#E.coli Flashcards

1
Q

The Enterobacteriaceae are what kinds of bacteria? (GP/GN, areobic/anaerobic)?

Where do these bugs live and how do they get their energy?

A

Gram-negative facultative anaerobes

Live in gut

Ferment sugars

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

What do the following antigens represent in serotyping of E.coli?

O antigen

H antigen

K antigen

A

O antigen – repeating carbohydrate side chains of LPS

H - flagellar antigen (think about the girl in the Sketchy video who had the red hair ties to represent flagella - H (hair) = flagella (red hair tie)

K or capsular antigen – carbohydrate side chains that are removed by heat

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

Name the types of diarrheagenic E. coli (e.g. EAEC)

A

Enterotoxigenic (ETEC)

Enteropathogenic (EPEC)

Enterohemorrhagic (EHEC) and other Shiga toxin producing (STEC)

Enteroaggregative (EAEC)

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

What are the types of extraintestinal E. coli?

A

Uropathogenic (UPEC) (recall from Sketchy that E.coli is actually the most common cause of UTI)

Strains associated with neonatal meningitis (MAEC) (also remember that baby reaching for the milkshake or whatever in the Sketchy video)

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

E.coli’s virulence factors are encoded on mobile genetic elements. Name them

A

Plasmids

Bacteriophages

Pathogenicity islands

Transposons

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

The main manifestation of infection with ETEC (enterotoxigenic e.coli) is acute onset of ___

ETEC is the leading cause of ___

A

Traveler’s diarrhea

Watery diarrhea: Rarely fatal but can be as severe as cholera

mild in adults and short duration (less than 5 days)

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

ETEC infection is typically acquired by ___

ETEC virulence factors include a heat-labile enterotoxin, ___ and ___, all encoded on a virulence plasmid

A

Ingestion of contaminated food or water

**note that you need a lot to cause disease**

Plasmid-encoded virulence factors:

Heat-labile enterotoxin (remember that this causes cAMP increase)

Heat-stable enterotoxin (remember that this is ass’d with increased cGMP)

Colonization Factor Antigens (pili / fimbriae) - important for adherence

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

The Heat-labile enterotoxin in E. coli is similar to cholera toxin and has __ A subunit(s) and __ B subunit(s)

This toxin works to increase __ levels which leads to opening of the CFTR channel and increased __ secretion

A

The Heat-labile enterotoxin in E. coli is similar to cholera toxin and has 1 A subunit(s) and 5 B subunit(s)

After the subunits get internalized, the toxin works to increase cAMP levels which leads to opening of the CFTR channel and increased chloride secretion (the buildup of chloride - and Na+ - is what leads to diarrhea because then water follows wherever the ions go)

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

What is the function of the heat-stable enterotoxin in E. coli and what’s the mechanism?

A

The heat stable enterotoxin binds to guanylate cyclase receptor and causes increased cGMP levels (then by some similar downstream signaling pathway you get activation of the CFTR channel and secretion of chloride and the diarrhea thereof)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the clinical features of Enteropathogenic E. coli

A

Watery diarrhea and vomiting; Usually short duration, but can be protracted and deadly

**think of the Sketchy video and imagine a kid coming into the shop and gets a milkshake (reminder that this is E.coli) that makes him vomit - vomiting - and start to pee himself (watery diarrhea)**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

The pathogenesis of EPEC can generally be described in two phases: adherence - mediated by plasmid encoded __, and attachment to gut cells via ___ of microvilli

A

The pathogenesis of EPEC can generally be described in two phases: adherence - mediated by plasmid encoded pilus, and attachment to gut cells via effacing of microvilli

**Bacteria intimately attached to “pedestals” of polymerized actin and other cytoskeletal proteins

Encoded by Type III secretion system on pathogenicity island

Dozens of injected effector proteins disrupt a variety of cellular functions with multiple potential mechanisms of diarrhea**

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

EPEC virulence factors are encoded on a ___ and include a Type III secretion system and the protein ___ which is necessary for adherence

A

EPEC virulence factors are encoded on a Type 3 secretion and include a Type III secretion system and the protein intimin which is necessary for adherence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The primary way to get EHEC infection is thru ___, the main resevoir being ___

A

The primary way to get EHEC infection is thru contaminated food, the main resevoir being cattle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

The main factor contriinuting to the pathogenicity of EHEC is ___, which damages intestinal epithelial cells and endothelial cells in the glomerulus

There’s also the LEE pathogenicity island that’s responsible for ___

A

The main factor contributing to the pathogenicity of EHEC is Shiga toxin, which damages intestinal epithelial cells and endothelial cells in the glomerulus

There’s also the LEE pathogenicity island that’s responsible for producing attaching and effacing lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does Shiga toxin contribute to EHEC virulence?

A

Basically the protein binds to GB3 that’s present on a variety of cells and depurinates the 28S ribosomal subunit, thereby inhibiting protein synthesis >> cell death

**in the sketchy video, think of the little boy eating the contaminated burger (EHEC) holding his Shiga-gorilla and the gorilla has a sign that says GB3 (the protein that shiga toxn binds to) and a price tag of 28 Sents (Shiga toxin binds and depurinates 28S ribosomal subunit and inhibits protein synthesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

The clinical presentation of EHEC infection includes water diarrhea, ___ diarrhea, colonic inflammation and ___, and HUS

A

Cramps, pain

Watery diarrhea; Bloody diarrhea

Inflammation and edema of colon leading to tissue necrosis in severe cases

HUS (hemolytic uremia syndrome)

17
Q

The diagnostic triad that clues you into hemolytic uremia syndrome includes hemolytic anemia, ___ and ___

___ can affect any organ and lead to ischemic organ infarcts

A

The diagnostic triad that clues you into hemolytic uremia syndrome includes hemolytic anemia, thrombocytopenia and renal failure

Thrombotic microangiopathy can affect any organ and lead to ischemic organ infarcts

18
Q

The risk factors for HUS include age, WBC count, ___ and (two types of drugs)

Typical HUS is associated with ___

Atypical HUS is associated with ___

A

Age (young kids and the elderly)

WBC count

Vomiting

Anti-motility agents

Antibiotics

**note that antibiotics and anti-motility agents are contraindicated in HUS treatment**

19
Q

How do you Dx EHEC infection?

A

Dx: usual McConkey agar (see which strains ferment sorbitol or not), ELISA, and PCR for toxin genes

20
Q

Describe the clinical features of EAEC

A

Watery diarrhea with mucous +/- blood; intestinal “colic”, growth retardation

21
Q

The pathogenesis of EAEC is mediated by ___ which help with the formation of biofilm on intestinal epithelial cells

A

Aggregative adherence mediated by plasmid-encoded fimbriae

Biofilm formation on intestinal epithelial cells

**note that there’s also damage to epithelial cells due to several toxins such as Pet and EAST**

22
Q

Describe the functions of the Pet and EAST toxins in EAEC

A

Plasmid-encoded toxin (Pet): Induces exfoliation of cells and elicits fluid secretion

EAST (some strains): Heat-stable toxin related to that of ETEC

**think PETs are always shedding (exfoliation of cells) and they always pee everywhere or drool etc (fluid secretion)**

**EAST is ETEC’s heat-stable toxin cousin from the far east**

23
Q

___ is one of the two most common causes of meningitis in neonates (the 2nd being Group B Strept)

Describe how this bug causes disease, and state which drug you would use to treat infection with this bug

A

K1 capsule (homopolymer of sialic acid that is identical to Group B meningococcus capsule): Masks activation of alternative complement pathway

Fimbriae and invasiveness contribute to pathogenesis

3rd generation cephalosporins

24
Q

What are the clinical indications of Klebsiella infection?

T/F Kleibsiella is always resistant to cephalosporins so you treat with penicillins

A

Occasional cause of UTI, severe pneumonia, nosocomial infections

Falsehood. Always resistant to penicillins, usually sensitive to cephalosporins

25
Q

___ and ___ are two bugs that are also responsible for nosocomial infections and exhibit inducible resistance to cephalosporins

A

Enterobacter and Serratia

26
Q

How would you treat infection with Enterobacter and Serratia?

A

Carbepenems and 4th gen. cephalosporins

27
Q

___ is another cause of UTIs, especially in association with catheters

(hint: this bug is highly motile and has peritrichous flagella?, which may aid in ascending the UG tract and getting to the kidneys)

How does this bug cause kidney stones and staghorn caliculi in the renal pelvis?

A

Proteus

Produces urease >> Converts urea to NH3 (ammonia), CO2 and H2O >> elevated urine pH >> precipitation of magnesium ammonia phosphate (struvite) and calcium phosphate (apatite) >> formation of kidney stones and staghorn calculi in renal pelvis

•Augments colonization and makes eradication difficult

28
Q

How would you treat P mirabilis vs P vulgaris?

A

P. mirabilis: Ampicillin, TMP-SMX, cephalosporins, fluoroquinolones

P. vulgaris often more resistant: 3rd generation cephalosporins + Fluoroquinolones

•All Proteus unusual among GNB

Resistant to tigecycline and polymixin