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MICROBIOLOGY II > Lecture 7 - Campy And Helicobacter > Flashcards

Lecture 7 - Campy And Helicobacter Flashcards

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Biology 101 flashcards
1
Q

Describe key feature of campy group

A
  • gram negative
  • Motile
  • spirilla
  • microaerophilic (need approx 5% of oxygen) - small amounts
  • oxidase positive
  • catalase positive
  • urease negative
  • polar flagella
  • Aw >0.98 high water activity needmoist environment
  • unusual optimum for growth temp (hence called thermophile due to 42deg) optimum 37 (human) & 42 deg (chicken and probs other poultry)
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2
Q

What type of flagella does it have

A

Amphitricious - flagella either end

Slight spiral curved rod

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3
Q

What was campy first described as

A

Vibrio - bent rod (common shape - vibrio cholera)

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4
Q

Thought to be vetinary disease until what year and why

A

1946 - breakout in prison in Illinois jail - eat same food track disease - unpasteurised milk found campy

ZOONOSIS transmission proved

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5
Q

What is a type strain

A

Organism that represents all general features you’d expect an organism to have.
Campy fetus

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6
Q

Name 5 KEY species in campy enteropathogenic group

A

Jejuni - poultry
Coli - associated pork
Lari - seagulls and other birds - faeces in wind.
Upsaliensis and helveticus in pets particularly kittens and puppies (diarhoel disease) - interact with pet

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7
Q

What are the microaerophilic conditions to grow campy

A

5% O2
10% CO2
85% N2

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8
Q

What temp will campy not grow below

A

25 deg

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9
Q

What is a fastidious organism

A

Need a lot of love to grow

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10
Q

What bacteria is only one to be able to hydrolyse hippurate and what happens

A

C. Jejuni

Glycine formed (and benzoic acid) and glycine react with Ninhydrin and blue colour occur

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11
Q

What does VNC stand for

A

Viable but non culturable

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12
Q

What other organisms can VNC occur

A

Ecoli, pseudo, vib

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13
Q

What morphology does campy form when oxygen levels rise

A

Form coccoid

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14
Q

What stains were used to prove VNC

A

Cyto 9 - GREEN. go in live cells but some cant be cultured.
Propidium iodide - RED. in dead cells. In live cells membrane potential keep it out of cell but when dead lose this and overtake green

Unlike vib and pseudo cannot get campy back from coccoid VNC

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15
Q

Where does campy affect

A

GI pathogen

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16
Q

Describe pathogenesis of camp

A

Lots of pus
Mucus lining overlay gut endothelial cells
Use spiral morphology to corkscrew through (NOT FLAGELLA)
Anchor flagella band rotate spiral body through mucus lining of gut
CDT toxin increase tight junction between cells allow to get through easier

CAMPY CAN GO INTO CELL.
Once campy in cell directly interact with nucleus bring about interleukins which stimulate neutrophil, DC and macs - early immune response

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17
Q

What does CDT stand for

A

Cytolethal distending toxin

Increase tight junctions between cells. Get through easier

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18
Q

In what animal does campy live asymptomatically

A

Poultry - good carrier

Held in mucus lining

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19
Q

Is campy more sporadic or outbreaks

A

Sporadic
Low secondary transmission
Not in form to pass on to someone else in faeces

20
Q

What percentage of chick tested positive and how many pieces does this equate to

A

76%

Every 8 pieces of chicken we touch is infected

21
Q

What is tested for campy with chickens

A

Neck skins
Packaging
Skin/meat

22
Q

What is a campy infection called and what does it cause

A

Campylobacteriosis and cause acute enteritis

23
Q

Describe the campylobacteriosis infection

A

Last 2-7 days
Onset after 2-5 days feel unwell
Affect children & young adults

24
Q

What is infectious dose of campy

A

500- 10^9

25
Q

What is predicted cases of campy per year and how many die

A

280,000 and 110 deaths

26
Q

Why does demyolinaion occur in Guillain Barré syndrome and how frequently does this disease arise due to campy

A

1 in 1000-3000

Antibodies raised agains LPS cross react with myelin sheath on neurones - demyelination. Body cannot move impulse so lead to temporary paralysis

27
Q

What agar is used and why

A

Blood agar or CCDA (charcoal based medium ) to bind up O2

Selective supplements - suppress other organisms (may use faecal sample -have lots of bacteria)

28
Q

What are the antibiotics used in agar

A

Vancomycin
Polymixin B
Trimethoprim

29
Q

What temp is it incubated at

A

42 deg

30
Q

What is used to get co2 environment

A

Gas jars and gas generation pouches - rip open pouch and put lid on.

31
Q

Why is campy called self limiting infection hence supportive treatment

A

Once been ill tend to get better

32
Q

What treatments are available for campy

A

Rehydration
Ciprofloxacin but not that effective
Becoming massively resistant to antibiotics due to poultry industry using them

33
Q

For helicobacter who conducted stomach ulcer biopsy to discover helicobacter (spiral bacillus in 60%) of ulcer biopsy patients

A

Warren and marshall 1982

34
Q

Why did warren and Mitchell achieve a nobel prize in 2005

A

Drank culture of helicobacter pylori, isolate organism, prove it is there, take antibiotics and show it disappeared

35
Q

What two tissue trophisms does helicobacter have

A

1- Liver e.g. H.hepaticus
2- Gut - H. Pylori

Can lead to hepatic and gastric cancer respectively (not organisms stated)

36
Q

What differs helicobacter to campylobacter

A

Helicobacter is UREASE POSITIVE

Metabolise urea to get ammonia to neutralise low pH of stomach

37
Q

Helicobacter has 7 flagella out one side. What type of flagella is this

A

Lophotricious

38
Q

Describe overview of pathogenicity of helicobacter

A

Gastric fluid low pH protected from epithelial cells by mucus layer
Helicobacter bind epithelial cells use urease to create light area (use as protective bubble)
Means pepsin CAN get to stomach and burn cells - like continuous heartburn

Continuous lead to cancer - constant replication can lead to errors

39
Q

Helicobacter 3 toxin (cagA, HP-NAP, VacA, ROI) pathogenicity process

A

1- flagella propel pylori to epithelial cells stick via adhesins
2- pylori inject cagA via type IV secretion in host cell and release other toxins such as H.pylori neutrophil activating protein (HP-NAP) and VacA
3- VacA form large vacuoles and alter tight junctions
4- HP-NAP cross epithelial lining and recruit neutrophils and monocytes and cause damage by releasing reactive oxygen intermediates ROI’s
5- Cag A cause alteration of cytoskeleton, pedestal formation and signal to nucleus to release inflammatory lymphokines - amplify inflammation with recruitment of lymphocytes and further induce ROI release
6- this leads to acid permeation

40
Q

What is type IV secretion analogous to

A

Bacterial conjugation method

41
Q

What is helicobacter route of transmission

A

Oral-oral, faecal -oral

(Toothbrushes, if one person in family has genotype typical people in family also have it

42
Q

What percentage of world is infected

A

50%

43
Q

What agar is used for helicobacter (same antibiotic supplements) BUT RARELY USED

A

Brucella or Columbia

44
Q

What methods used to be used to detect helicobacter

A

Isolation on agar
Biopsy - but invasive - false negative as stomach huge.
Urea Breath test - use C13 or C14 (carbon) to test for urease enzyme - detect radioactive co2 breathed out.

45
Q

What method is used NOW to detect for helicobacter

A

Faecal antigen tests
95-98% sensitive
Take faecal sample and test. Non invasive

46
Q

How to treat helicobacter

A

Treat with proton pump inhibitor (reduce acid production)
Take a while - can be up to months - some people stop.
1- metronidazole - Not nice to be on for long time
2- amoxicillin
3- tetracycline or Clarithromyocinin (10% failure due to resistance)

MICROBIOLOGY II (9 decks)

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