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Microbiology Exam III > Bacterial Infections of the GI Tract I > Flashcards

Bacterial Infections of the GI Tract I Flashcards

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1
Q

How are most/all GI infections transmitted?

A

Fecal-oral route

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2
Q

GI Host Defenses

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

A

Mucus and Bile

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4
Q

Gastritis

A

Inflammation of the stomach

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5
Q

Gastroenteritis

A

Inflammation of the stomach and intestines (characterized by nausea, vomiting, diarrhea, and abdominal pain/discomfort)

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6
Q

Dysentery

A

Inflammatory disorder of the GI tract associated with:

  1. Diarrhea with BLOOD and PUS in the feces
  2. Pain, fever, abdominal cramps
  3. Usually results from disease of the LARGE INTESTINE
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7
Q

Enteritis

A

Inflammation of the intestines, especially the SMALL INTESTINE

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8
Q

Enterocolitis

A

Inflammation of the mucosa of the SMALL and LARGE INTESTINES

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9
Q

Colitis

A

Inflammation of the COLON

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10
Q

Inflammatory GI Bacteria (Signs)

A
  • More likely to see occult or visible BLOOD
  • More likely to see fecal LEUKOCYTES
    e. g. Salmonella spp., Campylobacter jejuni, C. difficile, EHEC, EIEC, Shigella spp., Vibrio parahaemolyticus, Yersinia enterocolitica
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11
Q

Non-Inflammatory GI Bacteria (Signs)

A
  • Bacteria passing through the intestine or adherent to intestinal epithelium
  • Either:
    1) No known toxins
    2) Produce non-cytotoxic toxin (increase electrolyte and water efflux)
    e. g. EPEC, ETEC, Vibrio cholerae, Listeria monocytogenes
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12
Q

General Characteristics of GI Pathogens

A
  • Many can cause disease OUTSIDE of the GI tract
  • Fecal-oral transmission
  • Varied virulence factors (Toxin production)
  • Prevalent infections (Food poisoning and GI infection)
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13
Q

Bacterial Food Poisoning (Two Types)

A
  1. Toxins produced by bacteria in the food before the food is consumed
  2. Large numbers of spores ingested, spores germinate in intestine and vegetative bacteria produce toxins, there is no implied colonization or adherence to the GI tract
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14
Q

Bacterial Food Poisoning (Symptoms and Four Bacterial Causes)

A

Symptoms: Diarrhea, vomiting, or both. NO FEVER

Bacterial Causes:

1) Staphylococcus aureus
2) Clostridium botulinum
3) Clostridium perfringens
4) Bacillus cereus

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15
Q

Staphylococcus aureus (Characteristics)

A
  1. Gram-positive cocci in clusters

2. NOT spore-forming

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16
Q

Staphylococcus aureus (Disease)

A
  1. Ingestion of preformed toxin

2. Severe vomiting, diarrhea, and abdominal pain within 1-8 hours after consumption

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17
Q

Staphylococcus aureus (Pathogenesis)

A

HEAT STABLE TOXIN (Can bake food or reheat, but toxin remains stable)

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18
Q

Staphylococcus aureus (Treatment)

A

Supportive Therapy

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19
Q

Clostridium botulinum (Characteristics)

A
  1. Gram-positive rod

2. SPORE-FORMING

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20
Q

Clostridium botulinum (Disease)

A
  • Botulism mediated by BOTULISM TOXIN (active ingredient in botox)
    1. Early: onset of vomiting, diarrhea, abdominal pain 1-8 hours post ingestion of PREFORMED TOXIN or 8-16 hours post ingestion of SPORS
    2. Late: FLACCID PARALYSIS –> Progressive muscle weakness and respiratory arrest (can lead to death)
21
Q

Clostridium botulinum (Pathogenesis)

A

Ingestion of:

  1. Preformed toxin
  2. Large number of spores –> germinate in intestine –> produce toxin

Botulism Toxin:
1. Toxin acts at NEUROMUSCULAR JUNCTIONS, interferes with signaling at synapses (i.e. blocks Acetylcholine release)

22
Q

Where is Clostridium botulinum an especially big issue?

A

With infants and honey

23
Q

Clostridium botulinum (Epidemiology, Complications, and Treatment)

A

Epidemiology: often seen in HOME-CANNING (improperly canned food items)

Complications: if patient survives, lingering weakness, dyspnea up to 1 year after primary disease

Treatment: Supportive therapy; IV anti-toxin administration

24
Q

Infant Botulism (i.e. Floppy Baby Syndrome)

A

Occurs between between birth and 1 year
-Germination of C. botulinum spores in intestins –> growth –> toxin production (often ingested when infants are fed HONEY (tight junctions are not formed enough yet to prevent toxin from coming through until 6+ months old)

***Milder and lower mortality than adult botulism

25
Q

Clostridium perfringens (Characteristics)

A

Gram-positive rod

SPORE-FORMING

26
Q

Clostridium perfringens (Disease)

A
  1. Mediated by C. perfringens enterotoxin NOT endotoxin/LPS (Enterotoxin = protein toxins produced within the body)
  2. Associated with contaminated meat products/gravies held at below recommended temperatures
  3. Onset of diarrhea and abdominal cramps 8-16 hours post-ingestion and lasts for ~24 hours
27
Q

Clostridium perfringens (Treatment)

A

Supportive therapy

28
Q

Clostridium perfringens (Pathogenesis)

A
  1. C. perfrigens spores survive cooking of food
  2. Bacteria grow in food (not kept heated properly)
  3. Ingestion of organisms
  4. Organisms sporulate in the intestine
  5. Sporulation leads to enterotoxin production
  6. Toxin alters enterocyte membrane permeability
  7. Diarrhea
29
Q

Bacillus cereus (Characteristics)

A

Gram-positive

SPORE-FORMING

30
Q

Bacillus cereus (Emetic Form: Disease and Pathogenesis)

A
  • Onset of vomiting, nausea, and abdominal cramps 1-8 hours after ingestion of PREFORMED ENTEROTOXIN
  • Ingestion of preformed-heat stable enterotoxin
  • Associated with improper storage of COOKED RICE (spore survive cooking –> bacteria multiply –> produce a heat-stable enterotoxin that is not inactivated upon reheated)
31
Q

Bacillus cereus (Diarrheal form: Disease and Pathogenesis)

A
  • Onset of diarrhea, nausea, and abdominal cramps 8-16 hours post-ingestion of food contaminated with organisms
  • Production of heat-liable enterotoxin in the intestine
32
Q

Bacillus cereus (Treatment)

A

Supportive Therapy

33
Q

Bacillus cereus (Emetic vs Diarrheal Forms: Food, Cause, Onset of symptoms post-ingestion, Symptoms, Enterotoxin)

A

Food: Rice vs Meat, Vegetables
Cause: Preformed toxin vs Toxin production in the intestine
Onset of symptoms post-ingestion: 15 min-8 hours vs 8-16 hours
Symptoms: Vomiting, nausea, abdominal cramps vs Diarrhea, nausea, abdominal cramps
Enterotoxin: HEAT-STABLE vs Heat Liable

34
Q

Helicobacter pylori (Characteristics)

A
  • Gram-negative, curved rod

- Microaerophilic (5% oxygen)

35
Q

Helicobacter pylori (Disease)

A
  • Ulcers

- Chronic gastritis (***STOMACH CANCERS in <1% of infections, TYPE I CARCINOGEN)

36
Q

Helicobacter pylori (Pathogenesis)

A
  • Not completely understood
  • Flagella
  • UREASE
  • Cytotoxin-VacA
  • Adhesins
37
Q

Who linked H. pylori to ulcers rather than stress, smoking, and spicy foods?

A

Barry Marshall and Robin Warren (Marshall ingested H. pylori to prove it then treated with abx)

38
Q

Helicobacter pylori (Stomach: MOA)

A
  1. H. pylori penetrate the mucous layer lining the stomach’s epithelium, attracted to the chemotactic substances HEMIN and UREA
  2. H. pylori recruit and activate inflammatory cells. It also releases UREASE that cleaves urea, producing NH3 that neutralizes stomach acid in its vicinity
  3. H. pylori cytotoxin and the ammonia produced by its urease cause destruction of the mucus-producing cells, exposing the underlying connective tissue to stomach acid
39
Q

Helicobacter pylori (Diagnosis)

A
  1. Urea breath test

2. Biopsy

40
Q

Helicobacter pylori (Treatment)

A
  1. Only after a POSITIVE test for H. pylori
  2. Combination of:
    Antibiotics and Proton Pump Inhibitor (controls acid/further mucosal damage)
41
Q

Listeria monocytogenes (Small Intestine) (Characteristics)

A

Gram positive, facultative anaerobe
Short rods, sometimes occur in pairs
Intracellular pathogen

42
Q

Listeria monocytogenes (Key Survival Traits)

A
  1. Wide growth range (1 to 45 degrees C) Psychrophilic = cold-loving
  2. Resistant to high salt concentrations
  3. Wide pH range
43
Q

Listeria monocytogenes (Epidemiology)

A
  • Animal Reservoirs (mammals, birds, fish)
  • CONTAMINATED FOOD is primary source (ready to eat meats, raw vegetables)
  • High risk of infection in YOUTH, ELDERLY, IMMUNOCOMPROMISED, and PREGNANT
  • Human to Human transmission is possible; primarily from MOTHER TO FETUS
44
Q

Listeria monocytogenes (Clinical Manifestation)

A

-Healthy adults: usually asymptomatic (may have fever, nausea, and/or diarrhea; usually not severe)

  • Immunocompromised adults:
    1) BACTEREMIA- fever, malaise, and chills with no obvious focus
    2) MENINGITIS and ENCEPHALITIS- symptoms not distinct from other causes (fever, persistent headache, stiff neck, vomiting, and/or confusion); 20-50% mortality rate, significant neurologic sequelae in survivies
45
Q

Listeria monocytogenes (Clinical Manifestations Continued)

A

3) Infections in Pregnant Women- may develop nausea, fever, and/or diarrhea; fever with no obvious infection; risk of disease transmission to neonate

4) Neonatal infection- GRANULOMATOSIS INFANTISEPTICA (pyogenic granulomas distributed over the whole body, meningitis, encephalitis)
- Earl onset (in utero transmission): can result in premature birth, abortion, or still-birth
- Late onset: 2-3 weeks after birth

46
Q

Listeria monocytogenes (Pathogenesis)

A

1) Adherence and uptake (mediated by Internalin-A (IntA)
2) Internalized in endocytic vacuole
3) Acidification of vacuole/phagosome activates: Listeriolysin O (LLO)- disrupt vacuole membrane to allow for escape to the cytosol
4) Replication in host cell cytosol
5) ActA mediated actin polymerization (Spread to: neighboring cells and bloodstream by PUSHING THROUGH MEMBRANES)
5) Dissemination infection (Liver, Spleen, and CNS)

47
Q

Listeria monocytogenes (Diagnosis)

A

Microscopy of clinical samples is insensitive (too few bacteria, other gram + bacteria cause bacteremia and infect the CNS)

  • **Culture of cerebral spinal fluid and blood:
  • COLD ENRICHMENT SELECTION
  • Weak B-hemolysis on blood agar
  • Motility test
48
Q

Listeria monocytogenes (Treatment and Prevention)

A

Treatment:
1. Beta-Lactam or Trimethoprim-Sulfamethoxazole

Prevention:

  1. NO VACCINE AVAILABLE
  2. Properly cook animal products including ready-to-eat meats, wash raw vegetables (especially if immunocompromised or pregnant)

Microbiology Exam III (9 decks)

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