Travel Associated Illnesses Flashcards

1
Q

Describe the structure of Vibrios

A

Gram -
Comma Shaped
Polar Flagellum

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2
Q

How does the DNA of vibrios appear?

A

2 circular chromosomes

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3
Q

Vibrio pH happy place?

A

Highly alkali tolerent, but acid sensitive

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4
Q

How do vibrio feel about salinity?

A

Halotolerant, some halophilic

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5
Q

How are Vibrio cholerae classified?

A

Capsule, Biotypes, Serotypes

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6
Q

Disease state Vibrio cholerae has what capsule type?

A

O1 (no capsule)

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7
Q

Disease state Vibrio cholerae has what biotypes?

A

Classical

El Tor

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8
Q

What serotypes are associated with both biotypes? With One?

A

Both – Ogawa, Inaba

Only El Tor – O139

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9
Q

What medication is prone to promote Vibrio cholerae growth?

A

Antacid

Normally 10^6 needed, with AA only 10^3

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10
Q

Vibrio cholerae presents in what part of the body?

A

Small Intestine

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11
Q

Clinical presentation of Vibrio cholerae infection?

A

1-4 day incubation
Nausea, Vomiting, 1-2 loose stools
Acute, Profuse diarrhea – “Rice Water Stool”
No Pain, Fever

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12
Q

Describe the “Rice Water Stools” seen in Vibrio cholerae infection.

A

Contains lots of mucus
10^8 vibrios/mL
No Blood

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13
Q

How does Vibrio cholerae tend to become a fatal disease?

A

Dehydration and Electrolyte loss

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14
Q

Vibrio cholerae is distributed where?

A

Around the world in water supplies via copepods

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15
Q

Hosts of Vibrio cholerae?

A

Only humans

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16
Q

What do we know about chronic Vibrio cholerae?

A

Very rare

“Cholera Delores”

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17
Q

Explain the pathogenesis of Vibrio cholerae.

A

Fibriae bind gut epithelium
AB5 Toxin expressed (Toxin/Pilus regulated by riboswitch)
B binds to receptor ganglioside G-m1 of epithelial cells
A-A’s SS bond is reduced
A1 uses NAS to ADP-Ribosylate a Gs Protein

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18
Q

How does ADP-ribosylating a Gs protein influence host function?

A

Activates adenylyl cyclase
Increased cAMP causes ion secretion into gut
Water follows ions

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19
Q

Relationship between pertussis and cholera?

A

Similar mechanism
Per. blocks the inhibitor
Cholera locks in active state

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20
Q

Explain how the Vibrio cholerae riboswitch works

A

The switch weakly blocks the genes for toxin and pilus at low temperatures (ocean). When moved to higher temperatures (stomach), unstable base pairings fall apart, allowing transcription of the toxin and pilus

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21
Q

Most important component of treatment for Vibrio cholerae?

A

Rehydration and Electrolyte Replacement

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22
Q

An Oral Rehydration Salts (ORS) formula contains…

A

NaCl (3.5g/L)
KCl (1.5g/L)
NaHCO3 (2.5g/L)
Glucose (20g/L)

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23
Q

What medicinal treatment might be used for Vibrio cholerae?

A

Doxycycline can limit shedding, but can’t stop the diarrhea

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24
Q

Describe Vibrio cholerae vaccines.

A

not very effective – about 6 months
Use heat-killed O1 Classical Strain
Few doses available, used in outbreaks

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25
Clinical presentation of Vibrio parahemolyticus
- 12-24 hour incubation | - Nausea, vomiting, watery-bloody diarrhea, maybe gastroenteritis
26
Where can Vibrio parahemolyticus be found? How is it typically spread?
Worldwide in Oceans | Raw/Undercooked Seafood
27
Pathogenesis of Vibrio parahemolyticus?
Biofilms Type 3 and 6 Secretion Systems Hemolytic/Cytotoxic Enterotoxin
28
How is Vibrio parahemolyticus treated?
Rehydration and electrolyte replacement | Doxycycline if necessary
29
Typical origin of Vibrio vulnificus infection?
Infected would from handling contaminated seafood | Bacteremia from eating raw oysters
30
Symptoms of Vibrio vulnificus infection?
Infected wounds from handling Within hours, cellulitis and necrosis Eventual liver damage 50% Fatal
31
What is cellulitis?
Inflammation of subcutaneous connective tissue
32
Vibrio vulnificus is always associated with contaminated ________ or _______.
Seawater or Seafood
33
Vibrio vulnificus has foci in what three US states?
TX LA AL
34
Describe the pathogenesis of Vibrio vulnificus
Antiphagocytotic capsule prevents control | Necrotizing cytotoxin release
35
What do you do if you suspect a patient has Vibrio vulnificus infection?
Doxycycline immediately | Takes 18 hours to get culture -- too late.
36
Describe the structure of campylobacter
G- Curved, Helical, or Gul-Winged Polar Flagella
37
What oxygen tolerance is campylobacter?
Microaerophile
38
How can you differentiate different campylobacter species?
Growth temperature
39
Temperature campylobacter jejuni can grow in?
42C, but not 25C
40
Clinical presentation of Campylobacter jejuni infection?
Abdominal Pain, Cramps, Fever Very Bloody Diarrhea (Sometimes Blood Red) May invade bloodstream and cause enteric fever in IC
41
Campylobacter jejuni is a disease of what part of the body?
Large Intestine
42
Secondary concern that may arise 1-4 weeks after Campylobacter jejuni infection?
Guillain-Barre syndrome
43
What is Guillain-Barre Syndrome?
A demyelinating neural disease Causes Progressive flaccid paralysis Causes by molecular mimicry/autoantibodies to G-M1
44
Campylobacter jejuni is primarily spread through what two methods?
Fecal-Oral Route | Contaminated Poultry and Milk
45
When do people tend to get Campylobacter jejuni in the US?
Summer
46
Who is most prone to suffer from Campylobacter jejuni ?
Infants and Young Adults
47
Top two bacterial causes of gastroenteritis?
Salmonella | Campylobacter jejuni
48
Campylobacter jejuni pathogenesis?
Inflammatory enterotoxin | Bacteremia indicates invasive potential
49
How is Campylobacter jejuni treated?
Rehydration therapy | Tetracycline, Quinolones, Clarithromycin if systemic infections
50
What temperature does Campylobacter fetus grow at?
Grows at 25C, but not at 42C
51
Clinical presentation of Campylobacter fetus?
Systemic infections, septicemia
52
How is Campylobacter fetus typically acquired?
Eating contaminated/Undercooked Beef
53
Who is most susceptible to Campylobacter fetus?
Elderly, Ill, IC
54
Pathogenesis of Campylobacter fetus?
S-layer protein inhibits complement fixation --> Less Phagocytosis
55
How is Campylobacter fetus controlled?
Tetracyclines, Macrolides, and Quinolones
56
Describe the Helicobacter pylori organizm structure.
Gram- | Spirillum (Lazy S)
57
Oxygen sensitivity of Helicobacter pylori?
Microaerophile
58
Helicobacter pylori produces huge amounts of ______
Urease | Detectable within minutes-hours
59
Is Helicobacter pylori infection typically acute or chronic?
Chronic
60
Helicobacter pylori colonizes where? How?
Gastric Mucosa esp. antrum | via Lewis Blood Group Adhesin
61
Helicobacter pylori is associates with what two pathologies?
Gastric/Duodenal Ulcers | Gastric Adenocarcinoma
62
How is Helicobacter pylori detected?
Serological Test Gram Stain/Culture of Gastric Biopsy Urea Breath Test
63
Which test for Helicobacter pylori is most effective?
Urea Breath Test
64
How does a Urea Breath Test work?
C14 Urea is fed, detection of 14-CO2 in breath indicates urease activity of the stomach
65
___% of people are Helicobacter pylori carriers
Approx. 50%
66
Helicobacter pylori infection is most commonly seen in which patients?
Middle-aged and older
67
What may mask Helicobacter pylori infection?
Long-term proton pump inhibitors seen in GERD patients
68
Helicobacter pylori is heavily correlated with a particular _____ allele?
TLR1
69
Describe the pathogenesis of Helicobacter pylori.
- Bind to base of gastric mucosal cells (pH=7.4) - Bind Lewis Antigen - Huge amounts of urease buffer pH - Produce VacA (Vacuolating Toxin)
70
Helicobacter pylori is especially prevalent in people with Type __ Blood.
O | Lewis Antigen = O Blood group Antigen
71
How does urease activity buffer pH in the stomach?
Forms NH3 from Urea
72
Effects of vacuolating toxin (VacA)
- Activated by stomach acid - binds to lipid rafts of gastric epithelium - Inserts into cell as selective anion channel - Extensive vacuolation of epithelial cells and urea release while inhibiting immune response
73
Ulcer associated strains of Helicobacter pylori also produce what toxin...
Cytotoxin (CagA)
74
CagA is secreted by... | It has what primary effect? What potential secondary effect?
Type 4 secretion system Induced apoptosis of host cells It may be an oncoprotein
75
Production of VacA and CagA virulence factors of Helicobacter pylori is enhanced by ______.
Salt
76
How are Helicobacter pylori ulcers treated?
Bismuth subsalicylate
77
How is Helicobacter pylori infection treated?
Tetracycline (or) | Macrolide+Metronidazole
78
How is Helicobacter pylori acid treated?
PPI
79
Why is bicarbonate alone an ineffective treatment for stomach ulcers?
It allos Helicobacter pylori to spread