E. Coli and Related Organisms Flashcards
Describe some characteristics of E. Coli
- Gram negative or Positive?
- aerobic or anaerobic?
- where does it colonize? -
- what does it ferment?
- is it motile? how so?
- Gram negative
- Facultative anaerobe
- colonizes the Gut
- Ferments Glucose
- Very motile – flagella
Part of enterobacteriaceae family
What is the serotypic schmeme for ecoli?
- O antigen: polysaccharide at the distal end of the LPS
- H antigen: Flagellar antigen
- K antigen: capsule (not used any more)
What are the good guy (Dr. Jekyl) effects of e coli
_ majority of ecoli do not cause diseases
- colonize the gut;
produce helpful metabolites
Describe the classification of the disease causing types of E coli ?
Extra Intestinal (ExPEC)
- Uropathogenic
- MAEC - associated with neonatal meningitis
Diarrheagenic Strains: - ETEC - enterotoxigenic EHEC - Entero-hemorrhagic (and other STEC) EPEC -enteropathogenic EAEC -- enteroaggregative
what allows for the diverse profile of e coli?
Genomic Plasticity
- Bacteriophage
- conjugation (plasmids)
- Pathogenicity islands
What are the manifestations/presentation of Enterotoxigenic (ETEC)?
What symptom is notably absent
how long does it last?
How is it spread
- Common cause of travelers diarrhea and children diarrhea in 3rd world countries
Sx: Diarrhea, N, V, malaise,cramping
lasts 1 - 5days
NO FEVER
Spread by oral/fecal route; contaminated water supply (eg drinking tap water abroad)
What are the virulence factors of ETEC strains?
- Plasmid encoded Adherent Pili (23 different types)
- Heat labile enterotoxin
- heat stable enterotoxin
What is the mechanism for heat labile and heat stable enterotoxins ?
Heat Labile (same as cholera toxin):
- A/B Toxin. A is transported retrograde to the Golgi-
- ADP ribosylation of G protein
- Activation of AC —cAMP—PKA
- Phospho and opening of CFTR channel — chloride and water secretion = Diarrhea
Heat Stable Toxin:
- Analogous to Guanyline
- BInds G protein on apical surfface
Phospho and opening of CFTR
Treatment and Prevention of ETEC?
Prevention: use only bottled water and eat thoroughly cooked foods
Treatment: oral rehydration
Abx: FQs +/- immodium
- Rifaximine
Enteropathogenic (EPEC)
- Who gets this disease ?
- What are the manifestations?
- How is it transmitd
- Only infants contract the disease
Manifestations: short duration watery diarrhea, +FEVER + vomiting
Transmitted person to person
EPEC:
- virulence factors
- how does EPEC delay the immune response ?
- What proteins are endoced?
-
- LEE Pathogenicity Islands
- Bundle forming Pilus -
- Intimin
- Type 3 sections: TIR, NFkB suppression
- Type IV Pilus – allows for tighter binding of the bacteria to the host
- some effector proteins of the type 3 sections cleave NFkB or block its activation upstream
Treatment and Prevention of EPEC?
Prevention: Breast feed has been shown to protect
Treat: IV/Oral rehydration
Supportive care
Abx: possibly effective but the plasmids with the bundle forming pili genes also care resistances
Enterohemorrhagic (EHEC) and other Shiga toxin producing (STEC):
- Manifestations of disease (symptoms and complications)
- what symptom is notably absent?
- How is transmitted?
- Sx: cramps, pain, watery and blood diarrhea
NO FEVER (or mild fever)
- Hemolytic Uremic Syndrome:
TTP, microangiopathy, leading to renal failure - # 1 cause of renal failure in children
- Cattle are the most important reservoir, but also drinking water, petting zoos,
Diagnosis of EHEC
- what strain is associated with Outbreaks?
- what agar can be utilized to help diagnose this?
- what are other diagnositic test can be used?
- What are the findings of HUS
Agar: Sorbitol MacConkey –
- O157 H7: does not ferment sorbitol; does not turn pink
- ELISA for Shiga Toxin
PCR for toxin genes
HUS: TTP, Shistocytes; leading to kidney failure
describe Virulence Factors for EHEC (STEC)
what is the mechanism of the toxin?
- LEE pathogenicity Island: have genes for adherence
- Shiga Toxin (encoded for by bacteriphage)
- A/B toxin
- A removes adenine from 28S rRNA and stops protein synthesis
- Damage to endothelial promotes clotting – TTP and ischemia
:
What is unique about the use of ABX with EHEC Strains ?
DO NOT USE ABX FOR EHEC STRAINS
- induces SOS response from the cells which promotes the lytic phase of the bacteriophage
- further spread of the Shiga Toxin
Treatment / Prevention of EHEC/STEC strains
- Don’t eat pink ground beef
- OK to eat pink steak (inside is sterile)
- Avoid cross contamination
- Supportive care
Enteroaggregative (EAEC)
- manifestations
- how long does it last
- ## long term consequences
- Manifestions: watery diarrhea
- Childhood and traveler’s diarrhea
- Can be persistent
- Associated with growth retardation, poverty
Pathogenesis of EAEC
- Virulence Factors
-
Aggregative Adherence: (plasmid with pilus)
Toxins
- Pet – elicits fluid secretion
- EAST (Heat stable)
Extra Intestinal Pathogenic EC:
(ExPEC)
- what diseases are caused by these bugs?
- -
UTI
Neonatal Meningitis (MAEC)
Meningitis Associated EC (MAEC) –
- how is it obtained?
- What are some virulence factors?
- How is it treated
- common cause of meningitis is in neonates
- mothers are colonized by the bug and transmit it during delivery
- Child gets bacteremia
Virulence Factors: Capsule, Fimbriae, and able to cross the BBB
- Tx; 3rd Generation Cephalosporins
Klebsiella
- What is it’s primary virulence factor
- what can it cause?
- What is it resistant to?
- What is it sensitive to?
- Encapsulated
- UTIs, severe pneumonia, nosocomial infections
- Resistant to PCN
- Sensitive to cephalosporins (usually)
Enterobacter & Serratia
- Virulence Factors
- What can it cause
- what should you know about treating it?
- what works for treatment?
- Encapsulated
- Nosocomial infections; never really cause out patient infections
- Treatment: Cefepime or Carbapenem
- If sensitive: TMP/SMX; FQ
- inducible resistance to Cephalosporins (Cephalosporinases)
Proteus Mirabillis
- What is unique about its motility ? how does this appear on a plate? why does this complicate things
- What are other virulence factors?
- how is it treated
- Swarming Motility
- On culture, extends across the entire plate (unable to detect if infection is poly microbial)
- other virulence:
urease; Hemolysins, and fimbriae
Tx: ampicillin, 1st gen cephalosporins, TMP/SMX
How does the production of urease lead to further complications in patients with Proteus infections?
Urease:
conversion of urea to ammonia and Co2. Co2 diffuses away immediately, and ammonia makes the urine alkaline, making the minerals precipitate and clog catheters and form stones. Protease gets embedded in stone and you never get rid of it until you get rid of the stone.
Proteus Vulgaris –
how is this treated?
– usually more resistant
– Tx: Ciprofloxacin, 3rd generation cephalosporins