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Bacteriology F > Helicobacter Pylori > Flashcards

Helicobacter Pylori Flashcards

1
Q

How helicobacter pyori are transmitted?

A

By ingestion of food or water

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2
Q

What is the clinical presentation?

A

Chronic inflammatory gastritis = duodenal ulcer

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3
Q

What are their virulence factors?

A

Urease, motility, adherence factors, heat labile cytotoxin, gastric mucin protease, hemolysin, lipopolysaccharides

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4
Q

What’s the importance of the adherence factors?

A

For colonization

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5
Q

Which 2 different products are coded by the bacterial chromosome?

A

One product has a cytotoxic activity, the other has a vacuolating activity of glands, leading to their atrophy

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6
Q

What’s the importance of the gastric mucin protease?

A

To buffer the pH of the gastric mucin

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7
Q

What’s the function of hemolysins?

A

Break down RBCs

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8
Q

What is the optimal pH? Which part of the stomach has this pH?

A

Their optimal pH is 7

The mucosa of the stomach is the area of optimal growth of H. pylori

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9
Q

What is the site of infection during the acute stage? Where bacteria colonize?

A

The gastric antrum
Bacteria are present in the mucus overlying the mucosa. Colonization extends to the gastric glands but the mucosa isn’t invaded by bacteria

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10
Q

What is the outcome of the acute stage?

A

There is a superficial active gastritis infiltrated with inflammatory cells and PMN

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11
Q

What does the hemolysin?

A

It breaks the hemoglobin releasing hemin

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12
Q

How the medium become more alkaline and protecting the bacteria?

A

Ammonia by urease activity covers the bacteria to make the medium more alkaline, along with the gastric mucin protease, this creates a buffering, protecting the bacteria.

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13
Q

What are the symptoms of the acute stage?

A

Acute achlorhydric gastritis, nausea, abdominal pain, flatulence and bad breath because of the ammonia

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14
Q

When there is a progression to chronic gastritis and atrophic gastritis?

A

When achlorhydric gastritis stays for a year even after recovery

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15
Q

Which virulence factors are associated with the bacteria in peptic ulceration during the chronic stage?

A

Vac A (vacuoating protein) and Cag A (cytotoxicity associated protein)

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16
Q

What can influence the outcome of infection during this stage?

A

Host factors like age (when age increases infection increases), how many times we have been infected and if we had developed Ab

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17
Q

Where are present genes for Vac A and Cag A?

A

on the pathogenicity island of H. pylori.

18
Q

Where the bacteria invades? What is the outcome?

A

To lower layers

There will be atrophic gastritis

19
Q

What will happen if individuals don’t take the proper treatment?

A

Manifestations would last longer, especially abdominal pain and achlorhydric gastritis

20
Q

Where bacteria invades during gastric cancer?

A

Bacteria are no more between the mucus layer and the mucosa, they invade the mucosa layer

21
Q

What causes the formation of cancer?

A

Bacteria will multiply for a short period, they direct the cells causing them to replicate

22
Q

Why antibiotics or no longer effective in this period?

A

Since bacteria will disappear after that cancer is established

23
Q

Which type of cancer we will have?

A

MALT lymphoma

24
Q

What’s the cure when individuals reach the stage of cancer?

A

Once cancer state is reached there is no longer cure

25
Q

What is done to make the invasive tests?

A

A biopsy is taken from the pyloric end of the stomach or the surrounding by 5 cm. We use a part of the biopsy for each test

26
Q

For which tests the biopsy is used?

A

Histopathology and microscopy
Culture
Biopsy urease test

27
Q

What is the importance of histopathology even when bacteria can’t be found?

A

It allows us to see the tissue changes during carcinoma

28
Q

On which medium H. pylori can grow?

A

On blood agar plate

29
Q

What are the results of the oxidase and catalase tests?

A

Oxidase positive and catalase positive

30
Q

Are they gram negative or positive?

What is their shape?

A

They are gram-negative spiral bacteria

31
Q

Where biopsy is put in the biopsy urease test?

A

A piece of biopsy is put into urea with an indicator

32
Q

What indicates the presence of urease?

A

If there is a pH change, there was production of ammonia, so there is urease

33
Q

Why biopsy urease test is better than culture and histopathology?

A

Since it is a very quick method that gives results within 2 hours

34
Q

Which one are non-invasive tests?

A

Serology
Urea breath test
Fecal antigen test
PCR

35
Q

Which test is used in serology? Which antibodies are detected?

A

ELISA to detect certain Ab (IgM, IgG, IgA) against certain antigens

36
Q

What is the procedure of the urea breath test?

What happens if H. pylori is present?

A

The patient swallows in a capsule containing an isotope of carbon C13 or C14
If H. pylori is present, the isotope will be in the exhaled CO2 (urea + water + urease —> CO2 + ammonia). For detection, we need a spectrophotometer.

37
Q

What is the danger concerning this test?

A

The danger is that C14 is radioactive

The test is not as easy as the biopsy urease test, though it is not invasive

38
Q

What detects the fecal antigen test?

A

We have kits containing Ab to different Ag to detect H. pylori antigens in fecal specimens.
It gives quick results.

39
Q

Which specimens can be taken for PCR?

A

Saliva, dental plaques, water and fecal specimens

40
Q

Is there production of protective Ab after the first time of infection?

A

No protective Ab after the first time of infection

41
Q

When protective Ab are produced?

At which age individuals become protected?

A

The second time of infection

At the age of 60, enough Ab are produced so individuals are protected. It is an additive effect.

42
Q

What’s the antibiotic treatment?

Is there any vaccine?

A

A combination of 3 drugs for at least one week: omeprazole (which is a proton lowering pump inhibitor, increases the activity of the 2 other antibiotics, it is not an antibiotic but a drug), Clarithromycin and metronidazole
No vaccine

Bacteriology F (16 decks)

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