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Infectious Disease > Enteric Bacteria > Flashcards

Enteric Bacteria Flashcards

1
Q

Is vibrio cholera invasive?

A

no - noninvasive

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2
Q

Vibrio cholerae clinical symptoms

Incubation period

A

2-5 days

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3
Q

Vibrio cholerae clinical symptoms

A

abrupt onset of diarrhea, abdominal cramps, some vomiting
Milder to severe watery diarrhea - up to 15/20 liters per day leads to severe dehydration, blood pressure drop, and vascular collapse

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4
Q

Is there fever with cholera?

A

no

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5
Q

pathogenesis of vibrio cholera

A

colonization of the small bowel and toxin production are essential prerequisites to disease

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6
Q

Is bacteriophage conversion important in cholera?

A

Yes - both the colonization of the small bowel and the toxin production are essential prerequisites to disease that are both encoded by different lysogenic phages

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7
Q

How does vibrio cholerae colonize?

A

requires surface expressed adherence factor (TCP pilus) which I is also the coat protein of a phage encoding cholera toxin (CTX)

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8
Q

Cholera toxin production

A

genes chromosomal encoded as part of genome of phage CTX; this page use TCP pilus as its receptor

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9
Q

Cholera toxin structure and function

A

prototypical A-B type toxin
B subunit binds to cell surface receptors (ganglioside GM1) of enterocytes. A subunit then enters the cell cytoplasm where it transfers ADP ribose from NAD to a regulatory G protein
This then constitutively activates adenylyl cyclase, leading to increased cAMP concentration which leads to increased chloride secretion, decreased Na absorption, and net secretion of lucid into the gut lumen

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10
Q

Does cholera toxin kill the cell?

A

no it is cytotonic (does not kill cell) - an intoxicated enterocyte continues to secrete until it is replaced naturally

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11
Q

Epidemiology of cholera

A

cholera occurs in pandemics
most cases of cholera in the US are imported from endemic areas
cholera returned to the Americas in 1991 with nearly one million cases mostly in peru

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12
Q

Mode of transmission of cholera

A

fecal/oral - generally through ingestion of contaminated food
environmental - V cholerae can be found in aquatic environments

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13
Q

Treatment of cholera

A

treatment is aimed to restore fluid and electrolyte loss - milder cases can be orally rehydrated with salt/sugar solution - ORS - isotonic Na/K, Cl, Citrate, or bicarb buffer and glucose. If ORS is not tolerated, intravenous rehydration with Ringers lactate + KCl.
Antibiotics shorted the course of infection, number and volume of stools, and number of Vibrios excreted in the stool, and may help reduce carrier state

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14
Q

The three main Enteric E coli

A

ETEC
EPEC
EHEC

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15
Q

ETEC

clinical/epidemiology/virulence

A

traveler’s diarrhea
worldwide
heat-labile and heat stable toxins

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16
Q

EPEC

clinical / epidemiology / virulence

A

watery and persistent diarrhea
infants under 1
attaching and effacing (AE)

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17
Q

EHEC

clinical / epic / virulence

A

bloody dysentery
developed world
attaching and effacing / shiva-like cytotoxins

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18
Q

What is the leading cause of traveler’s diarrhea for adults

A

ETEC

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19
Q

Symptoms of ETEC

A

Watery diarrhea, no blood or pus, rarely have low grade fever, abdominal cramps, and vomiting. Can be severe, cholera like diarrhea, even in adults

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20
Q

treatment of ETEC

A

Supportive bc self limiting
replace fluids and salt
usually do not rec ab

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21
Q

pathogenesis of ETEC

A

toxigenic diarrhea - no tissue invasion

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22
Q

What are the 2 types of ETEC toxins

A

Heat labile enterotoxin - very similar to cholera toxin (same mechanism)
heat stable enterotoxin - small peptide toxin that activates guanalyl cyclase, raising cGMP levels and leading to increased fluid secretion

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23
Q

EPEC

predominately seen in

A

infants

24
Q

symptoms of EPEC

A

watery stools, no blood, or mucus,
no tissue invasion
vomiting
low grade fever

25
Q

Treatment of EPEC

A

restore hydration - usually responds rapidly to ab therapy

26
Q

Pathogenesis of EPEC

A

intimately adhere to enterocyte surface. A type III secretion system secretes the translocated-intimin receptor, initiating the characteristic “attaching and effacing lesion” microvilli destruction, pedestal formation. this probably interferes with absorption leading to diarrhea

27
Q

EHEC

Characteristics

A

associated with food and water borne outbreaks of bloody diarrhea and hemorrhagic colitis - leading to the development of hemolytic uremic syndrome (HUS)

28
Q

how can we easily detect EHEC?

A

colorless colonies on sorbitol MacConkey media.

29
Q

EHEC infectious dose?

A

low

30
Q

EHEC clinical course

incubation?

A

3-9 day incubation
initial watery diarrhea, developing to grossly bloody liquid stools with abdominal cramps. Colonizes large intestine. Fever seen in more severe cases. Fecal leukocytes uncommon - important diagnostic feature

31
Q

Do enterics cause disease outside the intestine?

A

yes! enterics can also cause pneumonia, sepsis, meningitis, UTI, etc.

32
Q

Host defenses (4)

A

gastric acidity
intestinal motility
local antibody
normal gut flora

33
Q

Which enteric looks like curved rods?

A

Vibrio

34
Q

which enteric looks like gull-wings?

A

Campylobacter

35
Q

all enterics are (stain?)

A

gram negative bacilli

36
Q

3 key antigenic structures of enterics?

A

lipopolysaccharides
H antigens
K antigens

37
Q

Lipopolysaccharides

3 components

A

LPS is in the outer membrane of all gram negative bacteria

  1. Lipid A
  2. Core polysaccharide
  3. O antigen
38
Q

Lipid A of LPS

A

Toxic part of LPS (endotoxin) - the lipid (fatty acid portion) forms the outer half of the lipid bilayer of the outer membrane

39
Q

Core polysaccharide of LPS

A

Constant region of LPS within a genus - different genera

40
Q

O antigen of LPS

A

repeating subunits of oligosaccharides (up to 40) - variable within genus - helps species ID (e.g. shigella sonnet vs shigella dysenteriae) or antigenic types as in Salmonella or E coli

41
Q

H antigens

A

flagellar protein antigens associated with motile organisms - not all enterics have this

42
Q

K antigen

A

consist of capsular polysaccharide - not found in all strains - when it is, it is usually associated with increased virulence. Capsules are most significant when the organism produces extra intestinal infections (e.g. bacteremia)

43
Q

Are all enterobacteriaceae oxidase negative?

A

yes

44
Q

Do all enterobacteriaceae ferment glucose?

A

yes

45
Q

What distinguishes vibrios from enterobacteriaceae?

A

oxidase positive

46
Q

whether an organisms produces a secretory or inflammatory diarrhea depends on (2)

A

virulence factors
AND
site of action in gut

47
Q

Watery diarrhea - small intestine - likely bacterial cause? (3)

A

ETEC
EPEC
Campylobacter

48
Q

Dysentery - large intestine - likely bacterial cause? (3)

A

Shigella
EIEC
Campylobacter

49
Q

Protracted diarrhea (lasting more than 14 days) likely cause?

A

EPEC

50
Q

Bloody watery diarrhea - ileum - likely cause?

A

Salmonella
Campylobacter
Yersiniae

51
Q

Hemorrhagic colitis - likely cause?

A

EHEC

52
Q

Cholera incubation period

A

2-5 days

53
Q

Does cholera have fever?

A

no

54
Q

colonization by cholera?

A

requires TCP pillus - which is also the coat protein of a phage encoding cholera toxin (CTX)

55
Q

Cholera toxin production

A

genes chromosomally encoded as part of phage CTX - This phage uses the TCP pilus as its receptor

56
Q

Cholera toxin function

A

AB type toxin - constitutively activate adenylate cyclase - increased cAMP - leading to increased Cl secretion and decreased Na absorption

57
Q

Does cholera kill cell?

A

no. cytotonic

Infectious Disease (5 decks)

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