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Bacteriology Lectures > Vibrio, Camphylobacter, Helicobacter > Flashcards

Vibrio, Camphylobacter, Helicobacter Flashcards

1
Q

Vibrio shape and genome

A

Gram negative

Comma shaped rod with a Polar Flagellum

2 circular chromosomes

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2
Q

Vibrio are ____ tolerant and ______ -tolerant

A

alkali-tolerant

Halo-tolerant

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3
Q

Vibrio can reside on _____. This allows….

A

Copepods

–> we can filter the copepods through a folded cloth

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4
Q

Vibrio antigens (and types)

A

Strains share H antigens, but have different O antigens

2 of the O antigens cause cholera

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5
Q

Vibrio are sensitive to…

A

acid

(pH less than 6)

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6
Q

Two strains of vibrio cholerae

A

O1 and O139

O1 (no capsule) = causes the majority of outbreaks

O139 (polysaccharide capsule)

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7
Q

Two biotypes of O1 V. cholerae

A

classical + El Tor

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8
Q

Two serotypes of V. cholerae

A

Ogawa + Inaba

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9
Q

V. cholerae - El Tor characteristics (3)

A
  1. Polymixin resistant
  2. produces hemolysin
  3. LESS toxin is produced –> better colonization (less cytotoxicity)
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10
Q

Classical O1 vibrio cholerae is responsible for…

A

6 pandemics

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11
Q

V. cholerae requires ___________ to colonize

A

LARGE numbers of bacteria (10^6)

** This can be reduced to 10^3 if an antacid is being used

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12
Q

V. cholerae is essentially a _____ disease

A

small intestine

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13
Q

V. cholera timeline of symptoms

A
  1. 1-4 days incubation
  2. nausea, vomiting, 1-2 loose stools
  3. 20L/day ricewater stool (contains high numbers of vibrios but no blood)

*no fever/pain

*dehydration and electrolyte loss causes circulatory collapse and death

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14
Q

V. cholerae present in ________

A

water (especially estuarine water), carried by copepods

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15
Q

V. cholerae hosts?

A

humans only natural host

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16
Q

Vibrio spread via…

A

fecal-oral

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17
Q

V. cholerae long-term carriers are ______

A

rare

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18
Q

V. cholerae pathogenic factors

A
  • Fimbriae bind to gut epithelium
  • Toxin
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19
Q

V. cholerae toxin:

  • Genetics/structure?
  • How does it function? (steps)
A
  • AB5 toxin
    • expressed by ctxAB operon on PAI on chromosome 1
    • Toxin and pilus genes regulated by ToxT (temperature-sensitive riboswitch)
    • A is in two subunits joined by disulfide bond
    • B binds as pentamer to ganglioside Gm1 (epithelial cells)
  • The Disulfide bond is reduced, and A1 uses NAD to ADP ribosylate a stimulatory G protein (Gs) = ACTIVATES adenyl cyclase, which increases cAMP-mediated ion secretion into the gut lumen (with water following)
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20
Q

V. cholerae treatment and antibiotics

A

Oral rehydration Salts formula

Doxycycline can limit shedding but not diarrhea

  • WHO recommends only use if more than 10% dehydrated
  • CDC recommends one dose for all hospitalized cases
  • AZITHROMYCIN for pregnant patients!
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21
Q

V. cholerae vaccine?

A

(not very effective)

–3 oral vaccines using heat-killed O1 classical strain

(Dukoral, Shanchol, mORC-VAX)

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22
Q

V. parahemolyticus is a ________ organism

A

halophilic

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23
Q

V. parahemolyticus infection sequence

From where does someone get this infection?

A

Self limiting infection

nausea > watery > bloody (w/ or w/o gastroenteritis) > resolution in 1-4 days

Ocean waters, consumed in contaminated undercooked seafood

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24
Q

V. parahemolyticus pahtogenic factors (3)

A
  1. Biofilms
  2. Type 3 and 6 secretion systems
  3. Hemolytic/cytotoxic enterotoxin
25
Q

V. parahemolyticus control measures (Tx and antibiotics)

A

Rehydration

Doxy if necessary

26
Q

V. vulnificus is a ______ organism

A

halophilic

27
Q

Where do you get V. vulnificus?

What kind of infection does it cause?

A
  • From handling contaminated seafood (shellfish)…. Bacteremia from eating raw oysters
  • VERY rapid cellulitis and necrotic infection, eventual liver damage. 50% fatal
28
Q

V. vulnificus especially associated with ______.

In the United States, endemic foci are in ___, ___,and ____

A

Oysters

Texas, Louisiana, Alabama

29
Q

The two pathogenic factors for V. vulnificus

A
  1. Antiphagocytic capsule
  2. necrotizing cytotoxin
30
Q

V. vulnificus Treatment

A

Doxy right away! —Cipro if pregnant

DO NOT CULTURE – it takes too long, will be too late by the time results come back

31
Q

Camphylobacter organism and shape

A

Gram negative

Curved, helical, or gull-winged

Polar flagella (sometimes bipolar)

32
Q

Two camphylobacters that cause infection, and their growth characteristics

A

jejuni = high temp

fetus = low temp (much more serious infection)

33
Q

Camphylobacter organism is a ___________

A

microaerophile

34
Q

C jejuni grows at ______.

It requires ____ ingestion of ______ organisms to grow.

It is a disease of the ________

A

42 degrees, but NOT at 25 degrees

orally ingest 10^4 organisms

disease of the large intestine

35
Q

C jejuni presentation

A
  • Gastroenteritis - abdominal pain
  • Cramps, fever, VERY bloody diarrhea (INVASIVE organism)
  • Self limiting within a week
  • May result in GBS because of Molecular mimicry (antibodies to GM1 gangliosides)
36
Q

C jejuni source, transmission, and epidemiology

A

Zoonosis from chickens and turkey

Fecal-oral transmission (consumption of contaminated poultry or milk)

Peaks in summer

37
Q

C. jejuni pathogenic factor?

What does bacteremia indicate with this organism?

A
  • Pathogenic factor = inflammatory enterotoxin
  • Bacteremia indicates an invasive potential
38
Q

C.jejuni treatment?

When are antibiotics used, and which ones?

A

Oral rehydration

Systemic infections:

  • Tetracycline
  • Quinolones
  • Clarithromycin
39
Q

C. fetus grows at…

A

25 degrees, but not at 42

40
Q

C. fetus usually causes ____ infections.

It rarely causes _______

A

Systemic

Diarrhea

41
Q

C. fetus source? Who does it infect?

A

Undercooked/contaminated beef

Infects elderly & immunocompromised patients

42
Q

C. fetus major virulence factor?

A

S-layer protein

**inhibits complement fixation by C3b = less opsonization

Lowered CMIR

43
Q

C. fetus antibiotics?

A

Tetracyclines, macrolides, quinolones

44
Q

H. Pylori appearance?

Motile/nonmotile?

A

gram negative spirillum — “Lazy S”

motile at 37 degrees?

45
Q

H. Pylori growth characteristics (plates)

A

Oxidase + and catalase +

Microaerophile

acid sensitive at pH 4.0

46
Q

Major virulence factor of H. Pylori

A

Huge amounts of urease

(Urease test positive in minutes to hours)

47
Q

H. pylori usually considered a ____ infection

A

chronic, non-invasive

48
Q

Colonization of H. Pylori is associated with

A

Lewis blood group adhesin

–> stimulation of GASTRIN production, which stimulates ACID production in fundus

49
Q

H. Pylori infection is associated with…

A
  • gastric/duodenal ulcers
  • gastric adenocarcinoma
50
Q

Detection of H. Pylori (methods?)

A

Serology, Gram stain, culture

Urea breath test = most effective

  • 14C urea is fed ->> detect 14CO2 in breath (can happen within minutes)
51
Q

H. Pylori carrier rate?

A

50%

(80% in ulcer patients)

52
Q

H. Pylori has a strong corrleation with ___ allele

A

TLR1

53
Q

What doyou have to look out for regarding H. Pylori infections?

A

They may be masked by PPI’s in patients undergoing long term GERD treatment

54
Q

H. Pylori Pathogenic steps

A
  1. Binds to base of mucosal cells (pH is 7.4 instead of 2)
  2. Binds to Lewis antigen (O)
  3. Urease buffers pH by forming NH3 from urea
  4. Produce vacuolating toxin VacA
55
Q

What is the VacA toxin?

A
  1. activated by stomach acid
  2. binds to lipid rafts (sphingomyelin) in epithelial cells
  3. inserts into cell as selective anion channel
  4. causes vacuolation and urea release, and inhibits antigen presentation (and thus T cells activation)
56
Q

Ulcer strains of H. Pylori produce ______.

What is it (three things)?

A

CagA

  • secreted by T4SS
  • induces apoptosis
  • Potential oncoprotein
57
Q

Treatment of H. Pylori?

A

Three-pronged approach

  1. Treat ULCER with bismuth subsalicylate
  2. Treat INFECTION with Tetracycline or Macrolide+Mzole
  3. Treat ACID with PPI
58
Q

H pylori ulcer only recovers if…

A

The infection is treated

(bicarbonate only allows H. pylori to spread)

Bacteriology Lectures (14 decks)

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