16: Diseases Of The GI Tract & CNS Flashcards
Vibrio Cholerae
-gram +/-
-flagella?
-w/ or w/o O2
-Lab identification
Gram negative curved rod
Polar flagella
Facultative anaerobe
Sucrose fermentation (+)
Vibrio cholerae ID50 ?
ID50 is high therefore low virulence
How many serogroups/biotypes identified based on their O antigen
2 groups based on their O antigen
O1 el Tor - major pandemics (outbreak in Haiti)
O139 - have a capsule (SE Asia)
Cholera epidemiology
-found where?
-spread by?
natural habitat is brackish water (sea water + fresh water) and coastal seawater
Spread by contaminated food (seafood) or water
US cases are travel related or shellfish in gulf of Texas and Louisiana
Cholera toxin pathogenesis
Cholera toxin (CT) is a protein exotoxin with an A-B subunit structure:
The A subunit (active subunit) is responsible for enzymatic activity.
The B subunit (binding subunit) consists of five identical units that form a pentamer. This subunit binds to the surface of the host’s intestinal epithelial cells, facilitating the entry of the A subunit.
Binding to the Intestinal Cells:
The B subunit binds to a specific glycolipid receptor on the surface of intestinal epithelial cells called GM1 ganglioside.
Once the B subunit has bound to the GM1 receptor, the entire toxin is internalized into the cell through endocytosis.
Activation of the A Subunit:
After entry into the cell, the A subunit undergoes cleavage into A1 and A2 fragments. The A1 subunit is the active enzymatic portion of the toxin.
The A1 subunit is released into the cytoplasm, where it activates the adenylate cyclase (AC), stimulating cAMP by using ATP.
**efflux of Chloride, sodium, potassium, bicarbonate and Water:
The increase in cAMP causes channels to open, leading to the massive secretion of ions into the intestinal lumen of the gut. Water follows = watery diarrhea
Cholera clinical manifestations
he hallmark of cholera is profuse, watery diarrhea, often described as “rice-water stools” due to its appearance. This diarrhea can lead to rapid and severe dehydration and electrolyte imbalances.
Hypovolemia and Hypotension
Children more at risk of dehydration and can die w/n 12hrs
An adult can lose up to 20 L/day
Cholera diagnosis
Stool culture = TCBS agar
Thiosulfate-citrate-bile-sucrose agar.
On this medium, vibrio cholera usually produces a yellow colony (indicative of the fermentation of sucrose)
Cholera treatment
Rehydration w/ fluids and electrolytes
Azithromycin can reduce duration and severity
Hemorrhagic colitis (EHEC)
-caused by
-most common strain in the U.S
-often referred to as
Caused by a strain of E.coli = EHEC
EnteroHemorrhagic Escherichia coli
O157:H7
Because this strain of E.coli produces a shiga toxin, they are often referred to as STEC (shiga toxin-producing E.coli)
EHEC (Enterohemorrhagic E.coli)
-gram -/+
-toxin
-ID50
-Lab identification
Gram -
Shiga-like toxin
ID50 = low
Lactose & sorbitol, fermentation
H2S
Lactose fermentation = distinguishes E.coli from other enteric pathogens
Sorbitol fermentation = Distinguishes EHEC from other strains of E.coli
H2S = distinguishes E.coli from salmonella
EHEC transmission
O157:H7 is part of the normal gut flora of cattle
This bacteria gets on the beef during the rendering process. Bacteria can be killed w/ heat if it stays on the surface of the meat.
Hamburgers = mixed bacteria w/ meat = must fully cook
Unpasteurized milk, animal contact, and person-to-person
EHEC pathogenesis
One of the hallmark features of EHEC pathogenesis is the production of Shiga toxin (Stx)
intestinal effect
The action of Shiga toxin disrupts the normal function of the intestinal epithelial cells, contributing to inflammation, cell death, and the characteristic bloody diarrhea.
systemic effect
When absorbed into the bloodstream, Shiga toxin can damage endothelial cells in the kidneys, leading to hemolytic uremic syndrome (HUS), a severe complication characterized by glomerular swelling and deposition of fibrin and platelets (kidney damage)
Characterized by hemolytic anemia, acute kidney failure, and thrombosis.
Enterohemorrhagic Escherichia coli (EHEC), also known as Shiga toxin-producing E. coli (STEC), is a pathogenic strain of E. coli that can cause severe gastrointestinal illness, primarily characterized by bloody diarrhea and abdominal cramps. The most notable serotype associated with EHEC infections is E. coli O157
EHEC clinical manifestations
Diarrhea, abdominal pain, vomiting (fever is not prominent, although may occur)
Diarrhea starts out watery then becomes grossly bloody (90%) by day 2/3
Most common in young children
Children = develop HUS
EHEC diagnosis
Sorbitol MacConkey (SMAC) agar contains sorbitol which EHEC strain cannot ferment but others strains of E.coli can
O157:H7 E.coli no fermentation of sorbitol on SMAC media
EHEC treatment
Antibiotics are controversial
They may shorten the length of the illness, but may increase the risk of HUS
Supportive measures
What is the main difference between food infection and food intoxication?
In food infection, live bacteria or pathogens cause illness after being ingested, while in food intoxication, toxins produced by bacteria in food cause illness.
-Do not require the bacteria to be present to cause illness
-Performed toxin is present in food when ingested
-The bacteria are generally killed when food is prepared, but -some toxins are heat stable.
Antibiotics are not warranted
No inflammatory process
Not transmissible from person-to-person
Most common food intoxication in the U.S. is from what bacteria?
What foods is it commonly found?
S.aureus has an Enterotoxin that is heat stable and this toxin stimulates nerves leading to nausea, cramping, mild diarrhea and severe vomiting (diarrhea not a main feature)
-Commonly found in high lipid content food (mayonnaise) and processed meats (high-salt)
-Food that has been left un refrigerated for a few hours
-incubation period is 1 to 6 hours
Bacillus cereus
Gram +/-
Most commonly associated with what food group?
Gram +
Fried rice
**foods that are held at warming temperatures for a long time*
The spores germinate in food and secrete toxins depending on the type of food.
It is an opportunistic pathogen and is most notorious for causing two distinct types of foodborne illnesses: the emetic (vomiting) form and the diarrheal form. Both forms of food poisoning result from the production of enterotoxins by the bacteria.
What are the two types of foodborne illnesses caused by Bacillus cereus?
It is an opportunistic pathogen and is most notorious for causing two distinct types of foodborne illnesses: the emetic (vomiting) form and the diarrheal form. Both forms of food poisoning result from the production of enterotoxins by the bacteria.
What is the incubation period for the emetic form of Bacillus cereus food poisoning?
1 to 6 hours after consuming contaminated food.
What is the incubation period for the emetic form of Bacillus cereus food poisoning?
1 to 6 hours after consuming contaminated food.
While the diarrheal form incubation period is 8-16hrs
What is the main symptom of the emetic form of Bacillus cereus food poisoning?
vomiting, and Nausea, often accompanied by abdominal cramps.
What type of food is commonly associated with the emetic form of Bacillus cereus food poisoning?
Starchy foods like cooked rice, pasta, and noodles.
What type of food is commonly associated with the emetic form of Bacillus cereus food poisoning?
Starchy foods like cooked rice, pasta, and noodles.
What type of food is commonly associated with the emetic form of Bacillus cereus food poisoning?
Starchy foods like cooked rice, pasta, and noodles.
What kind of toxins are produced in the diarrheal form of Bacillus cereus food poisoning?
Heat-labile enterotoxins
The enterotoxin for the emetic form of bacillus cereus is heat stable
What type of foods are typically associated with the diarrheal form of Bacillus cereus food poisoning?
Meat, poultry, vegetables
