Bacterial infection of GI I Flashcards
Diarrhea
- 3+ loose or liquid stools per day-usually result of probs in small intestine
Gastritis gastroenteritis enteritis enterocolits colitis
Gastritis- inflammation of the stomach
gastroenteritis- inflammation of stomach and intestines-nausea, vomiting, or diarrhea and ab pain
enteritis-inflammation of the intestines; usually small intestine
enterocolits-inflammation of the mucosa of the large and small intestine
colitis- inflammation of the large colon
dysentery
dysentery- inflammatory disorder of GI tract often associated with blood and pus in the feces
pain, fever and abdominal cramps
results usually from prob in LARGE intestine
what should you expect to see in stool that is infected by inflammatory bacteria
- leukocytes and fecal occult (not visible blood) and blood
in what hrs of digestion do performed (already made toxins) toxins work? Toxins produced after ingested? when adhered, grew and then release toxin.
1-8 hr
8-16
16 + hrs
what are the two types of bacterial food poisoning
1) Toxins produced by bacteria BEFORE food consumed
2) large numbers of spores ingested, spores germinate in intestine and vegetative bacteria make toxins- no implied adherence/colonization to GI tract
symptoms of bacterial food poisoning
- diarrhea, vomiting, both
- no fever
four bacteria that cause bacterial food poisoning
s. aureus
c. botulinum
c. perfingens
bacillus cereus
staphylococcus aureus type: spores? how does it cause disease? symptoms inflammation? time pathogenesis treatment
type: Gram pos cocci spores? no how does it cause disease? performed toxin symptoms- severe vomiting, diarrhea, and ab pain inflammation? no time 1-8 hrs post consumption pathogenesis- heat stable treatment-supportive
Clostridium botulinium type: spores? how does it cause disease? symptoms inflammation? time pathogenesis Mechanism
type: gram pos rod
spores? yes
how does it cause disease? botulinium toxin by preformed toxin
symptoms: early- onset of vomit, diarrhea, ab pain (1-8 h post ingestion)/8-16 hrs post late- flaccid paralysis and progressive muscle weakness and respiratory arrest
inflammation? no
time- 1-8/8-16- late
pathogenesis- ingest preformed toxin and large numbers of spores form and germinate the intestine to produce toxin
mechanism- acts as a neuromuscular nerve junction signaling blocker- blocks Ach from binding and muscle stim is blocked
clostridium botulinium found where?
complications of infection
treatment
- found in home canning
- patient survives- lingering weakness and sypnea up to year after primary disease
- treatment- supportive therapy, IV antitoxin administration
floppy baby syndrome
infant botulism
occurs between birth and 6 mo
germination of C. botulinium spores in intestines with toxin production
usually found when infants given honey
milder and lower mortality than adult botulism
clostridium perfringens type: spores? how does it cause disease? symptoms inflammation? time pathogenesis treatment
type: gram pos rod
spores? yes
how does it cause disease? mediated by C. Perfringens enterotoxin (toxins produced in the body)
symptoms? diarrhea and ab cramps 8-16 h post-ingestion and lasts for 24 h
inflammation? NO
time- 8-6 hrs post ingestion
pathogenesis- associated with contaminated meat products/gravies held below recommended temps
treatment- supportive
Bacillus Cereus type: spores? Inflammation? what are the two forms?
type: gram pos rod
spores: yes
inflammation- no
Forms: emetic (vomiting) form and diarrheal form
Diarrheal form of B. cereus implicated food- cause of disease- onset of symptoms- enterotoxin vs heat-
implicated food- meats and vegis
cause of disease-toxin made in intestine
onset of symptoms- 8-16 hrs post ingestion
enterotoxin-heat liable (dies in heat)
emetic form of B. cereus implicated food- cause of disease- onset of symptoms- enterotoxin vs heat-
implicated food- Rice (improperly stored) (cereus sounds like cereal and that is a grain and so is rice)
cause of disease-preformed toxin
onset of symptoms- 15 min-8h
enterotoxin vs heat- heat-stable
-spores survive cooking, bacteria multiply and make heat-stable enterotoxin that is not inactivated upon reheating
treatment for B. cereus
- supportive
Helicobacter pylori
how does it infect
- attracted to chemostatic substances HEMIN AND UREA of the stomach’s epithelium and it’s mucus that lines it
- recruits and inactivates inflammatory cells and also releases urease that cleaves urea, producing NH3 that neutralizes stomach acid in its vicinity
- H pylori cytotoxin and ammonia from urease cause destruction of mucus-producing cells, exposing the underlying connective tissue to stomach acid
Diagnosis and treatment of of H. pylori
type of bacteria and what does it cause
urea breath test or biopsy
antibiotics and proton pump inhibitor- to control acid
gram neg rod
causes stomach ulcers
listeria monocytogenes
type, oxygen and traits
- gram pos
- facultative anaerobe
- key traits: wide growth range *1C-45C
- resistant high salt concentrations
- wide pH range
why would you find listeria monocytogenes in processed food? what type of food would you see it the most?
- processed food often have a lot of salt in them to kill bacteria but listeria monocytogenes is resilient to high salt conc.
- food- processed meat and raw vegis
symptoms of listeria monoytogenes for
healthy people
immunocompromised
pregnant women
healthy adults- usually asymptomatic but may have fever, nausea, diarrhea
immunocompromised pt- Bacteremia (fever, chills and malaise)
or Meningitis and encephalitis- fever, headache, stiff neck, vomiting and confusion
pregs- fever with no obvious infection =blood culture- may tx to neonate
20-50% mortality rate and significant neuro sequelae in survivors
what occurs if a neonate is infected by listeria monocytogenes
- granulamatosis infantiseptica- pyogenic granulomas distributed over the whole body
- meningitis
- encephalitis
- pre mature birth, abortion or still-birth
how does listeria monogenes work
-adherence and induced uptake via internalin-A
-internalized into endocytic vacuole
-acidification of vacuole/phagosome activated listeriolysin O- disrupts vacuole membrane to allow for escape to the cytosol
int A -> LLO -> ACT A-> blood (CNS)
