Bacterial Infections of the GI Tract II Flashcards by Christopher Hauglid

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

Tests: Lactose Fermentation

Positive = Red
-E. coli

Negative = White
-Salmonella and Shigella

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Indole Test (Positive spp. and Negative spp.)

Positive = Red
-E. coli and Vibrio spp.

Negative = No color change
-Salmonella

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Hydrogen Sulfite Production (Characteristics)

A BLACK precipitate

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

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Hydrogen Sulfite Production (Differentiates Between)

Salmonella –> BLACK precipitate = H2S producer

Shigella –> No precipitate = does NOT produce H2S

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

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

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

P: Bacteriophage-mediated Shige-like toxin

SOA: Large intestine

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

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

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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EPEC (Small Intestine) (Characteristics)

Gram-negative
Facultative anaerobe
Moderately invasive

Mnemonic: EPEC –> think “P” = Pediatric

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EPEC (Small Intestine) (Disease)

Watery diarrhea

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

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EPEC (Small Intestine) (Epidemiology)

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

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EPEC (Small Intestine) (Pathogenesis)

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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EPEC (Small Intestine) (Diagnosis and Treatment)

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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ETEC (Small Intestine) (Characteristics)

Gram-negative
Facultative anaerobe
Non-invasive

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ETEC (Small Intestine) (Disease)

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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ETEC (Small Intestine) (Epidemiology)

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

ETEC (Small Intestine) (Pathogenesis)

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

ETEC (Small Intestine) (Diagnosis and Treatment)

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

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

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

Salmonella Typhi (Characteristics)

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

Salmonella Typhi (Epidemiology)

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

Salmonella Typhi (Clinical Manifestations)

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

Salmonella Typhi (Pathogenesis)

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

Salmonella Typhi (Pathogenesis Summary)

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))

Salmonella Typhi (Diagnosis)

Culture of stool and blood samples

Salmonella Typhi (Treatment)

Antibiotic therapy based on susceptibility profile | -Fluoroquinolones, Trimethoprim-sulfamethoxazole or broad-spectrum Cepholosporin

Salmonella Typhi (Prevention)

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

Non-Typhoidal Salmonella (Small Intestine) (Characteristics)

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

Non-Typhoidal Salmonella (Small Intestine) (Epidemiology)

- ~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

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

- 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)

Non-Typhoidal Salmonella (Small Intestine) (Pathogenesis)

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.

Non-Typhoidal Salmonella (Small Intestine) (Diagnosis)

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

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

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***

Campylobacter jejuni (Characteristics)

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

Campylobacter jejuni (Disease)

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

Campylobacter jejuni (Pathogenesis)

- Not much is known | - Mechanism similar to Salmonella***

Campylobacter jejuni (Sequelae)

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***

Campylobacter jejuni (Diagnosis and Treatment)

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)

Which bacteria are inflammatory?

Salmonella typhi, Non-typhoidal Salmonella, Campylobacter jejuni