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

Bacterial Infections of the GI Tract II Flashcards

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1
Q

MacConkey Agar (Tests, Positive Spp. and Negative Spp.)

A

Tests: Lactose Fermentation

Positive = Red
-E. coli

Negative = White
-Salmonella and Shigella

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2
Q

Indole Test (Positive spp. and Negative spp.)

A

Positive = Red
-E. coli and Vibrio spp.

Negative = No color change
-Salmonella

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3
Q

Hydrogen Sulfite Production (Characteristics)

A

A BLACK precipitate

-A variety of medias can test for this (e.g. S-S agar; Salmonella and Shigella agar)

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4
Q

Hydrogen Sulfite Production (Differentiates Between)

A

Salmonella –> BLACK precipitate = H2S producer

Shigella –> No precipitate = does NOT produce H2S

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5
Q

Enterotoxigenic (ETEC) (Pathogenesis, Site of Action, Disease and Epidemiology)

A

P: Enterotoxin LT and/or ST, cause fluid and electrolyte loss

SOA: Small intestine

D and E: Traveler’s diarrhea, infant diarrhea, watery diarrhea, cramps, nausea, low-grade fever

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6
Q

Enteropathogenic (EPEC) (Pathogenesis, Site of Action, Disease and Epidemiology)

A

P: Plasmid-mediated adherence and destruction of epithelial cells

SOA: Small intestine

D and E: Infant diarrhea and fever, nausea, vomiting, non-bloody stool

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7
Q

Enterohemorrhagic (EHEC) (Pathogenesis, Site of Action, Disease and Epidemiology)

A

P: Bacteriophage-mediated Shige-like toxin

SOA: Large intestine

D and E: Hemorrhagic colitis; Hemolytic uremic syndrome (HUS)

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8
Q

Enteroinvasive (EIEC) (Pathogenesis, Site of Action, Disease and Epidemiology)

A

P: Plasmid-mediated invasin, destruction of epithelial cells lining colon

SOA: Large intestine

D and E: Fevers, cramps, watery diarrhea followed by development of dysentery

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9
Q

EPEC (Small Intestine) (Characteristics)

A

Gram-negative
Facultative anaerobe
Moderately invasive

Mnemonic: EPEC –> think “P” = Pediatric

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10
Q

EPEC (Small Intestine) (Disease)

A

Watery diarrhea

-Symptoms caused by TISSUE DESTRUCTION (i.e. MICROVILLI)

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11
Q

EPEC (Small Intestine) (Epidemiology)

A
  • Important pathogen in infants (INFANTILE DIARRHEA) in developing countries
  • 5-10% of PEDIATRIC DIARRHEA in developing countries
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12
Q

EPEC (Small Intestine) (Pathogenesis)

A
  • Adhesins
    1) BfpA (Bundle forming pilus)
    2) Type III secretion system, Tir (injects proteins directly into the host cell

NO toxins (watery diarrhea, no toxins)

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13
Q

EPEC (Small Intestine) (Diagnosis and Treatment)

A

Diagnosis:

1) Culture and Biochemical Tests (False positives are common)
- Ferments lactose (RED on MacConkey Agar)
- Indole POSITIVE
2) PCR (More Accurate Method)

Treatment:
-Supportive Therapy

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14
Q

ETEC (Small Intestine) (Characteristics)

A

Gram-negative
Facultative anaerobe
Non-invasive

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15
Q

ETEC (Small Intestine) (Disease)

A
  • TRAVELER’S DIARRHEA: associated with travel to developing countries and consumption of contaminated WATER or ICE
  • Watery Diarrhea

Mnemonic: ETEC –> “T” = Travelers

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16
Q

ETEC (Small Intestine) (Epidemiology)

A
  • Leading bacterial cause of diarrhea in children in the developing world
  • ~200 million cases of diarrhea and 380,000 deaths per year worldwide, mostly in children in developing countries
17
Q

ETEC (Small Intestine) (Pathogenesis)

A

1) Fimbriae (Pili): adherence to epithelial cell

2) Toxins:
- LT: Heat Liable Toxin = AB toxin, INCREASES cAMP
- ST: Heat Stable Toxin = Non-AB toxin, does NOT enter cell, INCREASES cGMP
* **Both lead to INCREASED EFFLUX of ions/electrolytes/water
- Plasmid encoded

3) NOT invasive

18
Q

ETEC (Small Intestine) (Diagnosis and Treatment)

A

Diagnosis:

  • Clinical history
  • DNA probes detect LT and ST encoding genes in clinical samples and cultures (Research labs or reference labs; not common but becoming more so)

Treatment:
-Supportive Therapy

19
Q

Salmonella spp. (Small Intestine) (Typoidal vs Non-Typhoidal)

A
  • Over 2500 serotypes
  • Salmonella enterica serovar

1) Typhoidal
- S. Typhi: Salmonella enterica serovar Typhi

2) Non-Typhoidal Salmonella (Enteric)
- Salmonella enterica serovars Cholerasuis, Enteritidis, and Thypimurium

20
Q

Salmonella Typhi (Characteristics)

A
  • Gram negative, facultative anaerobe
  • MOBILE rods, Flagellated (H-ANGITEN)
  • ACID TOLERANT
  • Intracellular pathogen
  • Highly adapted to humans
21
Q

Salmonella Typhi (Epidemiology)

A
  • Humanes are the ONLY RESERVOIR
  • 400-500 cases per year in the US
  • 21 million cases per year, 200,000 deaths worldwide
  • FECAL-ORAL TRANSMISSION
  • Infections dose 10^5 to 10^6 bacteria
22
Q

Salmonella Typhi (Clinical Manifestations)

A

1) ~13 day incubation

2) Symptom progression
- Fever with headaceh
- Rising fever over 3 days*
- TYPHOID FEVER (prolonged fever of ~4 weeks)*
- Followed by GI symptoms (chronic colonization of the GALLBLADDER and Re-infection of the intestines)***
* ** = Sustained BACTEREMIA

3) Shedding of S. Typhi in stool

23
Q

Salmonella Typhi (Pathogenesis)

A

Adherence to M-cells and enterocytes

1) M-Cells
- Sample and present intestinal contents to immune cells
- Associated with PEYER’S PATCHES in the ileum
2) Type III secretion system (T3SS) mediated uptake into M-cell:
- Ssps- Salmonella-secreted invasion proteins
- MEMBRANE RUFFLING
- Escape from vacuole
3) T3SS
- Bacterial molecular SYRINGE
- Direct injection of proteins into host cell

24
Q

Salmonella Typhi (Pathogenesis Summary)

A

1) Phagocytosis or T3SS mediated uptake into macrophage
2) Macrophage transit to draining lymph nodes
3) Salmonella escape from macrophage
4) Bacteremia (Fever from septicemia (LPS aka endotoxin))

25
Q

Salmonella Typhi (Diagnosis)

A

Culture of stool and blood samples

26
Q

Salmonella Typhi (Treatment)

A

Antibiotic therapy based on susceptibility profile

-Fluoroquinolones, Trimethoprim-sulfamethoxazole or broad-spectrum Cepholosporin

27
Q

Salmonella Typhi (Prevention)

A

1) Avoid potential sources of infection
- Drink only bottled water, NO ICE, thoroughly cook foods, avoid raw fruits and vegetables
2) Vaccination for travelers to endemic areas
- Ty21A- capsul by mouth, 4 doses
- ViCPS- injection, 1 dose

28
Q

Non-Typhoidal Salmonella (Small Intestine) (Characteristics)

A
  • Gram negative, facultative anaerobe
  • Motile rods, Flagellated (H antigen)
  • Acid tolerant
  • Intracellular pathogens
  • **Same as S. Typhi except not as human adapted
29
Q

Non-Typhoidal Salmonella (Small Intestine) (Epidemiology)

A
  • ~50,000 cases per year in US
  • Disease of INDUSTRIALIZED COUNTRIES
  • Higher incidence in YOUNG CHILDREN/ELDERLY
  • Source of infection = 1) Contaminated food (poultry, eggs, dairy products, lettuce, brussel sprouts, etc.), 2) Human to human transmission UNLIKELY
  • Infectious dose is 10^6 to 10^8 bacteria
30
Q

Non-Typhoidal Salmonella (Small Intestine) (Clinical Manifestations)

A
  • Occur between 6-48 hours post-ingestion
  • Nausea and vomiting with/followed by abdominal cramps and watery diarrhea
  • Persistent diarrhea for 3-4 days (with or without blood; spontaneous resolution within 7 days)
  • 50% of cases present with FEVER
  • Symptomatic range (Loose stool –> severe DYSENTERY-LIKE diarrhea)
31
Q

Non-Typhoidal Salmonella (Small Intestine) (Pathogenesis)

A

1) Initial stages of infection VERY SIMILAR to S. Typhi pathogenesis
2) After enter into macrophage, 2 scenarios:
- 1. Rapid killing of macrophage via multiple mechanisms (Massive INFLAMMATORY response that: confines infections; active fluid secretion (diarrhea))
* Most cases are the first scenario*
- 2. Carriage in macrophage (IMMUNOCOMPROMISED individuals): a) Systemic DISSEMINATION, Bacteremia, b) Focail infections - arthritis, osteomyelitis, endocarditis, etc.

32
Q

Non-Typhoidal Salmonella (Small Intestine) (Diagnosis)

A

1) Serology: Detection of anti-Vi antigen antibodies

2) Culture from blood and stool:
Selective/Differential media
-Non-lactose fermenting (WHITE on MacConkeys)
-Produces H2S = BLACK precipitate

33
Q

Non-Typhoidal Salmonella (Small Intestine) (Treatment and Prevention)

A

1) Salmonella gastroenteritis
- Electrolyte replacement
- Antibiotic therapy NOT RECOMMENDED (as it enhances carrier state; ONLY for SEVERE cases to prevent septicemia)

2) Salmonella systemic infection
- Antibiotic therapy depending on resistance profile

Prevention:
NO VACCINE AVAILABLE

34
Q

Campylobacter jejuni (Characteristics)

A
  • Gram negative rod, curved or SEA GULL-SHAPED
  • Microaerophilic
  • Many ANIMAL RESERVOIRS (Turkeys, Pets)
  • INVASIVE (jejunum, ileum, and colon)
35
Q

Campylobacter jejuni (Disease)

A
  • Ulceration and acute enteritis (watery diarrhea (most common bacterial cause))
  • Sepsis
  • LONG incubation time (2-11 days)
  • Sequelae –> GUILLAIN-BARRE SYNDROME
36
Q

Campylobacter jejuni (Pathogenesis)

A
  • Not much is known

- Mechanism similar to Salmonella***

37
Q

Campylobacter jejuni (Sequelae)

A

Guillain-Barre Syndrome (GBS)

  • Now recognized as a HETEROGENOUS syndrome
  • Acute immune-mediate polyneuropathy
  • Progressive, fairly symmetric muscle weakness accompanied by absent or depressed DEEP TENDON REFLEXES
  • Symptoms vary: Difficulty walking –> Nearly complete paralysis (extremity, facial, respiratory, and bulbar muscles)
  • ~30-40 of GBS is attributable to Campylobacter infection

See NERUOLOGIC symptoms, think Campylobacter

38
Q

Campylobacter jejuni (Diagnosis and Treatment)

A

Diagnosis
-Culture (done routinely): selective media in a MICROAEROPHILIC environment

Treatment

  • Supportive Therapy
  • Antibiotic Therapy (only used for INVASIVE disease; based on susceptibility profile –> MACROLIDE)
39
Q

Which bacteria are inflammatory?

A

Salmonella typhi, Non-typhoidal Salmonella, Campylobacter jejuni

Microbiology Exam III (9 decks)

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