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M1 Micro Quiz 2 > Cholera, Campylobacter, Helicobacter > Flashcards

Cholera, Campylobacter, Helicobacter Flashcards

1
Q

What are the general physical properties of Vibrio cholerae?

A

Motile gram-negative fermenter
Comma shape
Polar flagellum

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2
Q

How does Vibrio cholerae appear on medium?

A

Yellow opaque colonies on special TCBS medium

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3
Q

What strain of Vibrio cholerae causes epidemic cholera?

A

O1; There are two biotypes: classical and El Tor (hemolytic). El Tor is responsible for all epidemic cholera in the last decade

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4
Q

What is the major colonization factor of Vibrio cholerae?

A

toxin coregulated pilus (TCP)

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5
Q

How does TCP contribute to Vibrio cholerae pathogenesis?

A

It is expressed once the bacteria enter the intestinal crypts and causes the formation if microcolonies

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6
Q

How does Cholera Toxin contribute to Vibrio cholerae pathogenesis?

A

After microcolonies are formed, Cholera toxin is expressed and secreted and binds to GM1 gangliosides of intestinal cell membranes
It then enters the intestinal cells by endocytosis and stimulates adenylate cyclase and cAMP production resulting in massive intestinal fluid loss

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7
Q

How does neuramidinase contribute to Vibrio cholerae pathogenesis?

A

It converts other gangliosides to GM1 and thereby increases the amount of Cholera toxin binding sites

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8
Q

How does Cholera Toxin result in massive intestinal fluid loss? (2 mechanisms)

A

Increased adenylate cyclase and cAMP production leads to:

  1. villus cells: decreased NaCl absorption from the gut
  2. secretory cells: increased Cl, HCO3, and H20 secretion into gut
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9
Q

What are the clinical features of Vibrio cholerae?

A

painless, odorless, profuse watery diarrhea (watery rice stool)
Isotonic volume loss (10-15L/day) and dehydration
Low blood pressure - shock

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10
Q

What are the stool electrolyte concentrations present during infection with Vibrio cholerae?

A

Na: 135
K: 15
Cl: 100
CO2: 45mEq/L

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11
Q

What is the treatment for Cholera?

A

Isotonic fluid replacement - oral or IV
Antibiotics reduce duration:
Doxycycline for adults: Azithromycin for children and pregnant women

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12
Q

In what regions is Cholera endemic?

A

South-central and Southeast Asia
African refugee camps
South America
Haiti

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13
Q

What are Cholera outbreaks related to?

A

contaminated water, shellfish, other seafood, rice

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14
Q

What are the two Cholera vaccines in current use and how are they given?

A

1 - inactivated vaccine: 2 oral doses, 70% effective, not recommended for travel, in use in Haiti
2 - live attenuated vaccine: effective in N.A. clinical trials but unproven in field studies

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15
Q

What condition is Vibrio parahaemolyticus associated with?

A

invasive gastroenteritis from contaminated shellfish

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16
Q

What condition is Vibrio vulnificus associated with?

A

infections in wounds contaminated by seawater or shellfish. Limited to individuals with underlying liver disorder

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17
Q

What are the general physical properties of Campylobacter?

A

curved or comma-shaped microaerophilic gram negative rod

18
Q

Describe the pathogenesis of Campylobacter

A

Ingested in contaminated food/water, most organisms are killed by gastric acid but some survive and cause invasive inflammation in small and large bowel. Rarely enter the bloodstream. Generally recover

19
Q

How is Campylobacter transmitted?

A

zoonotic disease, more than half of raw chicken in US grocery stores, cases peak in summer and fall

20
Q

What is the most common etiologic agent of diarrhea in the world?

A

Campylobacter

21
Q

What is the clinical syndrome of Campylobacter

A

3-5 day incubation with prodromal fever, malaise, headache

then fever, abdominal pain and diarrhea lasting up to 1 week

22
Q

What is a major complication of Campylobacter?

A

Giullaim-Barre syndrome

1/1000 people will develop autoimmunity to their own nerves leading to temporary paralysis

23
Q

What is the infectious dose of Camplylobacter?

A

500 organisms; as little as a drop of raw chicken juice

24
Q

How is Camplylobacter diagnosed?

A

stool culture on selective media (campy-BAP with caphalothin) incubated in 5-10% O2 at 37 or 42 degrees (42 is better because it is the body temperature of poultry)

25
Q

How is Campylobacter treated?

A 
Supportive therapy (fluids) 
Some get antimicrobials - Erythromycin/ciprofloxacin
26
Q

How is Campylobacter prevented?

A

Pasteurization of milk; avoid undercooked poultry

27
Q

What are the general physical properties of Helicobacter?

A

spiral shaped, gram negative

28
Q

How does Helicobacter survive gastric acid?

A

Once in the mucous lining of the stomach, it secretes urease which converts urea to bicarbonate and ammonia

29
Q

What are the virulence factors of Helicobacter?

A

Urease
Adhesins (BabA)
CagA
VacA

30
Q

What do Helicobacter adhesins bind to?

A

membrane associated lipids and carbohydrates of epithelial cells

31
Q

What is BabA?

A

A Helicobacter adhesin that binds to the Lewis b antigen on the surface of stomach epithelial cells

32
Q

What is CagA?

A

cag PAI-encoded protein injected by Helicobacter into stomach epithelial cells. It is phosphorylated and disrupts the cytoskeleton, adherence to adjacent cells, intracellular signaling, and cell polarity

33
Q

What is VacA?

A

a vacuolating cytotoxin secreted by Helicobacter into stomach epithelial cells that damages the epithelial lining

34
Q

Why is Helicobacter able to evade the immune system?

A

It exists in the mucous lining of the stomach where white cells, CTLs, and other immune cells cannot penetrate

35
Q

How does Helicobacter lead to the development of stomach ulcers?

A

As immune cells attempt to penetrate the mucus lining and die, they release superoxide radicals that destroy stomach cells. This can lead to chronic gastritis and ulcers.

36
Q

How does Helicobacter infection lead to gastric cancer?

A

chronic gastritis leads to intestinal metaplasia then malignant change. Typically MALT lymphomas

37
Q

How is Helicobacter transmitted?

A

Orally via fecally contaminated food and water

Oral contact after traveling from the stomach to mouth from gasto-esophageal reflux

38
Q

What is the clinical appearance of Helicobacter infection?

A

recurrent upper abdominal pain frequently accompanied by GI bleeding

39
Q

What are the 5 techniques for diagnosis of Helicobacter infection?

A
  1. Radiolabeled urea test (Breath Test)
  2. Stool culture with a rapid urease test
  3. Seroconversion
  4. PCR from stool or dental scrapings
  5. Endoscopy followed by histology of the biopsy is definitive
40
Q

Describe the Radiolabed urea test (Breath Test)

A

The patient swallows a capsule containing 1 micro-Curie of C14 urea. If the urea is cleaved by urease the C14 is then released as aerosol and can by detected in the patient’s breath

41
Q

How is Helicobacter treated?

A

A variety of antibiotics are effective and are supplemented with bismuth salts.
Antibiotics are contraindicated for asymptomatic individuals

M1 Micro Quiz 2 (12 decks)

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