GI disease Flashcards
(22 cards)
What are the two options for GI bacterial disease
either toxin-mediated or organism-mediated
describe the presentation and cause of toxin-mediated foodborne disease
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.
What are two common organisms to suspect of toxin-mediated foodborne disease
Staph aureus and bacillus cereus
What often causes heartburn
H. pylori
how is h. pylori spread
fecal oral
How does it create it’s survivable niche
it secretes urease to increase the pH of its environment and allow it to survive
What is a virulence factor for the H. pylori
CagA. It is injected into cells causing inflammation
Decribe the course of H. Pylori and the sequelae
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)
What are the pathogens that cause dysentery, leukocytosis, and PMN’s in stool
C. difficile, STEC, salmonella, shigella, C. jejuni, Y. enterocolitica
What are the pathogens that cause diarrhea and fever
C. difficile, salmonella, shigella, C. jejuni, and yersinia enterocolitica. viral diarrhea (sometimes). STEC (sometimes
What never causes fevery diarrhea
ETEC
Describe the pathogenesis of C. difficile
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
describe the pathogenesis of STEC
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.
Describe the mechanism of EHEC adhesion
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
Describe the laboratory testing for EHEC
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
How do the virulence factors of STX-1/2 get transferred
by bacteriophages.
What will an antibiotic do to STEC
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
how does Salmonella infect and invade
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).
What is the mechanism of Salmonella invasion
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
What does the lactose + pH indicator on a MacConkey say
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
What is the most common cause of traveler’s diarrhea
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
For ETEC and cholera what is the mechanism
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
