Gi Pathogens I And Ii

Front 1

How are GI pathogens generally acquired?

Back 1

Usually by the fecal-oral route

Front 2

T/F GI Infection may be confined to the GI tract or may spread from the gut to other parts of the body.

Back 2

T

Front 3

inflammation of intestinal mucosa

Back 3

enteritis

Front 4

inflammation of large intestine

Back 4

colitis

Front 5

inflammation of small and large intestines

Back 5

enterocolitis

Front 6

inflammation of stomach and intestinal linings

Back 6

gastroenteritis

Front 7

inflammation of the GI tract with <b>blood and pus</b> in the feces

Back 7

dysentery

Front 8

Common features of bacteria causing GI diseases

Back 8

Gram-negative rods

Grow in simple media
Facultative anaerobes (ferment glucose)

Front 9

Two families of enteric bacilli

Back 9

Enterobacteriaceae; Vibrionaceae

Front 10

Characteristics of Enterobacteriaceae

Back 10

Peritrichious flagella  (if flagella present)
Oxidase-negative  (a cytochrome test)
Common normal flora ofthe vertebrate gut

Front 11

Enterobacteriaceae: oxidase pos or neg?

Back 11

neg

Front 12

Two types of Enterobacteriaceae

Back 12

1) Lactose fermenting (coliform bacteria)
2) Lactose non-fermenting

Figure this out thru MacConkey test and EMB Agar test

Front 13

Characteristics of Vibrionaceae

Back 13

Polar flagella
Oxidase-positive

Front 14

Vibrionaceae: oxidase positve or negative?

Back 14

positive

Front 15

Difference in flagella between Vibrionaceae and Enterobacteriaceae

Back 15

Enterobacteriaceae: flagella evenly distributed over the entire surface of the cell (petrichous)

Vibrionaceae: a polar flagella (one)

Front 16

Escherichia, Klebsiella, Enterobacter, Serratia, Citrobacter: what do they have in common?

Back 16

They are enterobacteriaceae that ferment lactose.

Front 17

Salmonella, Shigella, Proteus, Yersinia (SPYS)

Back 17

They are enterobacteriaceae that do not ferment lactose.

Front 18

When is E coli pathogenic?

Back 18

When it has virulence factors not normally found in normal flora strains. Often they're plasma encoded.

Front 19

Specific Antibody + Bacteria surface antigens =

Back 19

Agglutination

Front 20

E. Coli: class and MacConkey result

Back 20

Enterobacteriaceae / Lac+

Front 21

ETEC: Enterotoxigenic E Coli can cause what illnesses?

Back 21

Diarrheal Disease
Urinary Tract Infection
Nosocomial Bacteremia
Neonatal Meningitis

Front 22

Adult Traveler's Diarrhea: Source, prevention, treatment

Back 22

Caused by e. coli

Source: contaminated food/water.
Prevention: avoid uncooked foods, unpeeled fruit, salads, cold drinks or local water (hot or carbonated OK).
Treatment: oral rehydration

Front 23

Colonization Factor Antigen (CFA) in E coli: what does it mediate?

Back 23

Adherence to intestinal surface

Front 24

Heat-Stable Toxin (ST) in E coli: what does it mediate?

Back 24

Called this because it isn't destroyed at high temps.

Causes watery diarrhea.

Front 25

Heat-Stable Toxin (ST) in E coli: How does it work?

Back 25

Stimulates membrane guanylate cyclase in intestinal cells. Increased cGMP inhibits NaCl transport into intestinal wall (anti-absorptive mech), leads to secretion of fluid and electrolytes => diarrhea

Front 26

Heat-Labile Toxin (LT) in E coli: what does it mediate?

Back 26

Causes a profuse, watery, non-inflammatory diarrhea

Front 27

Heat-Labile Toxin (LT) in E coli:How does it work?

Back 27

SAME as cholera toxin.

Stimulates membrane adenylate cyclase, increase production of cAMP. This leads to secretion of Cl- and fluids across membrane.

Front 28

Heat-Labile Toxin (LT) in E coli: What toxin is it identical to?

Back 28

Cholera toxin

Front 29

A major cause of infant diarrhea worldwide especially in developing countries

Back 29

Enteropathogenic e coli

Front 30

Symptoms of Enteropathogenic e coli (EPEC)

Back 30

Persistent watery diarrhea
(no leukocytes or RBCs in stool)
Signs of dehydration (weight loss), low fever, vomiting
Usually self-limiting; chronic in some infants.

Front 31

Treatment of Enteropathogenic e coli (EPEC)

Back 31

rehydration with water + salts + glucose

Front 32

Enteropathogenic e coli (EPEC): Virulence factors and pathogenesis (3 steps)

Back 32

1) Adherence to cells: Bundle forming pilus adhesin (BfpA) Pilus permits “localized adherence” of organisms to small bowel epithelial cells

2) Signal transduction: Type III-secreted proteins cause actin rearrangement

3) Intimate adherence: Surface protein Intimin mediates a tight A/E (attaching and Effacing) interaction.

Front 33

How is Enteropathogenic e coli (EPEC) intimately adhered to cells?

Back 33

Actin is rearranged at attachment point, forming pedestals. Then a bacterial surface protein, intimin, mediates very tight attachment (called Attachment and Effacing)

Front 34

Type III Secretion System/Proteins : What are they and what role do they play?

Back 34

protein appendage found in several Gram-negative bacteria.

In pathogenic bacteria, the needle-like structure is used as a sensory probe to detect the presence of eukaryotic organisms and secrete proteins that help the bacteria infect them. The proteins are secreted directly from the bacterial cell into the eukaryotic cell, also known as "the host" cell.

Front 35

Type III Secretion proteins used by E coli

Back 35

E. coli attaches to intestinal cells.

E. coli injects receptor protein, Tir (red),
which binds bacterial Intimin (blue cups).
(Type III secretion system)

Also EspB, D is injected into membrane, , triggers signals for actin rearrangements in host cells and A/E lesions.

E. coli now firmly bound to
Intestinal cell surface:
• strands of actin form below
• pushes cell membrane up,
forming a ‘pedestal’.

Front 36

EHEC-Enterohemorrhagic E. coli : Associated with what severe diseases?

Back 36

Hemorrhagic colitis; Hemolytic - Uremic Syndrome (HUS)

Front 37

Hemorrhagic colitis: symptoms

Back 37

Copious, bloody diarrhea (dysentery)

Front 38

Reservoir and transmission of Hemorrhagic colitis

Back 38

Reservoir: Cattle (can be asymptomatic) Uncooked hamburger and non pasteurized dairy and apple juice.

Also person-to-person contact (generally day care or family)

Front 39

Predominant pathogenic serotype
of EHEC (Enterohemorrhagic E Coli)

Back 39

O157:H7. Only need 10 bacterial cells...

Front 40

Virulence factors of O157:H7

Back 40

MOST IMPORTANT: Shiga-like (Vero) toxin (SLT); stops protein synthesis, destroys intestinal epithelial lining --> bloody diarrhea

Attaching & Effacing (A/E) lesions (like EPEC)

Acid Resistance - survive passage through stomach

Front 41

Virulence factor that stops protein synthesis, destroys intestinal epithelial lining leading to bloody diarrhea

Back 41

Shiga-like toxin (SLT)

Front 42

What is hemolytic-uremic syndrome?

Back 42

Kidney failure occurring in 5-10% of EHEC cases, usually kids.

May be due to Shiga toxin entering blood and carriage to kidney.

Often life-threatening, requiring transfusion and dialysis.

Front 43

Most common cause of acute renal failure in children in US

Back 43

Hemolytic Uremic syndrome due to Enterohemmorrhagic E coli

Front 44

How to diagnosis EHEC?

Back 44

Stool cultures contain sorbitol-nonfermenting E. coli (white on MacConkey-Sorbitol plates)

Serological tests with O157 and H7 antisera
Immunoassay for Shiga toxin in stool is commercially available and effective

Front 45

What is E coli strain O104:H4

Back 45

New shiga-toxin producing E coli (STEC). Illness similar to O157:H7 - severe cramps and bloody diarrhea mostly in kids.

900 cases may-june 2011.

Source: contaminated food

Treatment: cephalosporins

Front 46

EIEC - Enteroinvasive E. coli: what diseases does it cause?

Back 46

Diarrheal diseases (dysentery): similar to Shigella by invasion of epithelial cells. Symptoms are indistinguishable from shigellosis, but less severe. Seen in kids <5 years in develping countries

Front 47

T/F EIEC - Enteroinvasive E. coli has shiga toxin

Back 47

F. Symptoms are similar to shigellosis though

Front 48

What are virulence factors of EIEC - Enteroinvasive E. coli?

Back 48

Plasma-encoded invasion factors (same plasmid as Shigella). Secrete Ipa Proteins (invasion plasmid antigens) via type III mech. into host cells  - actin rearrangements /  - bacterial engulfment
actin-mediated intracellular motion, cell-cell spread.

Front 49

actin-mediated intracellular motion, cell-cell spread characteristic of what?

Back 49

virulence factors of EIEC

Front 50

EAggEC-Enteroaggregative E. coli: causes what disease primarily?

Back 50

Persistent pediatric watery-diarrhea in developing countries

Front 51

EAggEC-Enteroaggregative E. coli: what are virulence factors?

Back 51

Fimbrial adhesions, encoded by plasmids. Binds to small intestinal cells without causing obvious histological changes; enterotoxins possible but not understood

Front 52

UPEC - Uropathogenic E. coli: causes what disease primarily?

Back 52

UTIs (cystitis - bladder infection) in sexually active young women

Front 53

UPEC - Uropathogenic E. coli: what is virulence factor?

Back 53

P-fimbriae: an adherence factor associated with UTI permitting adherence to digalactoside (Gal-Gal) on uroepithelial cells in upper urinary tract.


Vaccine may become available.

Front 54

____ is the most common cause of nosocomial gram-negative bacteremia

Back 54

E. coli

Front 55

One of most common causes of neonatal meningitis due to infant being colonized during childbirth or from ruptured amniotic membranes

Back 55

E Coli

Front 56

E coli infant meningitis is usually caused by strains possessing what?

Back 56

K1 capsul (poly sialic acid); structurally identical to that on Group B Strep, another cause of meningitis in this population

Front 57

What is the Treatment for E coli?

Back 57

Cefotaxime, ceftriaxone, ceftazidime, cefepime

Front 58

How does the virulence factor K1 cause meningitis?

Back 58

Blocks complement and antibody deposition on bacterial surface

Front 59

3 major salmonella infections

Back 59

1. Gastroenteritis (Salmonellosis, Food poisoning)
2. Enteric Fever (Typhoid Fever)
3. Infection of organ systems

Front 60

What color are salmonella colonies on MacConkey agar?

Back 60

White (Lac-)
And gram neg

Front 61

most salmonella that are human pathogens are in what category?

Back 61

Salmonella enterica

Front 62

Salmonella: reservoir

Back 62

normal intestinal tract flora of many animals
often S. enterica Enteritidis or Typhimurium in chicken, cattle, turtles

Front 63

Salmonella: method of infection

Back 63

ingestion of animal fecal-contaminated food or water.
Poultry products most common source in USA (e.g., undercooked chicken, raw eggs, potato or chicken salad).
Common at summer picnics if food not refrigerated properly

Front 64

Salmonella: symptoms and time course

Back 64

begin ~1 to 2 days after eating fecal-contaminated products; include abdominal pain, headache, nausea, vomiting, diarrhea for 3-4 days

Front 65

T/F There is a large number of salmonella organisms needed to cause infection

Back 65

T. This is because they're senstiive to stomach acid

Front 66

Salmonellosis: treatment

Back 66

None. self-limited

Front 67

Salmonella: What are te virulence factors?

Back 67

Enterotoxin - Cholera-like, increases cAMP levels
Cytotoxin - inhibits protein synthesis (unlike Shiga toxin)

Front 68

80% of Salmonella cases come from what?

Back 68

egg shell contamination (S enterica Enteritidis

Front 69

Typhoid fever is aka

Back 69

Salmonella enteric fever

Front 70

What usually causes typhoid fever?

Back 70

ingestion food/drink contaminated with human fecal material due to poor sanitation.


S enterica Typhi, and Paratyphi

Front 71

What is the typical patient with typhoid fever?

Back 71

Traveler returning from endemic area (Latin America)

Front 72

When do symptoms of typhoid fever start?

Back 72

1-3 weeks after ingestion

Front 73

What are symptoms o typhoid fever?

Back 73

High fever
Abdominal pain (diarrhea rare)
Enlarged liver and spleen
"Rose Spots" (faint rash) on abdomen

Front 74

Typhoid fever: treatment

Back 74

Antibiotics effective (e.g., ampicillin, trimethoprim-sulfamethoxazole, or ciprofloxacin)
Without therapy: illness for 4 weeks, ~20% mortality

Front 75

Salmonella Typhi major virulence factors

Back 75

Cell invasion system - permits invasion across mucosal barrier and intracellular growth in monocytes where protected from antibodies and complement.

Proteins secreted via Type III secretion cause cytoskeletal rearrangements leading to membrane ruffling in M cells.

More minor factors:
Acid Resistance, Vi Capsule (resist complement-mediated lysis), PhoP, PhoQ (regulators of virulence determinants)

Front 76

Prevention of Typhoid fever

Back 76

2 Typhoid vaccines now available for travelers

Front 77

What are the virulence factors PhoP and PhoQ's action in salmonella?

Back 77

2-component regulator system
senses environment for adaptation
controls at least 40 genes
mutants defective in survival in macrophage, acid resistance, resistance to antimicrobial peptides and thus virulence.

Front 78

What is the host invasion system used by Salmonella?

Back 78

Ruffling of host cell membrane (indicating cytoskeletal rearrangement) before Salmonella invade an M cell.

Contact of the bacteria on the host cell surface causes the host cell to send up huge actin-rich ruffles or "splashes" that engulf the bacteria as they fold back over.
The bacteria are then trapped inside large vacuoles and replicate there.

Front 79

Which species of salmonella uses membrane ruffling?

Back 79

Salmonelle typhimurium invades Henle human epithelial cells

Front 80

part of a genome that has evidence of horizontal origins (any process in which an organism incorporates genetic material from another organism without being the offspring of that organism)

Back 80

Genomic island

Front 81

a distinct class of genomic islands which are acquired by horizontal gene transfer.

They are incorporated in the genome of pathogenic microorganisms but are usually absent from those non-pathogenic organisms of the same or closely related species. They usually occupy relatively large genomic regions ranging from 10-200 kb and encode genes which contribute to the virulence of the respective pathogen. Typical examples are adherence factors, toxins, iron uptake systems, invasion factors and secretion systems.

Back 81

Pathogenicity Islands

Front 82

What is encoded on the salmonella pathogenicity islands?

Back 82

Salmonella enterica harbours two Salmonella pathogenicity islands (SPIs) each encoding a type III secretion system for virulence proteins. SPI1 is required for invasion, while systemic infections and intracellular accumulation of Salmonella are dependent on SPI2 function.

Those for secretion (Type III) apparatus, genes for membrane ruffling, genes for macrophage cytotoxicity

Front 83

Salmonella Infection of Organ Systems: Which species?

Back 83

Usually Choleraesuis or Typhimurium

Front 84

Salmonella Infection of Organ Systems: pathogenesis

Back 84

Acute gastroenteritis (often w/o diarrhea) leads to infection of blood

Front 85

What is the Shigella reservoir?

Back 85

Only humans, but never found as normal flora

Front 86

What type of bacteria is Shigella?

Back 86

Lac– Enterobacteriaceae, non-motile, no H2S, no gas from glucose.

Closely related to E Coli (especially EHEC)

Front 87

Which Shigella species is cause of most serious disease

Back 87

Shigella dysenteriae

Front 88

Which Shigella species is cause of most common in US?

Back 88

S. sonnei

Front 89

Shigellosis : symptoms

Back 89

Occur 1-3 days after ingestion of human-fecal contaminated food / water or by direct personal contact. Frequent diarrhea with blood and mucus, cramps, tenesmus

Front 90

In what populations is shigellosis seen?

Back 90

Mostly seen in children in the US; 30,000 cases/yr USA reported (10-fold underestimate).
Common in male homosexuals

Front 91

Shigella: (High, Low) infectivity / (high, low) infectious dose

Back 91

High; low

Front 92

How is Shigella treated?

Back 92

Self-limiting (usually)
Oral replacement of fluids and electrolytes
Antibiotics may be given to shorten duration, excretion of organisms and reduce person-to-person spread. Antibiotic resistance is common

Front 93

How is Shigella diagnosed?

Back 93

Patient shows bloody diarrhea (dysentery) suggests Shigella, or EHEC or Entamoeba histolytica.
Clinical lab identification
Isolated from stool sample.
DNA probes for PCR tests may be available soon

Front 94

Significance of Type III Secretion systems

Back 94

Widely distributed, essential virulence determinants of Gram-negative bacteria.

Translocate, upon contact with eukaryotic host cells, proteins from the bacteria cytoplasm into the host cell cytoplasm.

Front 95

The Shigella flexneri type III secreton is composed of three parts:

Back 95

1) an external needle
2) a transmembrane or neck domain
3) a large proximal bulb positioned within the bacterial cytoplasm.

Front 96

What is EMB agar?

Back 96

Eosine Methylene Blue. It inhibits gram positive bacteria and colonies of lactose fermenters become deep purple to black in this medium. E coli becomes metallic green

Front 97

What does E coli look like in EMB agar?

Back 97

Metallis green sheen

Front 98

What are the 3 major surface antigens of the enterics that differ from bug to bug?

Back 98

O antigen, K antigen, H antigen

Front 99

Most external component of LPS. Differs from organism to organism.

Back 99

O Antigen. O for Outer

Front 100

Capsule antigen that covers the O antigen

Back 100

K antigen. K for Kapsule

Front 101

Antigenic determinant making up subunits of bacterial flagella, so only motile bacteria possess it.

Back 101

H antigen

Front 102

If there is no cell invasion (ie, bacteria bind to intestinal epithelial cells but don't enter the cell), what will diarrhea look like?

Back 102

Watery diarrhea without systemic symptoms. Diarrhea is caused by exotoxins

Front 103

Examples of bugs that cause watery diarrhea thru toxins alone (no cell invasion)

Back 103

E coli, Vibrio cholera

Front 104

If there is <b>intestinal epithelial cell invasion</b> (ie, bacteria have virulence factors that allow cell penetration), what will diarrhea look like?

Back 104

WBC infiltrates in diarrhea as well as fever. RBC leakage into stools.

Front 105

Examples of bugs that cause diarrhea thru cell invasion

Back 105

Enteroinvasive E coli, Shigella, Salmonella enteritidis

Front 106

If there is <b>invasion of lymph nodes and blood stream</b> what symptoms will patient have?

Back 106

Systemic symptoms - fever, headache, WBC elevation. Lymph node enlargement, sepsis, bacteremia.

Front 107

Examples of bugs that invade lymph nodes/blood stream from GI tract

Back 107

Salmonella typhi, Yersinia enterocolitica, Campylobacter jejuni

Front 108

T/F Shigella is motile like Proteus

Back 108

F. NONmotile

Front 109

How can Shigella be distinguished from E coli and Salmonella?

Back 109

Shigella does not ferment lactose (E Coli does) and does not produce H2S (Salmonella produces H2s)

Front 110

How is Shigella similar to E Coli (Enteroinvasive)?

Back 110

They both invade intestinal epithelial cells and release Shiga toxin that causes cell destruction

Front 111

How do Shigella get from cell to cell?

Back 111

IcsA Protein (an ATPase) is at one pole of the rod. It causes polymerization of host actin to propel nonmotile Shigella through cytoplasm and into adjacent cell. Projection lyses releasing bacteria into cell.
More cell-to-cell invasion - protected from Ab.

Front 112

What is the advantage of more cell to cell invasion for Shigella?

Back 112

Protected from antibody deposition

Front 113

How does Shiga toxin work? What part of intestinal epithelial cell is targeted?

Back 113

(Same toxin as in EHEC and EIEC). There is an A subunit bound to 5 B subunits. The B subunits (B for binding) bind to the microvillus membrane in the colon, allowing entry of the deadly A subunit (A for Action). The A subunits inactivate the 60S ribosome, inhibiting protein synthesis and killing intestinal epithelial cells.

(a) fluid secretion by blocking fluid adsorption in the intestine, and
(b) more mucosal damage and bleeding. Only produced by S. dysenteriae species, which also causes most severe disease.

Front 114

Responsible protein for intracellular spread thru actin polymerization in shigella

Back 114

IcsA

Front 115

Curved gram-negative rod with a single polar flagellum

Back 115

vibrio cholera (visualize a curved C)

Front 116

What is the cholera toxin?

Back 116

Choleragen

Front 117

How does cholera cause death?

Back 117

dehydration. Diarrhea loss of up to 1 L/hour

Front 118

How is cholera spread?

Back 118

fecal-oral route

Front 119

US infections of cholera: most common cause

Back 119

mostly from eating raw shellfish from the Gulf.

Front 120

What are the 3 cholera biotypes?

Back 120

O1 classical; O1 El Tor biotype: produces hemolysis; O139 Bengal (new)

Front 121

Antibiotic given in cholera

Back 121

Tetracycline can shorten duration and excretion of organisms.

Front 122

What is achlorhydria and how does it affect cholera infection?

Back 122

(reduced gastric acidity) from malnutrition increases susceptibility

Front 123

Why is a large dose of cholera needed to cause disease?

Back 123

It's sensitive to stomach acid. Less of a dose needed if achlorhydria is present

Front 124

Cholera toxin mechanism of action

Back 124

Similar to E Coli LT toxin. On Chromosome.

ADP-ribosylating toxin that modifies a Gs protein, stimulating membrane adenylate cyclase, leading to increased cAMP.


Increased cAMP stimulates Cl- secrtion and inhibits Na+ absorbtion. Since water follows Na+, there is an outpouring of fluids

Front 125

T/F on microscopic exam of stool, will see leukocytes in cholera

Back 125

F. Should NOT see them but may see curved rods with darting movements

Front 126

Which cholera virulence factors permit penetration of surface mucus covering intestinal mucosa?

Back 126

Mucinase and motility of the flagellum

Front 127

Which cholera virulence factors allows adherence of the organisms to the epithelial surface despite large outpouring of fluid?

Back 127

TCP = Toxin Co-regulated Pilus

Front 128

Vibrio parahaemolyticus : What disease does it cause?

Back 128

A Marine bacterium that requires high NaCl for growth, and is common to coastal waters
Causes 1/2 of all food poisonings in Japan where eating uncooked seafood is common.
In U.S., associated with under cooked shellfish.
24-48 hrs after ingestion
acute enteritis (severe cramping, abdominal pain, vomiting, watery diarrhea)

Front 129

Vibrio vulnificus : what disease does it cause?

Back 129

Rapidly progressive wound infections - cuts usually contaminated with seawater; can produce life-threatening bacteremia (typically in fishermen or seashore bathers).
Diarrhea following ingestion of raw shellfish (e.g., oysters), may produce bacteremia

Front 130

Camping bacteria in the jejunum with nothing better to do than cause diarrhea!

Back 130

Campylobacter jejuni

Front 131

What other bacteria does Campylobacter Jejuni look like?

Back 131

Looks like vibrio cholera

Front 132

3 most common causes of diarrhea in the world

Back 132

Campylobacter jejuni, ETEC, Rotavirus

Front 133

Campylobacter Jejuni Campylobacteriosis: where it comes from

Back 133

It's zoonotic. Found in wild and domestic animals and poultry.

consuming contaminated:
Food (often poultry), raw milk
Contaminated water
contact with infected animals (especially sick cats and dogs)

Front 134

When do symptoms of C jejuni infection start?

Back 134

2-5 days after ingestion of only 500 bacteria

Front 135

What are symptoms of campylobacter jejuni

Back 135

Diarrhea - (watery or sticky) containing blood and fecal leukocytes
Fever
Abdominal pain and nausea
Headache and muscle pain

Front 136

Virulence factors of campylobacter jejuni

Back 136

1) Enterotoxin: heat labile adenylate cycle activating toxin, related to cholera but doesn't cause inflammatory signals
2) Cytotoxin - may have role in inflammatory colitis
3) Adhesin - to intestinal mucosa

Front 137

Relation of helicobacter pylori to cancer

Back 137

Chronic infection can cause active gastritis, gastric MALT lymphoma, and gastric adenocarcinoma.

Front 138

Transmission of H pylori

Back 138

Suspected oral-oral or fecal-oral. Humans only known reservoir.

Front 139

Morphology/characteristics of H pylori

Back 139

Gram-negative spiral microaerophilic bacterium.

Front 140

What are the virulence factors of H pylori?

Back 140

1) Urease: converts urea to ammonia and CO2 creating a more alkaline envt and allows organisms to survive the extreme acid (pH 2) of the stomach. Ammonia is also toxic to eukaryotic cells and causes inflammation of the gastric mucosa.

2) Adherence mechanism: appears to be like EPEC strains of E coli

3) Cytotoxin: similar to E coli alpha hemolysin