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Bacteriology > E. Coli > Flashcards

E. Coli Flashcards

1
Q

E. coli characteristics

A

-Representative of order Enterobacterales (7 families, 88 genera)
-gram negative fermentative rods
-biocontainment level1-3 (Yersinia pestis level 3)
-on blood agar colonies are typically grey (range from small round colonies to swarming plate covering colonies)

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2
Q

How to divide Enterobacterales?

A

-commonly based in their ability to ferment lactose
*pink on MacConkey agar because lactose fermentation

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3
Q

Host or habitat

A

-Widely disseminated and ubiquitous (environment, intestinal tract, respiratory tract)

-sometimes specialized niches (humans only for Salmonella typhi=typhoid fever)

-some generalists (mostly plant pathogens but also cause disease in vertebrates)

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4
Q

Differential plates

A

-Can be used to differentiate
Ex. eosin methylene blue (lactose fermenters metallic)

Ex. XLT-4 H2S producers (black)

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5
Q

Biochemical tests

A

-Can use indole (positive=pink), citrate (Positive =blue), urease (positive=pink) tests

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6
Q

Motility test

A

-Will see spread/haze throughout the tube if motility present
Otherwise non-motility will appear as a line

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7
Q

E. coli taxonomy

A

-6 different species
-show variation between accessory genes

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8
Q

Virulence factors of E coli

A

**variations of virulence factors affect which type of infection occurs

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9
Q

Diarrheagenic E coli

A
  1. Shiga toxin- producing (STEC)
  2. Enterotoxigenic (ETEC)
  3. Enteropathogenic (EPEC)
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10
Q

Extraintestinal diarrheagenic E coli

A
  1. Uropathogenic (UPEC)
  2. Sepsis causing (SEPEC)
  3. Avian pathogenic (APEC)
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11
Q

Shiga toxin-producing (STEC) clinical signs

A

-bloody diarrhea, systemic disease
-cattle carriers
-edema disease in pigs

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12
Q

Virulence factors of Shiga toxin-producing (STEC)

A

-Shiga toxins
1. Stx- act by interfering with protein synthesis…causes edema and hemorrhage
2.Phage mediated- fluoroquinolones and TMS may increase expression

-Intimin- enterocyte attaching and effacing

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13
Q

Enterotoxigenic (ETEC)

A

-watery diarrhea
-neonatal colibacillosis diarrhea in pigs, calves, lambs (traveller’s diarrhea in people)

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14
Q

Enterotoxigenic (ETEC) virulence factors

A

**species and age specific pathogenicity based on receptors
F4 fimbriae- receptors in piglets up to 8weeks
F5 fimbriae- receptors in calved in first few days of life

Toxins:
1. Heat Labile Toxin (LT)- increase cAMP levels leading to increased fluid and electrolyte; similar to toxin produced by Vibrio cholerae
2. Heat Stable Toxin (ST)- interferes with enteric nervous system

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15
Q

Enteropathogenic (EPEC)

A

-watery diarrhea with characteristic attaching and effacing lesions

-all species; but increasingly recognized in dogs (mimics typical parvovirus presentation)

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16
Q

Enteropathogenic (EPEC) virulence factors

A
  1. See characteristic attaching and effacing lesions
    -bacteria seen closely adhered to enterocytes
    -heavily colonized enterocytes may have intracellular bacteria
    -mucosal erosions are also present
  2. eae (enterocyte attaching and effacing)- encodes intimin which allows attachment
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17
Q

Uropathogenic (UPEC)

A

**opportunistic infections, ascending from urethra

-intracellular infections
-urinary tract infections and urosepsis
-dogs and people

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18
Q

Uropathogenic virulence factors

A
  1. Fimbriae- P fimbriae protect against phagocytosis
  2. Flagella- swimming up to the kidneys from bladder
  3. Siderophores- aerobactin- acquisition of iron

4.Alpha hemolysin- pore forming

19
Q

Sepsis-causing (SEPEC)

A

-bacteremia and sepsis

20
Q

Sepsis-causing (SEPEC) virulence factors

A

**responsible for sepsis

1.Fimbriae- adhere and avoid phagocytosis
2. Capsule- prevent phagocytosis
3. Siderophores- aerobactin, salmochelin, yersinabactin= iron scavenging
4. Endotoxin- gram negative cell wall component
5. Colicin V- serum resistance (complement MAC)

21
Q

Avian pathogenic (APEC)

A

-affecting poultry and other birds

22
Q

Avian pathogenic virulence factors

A

1.Fimbriae- adherence and possibly avoidance of phagocytosis

  1. Invasins
  2. Hemolysins - prevents phagocytosis
  3. Siderophores- aerobactin, salmochelin and yersiniabactin= iron scavenging
23
Q

Piglet diarrhea

A

-F4 E coli

-Neonatal: 0-4 days old; affects gilt litters, mild to high mortality and extreme dehydration

-Young: until weaning

-Post weaning diarrhea

24
Q

Treatment for piglet diarrhea

A
  1. Antimicrobials
  2. Fluid therapy
  3. Management: keep barn clean, keep piglets warm (30-34 degrees) for unweaned and dry
25
Q

Calf scours in cattle and sheep

A

-F5 E coli; receptors are only expressed in first 1 week of life
-Leads to watery diarrhea (not bloody)= white scours

**other strains of E coli can cause systemic infections in calves (ascending from umbilicus)

26
Q

Calf scours and polymicrobial infections

A

Common. Some organisms can expose the F5 receptors in older calves allowing access
-Rotavirus
-Cryptosporidium parvum

27
Q

Edema disease in pigs

A

Peracute disease
-pigs often found dead
-edema of eyelids, forehead, stomach, spiral colon
-neuro signs- infarctions of brain

Fecal-oral transmission. Once attached to intestinal epithelium, produce shiga toxin resulting in systemic toxin absorption

28
Q

What is edema disease a differential diagnosis for?

A

Clostridioides difficile

29
Q

Hamburger Disease in people

A

Results in severe bloody diarrhea in people
-Hemorrhagic colitis
-Hemolytic-uremic syndrome (hemolytic anemia, kidney failure, thrombocytopenia)

Fecal-oral transmission-food and water
Foodborne pathogen associated with O157 somatic O antigen, and 7 flagella H antigen

30
Q

Mastitis in cattle

A

-Coliform mastitis
-major cause of mastitis in well managed herds
-mild to severe
-E coli is shed in feces and enters the teat from environment

31
Q

Cell multiplication of mastitis

A

Some cows respond to invasion early and clear E coli from teat, others are slower allowing cells to multiply

  1. Multiply in teat
  2. Endotoxin released from dead cells
  3. Leads to cytokine storm and systemic inflammation
32
Q

Colibacillosis in poultry

A

-Infection with Avian pathogenic E. coli resulting in Omphalitis including yolk sac, coli-septicemia, swollen head syndrome, air sacculitis

-believed to occur when E. coli makes it into egg

-found in environment from hens feces or exploding eggs (due to gas made from bacteria)

32
Q

Treatment of E coli causing mastitis

A

*30-40% of severely affected cows become bactermic

-Systemic and intrammammary antibiotics needed

-Need to remove organic bedding materials that support E coli growth

33
Q

Omphalitis in poultry

A

-Causes dead embryos, swelling and edema of navel, distended abdomen. Mushy chicks (body wall overlying yolk degenerates)

34
Q

Treatment of omphalitis

A

Antimicrobials

35
Q

Management of omphalitis

A

-keep things clean (discard floor eggs and exploders)
-disinfect eggs within 2 hours of laying
-good quality diets
-vaccination possible

36
Q

UTI in dogs

A

-Affect 14% of dogs; common when spayed. Less common in cats

37
Q

UTI classification

A

Based on anatomical site

  1. Lower UTI (bladder and urethra)
    >Recurrent Cystitis
    >Sporadic cystitis
  2. Upper UTI (kidney and ureter)
38
Q

Sporadic cystitis criteria

A
  1. female otherwise healthy, non pregnant
  2. no anatomical or functional abnormalities or relevant co-mobilities
  3. not a repeat infection
39
Q

Treatment of UTIs if sporadic cystitis

A

Can treat empirically BUT collecting urine to culture is still recommended

40
Q

Samples to collect

A
  1. Diarrhea- colonic tissue for histopathology
  2. Mastitis- milk
  3. Omphalitis- samples from dead chicks (inner viscera but avoid fecal contamination)
    4.Mortality event (whole animals)- ID lesions +histology/culture
    5.UTI- aseptically collected urine (prefer cystocentesis)
41
Q

Lab ID

A

1.Lab culture- easy to ID and grow
2. ID using biochemical tests, MALDI-TOF, Molecular methods
3.NAAT to ID/differentiate pathogenic types
4. Histology to ID lesions

42
Q

E coli zoonoses

A
  1. Foodborne transmission
    ex. E. coli O157 (cattle unaffected because lack toxin receptor, but affects humans)
    **Possible source for antimicrobial resistance
  2. Animal to human
    -less well defined
    **Preventative: hand washing, PPE
43
Q

Treatment options for E coli

A

**must be guided by susceptibility testing

AVOID:
-Benzylpenicillin, glycopeptides, fusidic acid, macrolides, lincosamides, streptogramins, rifampin

RESISTANCE is emerging with:
-broad spectrum beta-lactamases
-Fluoroquinolone resistance

Bacteriology (20 decks)

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