GI 1 Flashcards
what GI host defenses can trigger the expression of bacterial virulence factors (2)
1) mucus
2) bile
inflammation of the stomach
gastritis
inflammation of the stomach and intestines
gastroenteritis
frequent loose and fluid filled stools
diarrhea
inflammatory disorder of the GI associated with
- diarrhea with blood and pus
- pain, fever, abdominal cramps
dysentery
dysentery v. diarrhea
dysentery: usually disease of the large intestine
diarrhea: disease of the small intestine
inflammation of the intestines, especially small
enteritis
inflammation of the mucosa of the small and large intestine
enterocolitis
inflammation of the large colon
colitis
inflammatory GI bacteria (7)
1) campylocater jejuni
2) c. difficile
3) EHEC
4) EIEC
5) Shigella spp.
6) vibrio paraheaemolyticus
7) yersinia enterocolitica
more likely to see fecal occult or visible blood
more likely to see fecal leukocytes
inflammatory GI bacteria
bacteria passing through the intestine or adherent to the intestinal epithelium
non-inflammatory GI bacteria
non-inflammatory GI bacteria (4)
1) EPEC
2) ETEC
3) Vibrio cholerae
4) listeria monocytogenes
preformed toxin
1-8 hrs. after ingestion
production of toxin after ingestion
8-16 hr after ingestion
adherence, growth, and virulence factor production
16+ hr after ingestion
- staph. aureus
- bacillus cereus (emetic)
- clostridium botulinum
preformed toxin
1-8 hr after ingestion
- bacillus cereus (diarrheal)
- clostridum perfringens
- clostridium botulinum
production of toxin after ingestion
8-16 hr
- shigella spp.
- salmonella spp.
listeria monocytogenes - EHEC, EPEC, ETEC, EIEC
- campylobacter
- vibrio spp.
16+ hours after ingestion
adherence, growth and virulence factor production
two types of bacterial food poisoning
- preformed toxins in the food
- large numbers of spores ingested, germinate in intestine, produce toxins without colonization or adherence to GI tract
- diarrhea, vomiting or both
- NO FEVER
- 1-8 hrs or 8-16 hrs after ingestion
symptoms of bacterial food poisoning
four bacterial causes of food poisoning
- staph aureus
- clostridium botulinum
- clostridium perfringens
- bacilus cereus
- gram positive cocci in clusters
- not spore forming
- ingestion of a preformed,heat-stable toxin
- severe vomiting, diarrhea, and abdominal pain within 1-8 hrs of consumption
staph. aureus food poisoning
- gram positive rod
- spore forming
- early: vomiting, diarhea, abdominal pain 1-8hr after ingestion if preformed toxin, 8-16 hrs if spores
- late: flaccid paralysis
bacterial food poisoning with clostridum botulinum
MOA botulism toxin
acts at neuromuscular nerve junctions, blocks ach release, thus muscle stimulation is blocked
home-canning
clostridum botulinum
treatment clostridium botulinum
- supportive therapy
- IV anti-toxin administration
complications of clostridium botulinum
lingering weakness, dyspnea, up to 1 year after primary disease
floppy baby syndrome
clostridum botulinum
MOA infant botulism
germination of c. botulinum spores in intestines -> growth -> toxin production
- often when infant ingest honey
when can you feed baby honey?
after 1 year, the permeability of the intestinal mucosa decreases and changes
- gram positive rod
- spore forming
- meat products held at below recommended tempreratures
- onset of diarrhea and abdominal cramps 8-16 h post-ingestion and lasts 24 hr
clostridiym perfringens
etiology of clostridium perfingens
c. perfringens enterotoxin which mediates membrane permeability -> efflux of water
- gram-postive rods, spore forming
- onset of vomiting, nausea and abdominal cramps 1-8 hrs after ingestion of preformed heat stable enterotoxin
emetic form of bacilus cereus
associated with improper storage of cooked rice
bacillus cereus food poisoning
- spores survive cooking -> bac multiply -> produce heat stable enterotoxin
- gram positive rod, spore forming
- onset of diarrhea, nausea and abdominal cramps 8-16 hrs post ingestion
- production of heat liable enterotoxin in intestine
diarrheal form of bacillus cereus food poisoning
gram negative curved rod
- microaerophilic
- ulcers and chronic gastritis
helicobacter pylori
virulence factors of heliobacter pylori
- flagella
- urease
- cytotoxin- vacA
- adhesins
ulcers are caused by stress, smoking and spicy foods
false
gastric ulcers are mostly caused by helicobacter pylori
mechanism of h. pylori ulcers
1- h. pylori penetrates mucous layer attract to hemin and urea
2- h. pylori recruits and activates inflammatory cells and released urease which produces NH3 to neutralize the acid
3- h. pylori cytotoxin and NH3 destroy mucous cells and expose the underlying tissue to stomach acid
diagnosis of h. pylori
radioactive urea breath test
or biopsy
treatment of h. pylori
- antibiotics and proton pump inhibitor
- gram positive rod pairs
- intracellular faculative anaerobe
- cold loving and salt and pH resistant
listeria monocytogenes
large outbreaks concerning ready to eat meats and raw vegetables
listeria monocytogenes
fever
malaise
chills with no obvious focus
bacteremia from listeria monoctogenes in immunocompromised pateient
fever, persistent headache, stiff neck, vomiting and confusion
meningitis and encephalitis from listeria monocytogenes in immunocompromised patient
what should you do if a patient presents with a fever with no obvious infection
blood culture
granulomatosis infantiseptica
pyogenic granulomas distributed all over the body
symptom of neonatal infection with listeria monocytogenes (see 2-3 wks after birth)
MOA of listeria monocytogenes
- adherence and uptake mediated by internalin A
- intenalized into vacuole
- acidification of vacuole triggeres listeriolysisn O to allow escape into cytosol
- replicates in host cell cytoplasm
where besides GI does listeria monocytogenes infect
liver spleen CNS
how does listeria mono. spread?
sheer motility via ActA mediated actin polymerization allows them to push through membranes and spread to blood stream and neighboring cells
cold enrichment selection
also weak B hemolysis and motility test
listeria monocytogenes
treatment listeria mono.
beta lactam or trimethoprim-sulfamethoxazole
