Enterobacteriaceae (E.Coli-Specific)

Question 1

Describe the general structure of Enterobacteriaceae:

Answer 1

Gram negative rods
Many have flagella and a capsule
H and K Antigens
LPS

Question 2

What are the locations of H and K Antigens in Enterobacteriaceae?

Answer 2

H-antigen: located in peritrichous flagella

K-antigen: located in capsule

Question 3

Function of the capsule in Enterobacteriaceae?

Answer 3

Important in causing extraintestinal colonization, UTI, and invasive disease

Question 4

Describe the composition of LPS in the membrane of Enterobacteriaceae.

Answer 4

O-antigen: located on outer most domain
Core oligosaccharide
Lipid A: inner most region of LPS

Question 5

What is significant about of O-antigen?

Answer 5

Targeted antigen for detection in laboratory

Question 6

What is the pathogenesis of lipid A?

Answer 6

Causes toxicity: fever, diarrhea, and possible fatal endotoxic shock

Question 7

Name the 6 virulence factors of Enterobacteriaceae:

Answer 7

Endotoxin (LPS)
Capsule
Antigenic Phase Variation 
Type III secretion systems 
Sequestration of growth factors

Question 8

What is the significance of antigenic phase variation in Enterobacteriaceae?

Answer 8

Alte expression of H and K antigens to protect organisms from Ab mediated cell death

Question 9

What is the significance of Type III secretion systems in Enterobacteriaceae?

Answer 9

Facilitates secretion of virulence factors into host cells

Question 10

Morphology of Enterobacteriaceae

Answer 10

Gram-negative rods that stain red

Question 11

Culture Characteristics of Enterobacteriaceae

Answer 11

Grow on standard media (i.e. blood agar)

Question 12

5 Biochemical characteristics of Enterobacteriaceae

Answer 12

Facultative (aerobic & anaerobic)

Ferment glucose

Reduce nitrate to nitrite

Oxidase negative

Grow on MacConkey Agar (salt)

Question 13

What differentiates Enterobacteriaceae from other gram-negative rods?

Answer 13

Enterobacteriaceae is Oxidase negative

Question 14

Non-lactose fermenting Enterobacteriaceae

Answer 14

Salmonella 
Shigella 
Proteus 
Yersinia 
Serratia

Question 15

Lactose fermenting Enterobacteriaceae

Answer 15

E. coli
Klebsiella
Enterobacter
Citrobacter

Question 16

6 Escherichia Coli Clinical Syndromes:

Answer 16

Gram negative bacteremia and sepsis

Most common contributor to community-acquired UTIs

Wound infections

Pneumonia in immunocompromised hospitalized patients

Meningitis in neonates

Gastroenteritis

Question 17

Pathogenic Phenotype of Enterotoxigenic

E. coli (ETEC)

Answer 17

Elaboration of secretory toxins (LT, ST) that do not damage the mucosal epithelium but stimulate hypersecretion of fluids

Question 18

Signs and Symptoms of Enterotoxigenic

E. coli (ETEC)

Answer 18

Profuse, watery, secretory diarrhea is predominant symptom. Often accompanied by mild abdominal cramps. Dehydration and vomiting occur in some cases.

Question 19

Pathogenic Phenotype of Enteropathogenic E. coli (EPEC)

Answer 19

Adheres to epithelial cells in localized micro-colonies and causes attaching/ effacing lesions

Question 20

Signs and Symptoms of Enteropathogenic E. coli (EPEC)

Answer 20

Usually occurs in infants.
Characterized by low-grade fever, malaise, vomiting, and diarrhea, with a prominent amount of mucus, but with no gross blood

Question 21

Pathogenic Phenotype of Enteroinvasive E. coli (EIEC)

Answer 21

Invasion of epithelial cells

Question 22

Signs and Symptoms of Enteroinvasive E. coli (EIEC)

Answer 22

Inflammatory diarrhea (Dysentery) similar to Shigella. Hallmarks are fever and colitis. Symptoms are urgency and tenesmus; blood, mucus, and many leukocytes in stool

Question 23

Pathogenic Phenotype of Enterohemorrhagic E. coli (EHEC)

Answer 23

Shiga Toxin producing E. coli (STEC) -Carry cytotoxins (Shiga toxins, Stx1 and Stx2). Primarily caused by E.coli O157:H7

Question 24

Signs and Symptoms of Enterohemorrhagic E. coli (EHEC)

Answer 24

Bloody diarrhea without WBCs. Often no fever. Abdominal pain is common. May progress to hemolytic uremic syndrome (HUS) or hemorrhagic colitis.

Question 25

Pathogenic Phenotype of Enteroaggregative E. coli (EAggEC)

Answer 25

Adhere to epithelial cells in a pattern resembling a pile of stacked bricks

Question 26

Signs and Symptoms of Enteroaggregative E. coli (EAggEC)

Answer 26

Infants and travelers. Symptoms include watery diarrhea with blood and mucus, vomiting, dehydration and less commonly, abdominal pain.

Question 27

Two other names for Shiga Toxin Producing E. coli (STEC).

Answer 27

EHEC and E.coli O157:H7

Question 28

How is E.coli O157:H7 transmitted?

Answer 28

contaminated food or water direct contact with an infected patient

Question 29

E. coli O157 Reservoir

Answer 29

Reservoir in healthy dairy cattle

Question 30

Foodborne outbreaks of E. coli O157 are most commonly associated with ______________.

Answer 30

Foodborne outbreaks of E. coli O157 are most commonly associated with undercooked ground beef.

Question 31

Infections caused by E. coli O157:

Answer 31

Hemolytic Uremic Syndrome (HUS) | Hemorrhagic Colitis

Question 32

Hemolytic Uremic Syndrome triad of symptoms:

Answer 32

acute renal failure thrombocytopenia - low platelet count Microangipathic hemolytic anemia - the destruction of RBCs prior to their natural death cycle (shistocytes)

Question 33

Hemolytic Uremic Syndrome is usually preceded by:

Answer 33

bloody diarrhea

Question 34

HUS is the leading cause of ________________ in children.

Answer 34

HUS is the leading cause of acute renal failure in children.

Question 35

Treatment of HUS:

Answer 35

Mainly supportive Dialysis No antibiotics Plasmapharesis/IVIG

Question 36

Mechanism of Hemolytic Uremic Syndrome (HUS) - 3 steps

Answer 36

1. Toxin (STX2) binds to receptors in the intestinal villi and renal endothelial cells 2. The toxin causes damage to endothelial cells, which leads to platelet activation and thrombin deposition forming a clot at the region of endothelial destruction 3. Leads to decreased glomerular filtration and acute renal failure

Question 37

Describe the 2 Types of HUS:

Answer 37

Diarrheal-related: majority of cases Non-diarrheal HUS: occurs in association with pneumococcal infection, chemotherapy, or transplant immunosuppression

Question 38

Clinical Presentation of E. coli O157 Hemorrhagic Colitis

Answer 38

Abdominal cramps, watery diarrhea, bloody discharge (vomiting in 50%) Patients progress to bloody diarrhea within 2 days of onset of clinical symptoms of abdominal cramps No significant fever Absence of WBC in stool Symptoms resolve in 4-10 days

Question 39

How would you isolate E. coli O157 from other strains on agar?

Answer 39

Sorbitol MacConkey Agar is used because these organisms do not ferment sorbitol

Question 40

How would you detect E. coli O157 from other strains using surface antigens? Describe the process.

Answer 40

ProSpecT™ Shiga Toxin E. coli (STEC) Microplate - Remel 1. Direct fecal specimen detection by placing stool in sample well 2. If Shiga toxin and/or the O157 antigen are present, the lines will show 3. LPS antigen is used as a control 4. Enriched broth culture detection done overnight (more sensitive)

Question 41

How would you isolate E. coli O157 from other strains via toxin/antigen detection method?

Answer 41

BioFire FilmArray – Multiplex PCR Integrated Sample Preparation, Amplification, and Detection for 22 Enteric Pathogens Detects Shiga-toxin producing E. coli (STEC) stx1/stx2 and/or E. coli O157

Question 42

Treatment of STEC:

Answer 42

Oral rehydration (Gatorade, Pedialyte), supportive care, and careful monitoring of kidney function. HUS and renal failure: managed by dialysis

Question 43

What treatments should be avoided for STEC Diarrhea? Why?

Answer 43

Antibiotics and Anti-motility agents NOT given in STEC diarrhea because they will push patients toward HUS

Question 44

Is Treatment of E. coli O157 with Antimicrobial Agents useful?

Answer 44

Most strains are very susceptible, but Abx treatment has not been shown to shorten the duration or severity of disease. Treatment possibly increases the risk of developing HUS