Bacterial infection of GI3 Flashcards
Vibrio species like Vibrio cholera and parahaemolyticus
type, shape, oxygen, where live, pH and temps, what do they require for growth
- gram neg
- comma, curved shaped
- facultative anaerobes
- free living in water
- broad range of growth -temp/pH (susceptive to stomach acid)
- require sodium for growth
Vibrio cholera
- symptoms
- incubation
- duration
- how much diarrhea
- how does it spread
- inflammatory?
- asymptomatic to severe watery diarrhea
- 2-3 day incubation
- seven day duration
- 250 mL/kg rate of mucus, electrolyte and water-filled diarrhea
- spreads via contaminated water
- No
what’s important about immunity in regard to V. cholerae
- we can become immune to the particular O antigen type we were effected by but
- if bacteria use a different O antigen type then we are screwed!
what’s different in classic cholera biotype vs El Tor biotype
El tor is the current strain (7) that is more resilient and has a longer duration
pathogenesis of cholera toxin
- uses toxin co-regulated pilus to adherence to intestinal epithelial cells
- uses AB TOXIN to activate adenylate cyclase to increase cAMP and cause massive efflux of electrolytes and water with NO SIGNIFICANT CELL DAMAGE
how are Vibrio cholera diagnosed? Treatment?
- culture
- treat- rehydration-IV/Oral and without rehydration, mortality is 90%
Vibrio parahaemolyticus
symptoms
what causes V. parahaemolyticus
- symptoms- watery diarrhea TO BLOODY DIARRHEA, nausea, vomiting, abdominal cramps, low grade fever
- virulence is Kanagawa hemolysin- induces chloride secretion thus watery diarrhea
what is vibrio parahaemolyticus associated with eating
inflammatory?
treatment and prevention?
- shellfish and other seafood
- yes
- treatment- self limiting
- prevention- proper cooking of shellfish
Yersinia enterocolitica type of bacteria found in? symptoms? Inflammatory?
- gram neg coccobacilli
- found in contaminated water and food (improperly cooked pork)
- symptoms? FEVER, abdominal cramps and watery to bloody diarrhea
- last 1-2 wks
- yes
mechanism of Yersinia entercolitica
- not well understood but invades M cells in the terminal ileum like salmonella but invades via a different mechanism
- involves T3SS and injection of Yops (Yersinia outer proteins)
- products heat stable enterotoxin
diagnosis and treatment of Yersinia entercolitica
-diagnosis via culture of stool
treatment- self limiting
Clostridium difficile (C. diff)
type-
inflammatory?
symptoms
-gram pos anaerobe
-non invasive
-spore forming
-emerging nosocomial pathogen
-inflammation
symptoms-
1) asymptomatic,
2) CDAD (clostridium difficile associated diarrhea)
3) pseudomembrane colitis
4) fulminant colitis with toxic megacolon -which cause plaques on colon that may have to be removed
how does C diff work?
- Toxin AB causes damage to epithelial mucosa and causes host cell cytoskeleton to be damaged = BLOODY diarrhea
- this occurs when a pt is hospitalized and given many broad spectrum antibiotics that change the gut flora
- some hospital emplyees could have C diff on hands and touch them and they get c diff
- if immunosuppressed enough, get CDAD
diagnosis and treatment and prevention of C. diff
diagnosis- toxin in stool and culture is not helpful b/c it’s part of our normal biota
treatment- oral vanco and metronidazole
prevention- fecal transplant (EWW)
Enterohemorrhagic e. coli (EHEC) type reservoirs transmitted via inflammatory? body part?
- gram negative, facultative anaerobe
- animals like cattle
- transmitted via HAMBURGERS (eHec) and vegetables (washed with water from streams)
- yes
- large intestine
what disease does EHEC cause
- hemorrhagic colitis -bloody diarrhea
- no fever, marked ab pain and tenderness
- sequelae-*hemolytic uremic syndrome (HUS)- anemia and kidney failure
how does EHEC work?
- attaches and effaces lesion like EPEC HOWEVER:
- toxin like shiga toxin (verotoxin)- blocks translation by cleaving part of 60S subunit of the ribosome
- > attaches to brush border of intestinal mucosa, produces verotoxin that destroys microvilli, verotoxin enters blood causing vascular endothelial damage and increased plt aggregation, plt-fibrin thrombi form causing ischemic damage to colon, kidneys and other tissues =hemorrhagic colitis and hemolytic uremic syndrome (kidney disease) via attaching to GB3 kidney receptors that cows DONT have (so don’t get HUS)
diagnosis, treatment and prevention of EHEC?
-diagnosis- presumptive- bloody diarrhea WITHOUT fever, culture, PCR (stx gene that encodes the toxin)rapid test
treat- supportive, antibiotics not helpful and maybe hurtful because antibiotics cause bacterial cell damage and initiates a lysogenic phage to start working to get a lytic cycle going which leads to toxin production and increased HUS rate
prevention- cook raw hamburgers and raw vegis
Shigella spp Type? inflammatory? body part? reservoir? infectious dose how spreads?
- intracellular gram neg rod- anaerobe
- inflammatory
- large intestine effected
- res- only humans
- inf dose- very LOW (<10 organisms)
- poor sanitary infrastructure, crowded healthcare systems and DAYCARE CENTERS
where is shigella soneii found
s. flexneri
s. dysentarie
soneii- developed countries
flexneri- developing countries (in the middle-flexible)
dysentarie- underdeveloped countries tropical countries- worst
how long post ingestion does shigella toxin have effects?
how long does it last
symptoms
-1-3 days
-last 2-5 days post symptoms
-symptoms are strain specific
soneii = fever, malaise, WATERY diarrhea
flexerni and dysentarie- cause DYSENTERY- fever, malaise, watery diarrhea, cramps, bloody and pus filled stools, TENESMUS (NEED TO CONSTANTLY DEFECATE )
S. dysenteriae- POTENTIAL for hemolytic uremic syndrome (HUS)
pathogenesis of Shigella
acid resistant
1) -adheres selectively to and pass thru M cells
-phagocytosis by macrophages
-rapid escape from phagosome
-rapid induction of macrophage apoptosis = infection
OR
2)enter via another mech to get into M calls and then
- they interact with basolateral portion of enterocytes (small intestine)
-induce uptake via type 3 secretion system- injection of Ipa proteins and cause cytoskeletal rearrangement
-lysis of endocytic vacuole -unknown mech
-jump to neighboring cells via actin polymerization at a pole (evades host defense)- basically gets motile
-ulcers form
-diarrhea via inflammation
-toxin is shiga toxin that binds gb3 receptors and inhibits translation to cause cell death (glomerular endothelial cells rich in gb3 so get HUS)
diagnosis and treatment of shigella
diagnosis-culture of stool, serological test
treatment- rehydration, antibiotic treatment- ampicillin resistance is common, choice dependent on susceptibility profile
prevention- no vaccine, improve sanitation and hygiene
NOTE: INFECTION DOES NOT CONFER IMMUNITY
Enteroinvasive E. coli
mech:
-very uncommon
mechanism same as shiga-toxin but no shiga toxin so no HUS
appears that E. coli obtained pathogenicity island from shigella spp via horizontal transfer
