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GI II Exam 1 > Infectious Entercolitis > Flashcards

Infectious Entercolitis Flashcards

1
Q

INFECTIOUS ENTEROCOLITIS causes a broad range of symptoms including:

A
  • diarrhea, abdominal pain, urgency, perianal discomfort, incontinence, hemorrhage
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2
Q
  • ____________ commonly cause pediatric infectious diarrhea leading to_______ and _______
A
  • Enteric viruses
  • Severe dehydration and metabolic acidosis
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3
Q

What is the morphology of Vibrio cholerae?

A

Comma-shaped; gram (-) baccili

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4
Q

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

A

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

Reservoir = shellfish

MOT = fecal-oral; water

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5
Q

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

A
  • Non-invasive and remain in lumen
  • Cholera toxin
  • Flagella for motility and attachment
  • Hemagglutinin for detachment and shedding in stool
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6
Q
  • Symptoms in most patients with Vibrio Cholera?
  • Severe Cases?
A

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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7
Q

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

When do most deaths occur?

Treatment?

A
  • 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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8
Q

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

A

Campylobacteri jejuni

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9
Q

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

A
  • Comma-shaped gram (-) baccili; flagellated;
  • Poulty (undercooked), milk (unpasteurized), other foods
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10
Q

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

A
  1. Motility - flagella
  2. Adherence
  3. Toxin production - cytotoxin + cholera toxin-like enterotoxin
  4. Invasion
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11
Q

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

A
  • 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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12
Q

Complications of Campylobacter spp.?

A
  1. Reative arthritis (linked to HLA-B27)
  2. Erythema nodosum (not HLA-linked)
  3. Guillain-Barre syndrome (not HLA-linked)
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13
Q

Dx of Campylobacter infection

Which immune cell infiltrates predominate and where are they found?

A
  • Primarily by stool culture
  • Intraepithelial neutrophil infiltrates within superficial mucosa and crypts (=>cryptitis)
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14
Q

What is the affect of Campylobacter infection on crypt architecture?

A

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

HOWEVER; crypt architecture is preserved. **

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15
Q

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

A

Shigella toxin

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16
Q

ABX needed for Campylobacter?

A

No

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17
Q

What is the morphology of Shigella?

Mode of transmission?

Reservoir?

A
  • Gram (-) bacilli; Unencapsulated; Non-motile; Facultative anaerobes
  • Reservoir: Humans
  • MOT = fecal-oral, food, water
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18
Q

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

Most deaths occur in whom?

A

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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19
Q

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

A
  • Acid-STABLE
  • Able to resist the harsh acidic enviornment of the stomach
20
Q

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

A
  • 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
21
Q

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

What is the morphology of the mucosa?

A

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

  • Mucosa = ulcerated + hemorrhagic w/ pseudomembranes
22
Q

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

A

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
23
Q

What are the complications of Shigella and in whom?

A
  • In HLA-B27+ M 20-40 YO: Sterile reactive arthritis, urtheritis, conjuntivitis
  • In serotype 1 => hemolytic uremic syndrome
  • Rarely, toxic megacolon and intestinal obstruction
24
Q

Diagnosis and Treatment of Shigella Tocin

A

Dx: Stool culture

Tx:

  • ABX
  • DONT give anti-diarrheals => delay clearance
25
Q

Salmonellosis is usually due to which type of Salmonella?

A

Salmonella enteritidis (non-typhoid salmonella)

26
Q

Salmonella eneteritidis is a ___________ bacteria that is most commonly transmitted how?

Which age groups most affected?

Which time of year do infections peak?

A
  • Gram (-) baccilus
  • Meat, poultry, and eggs/milk
  • Young children and older adults
  • Peak incidence in fall and summer
27
Q

Who is more likely to get of Salmonella infection?

A
  1. Atrophic gastritis or on acid-suppressive therapy (PPIs)
  2. Genetic defects in TH17 –> Disseminated salmonellosis
28
Q

Which virulence factor allows for Salmonella invade and infect humans?

Explain the pathogenesis of invasion.

A
    • Type III secretion system transfers bacterial proteins –> M cells and enterocytes
    • Proteins (+) Rho GTPases –> rearrange actin and bacterial endocytosis, allowing growth
29
Q

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

A
    • Flagellin –> TLR5 –> Increased inflammtory response
    • LPS –> TLR4
30
Q

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

A

Secrete molecule inducing epithelial cells to release eicosanoid hepoxilin A3

31
Q

Which immune cells limit infection by Salmonella enteridis ?

A

TH1 and TH17

32
Q

What is essential for the diagnosis of Salmonella infection?

A

+ stool culture

33
Q
  • Salmonella enteritidis (salmonellosis) profuse watery diarrhea => dystentary that lasts _______ and treated how?
A
  • 1 week
  • Self limited; do not give ABX
34
Q

Typhoid fever (enteric fever) is caused by which organism and its 2 subtypes?

Which subtype is associated with endemic countries and which with travelers?

A

- Salmonella enterica

  • Subtypes:
  • Typhi (endemic countries)
  • Paratyphi (travelers)
35
Q

What is the reservoir for Salmonella enterica?

Mode of transmission?

A
  • Humans = reservoir
  • MOT = fecal-oral and water
36
Q

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

A

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

37
Q

S. typhi or S. paratyphi can colonize the _________, causing __________ and ________.

A

Gallbladder

Gall stones and chronic carrier state.

38
Q

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

A
    • Survive in gastric acid –> small intestine, where they are taken up by M cells =>
    • Engulfed by mononuclear cells in lymph tissue
    • Disseminate throughout the body via lymph and blood causing phagocyte and lymph tissue reactive hyperplasia
39
Q

Morphology of S. typhi infection (typhoid fever)?

A
    1. Enlarged/plateu-like Peyer’s patches in terminal ileum and draining mesenteric LN
    1. Acute and chronic inflammatory cells in lamina propria => necrotic debris and mucosal ulcers that may perforate.
    1. Liver forms tyhoid nodules (focal hepatocyte necrosis with MO aggregates)
    1. Spleen: elarged with red pulp and obliterated follcular markings
40
Q

What is the clinical course of Typhoid fever?

A
  • 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.
41
Q

Are ABX recommended for Typhoid Fever?

A

YES; can prevent progressiopn

42
Q

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

A
  1. Sustained high fevers
  2. Tender abdomen which may mimic appendicits
  3. Rose spots = erythematous maculopapular lesions on chest and abd.
43
Q

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

A
    • Encephalopathy/ Meningitis/ Seizures (Neuro)
    • Endocarditis/ myocarditis (Cardio)
    • Pneumonia (Pulm)
  4. - Cholecystitis
44
Q

Patients with _____________, who get S. typhi are more likely to get osteomyelitis.

A

Sickle cell disease

45
Q
A

GI II Exam 1 (19 decks)

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