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Bacteriology Lectures > Enterobacteriaceae > Flashcards

Enterobacteriaceae Flashcards

1
Q

Enterobacteria general characteristics (3)

A
  1. Facultative anaerobes
  2. Motile by peritrichous flagella (or nonmotile)
  3. Type 3 secretion system
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2
Q

Enterobacteriaceae are typed by…

A

Antigens: O, H, K/Vi

  • all have capsules but large only in Klebsiella

Biochemical tests

  • IMViC
  • CHO fermentation: especialy lactose (MacConkey’s Agar)
    • Lac+ are coliforms
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3
Q

What is IMViC?

A
  • Indole - tryptophanase
  • Methyl red - acid fermentation
  • Voges-Proskauer - neutral fermentation
  • Citrate - growth
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4
Q

Gut bacteria can respond to…

A

neuroendocrone hormone levels

(e.g. E. coli and norepinephrine)

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5
Q

Enterobacteria can inhibit the _______ in order to avoid immune detection

A

inflammasome

(Including NEMO,NFkB, IkBa, and MAPK)

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6
Q

In many cell types, bacterial manipulation of vesicular trafficking promotes bacterial survival. This occurs largely by the manipulation of…

A

GTPase signaling

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7
Q

E. coli metabolism and detection on growth medium

A
  • Lac +
  • Copius acid production
  • Detected by green metallic sheen on EMB agar
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8
Q

6 pathotypes of E. coli

A
  1. EPEC
  2. EHEC
  3. ETEC
  4. EAEC
  5. EIEC
  6. DAEC
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9
Q

___ are the most common extra-intestinal E. coli infection

They are primarily caused by _____

A

UTI’s

UPEC (uropathogenic E.coli)

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10
Q

___ is becoming an increasingly common pathotype for meningitis and sepsis

A

MNEC

(meningitis-associated E. coli)

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11
Q

Three main presentations of E. coli infections

A
  1. Enteric (diarrheal)
  2. UTI
  3. Sepsis/meningitis
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12
Q

E. coli causes ___% of UTI’s

These can spread to what organ?

This is associated with ____ (blood cell binding)

A

90% of UTI’s

spread to kidneys (vesicoureteral reflux) to cause pyelonephritis

Associated with P pilus

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13
Q

5 E. coli pathotypes that cause diarrhea

A

P, T, H, I, A

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14
Q

EPEC diarrhea

A

(attachment protein, bundle forming pili)

efface small intestine microvilli –> inhibit water uptake

  • Watery, self limiting diarrhea
  • common in young children
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15
Q

ETEC, a.k.a…

A

Traveler’s diarrhea

Watery, increased motility & cramping

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16
Q

Pathotype of E. coli that is associated with CFA adhesion protein for brush border membrane

A

ETEC

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17
Q

ETEC toxins

A
  • 2 LT toxins
    • LT1 is an AB toxin (like Cholera…increases camp to cause secretory diarrhea)
  • 2 ST toxins
    • activate cGMP production (water secretion)
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18
Q

EHEC causes ____ diarrhea, without…

A

Bloody diarrhea without fever

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19
Q

EHEC toxin name and 3 characteristics

A

verotoxin (Shiga-like toxin)

  • AB toxin
  • Protein synthesis inhibitor
  • acquired by phage conversion
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20
Q

EHEC has a tropism for what tissue?

A

Kidney

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21
Q

E. coli strain (EHEC) responsible for community epidemics from contaminated meat, water, or vegetable produce?

A

0157:H7

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22
Q

Disease caused by EHEC

What is its pathology? How is this handled?

A

Hemolytic Uremic Syndrome

  • Damage to glomerular enothelium (by systemic toxin) causes uremia and organ failure
  • You DO NOT GIVE ANTIBIOTICS for this disease – they upregulate the Stx gene (toxin)
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23
Q

EIEC diarrhea

A

“Invades” the colon, causing bloody diarrhea

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24
Q

EIEC is indistinguishable from…

A

Shigella dysenteriae (type 1)

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25
Q

EIEC colonization factor

A

Ipas

Produced from Shigella plasmid

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26
Q

This E. coli pathotype is known to form a biofilm on the intestine

A

EAEC

–causes malapsorptive-type diarrhea

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27
Q

When I say “noninflammatory pediatric diarrhea in developing countries, that is also the #2 cause of travelers’ diarrhea in most countries” you tell me that this is…

A

EAEC

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28
Q

EAEC form ______ via ______ in intestine

A

infective foci via “aggregative pili”

(hence, EAEC)

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29
Q

___, ___, and __ hit the small intestine

___ and ___ hit the large intestine

A

Small = EPEC, ETEC, EAEC

Large = EHEC, EIEC

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30
Q

The E. coli pathotypes that cause bloody diarrhea tend to hit where?

A

Large intestine

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31
Q

Major E. coli cause of neonatal meningitis?

What is it’s major pathogenic characteristic?

A

E. coli K1

  • most meningitis strains have K1 capsule
  • It functions as a molecular mimic of host’s NCAM receptors
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32
Q

E. coli K1 capsule is similar to…

A

N. meningitidis B capsular antigen

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33
Q

Salmonella metabolism and growth characteristics

A
  • Lac (-)
  • H2S (+) - S-S agar
  • Grows in selective media with Bile salts (deoxycholate)
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34
Q

All Salmonella belong to _____ species, with how many subspecies?

A
  • S. enterica
  • 6 subspecies (e.g. S. enterica ssp. arizonae)
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35
Q

It is only important (for us) to distinguish what two Salmonella subspecies?

A

Typhi + Paratyphi

36
Q

Salmonella diseases (and subspecies that cause)

A
  1. Typhoid fever (S. typhi or S. paratyphi)
  2. Bacteremia/Septicemia (S. cholerasuis)
  3. Enterocolitis / GE (S. Enteriditis)
37
Q

Typhoid fever is a ____ disease that disseminates via ______to liver, GB

Death is usually from _______

A

invasive disease, disseminates via macrophages

death from intestinal hemorrhage

38
Q

Salmonella septicemia mainly hits whom?

A

immunocompromised patients

39
Q

Salmonella enterocolitis/gastroenteritis clinical features (3)

A
  • nausea, profuse diarrhea, FEVER
  • self limiting within 2-5 days
  • may colonize GB and shed for weeks
40
Q

Salmonella Enteriditis is especially transmitted via…

A

egg and poultry products

41
Q

Two distinct features of Typhoid fever

A
  1. High sustained fever
  2. Roseate rash
42
Q

Salmonella spread via

A

fecal-oral

from contaminated water, endemic sources in eggs and poultry, crops fertilized with human excreta, and pets

43
Q

Salmonella pathogenic steps (4)

A
  1. Binds brush border
  2. invades gut epithelial cells
  3. invades deep tissues and bloodstream through the basal membrane
  4. produces cytotoxic enterotoxin
44
Q

Typhoid toxin characteristics and function

A

A2B5 toxin

can grow in bile using efflux pumps and DNA repair to survive

Uses phospholipids as a carbon source

  1. A1 = ADP ribosylates G protein
  2. A2 = Damages DNA and stops replication of cell
45
Q

Salmonella cytotoxin may cause _____

A

bloody diarrhea

46
Q

Salmonella survives within…

A

MQ’s

47
Q

Shigella metabolism and characteristics

A

Lac-, H2S- (S-S Agar)

Looks like other enterobacteriaceae

48
Q

Shigella types

A

dysenteriae

flexneri (3rd world)

boydii

sonnei (US)

49
Q

Shigella does not result in

A

systemic infection / sepsis

(only a GI pathogen)

50
Q

Shigella diarrhea timeline

A
  • acute onset watery diarrhea (WITH FEVER)
  • 2 days later the volume is less, but more mucus/blood in stool
  • Resolves in ~one week
51
Q

Shigella transmits via

A

fecal oral

Spread via 4 F’s!

  1. Food
  2. Fingers
  3. Feces
  4. Flies

Associated with crowded unsanitary conditions

52
Q

Shigella pathogenic steps

A
  1. Phagocytosed and transmitted by M cells
  2. engulfed by MQ
  3. Lyse MQ phagolysosome and replicate in cytoplasm
  4. MQ undergoes apoptosis
53
Q

How does shigella change the basal membrane/cell-cell interactions?

A

Releases IL-1 and other cytokines to permeabilize the cell junctions

Induces Basal membrane phagocytosis by lumenal cells

Can spread via actin tails

54
Q

What are shigella IPAS?

A

Invasion factors

secreted by T3SS

55
Q

How does shiga enterotoxin kill cells?

A

It disrupts protein synthesis

56
Q

“Classic symptom” of shigella

A

fecal leukocytes

(gaps opened up in the basal membrane by shigella cause leakage of polymorpholeukocytes, which show up in stool sample)

57
Q

Yersinia may or may not be…

A

GIT infection

58
Q

Yersinia appearance

A

Looks like other enterobacteriaceae, but may be coccobacillus

59
Q

Yersinia staining

A

Bipolar

(Wright-Giemsa stain, Wayson’s)

60
Q

Yersinia - three general pathogenic factors

A
  • YadA adhesin
  • YOP (T3SS encoded by plasmid)
  • V and W antigens (allow for intracellular growth)
61
Q

Non-GI version of yersinia

A

Y. pestis

  • Zoonosis
  • Bubonic = most common form
  • painful buboes in groin or other lymph node
62
Q

It is essential that yersinia buboes are differentiated from which other conditions/pathogens?

A

tularemia & pasteurella

63
Q

Less common form of Yersinia pestis?

What are the characteristics?

Symptoms?

A

Septicemic

  • may be primary/secondary to bubonic
  • (if secondary, it develops within a few days of the appearance of buboe

Sx = purpura, DIC, necrosis

64
Q

Third presentation of yersinia pestis?

What are the types/origin, symptoms?

What shows up on labs/imaging?

A

Pneumonic

  • Primary from inhalation, Secondary from DIC
  • X-rays show bilateral alveolar involvement
65
Q

Y. pestis spread via ____

A

rat flea (xenopsylla cheopis)

  1. Bacteria toxin blocks fleas gut - clot forms
  2. When flea bites again, the clot is transferred into the animal host
66
Q

Main reservoirs for Y. pestis in the US?

A

deer mice

ground squirrels (prairie dogs)

67
Q

Yersinia pestis pathogenesis (in flea and mammal)

A

Flea:

  1. YMT phospholipase helps survival within flea (key to expanding host range)

Human:

  1. Capsular genes turned on at 37 degrees
  2. Yop T3SS injects toxins
  3. MAPK pathway is inhibited by Yop-J
  4. Phagocytosis is prevented by Yop-E
  5. Platelet aggregation is inhibited by Yop-M
68
Q

Yersinia YopJ effects

A

Inhibits MAPK pathway

  • prevents cytokine production
  • prevents cell replication (apoptosis and necrosis)
69
Q

Y. pestis control is based around

A

prevention: insecticide kills fleas before infection

70
Q

Is there a Yersinia pestis vaccine?

A

Yes! Formalin-killed OR live attenuated

*must be boosted every year, so it’s only for people who are repetedly exposed

71
Q

Y. pestis post-exposure treatments

A

Oral tetracycline for those exposed but asymptomatic

streptomycin (i.m.) for symptomatic pts.

**pneumonic plague treatment is rarely successful (virtually 100% fatal within 24 hours)

72
Q

GiT version of yersinia

A

Y. enterocolitica

Y. pseudotuberculosis

73
Q

2 major Y. enterocolitica symptoms

A
  1. enterocolitis with intestinal abscesses (SEVERE bloody diarrhea)
  2. Mesenteric adenitis (mimics appendicitis)
74
Q

GIT yersinia reservoirs and spread

A

Cattle/hog reservoir

Spread in feces or via contaminated drinking water/milk

75
Q

Control for Yersinia enterocolitica/pseudotuberculosis

A

Ampicillin

*note: does NOT control y. pestis

Can also use Third Gen Ceph’s or Bactrim

76
Q

What are the “other” enterobacteriaceae?

A
  • Klebsiella pneumoniae
  • Klebsiella oxytoca
  • Klebsiella granulatomatis
  • Proteus mirabilis
  • Proteus vulgaris
  • Serratia marcascens
77
Q

K. pneumoniae virulence, symptoms/prognosis

A

virulence = large capsule

hemorrhagic, necrotizing infection (currant jelly)

50-100% fatal

78
Q

K granulomatis infection type

Possible presentation?

A

STD, not GIT

Donavonosis = “granuloma inguinale” = granulomatous infection that can mimic syphillis

79
Q

K. granulomatis may mimic…

A
  1. syphillis (genital granulomas)
  2. genital cancers (because of progressive destruction of tissue)
80
Q

What enterobacteriaceae exhibit “swarming motility” on agar?

What other pathogenic feature is present in this organism, and what happens as a result of it?

A

Proteus! (due to many flagella)

** this makes it ascent possible in the urinary tract – Associated with UTI

Proteus also makes UREASE (similar to mycoplasma)

  • causes alkaline urine, precipitates formation of BLADDER STONES
81
Q

Serratia marcescens:

  • Infection route?
  • What kinds of infections that tend to result?
A
  • Opportunistic nosocomial pathogen
  • PNA, bacteremia, endocarditis

** in immunocompromised patients

82
Q

General control for “other enterobacteriaceae”

What antibiotics can we use (if any)?

A

General control: isolate source and decontaminate (esp. for fecal oral)

Antibiotics: Ampicillin, Third Gen Ceph’s, Quinolones, Sulfas, Streptomycin

**Antibiotic resistance greatly influences ability to treat. (R plasmids are very common in enterobacteriaceae)

83
Q

Antibiotic guidelines for uncomplicated UTI (enterbacteriaceae)

A

BACTRIM is 1st choice, followed by Fosfomycin

DON’T use fluoroquinolones (resistance)

84
Q

Most common prophylactic for traveler’s diarrhea

A

Rifamixin

85
Q

What is MUC2? What are three things it does?

A
  • hyperglycosylated mucin
  • subdues inflammatory response from Dendritic cells
  • stimulates production of Treg cells (by DC signaling)
  • Normal flora use it as a carbon source –> non-inflammatory

Bacteriology Lectures (14 decks)

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