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Micro Exam #2 > Travel Associated Illnesses > Flashcards

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
Q

Clinical presentation of Vibrio parahemolyticus

A
  • 12-24 hour incubation

- Nausea, vomiting, watery-bloody diarrhea, maybe gastroenteritis

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26
Q

Where can Vibrio parahemolyticus be found? How is it typically spread?

A

Worldwide in Oceans

Raw/Undercooked Seafood

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27
Q

Pathogenesis of Vibrio parahemolyticus?

A

Biofilms
Type 3 and 6 Secretion Systems
Hemolytic/Cytotoxic Enterotoxin

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28
Q

How is Vibrio parahemolyticus treated?

A

Rehydration and electrolyte replacement

Doxycycline if necessary

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29
Q

Typical origin of Vibrio vulnificus infection?

A

Infected would from handling contaminated seafood

Bacteremia from eating raw oysters

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30
Q

Symptoms of Vibrio vulnificus infection?

A

Infected wounds from handling
Within hours, cellulitis and necrosis
Eventual liver damage
50% Fatal

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31
Q

What is cellulitis?

A

Inflammation of subcutaneous connective tissue

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32
Q

Vibrio vulnificus is always associated with contaminated ________ or _______.

A

Seawater or Seafood

33
Q

Vibrio vulnificus has foci in what three US states?

A

TX
LA
AL

34
Q

Describe the pathogenesis of Vibrio vulnificus

A

Antiphagocytotic capsule prevents control

Necrotizing cytotoxin release

35
Q

What do you do if you suspect a patient has Vibrio vulnificus infection?

A

Doxycycline immediately

Takes 18 hours to get culture – too late.

36
Q

Describe the structure of campylobacter

A

G-
Curved, Helical, or Gul-Winged
Polar Flagella

37
Q

What oxygen tolerance is campylobacter?

A

Microaerophile

38
Q

How can you differentiate different campylobacter species?

A

Growth temperature

39
Q

Temperature campylobacter jejuni can grow in?

A

42C, but not 25C

40
Q

Clinical presentation of Campylobacter jejuni infection?

A

Abdominal Pain, Cramps, Fever
Very Bloody Diarrhea (Sometimes Blood Red)
May invade bloodstream and cause enteric fever in IC

41
Q

Campylobacter jejuni is a disease of what part of the body?

A

Large Intestine

42
Q

Secondary concern that may arise 1-4 weeks after Campylobacter jejuni infection?

A

Guillain-Barre syndrome

43
Q

What is Guillain-Barre Syndrome?

A

A demyelinating neural disease
Causes Progressive flaccid paralysis
Causes by molecular mimicry/autoantibodies to G-M1

44
Q

Campylobacter jejuni is primarily spread through what two methods?

A

Fecal-Oral Route

Contaminated Poultry and Milk

45
Q

When do people tend to get Campylobacter jejuni in the US?

A

Summer

46
Q

Who is most prone to suffer from Campylobacter jejuni ?

A

Infants and Young Adults

47
Q

Top two bacterial causes of gastroenteritis?

A

Salmonella

Campylobacter jejuni

48
Q

Campylobacter jejuni pathogenesis?

A

Inflammatory enterotoxin

Bacteremia indicates invasive potential

49
Q

How is Campylobacter jejuni treated?

A

Rehydration therapy

Tetracycline, Quinolones, Clarithromycin if systemic infections

50
Q

What temperature does Campylobacter fetus grow at?

A

Grows at 25C, but not at 42C

51
Q

Clinical presentation of Campylobacter fetus?

A

Systemic infections, septicemia

52
Q

How is Campylobacter fetus typically acquired?

A

Eating contaminated/Undercooked Beef

53
Q

Who is most susceptible to Campylobacter fetus?

A

Elderly, Ill, IC

54
Q

Pathogenesis of Campylobacter fetus?

A

S-layer protein inhibits complement fixation –> Less Phagocytosis

55
Q

How is Campylobacter fetus controlled?

A

Tetracyclines, Macrolides, and Quinolones

56
Q

Describe the Helicobacter pylori organizm structure.

A

Gram-

Spirillum (Lazy S)

57
Q

Oxygen sensitivity of Helicobacter pylori?

A

Microaerophile

58
Q

Helicobacter pylori produces huge amounts of ______

A

Urease

Detectable within minutes-hours

59
Q

Is Helicobacter pylori infection typically acute or chronic?

A

Chronic

60
Q

Helicobacter pylori colonizes where? How?

A

Gastric Mucosa esp. antrum

via Lewis Blood Group Adhesin

61
Q

Helicobacter pylori is associates with what two pathologies?

A

Gastric/Duodenal Ulcers

Gastric Adenocarcinoma

62
Q

How is Helicobacter pylori detected?

A

Serological Test
Gram Stain/Culture of Gastric Biopsy
Urea Breath Test

63
Q

Which test for Helicobacter pylori is most effective?

A

Urea Breath Test

64
Q

How does a Urea Breath Test work?

A

C14 Urea is fed, detection of 14-CO2 in breath indicates urease activity of the stomach

65
Q

___% of people are Helicobacter pylori carriers

A

Approx. 50%

66
Q

Helicobacter pylori infection is most commonly seen in which patients?

A

Middle-aged and older

67
Q

What may mask Helicobacter pylori infection?

A

Long-term proton pump inhibitors seen in GERD patients

68
Q

Helicobacter pylori is heavily correlated with a particular _____ allele?

A

TLR1

69
Q

Describe the pathogenesis of Helicobacter pylori.

A
  • Bind to base of gastric mucosal cells (pH=7.4)
  • Bind Lewis Antigen
  • Huge amounts of urease buffer pH
  • Produce VacA (Vacuolating Toxin)
70
Q

Helicobacter pylori is especially prevalent in people with Type __ Blood.

A

O

Lewis Antigen = O Blood group Antigen

71
Q

How does urease activity buffer pH in the stomach?

A

Forms NH3 from Urea

72
Q

Effects of vacuolating toxin (VacA)

A
  • 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
Q

Ulcer associated strains of Helicobacter pylori also produce what toxin…

A

Cytotoxin (CagA)

74
Q

CagA is secreted by…

It has what primary effect? What potential secondary effect?

A

Type 4 secretion system
Induced apoptosis of host cells
It may be an oncoprotein

75
Q

Production of VacA and CagA virulence factors of Helicobacter pylori is enhanced by ______.

A

Salt

76
Q

How are Helicobacter pylori ulcers treated?

A

Bismuth subsalicylate

77
Q

How is Helicobacter pylori infection treated?

A

Tetracycline (or)

Macrolide+Metronidazole

78
Q

How is Helicobacter pylori acid treated?

A

PPI

79
Q

Why is bicarbonate alone an ineffective treatment for stomach ulcers?

A

It allos Helicobacter pylori to spread

Micro Exam #2 (15 decks)

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