____________ commonly cause pediatric infectious diarrhea leading to_______ and _______

Enteric viruses Severe dehydration and metabolic acidosis

Symptoms in most patients with Vibrio Cholera? Severe Cases?

Asypomatic or mild diarrhea - Abrupt onset of vomiting and severe, rice water diarrhea that smells like fish after 1-5 days

Infectious Entercolitis Flashcards by David Rendon

INFECTIOUS ENTEROCOLITIS causes a broad range of symptoms including:

diarrhea, abdominal pain, urgency, perianal discomfort, incontinence, hemorrhage

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____________ commonly cause pediatric infectious diarrhea leading to_______ and _______

Enteric viruses
Severe dehydration and metabolic acidosis

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What is the morphology of Vibrio cholerae?

Comma-shaped; gram (-) baccili

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What is the reservoir and mode of transmission for Vibrio cholerae?

Endemic to Ganges Valley in India and Bangledesh (India and Africa)

Reservoir = shellfish

MOT = fecal-oral; water

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Is Vibrio cholerae invasive and which components of the organism are related to its virulence?

Non-invasive and remain in lumen
Cholera toxin
Flagella for motility and attachment
Hemagglutinin for detachment and shedding in stool

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Symptoms in most patients with Vibrio Cholera?
Severe Cases?

Asypomatic or mild diarrhea

Abrupt onset of vomiting and severe, rice water diarrhea that smells like fish after 1-5 days

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What is the rate of diarrhea in severe cases of cholera and what problems can this create?

When do most deaths occur?

Treatment?

Up to 1L/hr
Dehydration, hypotension, electrolyte imbalance, cramping, anuria, shock, and LOC
Death usually within first 24 hours
Timely fluid replacement can save more than 99% of pts

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________ is the most common bacterial enteric pathogen in developed countries and an important cause of travelors diarrhea (food poisoning)

Campylobacteri jejuni

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What is the morphology and mode of transmission for Campylobacter spp.?

Comma-shaped gram (-) baccili; flagellated;
Poulty (undercooked), milk (unpasteurized), other foods

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What are the 4 major properties contributing to the virulence of Campylobacter jejuni?

Motility - flagella
Adherence
Toxin production - cytotoxin + cholera toxin-like enterotoxin
Invasion

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What are some of the signs and symptoms of Campylobacter infection?

Watery diarrhea, either acute or following an influenza-like prodrome after 8 day incubation period
- Dysentery (blood stool) in minority of patients
Fever: Enteric fever if bacteria prolif. in lamina propria and mesenteric LNs
Sheds bacteria for 1 month after resolution

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Complications of Campylobacter spp.?

Reative arthritis (linked to HLA-B27)
Erythema nodosum (not HLA-linked)
Guillain-Barre syndrome (not HLA-linked)

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Dx of Campylobacter infection

Which immune cell infiltrates predominate and where are they found?

Primarily by stool culture
Intraepithelial neutrophil infiltrates within superficial mucosa and crypts (=>cryptitis)

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What is the affect of Campylobacter infection on crypt architecture?

Neutrophils in crypts (cryptitis) and submucosa and may cause crypts abcess;

HOWEVER; crypt architecture is preserved. **

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What is one of the most common cause bloody diarrhea in the world?

Shigella toxin

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ABX needed for Campylobacter?

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What is the morphology of Shigella?

Mode of transmission?

Reservoir?

Gram (-) bacilli; Unencapsulated; Non-motile; Facultative anaerobes
Reservoir: Humans
MOT = fecal-oral, food, water

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Where are the most common sites for infection by Shigella and who is most at risk?

Most deaths occur in whom?

In US and Europe, daycares, migrant workers, travelers, and those in nursing homes; endemic in developing counties

Most deaths occurs in children <5YO

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Why is such a low dose of Shigella required to cause symptoms?

Acid-STABLE
Able to resist the harsh acidic enviornment of the stomach

Once Shigella are in the intestine how are they taken up and what do they do?

Taken up by Microfold (M cells) epithelial cells
Proliferate intracellularly, escape into LP => phagocytosed by MØ’s, in which they induce apoptosis
Inflammatory response => damages surface epithelia and allows Shigella in lumen to access to BL membrane in L colon/ileum for invasion

Shigella most prominently infect which part of the GI, likely due to what?

What is the morphology of the mucosa?

- Left colon and Ileum –> M cells prominent in Peyers patches here

Mucosa = ulcerated + hemorrhagic w/ pseudomembranes

What is the most common clinical presentation of a pt w/ Shigella infection?

After incubation period of 1 week, causes 1 week of diarrhea w/ fever and abdominal pain

Unitially watery diarrhea may progress to dysenteric phase w/ sx’s lasting up to a month

What are the complications of Shigella and in whom?

In HLA-B27+ M 20-40 YO: Sterile reactive arthritis, urtheritis, conjuntivitis
In serotype 1 => hemolytic uremic syndrome
Rarely, toxic megacolon and intestinal obstruction

Diagnosis and Treatment of Shigella Tocin

Dx: Stool culture

Tx:

ABX
DONT give anti-diarrheals => delay clearance

Salmonellosis is usually due to which type of ***Salmonella***?

**Salmonella enteritidis (non-typhoid salmonella)**

**Salmonella eneteritidis** is a ___________ bacteria that is most commonly transmitted how? Which age groups most affected? Which time of year do infections peak?

- **Gram (-) baccilus** - Meat, **poultry**, and **eggs/milk** - **Young children** and **older adults** - Peak incidence in **fall** and **summer**

Who is more likely to get of **Salmonella infection**?

1. **Atrophic gastritis** or on **acid-suppressive therapy (PPIs)** 2. Genetic **defects** in **TH17** --\> Disseminated salmonellosis

Which virulence factor allows for **Salmonella** invade and infect humans? Explain the pathogenesis of invasion.

1. - *Type III secretion system* transfers bacterial proteins --\> M cells and enterocytes 2. - Proteins (+) Rho GTPases --\> rearrange actin and bacterial endocytosis, allowing **growth**

What do the flagellin and LPS of **Salmonella** **enteritidis** activate inside humans are what does this result in?

* - **Flagellin** --\> TLR5 --\> Increased inflammtory response * - **LPS** --\> TLR4

How do Salmonella enteritdis indirectly cause increased neutrophils and potentiate mucosal damage?

Secrete molecule inducing epithelial cells to release **eicosanoid hepoxilin A3**

Which immune cells limit infection by Salmonella enteridis ?

**TH1** and **TH17**

What is essential for the diagnosis of Salmonella infection?

+ stool culture

* **Salmonella enteritidis (salmonellosis)** profuse watery diarrhea =\> dystentary that lasts _______ and treated how?

* 1 week * Self limited; do not give ABX

**Typhoid fever (enteric fever)** is caused by which organism and its 2 subtypes? Which subtype is associated with *endemic countries* and which with *travelers*?

**- Salmonella enterica** - Subtypes: - **Typhi (endemic countries)** - **Paratyphi (travelers)**

What is the reservoir for **Salmonella enterica?** Mode of transmission?

- **Humans** = reservoir - MOT = **fecal-oral and water**

**Typhoid fever** (Salmonella enterica) is strongly associated with travel to which countries?

India, Mexico, Philippines, Pakistan, El Salvador, and Haiti

**S. typhi** or **S. paratyphi** can colonize the \_\_\_\_\_\_\_\_\_, causing __________ and \_\_\_\_\_\_\_\_.

**Gallbladder** **Gall stones** and **chronic carrier state.**

Explain the pathogeneis of **S. typhi** infection (i.e., how do they invade?)

1. - **Survive in gastric acid** --\> small intestine, where they are taken up b**y M cells** =\> 2. - Engulfed by **mononuclear cells** in lymph tissue 3. - **Disseminate** throughout the body via lymph and blood causing **phagocyte and lymph tissue reactive hyperplasia**

Morphology of S. typhi infection (typhoid fever)?

* 1. **Enlarged**/plateu-like **Peyer's patches** in *terminal ileum* and draining **mesenteric LN** * 2. Acute and chronic inflammatory cells in lamina propria =\> necrotic debris and mucosal ulcers that may perforate. * 3. Liver forms **tyhoid nodules** (focal hepatocyte necrosis with MO aggregates) * 4. **Spleen**: elarged with red pulp and obliterated follcular markings

What is the clinical course of Typhoid fever?

* Dysentary, N/V, adominal pain =\> asympomatic phase =\> that leads to bacteremia in 90% of patients: fever, flu-like sx and abdominal pain that occurs without ABX.

Are **ABX** recommended for **Typhoid Fever**?

**YES**; can prevent progressiopn

In patients with **Typhoid Fever,** not treated w/ antibiotics what additional signs and symptoms may develop?

1. Sustained high **fevers** 2. **Tender abdomen** which may mimic appendicits 3. **Rose spots** = erythematous maculopapular lesions on chest and abd.

**Systemic dissemination** of S. typhi may lead to what complications?

1. - Encephalopathy/ Meningitis/ Seizures (Neuro) 2. - Endocarditis/ myocarditis (Cardio) 3. - Pneumonia (Pulm) 4. **- Cholecystitis**

Patients with \_\_\_\_\_\_\_\_\_\_\_\_\_, who get **S. typhi** are more likely to get **osteomyelitis**.

**Sickle cell disease**