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Unit 3 Micro and Immunology > Spirochetes and Vibrios > Flashcards

Spirochetes and Vibrios Flashcards

1
Q

How are spirochetes typically transmitted?

A

wide variety of methods

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2
Q

What is the primary virulence factor of spirochetes?

A

immune evasion

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3
Q

Which crosses into the blood stream more readily, Mycobacteria or Spirochetes?

A

Spirochetes, they do not need to establish a primary infection first. They also cross easily into the blood brain barrier

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4
Q

Can spirophetes be visualsed with a microscope?

A

Typically no, which makes lab diagnosis tricky

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5
Q

What is a Jarisch-Herxheimer reaction?

A

It is a spirochete reaction to treatment in which an individual developes flue like symptoms 24 hours after treatment. The reason for this reaction is unknown. The dead bacteria are possibly more virulent than the live ones.

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6
Q

How do spirochete diseases usually present?

A

In phases

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7
Q

What bacteria causes syphillis?

A

Treponema pallidum

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8
Q

What are the lab properties of T. pallidum?

A

1- Slow growing, cannot be cultured
2- too small to gram stain
3- Have “corkscrew” flagella

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9
Q

What type of cells does T. pallidum infect?

A

epithelium of small blood vessels (allows it to pass easily into the blood)

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10
Q

How is T. pallidum transmitted?

A

Usually sexual contact or transplacentally

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11
Q

What are the phases of a syphillis infection?

A

1- Primary Syphillis
2- Seconday Syphillis
3- Tertiary syphillis or latency

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12
Q

What is the main symptom of primary syphillis?

A

a cancre forms at the initial site of infectio and intiates bacteremia

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13
Q

What is the main symptom of secondary syphillis?

A

mucoutaenous lesions of various types, systemic symptoms and high antibody titres

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14
Q

After secondary syphillis what can happen?

A

1- resoultion
2- latency
3- tertiary syphillis

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15
Q

What are the three types of tertiary syphillis?

A

1- Gummatous syhpillis
2- Cardiovascular syphillis
3- Neurosyphillis

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16
Q

What is the main symptom of gummatous syphillis?

A

granulommas wuth rubbery necrotic center

17
Q

What is the main symptom of carviovascular syphillis?

A

aneurysm of the ascending aorta

18
Q

What is the hallmark sign of neurosyphillis?

A

Argyll-roberston pupil

19
Q

If a baby is born with congenital syphillis what are the typically outcomes?

A

stillbirth and many fetal abnormalities

20
Q

What agent causes lyme disease?

A

B. burgdorferi

21
Q

Can B. burgdorferi be visualized by microscope?

A

Yes, silver stain

22
Q

What is the vector of B. burgdorferi?

A

Tick

23
Q

About 6 months after infection with B. burgdorferi, what are the symptoms?

A

rash, flue like, lymphadenopathy, anti-spirochete and auto antibodies are raised

24
Q

What are the symptoms about 1 year after an infection with B. burgdorferi?

A

immune and neurological issues arise

25
Q

What are the symtoms of chronic lyme disease?

A

arthritis, encephalopathy, fibromyalgia, bells palsy, and aseptic memingitis

26
Q

How is lyme disease usually diagnosed?

A

Urine tests in pipeline, but for now it is serology and ELISA

27
Q

What are the typical lab properties of vibrios?

A

Gram -, curved bacteria that are also halophiles

28
Q

What is the primary route of intection for vibrios?

A

fecal-oral

29
Q

Is V. cholerae an obligate aerobe or a facultative anaerobe?

A

both

30
Q

What is the pathogenesis of V. cholerae?

A

1- Transmitted via fecal-oral route
2- surviving bacteria reach the small intestine
3- secrete mucinase to clear the brush boarder where they attach and colonize
4- secrete toxin

31
Q

What are the major causes of death due to V. cholerae

A

The bacteria is self limiting. So people die of dehydration and electrolyte imbalance (intersitital dehydration)

32
Q

What is the structure of the cholera toxin?

A

A and B subunit structure

33
Q

What is the mechanism of the cholera toxin?

A

B subunit binds the GM1 receptor on the intestinal lining and causes the loss of water and ions. The absorption via microvilli is blocked.

34
Q

What are the lab properties of H. pylori?

A

Curved, gram - rods that are urease +

35
Q

What is the pathogenesis of H, pylori?

A

1- attachment to mucous-secreting cells of the stomach with flagella
2- break down urea in stomach into ammonia which neutralies the pH of hte stomach

36
Q

How is H. pylori diagnosed?

A

1- urea breath test

2- antigen in stool

37
Q

How are spirocetes treated typically?

A

tetracycline

Unit 3 Micro and Immunology (25 decks)

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