Enteric Bacteria (Enterobacteriaceae) Flashcards
Enterobacteriaceae
Morphology:
1) Gram Negative Rods (Bacilli)
2) Anaerobic or Aerobic
3) Classified by *Serotypes According to the O, K, H Antigens
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Pathogenesis:
1) Outer Membrane LPS
= *O Antigen
2) Capsule or Amorphous Slime Layer
= * K Antigen
3) Flagella = *H Antigen
(Motile strains)
4) Surface Pili
_Antigenic
_Many strains
5) Toxins:
(1) *LPS Endotoxin
(All Gram Negatives)
(2) *Protein Exotoxins
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Epidemiology:
1) Most are Normal GI Flora
2) Many in Nature freely, Animals
3) Salmonella and Shigella are NOT normal flora, but there can be carrier states.
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Manifestations:
1) *Watery Diarrhea
=> Caused by Enterotoxin Strains.
(“The Runs”)
_Labile or Stable Toxins
2) *Dysentery
(Inflammatory Diarrhea)
_WBCs and/or Blood @ Stool
=> Caused by the Invasive and Cytotoxic Strains
("The Squirts")
3) Bloody Diarrhea:
_Shiga Toxin
4) Enteric (Typhoid) Fever
_Systemic Spread from GI.
=> Salmonella Typhi
5) Most Common Cause of UTI
_Most common is E. coli
_Localized @ Bladder: Dysuria, Urinary Frequency.
_Spread @ Kidney: Fever, Flank Pain, Dysuria, Urinary Frequency.
6) Abscess Formation
(like Bacteroides fragilis)
7) Bloodstream Spread:
Endotoxic Shock, often Fatal
8) Neonatal Meningitis
_E. coli
Most Virulent:
Escherichia, Shigella, Salmonella, Klebsiella, Yersinia
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Diagnosis: 1) Culture 2) => MacConkey Agar (Special Indicator Medium) _Pink Colonies = Ferment Lactose: E. coli, Klebsiella _Colorless Colonies = Doesn't Ferment Lactose: Salmonella, Shigella
Escherichia coli
Pathogenesis:
_Motile
1) *Type 1 Pili: Adhesion
_Binds to D-mannose residues @ host Epithelial cells
2) Alpha-*Hemolysin:
_Pore-Forming Cytotoxin
(Similar mechanism to GAS Strept Steptolysin O and to Staph aureus Alpha-Toxin)
3) *Shiga Toxin (Stx) _*A-B Toxin _E. coli and Shigella strains _A Subunit Blocks Protein Synthesis => Cell Death (Cytotoxic) _B Subunit Binds to cell
4) Heat-*Labile Toxin (LT): *A-B Toxin
=> Watery Diarrhea
(Via Secretion of Water and Electrolytes into Bowel)
5) Heat-*Stable Toxin (ST):
=> Watery Diarrhea
(Via Secretion of Water and Electrolytes into Bowel)
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Epidemiology:
Transmission:
(1) Food/Water Contaminated with Human Feces
(2) Person-to-Person Contact
1) #1 Cause of Cystitis
2) UTI way more common in Women than Men; esp. sexually active
**Uropathic E. coli (UPEC)
_The E. coli with enhanced potential to cause UTI.
3) Colonic E. coli Flora contaminate Perineal and Urethral area.
4) Extraintestinal E. coli infections are uncommon (except UTIs) unless there is a significant breach in host defenses:
=> Opportunistic infection may follow Mechanical Damage, e.g.
Ruptured Intestinal Diverticulum, Trauma, or involve a generalized impairment of Immune function.
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Manifestations:
1) Cystitis (Bladder):
(i) Urinary Frequency,
(ii) (Often) Painful, Burning Urination
_Self-Limiting
2) Pyelonephritis:
(i) Fever
(ii) General Malaise
(iii) Flank Pain
(iv) Frequent Urination
_Risk of Bloodstream Spread
_Leading Cause of Gram Negative Sepsis and Septic Shock
3) GI Infection
_Incubation Period: 2-4 Days
_Self-Limiting, 1-3 Days.
Exception:
(1) Enterohemorrhagic (EHEC):
3 - 10 Days, Unless Other Manifs:
Life-threatening manifestations outside of GI due to Shiga Toxin.
(2) Enteroaggregative (EAEC):
Prolonged Watery Diarrhea, more than 14 Days.
_Begins with Mild Watery Diarrhea
_ETEC and EPEC: Remain Watery
_EIEC, EHEC, EAEC:
Dysentery May Follow
(i) Watery Diarrhea:
=> Enterotoxigenic Strains (ETEC)
=> Enteropathogenic Strains (EPEC)
(ii) Bloody Diarrhea:
=> Enterohemorrhagic Strains (EHEC)
(iii) Dysentery w/ Blood, Pus @ Stool:
=> Enteroinvasive Strains (EIEC)
4) Neonatal Meningitis
=> Vaginal E. coli reach Infant via Ruptured Amniotic Membrane or During Childbirth
_One of most common causes of Neonatal Meningitis
_Many similar features to GBS Strept Meningitis
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Diagnosis:
1) Culture!!
2) Gram Stain
Isolation:
1) UTI: Urine
2) GI: Stool
Unique Features of E. coli:
1) *Ferment Lactose rapidly
2) *Produce Indole
EHEC Test: => EHEC Fails to Ferment Sorbitol => Sorbitol on MacConkey Agar (instead of lactose) => Colorless Colonies = EHEC
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Treatment:
1) Empirically for Acute, Uncomplicated UTIs
2) TMP-SMX
3) Fluoroquinolones
(Because widespread resistance to earlier agents like ampicillin)
1) Usually no treatment for Diarrhea b/c Mild and Self-Limiting
2) If Bad: Hydration and Supportive therapy
3) Hemodialysis or Hemapheresis may be Required for EHEC with Hemorrhagic Colitis and HUS.
4) TMP-SMX or Fluoroquinolones:
_Reduces Duration of Diarrhea
@ ETEC, EIEC, EPEC
_Contraindicated if EHEC is even suspected b/c antibiotics increase Risk of HUS.
_Anti-Motility agents Contraindicated in EIEC or EHEC
Enterotoxigenic E. coli
ETEC
Pathogenesis:
1) Strains produce Labile Toxin and/or Stable Toxin Enterotoxins @ Proximal Small Intestine
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Epidemiology:
High infecting dose
1) Most Important Cause of
* Traveler’s Diarrhea in Visitors to Developing Countries
_Residents of endemic area have immunity.
2) Transmission:
(i) Food/Water Contaminated by Infected Human
(ii) Convalescent Carriers
3) Uncooked Foods (e.g. Salads), Marinated Meats and Veggies
=> Greatest Risk
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Manifestations:
1) Watery Diarrhea
@ Small Intestine (Proximal)
Enteropathogenic E. coli (EPEC)
Epidemiology:
1) Seems to have disappeared in industrialized nations.
2) 20% of Diarrhea cases in Bottle-Fed Infants under 1 yr @ Developing Nations
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Manifestations:
1) Watery Diarrhea
Enterohemorrhagic E. coli (EHEC)
Pathogenesis:
1) Shiga Toxin (Stx)
=> Causes Multiple Extraintestinal Features,
e.g. Hemolytic Uremic Syndrome
_@ Colon:
Stx causes Capillary Thrombosis and Inflammation of Colonic Mucosa, leading to Hemorrhagic Colitis
_@ Circulating Stx:
Binds to Renal tissue, where its Glycoprotein Receptor is particularly abundant,
=> Causing Glomerular Swelling and Deposition of Fibrin and Platelets @ Microvasculature.
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Epidemiology:
Low infecting dose
(~100 organisms)
1) Consumption of Products from Infected Animals
2) Person-to-Person Transmission Also
_Secondary cases in Families during outbreaks
3) More Common in Developed Nations
4) Regional, National Outbreaks:
_Hamburger (rare, medium rare), Unpasteurized Juices and Dairy, Fresh Fruits and Veggies
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Manifestations:
1) Bloody Diarrhea
@ Colon, rather than small intestine
(i) Starts: Watery Diarrhea + Vomiting
(ii) 1-2 Days Later:
-Intense Abdominal Pain
+ Bloody Diarrhea
(Fever is Not prominent)
(iii) Some cases develop into Dysentery that is Less Severe than Shigellosis Dysentery.
Colonoscopy:
- Edema
- Hemorrhage
- Pseudomembrane
Resolves over 3-10 Days
2) Hemolytic Uremic Syndrome (HUS)
=> Due to Shiga Toxin!!
_10% of Cases
_Primarily Children under 10 yrs
Begins:
(i) Oliguria
(ii) Edema
(iii) Pallor
Progresses to Triad:
(iv) Microangiopathic Hemolytic Anemia
(v) Thrombocytopenia
(vi) Renal Failure
Systemic Effects are often Life-Threatening: Survival Requires:
_ Transfusion
_and Hemodialysis
Mortality: 5-30% for those with sequelae such as
- Renal Impairment or
- Hypertension
3) and other Extraintestinal Features
=> Due to Shiga Toxin!!
Enteroinvasive E. coli (EIEC)
Pathogenesis:
Same pathogenesis, genetics, and biochemistry essentially the same as Shigella
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Epidemiology:
1) Primarily Children Younger than 5 yrs @ Developing Nations
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Manifestations:
Basically is a Mild Version of Shigellosis
Enteroaggregative E. coli (EAEC)
Epidemiology:
Infants and Children @ Developing Nations
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Manifestations:
Prolonged (More than 14 Days) Watery Diarrhea
_ Occasionally w/ Blood and Mucus
Shigella
Morphology:
_Closely related to E. coli
1) Don’t Ferment Lactose
2) Lack Flagella (H antigen)
= All Shigella species are Non-motile.
3) All species Invade cells and Multiply within Epithelial Cells
=> Enterocyte
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Pathogenesis:
1) Acid-Resistant; Survives Stomach
2) Invades Enterocytes, Multiplies within them, Destroys them.
3) Creates Focal Ulcers in Colonic Mucosa
4) Ulcers Cause Hemorrhage and Allow Shigella to access Lamina Propria, where it triggers an Intense, Acute Inflammatory Response
5) Diarrhea results consisting of Small-volume stools containing WBCs, RBCs, Bacteria, and little else.
= Classic Dysentery
6) Disease Remains Localized @ Colonic Mucosa.
7) Shiga Toxin (Stx) is produced by some Shigella strains.
_Not essential for disease, but makes the disease more severe.
_S. dysenteriae Type 1 is the most potent producer of Shiga Toxin and is the only strain with a significant Mortality Rate in previously Healthy ppl.
8) Shiga Toxin reaches Bloodstream and causes Systemic Effects, including Hemolytic Uremic Syndrome (HUS). (Shiga Toxin inhibits protein synthesis, causing cell death.)
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Epidemiology:
1) Strictly Human
_No animal reservoirs
2) Developed and Developing Nations
3) Fecal-Oral Route
Person-to-Person
4) Very Low Infecting Dose (10 organisms!)
5) Also by Food/Water Contaminated by Humans
6) Sanitary Practices
7) Primarily Pediatric in Developed Nations
8) S. dysenteriae Type 1 is Most severe. (“Bacillary Dysentery”)
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Manifestations:
Begins as a Watery Diarrhea; evolves into an intense inflammatory colitis with fever and frequent small-volume stools containing blood and pus; Bloody Diarrhea.
Classic Dysentery Triad:
1) Cramps
2) Painful Straining to Pass Stools (Tenesmus)
3) Frequent, Small-Volume, Bloody, Mucoid Stools.
Remains Localized to Intestine
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Diagnosis:
1) Stool Culture
_using Selective Media
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Treatment:
Definitely Give Antibiotics!!
1) TMP-SMX, Fluoroquinolones, Ceftriaxone, Azithromycin, Nalidixic Acid
Do NOT use anti-diarrheals (e.g. Imodium, Lomitil)!!
Salmonella enterica Typhimurium
Gastroenteritis
Morphology:
1) Multiple types of Pili, including one very similar to the E. coli Type 1 Pili that binds D-mannose receptors on host cells.
2) Flagella (motile)
Serotypes
1) S. enterica Typhimurium: Gastroenteritis (Diarrhea)
2) S. enterica Typhi: Typhoid Fever
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Pathogenesis:
1) Invades Enterocytes + Increased Vascular Permeability and Inflammatory Response
=> Diarrhea
2) Spreads to Bloodstream and Distant Organs
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Epidemiology:
1) Industrialized Nations mostly
2) Improper Food Handling
=> Allows Transmission from Animal Reservoir to Humans
3) Higher infecting dose than Shigella
4) Grows in Contaminated Foods that are then Ingestion
(No direct contact human-to-human transmission)
5) Picnic
6) Poultry, Eggs, Turkey Dressing, Salads, Potato Salads
7) Peak incidence in Summer and Fall
8) Highest rates among
_Children Under Age 5
_Ages 20 - 30
_Elderly Older than 70
9) ~1/3 @ Nursing Homes, Hospitals, Mental Health Facilities, other institutions
10) Pet Turtles
11) Chronic Human Carriers who are Food Handlers
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Manifestations:
=> 24 - 48 hrs After Ingestion:
Acute Gastroenteritis:
1) Nausea and Vomiting
2) Abdominal Cramps and Diarrhea
=> Diarrhea:
_Predominant Symptoms fo 3 - 4 Days
_Usually Spontaneously Resolves ~ 7 Days
Fever in 50% of Patients
Bacteremia: Transient or Persistent.
Bacteremia => Bone Infections (part. the long bones) _Life-Threatening! _**Sickle Cell Pts (Osteomyelitis) _**AIDS Pts => Trauma => Skeletal Prosthesis
AIDS:
_Salmonella Common and Severe
_Bacteremia in 70%; Can Cause Septic Shock and Death
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Diagnosis:
1) Stool Culture
2) Blood Culture
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Treatment:
1) Avoid Antibiotics, unless Severe Infx or Underlying Risk Factors:
AIDS, Sickle Cell, Trauma, Bone Infection, Children, Bacteremia, etc.
2) Fluids and Electrolytes
Salmonella enterica Typhi
Typhoid Fever
Epidemiology:
1) Most Cases while Traveling Internationally
Transmission: Fecal-Oral
Strictly Human.
Primary Reservoir: Chronic Carriers
_ Can be chronic carrier for years (Typhoid Mary): usually b/c Chronic Infection @ Biliary Tract when Gallstones are Present
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Pathogenesis:
1) **Prolonged Intracellular Survival in Macrophages
(Unique to Typhi serotype)
2) Proliferate in Macrophages, carried through lymph to RES
3) Gram Negative LPS Endotoxin into Blood initiates Fever;
Fever slowly increases and persists with continued Seeding of Typhi.
4) Cycle Takes 2 Weeks: Starts in Small Intestine and Ends in Small Intestine (Hemorrhage of Peyer’s Patches)
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Manifestations:
=> Slow, insidious Onset; lasts for weeks if untreated.
_Primary Symptom is Slowly Rising Fever, often with Abdominal Pain; little else.
Ends by gradual resolution or in Death due to complications: e.g. Rupture of Intestine or Spleen and internal bleeding.
Enteric Fever: _Multi-organ System infx _Prolonged Fever _Sustained Bacteremia _Profound Involvement @ Mesenteric Lymph Nodes, Liver, Spleen
Incubation ~ 13 Days avg
1) First Sign: Fever + Headache
2) Fever Rises Stepwise over 72 Hours
3) **Slow Pulse!!!
(Normally, infections with Fever cause Elevated Pulse!!)
4) Faint Rash (Rose Spots) @ Abdomen and @ Chest During First Few Days
5) If Untreated, Fever Persists for Weeks
Chronic Bloodstream Infection:
1) Myocarditis, Encephalopathy, Intravascular Coagulation
2) Other Sites:
_Biliary Tree with Reinfection @ Intestine + Diarrhea Late in Disease
3) UTI, Metastatic Lesions @ Bone, Joint, Liver, Meninges
4) Most Important: Hemorrhages @ Peyer’s Patches due to perforations in wall @ terminal ileum or proximal colon
=> Occur if disease progresses for 2 weeks or more
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Diagnosis:
1) Culture: Blood or Stool
_Blood most likely to give Positive Culture @ Early on in course, than culture from any other site
_Stool Culture media is same as for Shigella.
2) **Fails to Ferment Lactose
3) **Produces Hydrogen Sulfides from sulfur-containing Amino Acids
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Treatment:
1) Ceftriaxone, Cefixime, Ciprofloxacin are all 1st Line
With antibiotics:
1) Feels better in 24 - 48 hrs
2) Temp returns to Normal in 3 - 5 Days
3) Well in 10 - 14 Days
