic uremic syndrome (HUS) a/w E coli 0157?
What do the onset sx look like?

A

Hemorrhagic colitis

  • Bloody watery diarrhea, abd cramps
  • No significant fever
  • Absence of WBC in stool
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18
Q

*List the triad of symptoms that defines hemolytic uremic syndrome (HUS).

A
  • Acute renal failure
  • Thrombocytopenia
  • Hemolytic anemia (schistocytes)
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19
Q

Does E coli enter the blood?

A

No, just shiga toxin

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20
Q

*Explain by shiga toxin causing HUS leads to - acute renal failure, thrombocytopenia and hemolytic anemia.

A

Shiga attaches to endothelial cells. The highest conc of receptors are in the renal endothelium, so this is where the dmg occurs bleeding, scar formation

  1. Scars forming on endothelium, lumen narrow, leading to schistocyte formation and loss of Hb (hemolytic anemia)
  2. Dmg and bleeding @ endothelium: clotting occurs, platelets used (thrombocytopenia)
  3. Eventually blood supply to kidney becomes narrower (acute renal failure)
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21
Q

What is causing bloody diarrhea in HUS?

A

Toxins → Damage of microcirculation → vasculitis → mucosal damage. Infarction of mucosa leads to bleeding into the bowel and bloody diarrhea

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22
Q

What was another E coli strain that lead to a flour recall this year?

A

E. coli 0121

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23
Q

In lab dx of E coli, when should you collect specimen?

From what type of sample?

A
  • 1st 4 days onset (any enteric illness); before abx

- Whole stool

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24
Q

What is the special type of plate used to ID E. coli 0157?

A

Sorbitol MacConkey Agar

rather than lactose

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25
Q

What are the antigens (2) for ProSpecT™ Shiga Toxin E. coli (STEC) Microplate - Remel?
What are it’s 2 alternate modes of detection (differing sample types)

A
  • Antigens: Shiga toxin or the O157 antigen (LPS)

- Direct fecal specimen detection or enriched broth culture detection (more sensitive)

26
Q

What’s a good way to amplify and quickly detect E coli?

A

BioFire FilmArray – Multiplex PCR (just know PCR?)

27
Q

What abx should you give to treat STEC?

A

*NONE!!!

28
Q

How would you treat STEC?

How would you manage HUS?

A
  • Oral rehydration (Gatorade, Pedialyte), supportive care, and careful monitoring of kidney function.
  • HUS and renal failure: can be managed by dialysis.
  • Chemoprophylaxis with SXT or ciprofloxacin for travelers’ diarrhea NOT recommended
29
Q

What else would you not give for STEC, besides not giving abx?

A

*Anti-motility agents!!

30
Q

What’s another name for ETEC?

A

Traveler’s diarrhea

31
Q

All shigella are a form of diarrheagenic ________. (pathogen)

A

E. coli

32
Q

*How does shigella differ from E. coli? (3)

A
  • Non-lactose fermenter
  • Non gas producer
  • Nonmotile
33
Q

How is shigella transmitted?

What are the 5 f’s (+w)?

A

Fecal-oral route

- Water, food, flies, fingers, fomites, feces

34
Q

What demo’s are at highest risks for shigella?

A
  • Young children in day care center, nurseries, custodial institutions
  • Siblings and parents of these children
  • Male homosexuals
35
Q

Explain the narrative of the pathogenesis of shigella. (too hard, but read a bunch of times)

A
  • Virulent strains carry plasmid for attachment and entry
    1. Enters cells by phagocytic vacuole
    2. Organism escapes in cytoplasm
    3. Intracellular replication
    4. Actin “tail” drives organism in cytoplasm
    5. Organisms enter adjacent cells
    6. Shigella phagocytosed into new cell and released into cytoplasm
    7. Shigella can kill phagocytic macrophages
    (8. ) Some strains produce Shiga toxin&raquo_space; more severe disease (Only in Shigella dysenteriae, not common in US)
36
Q

Describe the clinical syndrome of shigella.

A
  • Abdominal cramps, tenesmus, pus and blood in stool
  • Fecal leukocytes present
  • Incubation 1-3 days lasting 48 hrs.
37
Q

How deep does the shigella infection go? (layer of tissue)

A

Infection does not extend into lamina propria (tissue invasion limited to epith. cells and submucosa)

38
Q

What is the reservoir/host of shigella?

A

Humans

39
Q

What is the most communicable of form of bacterial diarrhea?

A

Shigella

40
Q

Define dysentery.

A

Inflammation of the intestines accompanied by bloody diarrhea.

41
Q

Define tenesmus.

A

A continual or recurrent inclination to evacuate the bowels, caused by disorder of the rectum or other illness.

42
Q

Where is Edwardseilla tarda found (reservoir)?
What are the clinical manifestations?
What could it be mistaken for?

(Enterobacteriaceae family)

A
  • Reptiles
  • Gastroenteritis (+ rarely septicemia)
  • Salmonellosis or IBD (Crohn’s)
43
Q

What is the habitat for non-typhoid salmonella strains?

What about for S. typhi?

A
  • Lower animals (*poultry, cows, pigs, pets, reptiles, egg shells) for nontyphoid strains.
  • Humans for S. Typhi
44
Q

Does salmonella ferment lactose?

Does it produce hydrogen sulfide?

A
  • Yes, lactose fermenter

- Yes, produces hydrogen sulfide

45
Q

Besides improper food handling, how else can salmonella be transmitted?

A

Secondary transmission person-to-person

46
Q

*List 5 important clinical manifestations of salmonella.

A
  1. Asymptomatic carrier state
  2. Febrile gastroenteritis
  3. Enteric fever
  4. Septicemia
  5. Focal infections
47
Q

Does the asymptomatic carrier state of salmonella have a longer duration w/the typhi or non-typhoid form?

A
  • S. typhi: Chronic or decades long

- Non-S. typhi: Relatively limited; occasionally prolonged over a year.

48
Q

What’s the most common form of salmonella clinical manifestation in man?
What are some of the sx?
How do you treat it?
How long does it last?

A

Febrile gastroenteritis

  • Malaise, nausea, sometimes w/ vomiting, followed by abd pain and diarrhea.
  • Self-limited.
  • Duration 3-5 days.
49
Q

What’s the best known eg of enteric fever a/w salmonella?
What serotypes cause it?
Explain the timing of the disease course and what sx a/w each stage.

A
  • Typhoid fever
  • Caused by S. typhi and S. paratyphi A and B, rare with other serotypes.
  • Incubation 1-2 weeks. Length of illness 4 weeks, characterized by increasing fever for 2 weeks (bacteremic stage) followed by gastrointestinal symptoms for 1-2 weeks.
50
Q

Only known reservoir of S. typhi is _________.

A

Man

51
Q

What salmonella-infected pt demo’s typically end up with the septicemic form (bactermia)?
What 3 other pathogens is this form a/w, frequently?

A
  • Pts w/ underlying leukemia, lymphoma, AIDS, SLE, SCC, and alcoholic hepatitis (relapses are common).
  • S. choleraesuis, S. dublin, and S. oranienburg
52
Q

What are some eg’s of focal infections a/w salmonella?

A

Osteomyelitis, meningitis, brain abscess, endocarditis

53
Q

Recall: Explain the pathogenesis of gastroenteritis a/w Salmonella.

A
  1. Salmonella produces an adhesion&raquo_space; stimulates rearrangement of plasma cell membrane to form ruffles
  2. Bacteria enter cell by pinocytosis associated with ruffles
  3. Organisms invade large and small bowel and lamina propria
  4. Large inflammatory response induced
54
Q

Recall: Explain the pathogenesis of enteric ever a/w Salmonella.

A
  1. Bacteria bind to M cells
  2. Infection kills cell, bacteria go to Peyer’s patches
  3. Organisms invade macrophages where they multiply
  4. Inhibition of oxidative metabolic burst allows organisms to survive intracellularly
  5. Bacteria spread from Peyer’s patches into RE (reticuloendothelial) system&raquo_space; bloodstream
  6. LPS (major virulence factor) causes septic shock
55
Q

Explain immunity in Salmonella (not sure how to work this question but should know the answer)

A

Immunity is humoral and cell mediated

56
Q

Explain the clinical manifestations of enteric fever.

A
  • Presents with fever, headache, rose spots, constipation [Rose spots: pink macules or prupuric lesions]
  • Fever; temp-pulse dissociation
  • Neuropsychiatric manifestations
57
Q

What is temperature-pulse dissociation, which is a/w enteric fever of salmonella?
What types of infections are they a/w?

A

Refers to relative bradycardia with a pulse rate less than expected at a given body temp.
- A/w specific infections, including intracellular organisms such as salmonella, legionella, and chlamydia

58
Q

What are some complications of enteric fever a/w salmonella?

A
  • GI bleeding
  • Perforation of ileal ulcers
  • Circulatory collapse
  • Relapse following treatment
  • Long term carriage
59
Q

Explain the clinical manifestations a/w septicemia/bacteremia of salmonella.

A
  • Clinically similar to other gram- neg bacteremias

- 10% localized suppurative infections (e.g. osteomyelitis, endocarditis, arthritis)

60
Q

How would you dx salmonella?

A

Positive blood cultures

61
Q

How do you treat salmonella?

A

Third generation cephalosporins