export_gi bacteria iii Flashcards
Vibrio features
Gram-negative, facultative anaerobes, curved
Broad temperature and pH range for growth, but susceptible to stomach acid, free living in water
Requires NaCl to grow
Vibrio cholerae range of disease
Asymptomatic to severe watery diarrhea
Vibrio cholerae incubation
2-3 days
Vibrio cholerae immunity
Appears to be O Ag specific
If the O Ag on the LPS on the Vibrio cholerae strain mutates, you lose immunity to that strain
Vibrio cholerae pathogenesis
Toxin co-regulated pilus (TCP)
Cholera toxin
TCP
Adherence of Vibrio cholerae to intestinal epithelial cells
Cholera toxin
AB toxin
Increase cAMP, mass efflux of water
Encoded on CTX-phi (prophage)
Vibrio cholerae diagnosis and treatment
Culture (differential media)
Rehydration therapy
Vibrio parahaemolyticus disease
Explosive watery diarrhea, nausea, vomiting, abdominal cramps
Vibrio parahaemolyticus epidemiology, treatment, and prevention
Raw shellfish
Self-limiting disease
Properly cook shellfish
Yersinia enterocolitica features and symptoms
Gram-negative coccobaccilli
Fever, abdominal cramps, water to bloody diarrhea, can last 1-2 weeks
Yersinia enterocolitica pathogenesis
Poorly understood
Binds to M-cells
Involves T3SS
Produces heat-stable enterotoxin
Clostridium difficile features
Gram-positive aerobe Non-invasive Spore forming nosocomial infection (people may get it from long stretches of taking broad-spectrum antibiotics)
Clostridium difficile disease
Wide range, asymptomatic to diarrhea to colitis to toxic megacolon
What is CDAD?
C. difficile-associated diarrhea
What is pseudomembrane colitis?
Raised, adherent yellow plaques in the colon
Can progress to fulminant colitis
C. diff. pathogenesis
Toxin A and toxin B
Damages the mucosa
Disrupt host cell cytoskeleton = diarrhea
C. diff. diagnosis, treatment, and prevention
Toxin detection in stool
Vancomycin or metronidazole
Culture NOT helpful (can be part of normal microbiota)
Fecal transplant
Enterohemorrhagic E. coli (EHEC) features
Gram-negative, facultative anaerobe, lots of animal reservoirs, generally non-invasive
EHEC disease
Hemorrhagic colitis = bloody diarrhea
Sequelae (hemolytic uremic syndrome)
EHEC pathogenesis
Attaching and effacing lesion (like EPEC)
Produces Shiga-like toxin (verotoxin)
Verotoxin
Cleaves part of the 60S subunit of the ribosome, resulting in cell death
EHEC and the kidneys
Glomeruli are rich in Gb3 (toxin glycolipid receptor) which will bind the verotoxin, resulting in kidney failure
EHEC diagnosis
Bloody diarrhea WITHOUT fever (presumption)
Culture
NAAT (stx genes that encode verotoxin)
EHEC treatment
Supportive therapy
NOT antibiotics - results in increased toxin production, which increases HUS rate
Shigella features
Gram-negative rods, facultative anaerobes, intracellular pathogens
Incredibly acid tolerant (few organisms needed for infection)
humans are only reservoir
Shigella transmission
Fecal-oral route
Shigella incubation period
1-3 days
Disease is self-limiting, resolving within 3-5 days
Shigella soneii disease
Developing countries
Fever, malaise, watery diarrhea
Shigella flexneri disease
Developing countries
Dysentery, fever, malaise, watery diarrhea, abdominal cramps, tenesmus, bloody/purulent excretions
Shigella dysenteriae disease
Underdeveloped countries
Dysentery, fever, malaise, watery diarrhea, abdominal cramps, tenesmus, bloody/purulent excretions
Potential for HUS
Shigella pathogenesis
Adhere to M-cells
T3SS
Escape from phagosome
Macrophage apoptosis
Actin polymerization - spread to neighboring cells
-ulcers form in infected areas
severe inflammation = diarrhea
Shiga toxin (binds Gb3 = kidney damage= hemolytic uermic syndrome
Shiga toxin
Binds to Gb3
Inhibits translation
HUS
Shigella diagnosis and treatment
Culturing and serology
Rehydration and antibiotic therapy
Shigella prevention
No vaccine
Infection does NOT confer immunity
Enteroinvasive E. coli features
Same as Shigella except NO Shiga-toxin
May have obtained pathogenicity island from Shigella via horizontal gene transfer
