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Enterics Flashcards

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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
Q

Vi antigen

A

Capsule polysaccharide
Specific to S typhi

May promote survival in endosome
Target of ViCPS vaccine (injection)

25
Q

Endotoxin

A

= 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
Q

Typhoid diagnosis

A

Week 1 = subclinical -> + stool culture
Week 2-3 = symptomatic -> + blood culture
Week 3 = gal bladder colonization -> + stool culture again

Characterize as Salmonella

27
Q

Typhoid treatment

A 
Generally treated due to bacteremia
Acute:
 Ciprofloxacin
 Cephalosporin (Ceftriaxone)
Chronic:
 Ampicillin
 Ciprofloxacin
 Cholecystectomy
28
Q

Typhoid prevention

A

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
Q

S cholerasuis

A

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
Q

E coli overview

A

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
Q

Enterohemorrhagic E coli

A

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
Q

STEC presentation

A

Very low toxic dose ( endothelial damage)
-> acute renal failure, anemia, thrombocytopenia

E coli is extracellular, localized to GI
Toxin is released -> kidney, etc

33
Q

STEC pathogenesis

A

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
Q

LEE pathogenicity island

A

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
Q

EHEC Shiga-like toxin

A

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
Q

Hemolysin

A

aka RTX toxin (“repeats in toxin”)

Plasmid
Pore-forming protein -> lysis
Common in other Gram (-), meningitis

37
Q

Enteropathogenic E coli (EPEC)

A

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
Q

Diarrheagenic E coli

A

Enteropathogenic (EPEC) - childhood in developing world
Enterotoxigenic (ETEC) - travellers, infants
Enteroaggregative (EAEC) - persistent -> weight loss
Enteroinvasive (EIEC)

39
Q

Enterotoxigenic E coli (ETEC)

A

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
Q

Enteroaggregative E coli (EAEC)

A

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
Q

Enteroinvasive E coli (EIEC)

A

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
Q

Diffuse adhering E coli (DAEC)

A

Older children, developing

Individual (diffuse) attachment
Poorly characterized pathogenesis and toxins

43
Q

E coli diagnostics

A

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
Q

E coli treatment

A

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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