Bacterial infection of GI I Flashcards

1
Q

Diarrhea

A
  • 3+ loose or liquid stools per day-usually result of probs in small intestine
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2
Q
Gastritis
gastroenteritis
enteritis
enterocolits
colitis
A

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

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3
Q

dysentery

A

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

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4
Q

what should you expect to see in stool that is infected by inflammatory bacteria

A
  • leukocytes and fecal occult (not visible blood) and blood
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5
Q

in what hrs of digestion do performed (already made toxins) toxins work? Toxins produced after ingested? when adhered, grew and then release toxin.

A

1-8 hr
8-16
16 + hrs

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6
Q

what are the two types of bacterial food poisoning

A

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

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7
Q

symptoms of bacterial food poisoning

A
  • diarrhea, vomiting, both

- no fever

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8
Q

four bacteria that cause bacterial food poisoning

A

s. aureus
c. botulinum
c. perfingens
bacillus cereus

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9
Q
staphylococcus aureus
type:
spores?
how does it cause disease?
symptoms
inflammation?
time
pathogenesis
treatment
A
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
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10
Q
Clostridium botulinium
type:
spores?
how does it cause disease?
symptoms
inflammation?
time
pathogenesis
Mechanism
A

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

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11
Q

clostridium botulinium found where?
complications of infection
treatment

A
  • found in home canning
  • patient survives- lingering weakness and sypnea up to year after primary disease
  • treatment- supportive therapy, IV antitoxin administration
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12
Q

floppy baby syndrome

A

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

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13
Q
clostridium perfringens
type:
spores?
how does it cause disease?
symptoms
inflammation?
time
pathogenesis
treatment
A

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

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14
Q
Bacillus Cereus
type:
spores?
Inflammation?
what are the two forms?
A

type: gram pos rod
spores: yes
inflammation- no
Forms: emetic (vomiting) form and diarrheal form

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15
Q
Diarrheal form of B. cereus
implicated food-
cause of disease-
onset of symptoms-
enterotoxin vs heat-
A

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)

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16
Q
emetic form of B. cereus
implicated food-
cause of disease-
onset of symptoms-
enterotoxin vs heat-
A

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

17
Q

treatment for B. cereus

A
  • supportive
18
Q

Helicobacter pylori

how does it infect

A
  • 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
19
Q

Diagnosis and treatment of of H. pylori

type of bacteria and what does it cause

A

urea breath test or biopsy
antibiotics and proton pump inhibitor- to control acid
gram neg rod
causes stomach ulcers

20
Q

listeria monocytogenes

type, oxygen and traits

A
  • gram pos
  • facultative anaerobe
  • key traits: wide growth range *1C-45C
  • resistant high salt concentrations
  • wide pH range
21
Q

why would you find listeria monocytogenes in processed food? what type of food would you see it the most?

A
  • 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
22
Q

symptoms of listeria monoytogenes for
healthy people
immunocompromised
pregnant women

A

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

23
Q

what occurs if a neonate is infected by listeria monocytogenes

A
  • granulamatosis infantiseptica- pyogenic granulomas distributed over the whole body
  • meningitis
  • encephalitis
  • pre mature birth, abortion or still-birth
24
Q

how does listeria monogenes work

A

-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)

25
Q

how does listeria monogenes replicate

A
  • replicates in host cell cytosol and does so via Act A mediated actin polymerization and spreads to neighboring cells and blood stream
  • disseminated infection-liver, spleen, CNS
26
Q

what is the best method for diagnosing listeria monocytogenes

A
  • NOT microscopy because too little bacteria

- instead use culture of cerebral spinal fluid and blood via cold enrichment selection (will grow in fridge)

27
Q

treatment and prevention of listeria monocytogenes

A

beta lactam or trimethyoprim-sulfamethoxazole

prevention- no vaccine- properly cook animal pdts including ready to eat meats and wash raw vegis