GI disease Flashcards

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1
Q

What are the two options for GI bacterial disease

A

either toxin-mediated or organism-mediated

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2
Q

describe the presentation and cause of toxin-mediated foodborne disease

A

acute onset of nausea and vomiting less than 6 hours after eating contaminated food. the pre-formed toxin is usually already in the food from bacterial food growth

NO fever. Diarrhea is rare.

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3
Q

What are two common organisms to suspect of toxin-mediated foodborne disease

A

Staph aureus and bacillus cereus

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4
Q

What often causes heartburn

A

H. pylori

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5
Q

how is h. pylori spread

A

fecal oral

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6
Q

How does it create it’s survivable niche

A

it secretes urease to increase the pH of its environment and allow it to survive

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7
Q

What is a virulence factor for the H. pylori

A

CagA. It is injected into cells causing inflammation

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8
Q

Decribe the course of H. Pylori and the sequelae

A

h. pylori will cause chronic superficial gastritis (weeks to months). Over the years it can lead to several things: peptic ulcer disease, chronic superficial gastritis, gastric lymphoma, gastric adenocarcinoma (from chronis atrophic gastritis)

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9
Q

What are the pathogens that cause dysentery, leukocytosis, and PMN’s in stool

A

C. difficile, STEC, salmonella, shigella, C. jejuni, Y. enterocolitica

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10
Q

What are the pathogens that cause diarrhea and fever

A

C. difficile, salmonella, shigella, C. jejuni, and yersinia enterocolitica. viral diarrhea (sometimes). STEC (sometimes

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11
Q

What never causes fevery diarrhea

A

ETEC

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12
Q

Describe the pathogenesis of C. difficile

A

fecal-oral spread. The C. dificile will overgrow and realease Toxins A and B. These will inactivate Rho which is an important cytoskeleton protein. this disruption of the cytoskeleton leads to cell apoptosis and inflammation leading to colitis

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13
Q

describe the pathogenesis of STEC

A

beef will get infected with it. This will adhere to the colon. leading to Stx 1/2 (shiga-like toxin) which will depurinate rRNA and inhibit protein synthesis. This leads to local GI inflammation and hemorrhage. Once it breaks through to a systemic ilness, there will be endothelial damage and deposition of immune complex in the kidney leading to hemolytic uremic syndrome.

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14
Q

Describe the mechanism of EHEC adhesion

A

It is a type III secretion system that will inject receptor AND effector proteins. This will rearrange the cytoskeleton to create a pedestal. This is a super-tight adherence. Remember, this does NOT leads to exotoxin injection

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15
Q

Describe the laboratory testing for EHEC

A

look at it on the sorbitol-mackonkey agar which will detect E. coli O157:H7 which does NOT ferment soritol. You can also do an immunoassay for Stx-1 and stx-2 which will detect all serotypes of EHEC

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16
Q

How do the virulence factors of STX-1/2 get transferred

A

by bacteriophages.

17
Q

What will an antibiotic do to STEC

A

It will damage the bacteria leading to release of lytic virus and increased toxin production. ALSO, this will be able to transfer to other E. coli strains. There is a significant serotype diversity among the EHEC

18
Q

how does Salmonella infect and invade

A

It will be passed zoonotically from a bird (only non-typhi salmonella) or from fecal-oral human hosts (S. typhi and paratyphi). It will infect M-cells in the GI mucosa leading to inflammation and diarrhea. If it gets into the blood via the lymphatics, it will cause disseminated disease leading to enteric fever (this really is only S. typhi and S. paratyphi).

19
Q

What is the mechanism of Salmonella invasion

A

It is similar to STEC in that it uses a secretion system that will inject effector proteins. It will lead to cytoskeletal rearrangement and membrane ruffling. Unlike the STEC, though, it will be ENGULFED by the cell leading to uptake

20
Q

What does the lactose + pH indicator on a MacConkey say

A

basically, the E. coli are all lactose fermentors, but salmonella and shigella are not. Therefore, if you have a non-lactose fermenting thing in a person with diarrhea, you know it is one of these

21
Q

What is the most common cause of traveler’s diarrhea

A

ETEC is the most common cause of traveler’s diarrhea. It is usually mid and self-limited. It is spread by fecal-oral.

also, don’t forget V. cholerae. This has a variety of presentation from mild to severe, life-threatening illness. spread fecally oroally. Also can be contracted from coastal water shellfish

22
Q

For ETEC and cholera what is the mechanism

A

Basically, there is growth of the ETEC or cholera in the GI. The toxin created is an A-B toxin which will get into the GI cells and activate cAMP. This leads to increased ion and H2O efflux OUT of the cell into the lumen leading to secretory diarrhea and dehydration