Enteric Bacterial Infections (NON-Inflammatory): Cross, Ryan Flashcards
List the 8 bugs causing Non-inflammatory diarrhea.
ETEC EPEC EAEC Vibrio cholerae Vibrio parahemolyticus Vibrio vulnificus S. aureus Bacillus cereus
ETEC causes:
How long does it last?
Traveler’s diarrhea! Remember bc of ‘T’ in ETEC
1-5 days
Discuss the pathogenesis of ETEC.
2 toxins:
Heat labile toxin- similar to cholera toxin. Stimulates adenylate cyclase–> ^ levels of intracellular cAMP–> secretion of Cl- from intestinal crypt cells and decreased reabsorption of NaCl at villous tips–> water follows–> diarrhea
Heat stable toxin- Same thing! stimulates enterocyte cGMP–> same course of events.
Pathogenesis of EPEC.
What age group does it effect?
T3SS–> bact. attaches to host cell–> effacement of mucosa–> profuse, watery diarrhea, vomiting, dehydration.
Affects babies.
What does EAEC do?
Causes diarrhea in kids and adults. That’s all we know.
Describe some other diseases that E. coli causes.
Neonatal meningitis caused by encapsulated strains.
UPEC causes 90% of UTIs
Describe the micro morph of the Vibrio genus.
Main animal reservoirs?
When/where do epidemics occur?
Curved, gram (-) rods w/ polar flagellum.
Marine shellfish
Natural disasters, overcrowding. Usually due to fecal contamination of drinking water.
Name the serogroups responsible for endemic and pandemic cholera.
O1 and O139
Outline the pathogenesis of Vibrio cholerae.
:: Bact. must colonize small intestine and secrete toxin.
:: High infectious dose
:: Bacteria secretes mucinase to break down mucous covering cells and allow adherence to enterocytes.
:: Once adhered, organism multiplies and secretes cholera toxin (AB toxin)
B subunit- binding subunit for binding gangliosides on enterocyte.
A subunit- causes persistent stimulation of adenylate cyclase–> Cl- secretion–> diarrhea
Describe the clinical presentation of Vibrio cholerae.
Incubate 1-3 days
Large volumes of watery diarrhea (up to 20L/day)
Rice water stools (due to consistency and mucus and bact. present in stool)
Vomiting
Dehydration- loss of fluids/electrolytes–> cardiac/renal failure. Acidosis and hypokalemia.
40% die if untreated
Vibrio cholerae.
Dx:
Tx:
Dx: clinical symptoms. Stool culture using MacConkey agar (colorless colonies) or thiosulfate citrate bile sucrose (TCBS), or taurocholate tellurite gelatin agar (TTGA).
Tx: aggressive volume replacement.
Abx as adjuvant tx for pts w/ moderate-severe volume depletion- Tet, eryth, azith, cipro
Vibrio parahemolyticus. Where? Why? Clinical presentation? Dx? Tx?
Japan. Bc they eat so much raw seafood Gulf coast of U.S. in warm months. n/v/d abd. cramps, fever Bacteremia in liver dz Wound infections Dx: culture Tx: volume replacement. Doxy in severe cases.
Vibrio vulnificus.
Clinical presentation?
Dx?
Tx?
Diarrhea
Severe skin and soft tissue infections (think like bullous pemphigoid)
Septicemia in immunocompromised people who ate shellfish containing organism.
Dx: culture
Tx: Doxy + cefataxime or ceftriaxone
Bacillus cereus.
Micro morph and gram stain?
Toxins produced?
Clinical presentation?
Spore-forming gram (+) rods
Diarrheal enterotoxin and emetic toxin
Diarrheal syndrome: Diarrhea that resolves in 2 days
Emetic syndrome: from ingesting toxin cereulide (heat stable). cramps n/v. Diarrhea in 1/3 of people. Onset within 1-5 hrs of ingestion.
Don’t leave starchy foods out for hours!
Describe the toxin produced by S. aureus and its related pathogenesis.
Clinical presentation?
Enterotoxin is heat stable.
Acts as superantigen to stimulate release of IL-1/2.
Symptoms begin within 1-6 hrs of ingestion w/ n/v and abd. cramps.
Fever/diarrhea in a minority
24 hrs or less, but can be longer