Bacterial Infection of the GI Tract 1 Flashcards

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1
Q

How are most GI tract infections transmitted?

A

Fecal-Oral route:

  1. Directly
  2. Feces-contaminated water
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2
Q

GI Host Defenses (8)

A
  1. Continuous Epithelium
  2. Mucus
  3. Low pH (stomach)
  4. Gut motility
  5. Shedding of epithelium
  6. Bile
  7. Secretory IgA
  8. Normal microbiota
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3
Q

Which two GI host defenses can trigger the expression of bacterial virulence factors?

A
  1. Mucus
  2. Bile
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4
Q

Characteristics of normal macrobiota (good and bad…4)

A
  1. Competitive exclusion of abnormal biota 2. Digest undigested or indigestible compounds 3. Effects on innate and adaptive immunity 4. Interplay between GI microbiota and host depression and hunger
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5
Q

Gastritis

A

Inflammation of the stomach

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6
Q

Gastroenteritis and syndrome

A

Inflammation of the stomach and intestines

Syndrome: N/V/D and abd pain

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7
Q

Diarrhea

A

Usually results from disease of small intestine

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8
Q

Dysentery and syndrome

A
  1. Inflammatory disorder of the GI tract with
    a. Diarrhea with pus and blood
    b. Pain, fever, and abdominal cramps/pain
    c. Usually results from disease of large intestine
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9
Q

Enteritis

A

Inflammation of the intestines, especially the small intestine

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10
Q

Enterocolitis

A

Inflammation of the mucosa of the small and large intestine

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11
Q

Colitis

A

Inflammation of the large colon

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12
Q

Two major causes of inflammation in GI tract

A
  1. Bacteria themselves
  2. Immune response to bacteria
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13
Q

More likely to see which two chacteristics of inflammatory GI bacteria on fecal tests?

A
  1. Fecal occult or visible blood
  2. Fecal leukocytes
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14
Q

Which pathogens cause are inflammatory GI Bacteria? (8)

Shagga found it difficult to catch salmon while camping.

Ursula vibed on invading ecology twice

A
  1. Salmonella spp.
  2. Campylobacter jejuni
  3. C. difficile
  4. Enterohemmorhagic E. Coli
  5. Enteroinvasive E. Coli
  6. Shigella
  7. Vibrio parahaemolyticus
  8. Yersinia enterocolitica
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15
Q

Movement patterns of non-inflammatory GI bacteria

A
  1. Pass through the intestine
  2. Adhere to intestinal epithelium
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16
Q

Non-inflammatory GI Bacteria produce what? (2)

A
  1. No known toxins
  2. Non-cytotoxic toxins
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17
Q

What is the effect of non-cytotoxic toxins produced by non-inflammatory GI Bacteria?

A

Increase in electrolyte and water efflux

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18
Q

Which pathogens are non-inflammatory GI bacteria (4)?

A
  1. Enteropathic E. Coli
  2. Enterotoxigenic E. Coli
  3. Vibrio cholera
  4. Listeria monocytogenes
19
Q

Pathogens that produce watery, sometimes bloody, or often bloody diarrhea (7)

CEECVYS

A
  1. EHEC
  2. EIEC
  3. Campylobacter jejuni
  4. Shigela spp.
  5. Yersinia enterocolitica
  6. C. difficile
  7. Vibrio parahaemolyticus
20
Q

Pathogens that produce watery, rarely bloody diarrhea (8)

FEELS PBV

Pretty Boobs FEEL Very Sublime

A
  1. EPEC
  2. ETEC
  3. food poisoning
  4. C. perfringens
  5. Bacillus cereus
  6. Vibrio cholerae
  7. Salmonella spp.
  8. Listeria monocytogenes
21
Q

3 vectors of fecal-oral transmission (3F’s)

A
  1. Food
  2. Fluid
  3. Fingers
22
Q

If organisms multiple and produce toxins but infection remains localized in GI tract, what is the most common symptom?

A

Diarrhea

23
Q

If organisms invade host or host absorbs toxins, then what are three common symptoms of disseminated, systemic infection?

A
  1. Fever
  2. Myalgia
  3. Jaundice
24
Q

1-8h after ingestion uses what kind of toxin?

Which pathogens (3)? (ABCs)

A

Preformed Toxin

Pathogens:

  1. Staphylococcus aureus
  2. Bacillus cereus (emetic form)
  3. Clostridium botulinum
25
Q

8-16hr after ingestion…toxin timing

What pathogens (3)?

A

Production of toxins after ingestion

Pathogens:

  1. Bacillus cereus (diarrheal form)
  2. Clostridium perfringens
  3. Clostridium botulinum
26
Q

16+ hours after ingestion– up to 11 days…toxin timing

Which pathogens (9)? 4 are related

A

Adherence, growth, and virulence factor production

Pathogens:

  1. Shigella spp
  2. Salmonella spp
  3. Listeria monocytogenes
  4. EHEC
  5. EPEC
  6. ETEC
  7. EIEC
  8. Campylobacter
  9. Vibrio
27
Q

What are the two types of bacterial food poisoning?

A
  1. Preformed toxins in food
  2. Large number of SPORES ingested, spores germinate, and produce toxins. There is no implied colonization or adherence to the GI tract
28
Q

Top three symptoms of bacterial food poisoning?

A
  1. Diarrhea
  2. Vomiting
  3. NO fever
  4. Probably nausea and abd. pain
29
Q

Top 4 bacterial pathogens causing food poisoning?

Short acting

A
  1. Staphylococcus aureus
  2. Clostridium botulinum
  3. Clostridium perfringens
  4. Bacillus cereus
30
Q

Staphylococcus Aureus:

  1. Gram stain and shape
  2. Spore forming?
  3. Preformed or produced toxin
  4. Common symptoms and timing
  5. How does the toxin work
  6. Treatment
A
  1. Gram stain positive cocci in clusters
  2. NOT spore forming
  3. Preformed toxin
  4. Severe V/D, abd pain within 8 hrs of consumption
  5. Heat-stable toxin with an unknown MOA
  6. Supportive Tx (hydration and symptom control)
31
Q

Clostridium botulinum

  1. Gram stain and shape
  2. Spore formation?
  3. Toxin production (2)
  4. Common symptoms (early and late)
  5. Pathogenesis
  6. Treatment
  7. Epidemiology
  8. Complication
A
  1. Gram-positive, rod
  2. Spore forming
  3. Botulism toxin is either preformed or produced
  4. Early onset of V/D and abd pain 1-8h after preformed toxin ingestion or 8-16h post spore ingestion.

Late: flaccid paralysis–> progressive muscle weakness and respiratory arrest

  1. Ingestion of preformed toxin or spores germinate and produce toxin
  2. Supportive and IV anti-toxin therapy
  3. Often seen in home-canning
  4. Lingering weakness and dyspnea up to 1 year after primary disease
32
Q

Infant Botulism:

  1. Other name
  2. Occurs when?
  3. Due to?
  4. Associated with which food
  5. Mortality differences than adult botulism
  6. Why is it ok to eventually given babies #4 food?
A
  1. Floppy Baby Syndrome
  2. Occurs between birth-6 months (up to 1 year)
  3. Due to C. botulinum spores growing and producing toxins
  4. Honey
  5. Milder and lower mortality than adult botulism
  6. After 6 months, permeability of the intestinal mucosa changes
33
Q

Clostridium perfringes

  1. Gram stain and shape
  2. Spore formation
  3. Primary toxin and associated food
  4. Common symptoms and timing
  5. Treatment
A
  1. Gram stain positive, rod
  2. Spore forming
  3. C. perfringens enterotoxin associated with contaminated meat/gravies held below recommended temps
  4. Diarrhea and abd pain 8-16h after ingestion, lasting 24 hours
  5. Supportive therapy
34
Q

Bacillus cereus: Emetic form

  1. Gram stain
  2. Spore formation
  3. Toxin production
  4. Symptoms and timing
  5. Associated with which food
A
  1. Gram positive
  2. Spore forming
  3. Preformed, heat-stable enterotoxin
  4. Voming, nausea, abd pain 1-8hr after ingestion of preformed toxin
  5. Improper storage of cooked rice
35
Q

Bacillus cereus: Diarrheal form

  1. Gram stain
  2. Spore formation
  3. Toxin production
  4. Common symptoms and timing
  5. Associated with which food
  6. Treatment
A
  1. Gram positive
  2. Spore forming
  3. Production of heat-liable enterotoxin

4+5 . Diarrhea, nausea, and abd pain 8-16hrs post ingestion of contaminated meat/vegetables

  1. Supportive therapy
36
Q

Helicobacter pylori

  1. Gram stain and shape
  2. Aerobic?
  3. Diseases?
  4. Primary pathogenesis
A
  1. Gram negative, curved rod
  2. Microaerophilic (5% O2)
  3. Causes ulcers and chronic gastritis (stomach cancers)
  4. Urease: H. pylori penetrate mucus layer and release urease which cleaves urea into carbon dioxide and ammonia. The ammonia destroys the mucus producing cells, exposing underlying cells to stomach acid, thereby causing ulcers
37
Q

Helicobacter pylori:

  1. Diagnosis
  2. Treatment
A
  1. Urea breath test or biopsy
  2. Antibiotics and proton pump inhibitor
38
Q

Listeria monocytogenes:

  1. Location in the body
  2. gram stain and shape
  3. Aerobic?
  4. Cellular location
  5. Survival traits/growth requirements (3)
A
  1. Small Intestine
  2. Gram positive, rod
  3. Facultative anaerobe
  4. Intracellular pathogen
  5. Wide growth temps (1-45 degrees C), high salt resistance, wide pH range
39
Q

Listeria monocytogenes:

  1. Epidemiology (#cases/year)
  2. Animal reservoirs (3)
  3. Primary source of pathogens (2)
  4. Vulnerable populations (4)
  5. Transmission routes
A
  1. 800 cases/year
  2. Mammals, birds, and fish reservoirs
  3. Contaminated food: ready to eat meats and raw vegetables
  4. Young, eldery, immunocompromised, and preggers
  5. Human to human transmission possible (mother to fetus)
40
Q

Listeria monocytogenes: manifestations

  1. Healthy adult
  2. Immunocompromised adult- 2 deadly, neurological symptoms/diseases
  3. Pregnant women
  4. Neonates and onset. (the primary condition assocaited with listeria and neonates)
  5. In utero transmission can cause what?
A
  1. Usually asymptomatic but may have fever, nausea, and diarrhea
  2. Bacteremia- fever, malaise, and chills.

Meningitis and Encephalitis- fever, HA, stiff neck, vomiting, confusion. 20-50% mortality rate

  1. Nausea, fever, diarrhea. Fever with no obvious infection = blood culture for listeria.
  2. Granulomatosis infantiseptic- pyogenic granulomas distributed over whole body. Meningitis and encephalitis possibly.

In utero transmission can result in premature birth, abortion, or still-born.

Late onset- 2-3 weeks after birth

41
Q

Listeria monocytogenes:

Pathogenesis (general steps)

Dissemination locations (3)

A
  1. Adherence and induced uptake mediated by Internalin-A
  2. Internalized into endocytic vacuole
  3. Breaks out of vacuole via Listeriolysin O
  4. Replicates in cytosol
  5. Internalin-A mediated actin polymerization
  6. Dissemination to liver, spleen, and CNS
42
Q

Diagnosis of Listeria monocytogenes:

  1. Wrong way
  2. Right way (correct selection and two tests)
A
  1. Wrong way: microscopy of clinical samples
  2. Right way: Culture of CSF and blood

*Cold Enrichment selection

*B-hemolysis

*Motility test +

43
Q

Lysteria monocytogenes

Which two antibiotics are used?

Prevention: vaccine? and one other thing

A
  1. Treatment: B-Lactams OR trimethoprim-sulfamethoxazole
  2. No vaccine available. Properly cook ready to eat meats and wash raw vegetables