Gi - Dickinson - Invasive Infections Of Ileum And Colon

Front 1

Which organisms cause watery ie non-invasive diarrhea?

Back 1

ETEC, EAEC, EPEC, Virbrio

Front 2

Which organisms cause bloody ie invasive diarrhea?

Back 2

Salmonella, Shigella, EHEC, Campylobacter, EIEC (C. perfringens and Listeria begin with watery then TURN TO bloody, classify them as bloody re: Dr. Dickinson)

Front 3

What do all the dif. types of E. coli infections stand for?

Back 3

EIEC = Enteroinvasive
EPEC = Enteropathogenic
EHEC = Enterohemorrhagic
EAEC = Enteroaggregative
ETEC = Enterotoxigenic

Front 4

Which organism is Enteroinvasive E. coli similar to in its pathogeneis and symptoms?

Back 4

Shigella sonnei

Front 5

Which organisms produce shiga toxin or shiga-like toxin?

Back 5

Shigella dysenteriae
Enterohemorrhagic E. coli

Front 6

Does Enteroinvasive E. coli do Type III secretion to enter cells?

Back 6

YES

Front 7

What types of bact. do Type III secretion?

Back 7

Shigella
Salmonella
EHEC
EIEC
EPEC

Front 8

Shigella and EIEC both do what?

Back 8

-Type III secretion to invade mucosal epi cells
-Assemble actin tails to propel laterally through epi
-Escape phagosome and multiply in cytosol

Front 9

Cleaves Adenine residue from 28S RNA of large 60S euk. ribosomal subunit --> Blocks protein synth --> Colonocytes die via apoptosis

This describes Shiga-toxin and what else?

Back 9

EHEC

Eneterohemorrhagic E. coli

(Also: shigella)

Front 10

When you hear about E. coli outbreaks, they are usually talking about what EHEC E. coli strain?

Back 10

O 157

O = an antigen in LPS

Front 11

How is Enterohemorrhagic E. coli O 157 transmitted?

Back 11

foods (unpasteurized), petting zoos, country fairs, dairy farms (found in feces), beef

Front 12

In what pt. populations is Enterohemorrhagic E. coli most severe?

Back 12

young children

Mortality can result in the elderly

Front 13

Does Enterohemorrhagic E. coli cause fever?

Back 13

NO

Front 14

T/F: HUS can result from infection by Enterohemorrhagic E. coli

Back 14

TRUE

HUS = Hemolytic Uremic Syndrome = Shiga toxin absorbed, gains access to blood, Diarrhea HUS = leading cause of acute renal failure in kids

Front 15

T/F: Diarrhea-assoc. HUS is the leading cause of acute renal failure in kids

Back 15

TRUE

Front 16

T/F: 90% of pts with HUS experience a diarrheal prodrome 1-2 weeks before symptoms of HUS appear

Back 16

TRUE

Front 17

How does Shiga toxin damage the kidney?

Back 17

Neutrophils, Platelets, Erythrocytes, Monocytes carry shiga toxin to kidney --> damages glomerular endo cells --> endo cells swell/detach from BM --> Platelet activation, activation of coag cascade, pro-inflamm cytokines --> renal pathology like proteinuria, hematuria, renal failure, oligoanuria

Front 18

Whats the hallmark finding of HUS?

Back 18

Microangiopathic hemolytic anemia ie endothelial dysfunction is the triggering event in development of microagiopathic process mainly affecting endo cells located in renal vasculature

Front 19

Whats the TRIAD for diagnosing HUS?

Back 19

Microangiopathic hemolytic anemia
Thrombotic Thrombocytopenic purpura
Acute Renal Failure

Front 20

IN what pt population does HUS (Microangiopathic hemolytic anemia, Thrombotic Thrombocytopenic purpura, Acute Renal Failure) usually occur?

Back 20

young kids

Front 21

Whats the primary target of HUS?

Back 21

renal vasculature

Front 22

Most common cause of HUS is what?

Back 22

Enterohemorrhagic E. coli, Esp. o 157:H7

Front 23

Define TPP, Thrombotic Thrombocytopenic Purpura

Back 23

Platelets consumed as a result of thrombi in microvasculature

Front 24

Pt has cranberry-sauce like stool. What is the cause of their infection?

Back 24

Enterohemorrhagic E. coli.

Front 25

Pt has eaten cheese that was non-pasteurized and presents with acute vomiting and diarrhea. You note liver and spleen abcesses on imaging and inflammatory colitis. What organism?

Back 25

Yersinia enterocoliticus

(Note: Entomoeba histolytica can also cause liver abcesses)

Front 26

Define Reiter's syndrome

Back 26

Reactive Polyarthritis


Symptoms in joints (arthritis) eyes or urogenital tract

Front 27

Diseases that cause Reiter's syndrome ie reactive polyarthritis?

Back 27

Yersinia, Camplylobacter, Salmonella, Shigella, Vibrio parahaemolyticus

Front 28

What trigger's Reiter's syndrome?

Back 28

Triggered by infection in a genetically susceptible person (ie those with HLA-B27)

Front 29

Whats the most common cause of inflammatory enteritis in US?

Back 29

Virus

Front 30

Whats the morphology of campylobacter?

Back 30

Gram neg. bacilli

Polar flagella

Front 31

Clinical symptoms of Campylobacter?

Back 31

Prodrome (=early symptoms) of fever, headache, mylagia, malaise

Cramps and abd pain with profuse bloody diarrhea

Front 32

T/F: Camplylobacter is self-limiting after 5-8 days

Back 32

TRUE

Front 33

How do we get Campylobacter?

Back 33

Food or Water

Front 34

What infections can present with Reiter's syndrome?

Back 34

Yersinia enterocoliticus, Camplylobacter, Salmonella, Shigella, Vibrio parahaemolyticus

Campylobacter jejuni (=can ALSO see bacteremia and Guillan-Barre syndrome)

Front 35

Define Guillan-Barre Syndrome

Back 35

Acute paralytic disease of peripheral nervous system
=Abs against LPS antigens cross-react with peripheral nerve tissue --> nerve damage --> muscle weakness/paralysis

Front 36

How might Guillan-Barre syndrome present? What organism preceeded it?

Back 36

Muscle weakness/paralysis due to nerve damage

Preceeded by a Camplyobacter jejuni infection

Front 37

A pt is started on an Abx. 4-14 days later they experience cramps, lower abd pain, and diarrhea. You stop the drug, and symptoms subside 7-10 days later. What was going on?

Back 37

They were suffering from Abx-associated pseudomembraneous colitis due to over-growth of a toxigenic strain of Clostridium difficile

Front 38

How do you Dx. pseudomembraneous colitis?

Back 38

presence of Clostridium difficile toxin in stool (toxin A and Toxin B)

Front 39

Where are the toxins of Clostridium difficile produced?

Back 39

Spores survive gastric acid and germinate upon exposure to bile acids --> move to COLON where toxins are produced --> toxins A and B produce the bloody diarhea

Front 40

Whats the purpose of toxin A in Clostridium difficile?

Back 40

Toxin A enters intestinal epi cells and disrupts tight junctions so Toxin B can get in, then BOTH induce cell death by apoptosis causing pseudomembraneous colitis

Front 41

Once in the cell, what does toxin A stimulate the release of in Clostridium difficile infection?

Back 41

Toxin A stimulates the release of neuropeptides from enteric nerves --> Substance P, Neurotensin, Calcitonin gene-related peptide --> Chloride secretion and water loss causing pseudomembraneous colits

Front 42

What makes the "pseudo-membrane" of the membrane in pseudomembraneous colitis?

Back 42

Neutrophils and Monocytes from vascular endothelium make the pseudomembrane then we get apoptosis

Front 43

What sources can we find Listeria monocytogenes obtained from?

Back 43

unpasteurized cheese (ex. = mexican cheese), unpasterized milk products, undercooked meat (ex = deli meat), Raw veggies

(Cyclospora cayetcunensis can also be from raw veggies...and fruit and contaminated water)

Front 44

Whats the pathogenesis of Listeria monocytogenes

Back 44

Listeria invades colonocytes and macrophages

Low pH of phagolysosome activates production of listeriolysin O

Listeriolysin O lyses the phagolysosome membrane and bact. escape into cytosol

Like shigella, moves cell to cell on actin tail