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Enterics Flashcards

0
Q

Strain vs serotype

A

Strain - genetically identical, single precursor

  • via mutation or horizontal acquisition
  • more specific than species, subspecies

Serotype - same antigenetic determinants

  • only surface proteins - may include different strains
  • O antigen = LPS (repeating oligosacch + side chains)
  • H antigen = flagellin
  • K antigen = polysacch capsule
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1
Q

Enteric bacteria

A

Enterobacteriaciae
All Gram (-) that live in gut
(other Gram + are NOT “enterics”)

Salmonella
Shigella
E coli

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2
Q

Typhoid epidemiology

A

22 million cases, 200,000 deaths
Mostly developing world, travellers

Fecol oral transmission (contaminated food, water)
Only humans (no reservoir)
Incubation 7-14 days

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3
Q

Salmonella clinical syndromes

A

S typhi -> typhoid/enteric fever
S cholerasuis -> septicemia
S enteriditis, typhimurium -> acute gastroenteritis

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5
Q

Typhoid presentation

A

Distinct phases of disease, NOT diarrhea

week 1 - fever, pain, constipation
week 1-2 - bacteremia, Rose spots (bacterial emboli), hepatosplenomegaly, leukopenia, fever
week 2-3 - bowel hemorrhage, rare perforation
can become chronic

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6
Q

Typhoid pathogenesis

A

Requires high dose (10’3-5 in immunocompetent)
Resistant to stomach pH
Adhesins -> endothelium -> induces endocytosis (via T3SS)
Survive and divide within macrophages (resistant to lysosomes)
Lysis/release -> bacteremia -> spleen, liver, gall bladder
(also endotoxic shock)
Reinfect GI -> bleed

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7
Q

Salmonella virulence factors

A

Pathogenecity islands - horizontal transposon sequences (aka SPI)
SPI encode for Type 3 Secretion Systems (T3SS)
- “needle” that injects effector protein across bacterial and host membranes

SPI1 -> invasion and endocytosis (“membrane ruffling”)
SPI2 -> protection in endosome

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7
Q

Shigella presentation

A 
Fever (LPS)
Bloody diarrhea with mucous (T3SS), cramps
Usu self-limiting
 - bacteremia rare
 - hemolytic uremic syndrome possible
Shed for 1-4 weeks post-sx
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8
Q

Shigella epidemiology

A

14,000 cases confirmed (likely 20x higher)
Spread: Feces -> Food, Fingers, Flies
No animal reservoir
Children more susceptible

Four species - similar presentation

  • dysenteriae - developing world
  • flexneri -
  • sonnei - most common US
  • boydii - India
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10
Q

Shigella pathogenesis

A

Low inoculum (100), acid tolerant
Specific phagocytosis into epithelium (T3SS, fimbrae)
Escape phagosome -> direct cell-cell spread (polymerize actin)
Apoptosis of macrophages

TNF, IL-1 -> systemic sx (fever)
Shiga toxi -> diarrhea

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10
Q

Shigella tx

A

Fluids, electrolytes
Antibiotics if severe
- Ciprofloxacin, Bactrim (trimethoprim-sulfonamide)
- resistance increasing

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11
Q

Shiga toxin

A

Only produced by S. dysenteriae
Exotoxin (released vs endotoxin)

Subunit B binds to intestinal receptor
Subunit A -> inhibits 60S ribosome -> inhibits protein synthesis

  • > fluid malabsorption -> diarrhea
  • > apoptosis or necrosis -> ulceration

Detect via immunochromatographic after growth in broth
(rare to have toxin +, culture -…wtf?)

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12
Q

Shigella prevention

A

Sanitation (only humans)
- pools, food, daycare, nursing homes
No effective vaccine (live attenuated not effective)
- possible O-antigen + inactivated Shiga toxin

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13
Q

Overview of enteric identification

A

Stool sample (blood or gall bladder for Salmonella)
Enrichment broth - bile suppresses non-enterics
Selective and differential media
- bile to suppress others, pH or metabolic indicators

Specific tests

  • MacConkey, Hektoen agar
  • Kligler agar
  • oxidase
  • motility
  • urease
  • Shiga toxin

All grow on glucose, oxidase negative, reduce nitrate

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14
Q

Hektoen agar

A

Bile + dyes - inhibit non-enteric
Lactose, sucrose, salicin + pH (acid = yellow)
Na2S2O3, Fe

E coli - ferments lactose -> yellow/salmon + bile precipitate (dt acid)
Shigella - non-lactose fermenter = green
Salmonella - non-fermenter, produces H2S -> black (with Fe)

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15
Q

MacConkey agar

A

Bile + dyes - inhibit Gram +
Lactose + pH (acid = red)

E coli - lactose fermenter -> pink with bile precipitate (dt acid)
Salmonella, Shigella - non-fermenters -> colorless colonies

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16
Q

Treatment for enterics

A

Treat with antibiotics if bacteremia common!

  • S typhi
  • S cholerasuis
  • NOT S typhimurium, Shigella
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17
Q

Differential diagnosis of diarrhea

A

Bacteria

  • Shigella
  • Salmonella
  • E coli
  • Campylobacter
  • C difficile
  • rare: Yersinia enterocolitica, Vibrio cholerae, Vibrio parahemolytica

Toxin: S aureus, Bacillus cereus

Viral: Rotavirus, Norwalk

Protozoa: Giardia
Helminths: Strongyloides

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18
Q

Kligler Iron Agar

A

Tube = anaerobic conditions
Some glucose (all grow)
Lots of lactose (-> more fermentation)
Na2S2O3, Fe

E coli - ferments lactose -> completely yellow + gas
Shigella - only glucose -> some yellow
Salmonella - only glucose, produces H2S, gas -> black (with Fe), gas

19
Q

Cytochrome oxidase

A

Final enzyme of electron transport chain
(for aerobic metabolism)
e- + O2 -> H2O (also pumps H+)

Redox dye (TMPD) -> purple if present

All enterics are negative (E coli, Salmonella, Shigella)
Positive for other Gram (-) (Pseudomonas, Neisseria)

20
Q

Sulfide identification

A

Specific sulfur metabolism enzyme
S2O3 + H20 -> H2S + SO4

Detect with ferric citrate
Fe + H2S -> Fe2S3 (black) + H+

Salmonella - positive
E coli and Shigella - negative

21
Q

Salmonella identification

A

Fecal (or blood for S typhi)
Lactose non-fermenter (black MacConkey, colorless Hektoen)
Motile (vs Shigella)
H2S producer (vs Shigella - black MacConkey and Kligler)
Gas producer from glucose (vs Shigella)
Urease negative (vs Proteus)
Indole negative (vs E coli)

Can serotype O and H antigens, PCR for epidemiology

22
Q

Shigella identification

A

Fecal sample
- PMNs in stool = invasive disease

Lactose non-fermenter (green MacConkey, colorless Hektoen)
No H2S (vs Salmonella)
Non-motile (vs Salmonella) - no H antigen (flagellin)
No gas production
Indole negative (vs E coli)
Urease negative

Shiga toxin can be tested via immuno-assay

23
Q

Overview of Salmonella vs Shigella

A

Antigens:
O (aka LPS) - both
H (aka flagellin) - Salmonella
Vi - S typhi only

Infectability
100,000 for Salmonella vs 100 Shigella

Reservoir
Salmonella poultry, reptiles, Shigella none

Bacteremia - common in S typhi, S choleraesuis

24
Vi antigen
Capsule polysaccharide Specific to S typhi May promote survival in endosome Target of ViCPS vaccine (injection)
25
Endotoxin
= lipid A component of LPS (lipopolysaccharide) Gram negative outer membrane Strong innate immune response even to low concentrations - macrophages -> TNFa -> phagocytes, permeability, PLT adhesion -> micro-emboli Gram (-) bacteremia -> endotoxic shock - 20-80% mortality dt fever, inflammation, hypotension, DIC
26
Typhoid diagnosis
Week 1 = subclinical -> + stool culture Week 2-3 = symptomatic -> + blood culture Week 3 = gal bladder colonization -> + stool culture again Characterize as Salmonella
27
Typhoid treatment
``` Generally treated due to bacteremia Acute: Ciprofloxacin Cephalosporin (Ceftriaxone) Chronic: Ampicillin Ciprofloxacin Cholecystectomy ```
28
Typhoid prevention
Epidemiology -> control food, water No animal reservoir -> identify carriers - may be chronic, assymptomatic gall bladder secretion - ex Typhoid Mary Vaccines - Ty21a = live attenuated (oral) - ViCPS (targets capsule polysacch) = injection
29
S cholerasuis
Rare - only source is contaminated pork Ingest 1000 organisms -> short incubation 6-72 hrs -> Bacteremia, fever, gastroenteritis, microabcesses -> High mortality Similar to typhoid (SPI1, SPI2 -> T3SS, endotoxin) Susceptibility if young, malaria, sickle cell, immunocompromised
30
E coli overview
Enteric Normal microflora -> Vitamin K, protective vs pathogens Pathogenic if acquired virulence genes via phage, plasmid, transposon - diarrheal - often endemic (25-50% of diarrheal mortality) - Shiga toxin - epidemic, high mortality - sometimes also need to lose commensal genes
31
Enterohemorrhagic E coli
Acquired Shiga toxins (STEC) (EHEC is specific type of STEC) ``` Labeled by O and H antigens - O = LPS polysaccharide - H = flagellin Most common is O157:H7 Also O111, O26, O157:H-, O104:H4 ``` vs Commensal (ex K12)
32
STEC presentation
Very low toxic dose ( endothelial damage) -> acute renal failure, anemia, thrombocytopenia E coli is extracellular, localized to GI Toxin is released -> kidney, etc
33
STEC pathogenesis
E coli common pilus -> weak attachment (similar to commensals) -> trigger A/E lesions -> effacement = loss of microvilli T3SS -> stronger attachment (Tir, Intimin) -> actin polymerization -> "pedestal" Hemolysin Shiga-like toxin Others - capsule (K antigen) - LPS -> inflammation -> sx - nutrient acquisition pathways
34
LEE pathogenicity island
Virulence genes + IS sequences -> E coli "Locus of Enterocyte Effacement" Type 3 Secretion system (T3SS) - "needle" and pore induced by contact - Tir -> host cell surface - Intimin -> bacterial surface - both on eae gene -> bind together for strong adhesion
35
EHEC Shiga-like toxin
aka verotoxin Acquired via phage (more than bacteria) Multiple different sequences Bloody (hemorrhagic) diarrhea Cytotoxic -> endothelium -> HUS, kidney, CNS Subunit B -> binding and uptake (cows don't have host target receptor CD77 -> immune to E Coli) Subunit A -> ribosome binding and RNA cleavage
36
Hemolysin
aka RTX toxin ("repeats in toxin") Plasmid Pore-forming protein -> lysis Common in other Gram (-), meningitis
37
Enteropathogenic E coli (EPEC)
Diarrheagenic E coli Usu person-person vs food Leading cause of childhood diarrhea in developing Pathogenesis: - Bundle forming pili (Bfp) -> adherence - A/E effacement lesions -> T3SS -> Tir, Intimin - No toxin in stool (diarrhea is direct effect of bacteria) "Moderately invasive"
38
Diarrheagenic E coli
Enteropathogenic (EPEC) - childhood in developing world Enterotoxigenic (ETEC) - travellers, infants Enteroaggregative (EAEC) - persistent -> weight loss Enteroinvasive (EIEC)
39
Enterotoxigenic E coli (ETEC)
Traveller's diarrhea and infants in developing Virulence factors - fimbriae - adherence to small intestine (NOT pili and T3SS) - heat labile toxin (LT) - similar to cholera toxin - > adenylate cyclase -> cAMP -> CFTR (transmembrane channel) -> Cl- secretion, less Na uptake -> watery diarrhea - heat stable toxin (ST) -> guanylate cyclase -> cGMP -> ion movement -> watery diarrhea Not invasive
40
Enteroaggregative E coli (EAEC)
Childhood -> persistent diarrhea -> weight loss Similar to EPEC with more aggressive epithelial adhesion (biofilm) No A/E effacement lesions Not invasive Virulence factors: Enteroaggregative stable toxin (EAST) - similar to heat stable Pet = plasmid-encoded toxin Hemolysin ex 2011 Germany outbreak = EAEC + Shiga-toxin phage
41
Enteroinvasive E coli (EIEC)
Mostly developing countries Non-fimbrial adhesions Invades cells -> multiplication -> spread to neighboring Watery diarrhea + blood/mucous (similar to Shigella) Not systemic Does not produce familiar toxins (ST, LT, etc)
42
Diffuse adhering E coli (DAEC)
Older children, developing Individual (diffuse) attachment Poorly characterized pathogenesis and toxins
43
E coli diagnostics
Stool enriched in Gram (-) bile broth Lactose fermenter -> yellow on MacConkey or EMB Sorbitol - O157:H7 negative vs commensals positive ``` Confirmation: O157 antigen -> latex agglutination H7 serology Shiga-toxin immunoassay PCR, DNA probe (vs stx1, stx2, eae, hlyA) ``` Epidemics (spinach outbreak): pulsed field gel electrophoresis ->
44
E coli treatment
Supportive fluid management (prevent dehydration, HUS pathology) STEC: Do NOT give antibiotics (more toxin released) or anti-motility ETEC: Loperamide, Fluoroquinolone (Cipro), Azithromycin, rifaximin EPEC: susceptible antibiotics if severe EAEC: fluoroquinolones for travellers, HIV

Microbiology (23 decks)

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