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Unit 1 ID+LC > Enteric Bacteria I+II > Flashcards

Enteric Bacteria I+II Flashcards

1
Q

Noninvasive bacteria

A
  1. V. Cholerae
  2. ETEC
  3. EPEC
  4. EHEC

*all ecoli other than EIEC

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2
Q

Invasive bacteria

A
  1. Shigella
  2. EIEC (enteroinvasive e.coli)
  3. Salmonella
  4. Yersinia
  5. Campylobacter
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3
Q

Sources of enteric pathogens

A
  1. vegetables
  2. beef
  3. milk
  4. eggs
  5. poultry
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4
Q

Which enteric bacteria infxns peak in the summer? Winter?

A

Summer:

  1. campylobacter
    - heat tolerant
  2. salmonella
  3. E. coli

Winter:
Yersinia

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5
Q

O157 is located where in e.coli?

A

present in flagellum

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6
Q

Pili are used for adhesion, what 2 special properties aid to this?

A

inhibits competition

tropism

  • tissue of host aides growth
  • by hanging on better, can use host to advantage
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7
Q

Shellfish

A

V. cholera

  • estuarine and marine environments
  • eat shellfish –> now you poop and spread in household if poor sanitation
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8
Q

Virulence factors of V. cholera

A

Colonization: TCP co-regulated pilus

Enterotoxin: cholera toxin

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9
Q

toxic part of LPS

A

Lipid A

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10
Q

Pathogenicity islands

A

specific regions of DNA found only in chromosomes of pathogenic strains encode virulence factors

  • ie: invasion genes, or toxins
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11
Q

Which is primarily toxigenic and which is primarily invasive?
V. Cholerae
Salmonella

A

Toxigenic: V. cholerae

Invasive: salmonlella

*note that shigella is both

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12
Q

Cholera causes profuse watery diarrhea using an ______. How long does it incubate?

A

enterotoxin
- an exotoxin that acts at intestines

*they incubate and prod. this over 2-5 days.

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13
Q

Does cholera cause:
vomiting?
fever?
abrupt or slow onset diarrhea?

A

Some vomiting
No fever
Abrupt onset diarrhea

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14
Q

Fxn of A-B type toxin of cholera

A

B subunit binds cell surface receptors (ganglioside GM1)

A subunit enters the cell cytoplasm and activates Gs –> adenylate cyclase –> cAMP

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15
Q

Heat-labile enterotoxin vs

Heat-stable enterotoxin

A

Heat labile: activates cAMP

Heat stable:
activates cGMP

*eL Agua
de
San Gabriel

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16
Q

Organisms with type III secretion systems

A

EPEC
Shigella
Salmonella
Yersinia

*secretes translocated-intimin receptor, allowing for attachment and effacement lesions –>
microvilli destruction –>
interferes with absorption

17
Q

antibiotics recommended for EHEC?

A

No

*also not recomm. for travelers diarrhea

18
Q

difference between shiga toxin and shiga like toxin

A

They are same:

Stx and SLT: Inactivates 60s by removing adenine from rRNA
- binds to sphingolipids of enterocytes and renal endothelial cells

  • only shigella is invasive
19
Q

Major initial targets of entry for invasive pathogens

A

Intestinal epithelial M cells:

- antigen-sampling cells that overly the lymphoid follicles of the gut

20
Q

Which type of Shigella makes Shiga toxin?

A

Only S. dysenteriae Type I

- causes epidemic dysentery

21
Q

Transmission of shigella

A

4 F’s

  1. Food
  2. Fingers
  3. Feces
  4. Flies
22
Q

First and second leading cause of bacterial gastroenteritis

A
  1. Campylobacter

2. Salmonella

23
Q

How long after ingestion does Salmonella induced gastroenteritis present?

A

24-48 hours after ingestion.

24
Q

Is N/V present in salmonella and shigella infxns?

A

Salmonella enteriditis only
- followed by chills, fever, cramps, watery diarrhea

  • self limiting, do not require ab tx
  • tx w/ S. typhi for tyhoid fever.
25
Q

Yersinia enterocoliticia affects which part of the intestines?

A

Terminal ileum

- pseudoappendicitis

26
Q

Organisms that can cause Reiters syndrome

A
  1. Yersinia
  2. Campylobacter

*commonly occurs in HLA B27 indiv.

27
Q

Complications of Campylobacter

A
  1. Guillain-Barre syndrome
    - ab response against O antigen –> cross react with sphingomyelin –> demyelinates nerves
  2. Reiters syndrome
    - autoimmune reactive arthropathy
28
Q

Treatment for campylobacter is usually fluid replacement, what about when it is severe?

A

Erythromycin or quinolones

29
Q

The most common hu bacterial pathogen

A

H. pylori

- primarily in gastric mucosa

30
Q

Virulence factors of H. pylori

A
  1. Highly motile
    - reach less acidic environment of gastric epithelium
  2. Powerful urease production
    - makes NH3 –> raises pH
  3. Has pathogenicity islands encoding virulence genes
31
Q

When are H. pylori infxns typically acquired?

A

In childhood

32
Q

Gold std of diagnosing H. pylori

A

histological examination of multiple biopsies

followed by culture and isolation of organism

33
Q

tx for H. pylori

A 
triple therapy
1. PPI
2. BIsmuth
3. Tetracycline (helidac)
for 14 days
34
Q

Which organisms have NADPH activity?

A
  1. Listeria
    - NADPH oxidase cannot be assembled to make O2 –> superoxide –> ROS
    and it lyses and escapes the phagosome
  2. Legionella
    - inhibits mobilization of cytosolic components of NADPH oxidase to membrane
  3. Salmonella
    - uses superoxide dismutase and catalase to detoxify ROS

Unit 1 ID+LC (32 decks)

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