Immunity And Infection Gi Infections

Front 1

What are the manners in which GI infections can cause disease?

Back 1

Toxin production
Adhesive/aggregative (occupy microvilli)
Invasive - Inflammation

Front 2

What organism requires very few organisms to cause disease? Which require many?

Back 2

S. dysenteriae = few hundered
ETEC = 10^8

Front 3

What are the GI defenses vs. pathogens?

Back 3

low pH in stomach
small intestine: large volume, preoteases, bile, IgA
Large intestine: large # flora produces inhibitory substancs and occupies adhesive sites

Front 4

How does cholera toxin work? How is it carried?

Back 4

Binds to ADP ribosylating enzyme and locks it "on"
Increased cAMP
-turns off Na+ absorption
-increase Cl secretion
-results in net loss water
Quickly causes dehydration
Carried on a phage

Front 5

What other species produces a cholera like toxin?

Back 5

Labile toxin of E. coli
Salmonella
Campylobacter
Yersina
Aeromonas

Front 6

What does the stabile toxin of E. coli do?

Back 6

Increases cGMP

Front 7

Vibrio Cholerae

Back 7

Lives in saline water but can grow in absence of salt.
Human pathogen.
Can adhere
Causes secretory rice water diarrhea
pandemics caused by O1 or O139
Spread by consumption of contaminated water/food
Person to person spread is unlikely
Antibiotics may shorten the duration of toxin secretion and decrease spread

Front 8

Vibrio parahemolyticus

Back 8

Gained through consuming improperly cooked seafood esp. raw oysters
Requires salt
Gastroenteritis year round
Cuases septicemia and wound infections in warm months (multiplies in seawater)

Front 9

Vibrio vulnificus

Back 9

Very virulent, has a capsule to protect against phagocytosis and complement mediated killing
Severe wound infections and sepsis
Sepsis can occur after eating oysters
Especially in cirrhosis, renal failure

Front 10

Describe the enterobacteriaceae
Lactose +
Lactose -
3 groups

Back 10

G- rods, most are motile (NOT shigella, Klebsiella, Yersina)
Lactose +: Citrobacter, serratia, E.coli, Enterobacter, Kleb
Lactose -: Salmonella, Shigella, Yersinia, Proteus

3 groups
1) Commensals: E. coli, Proteus, Kleb., May be opportunistic
2) Shigella, Salmonella, Yersinia
3) Acquired virulence: E.coli

Front 11

What are the pathogenic E. coli?

Back 11

ETEC
EPEC
EHEC
EAEC - enteroadhesive E. coli

Front 12

ETEC

Back 12

Traveler's diarrhea
Exposure induces mucosal immunity
Requires high dose of to cause infection
asymptomatic carrier states
Source is contaminated food/water
14-50 hours incubation
Labile toxin = cholera like (increases cAMP)
Stabile Toxin = like Yersinia and Vibrio cholerae, (increases cGMP stimulates Cl secretion, inhibits NaCl absorption), both cause secretory diarrhea
Therapy = Antibiotics decrease duration and severity, bismuth can prevent

Front 13

EPE

Back 13

Infant diarrhea in developing world
Hallmark: effacing of microvilli and attaching cell membrane leads to activation signal transduction
Transmission: oral/fecal, hands, foods, tabletops
Reservior: asymptomatic kids and adults
Diagnosis: culture HeLa cells, PCR
Mortality: 50%
Symptoms: diarrhea, sometimes vomiting

Front 14

EHEC

Back 14

E. coli 0157:H7
Shiga like or Vero like Cytotoxin associated with hemolitic uremic syndrome on phage (Stx)
Stx causes bloody diarrhea
Hemolytic uremic syndrome = hemorrhage and edema
Reservoior = animals and meats (beef, lamb-mostcommon, poultry)
Transmission = burgers, apple juice, salami, mayonnaise, radish sprouts
small infectious dose, (can be persone to person)
Clinical: 1st diarrhea, fever, cramps, then bloody diarrhea lasting 4-10 days, develop hemolytic uremic syndrom consisting of hemolytic anemia, oliguric renal failure, thrombocytopenia
More likely if very young/old, antimotility drugs, expression of Stx2, AB NOT indicated
Diagnosis = culture stule on sorbitol macconkey, or detecting Stx on PCR

Front 15

What causes dysentery and bloody diarrhea? What is dysentery and bloody diarrhea?

Back 15

Structural damage to intestine, invasion or damage to mucosa
Dysentery = frequent stools, small volume, gross pus with or without blood, caused by Shigella or Entamoeba
Organisms invide intestinal epithelium
Inflammatory leukocyte reaction in lamina propria
Release of inflammatory mediators or vascular abnormalities results in blood

Bloody diarrea = invasion of the gut mucosa, caused by nontyphoid salmonella, Campylobacter, Yersinia

Front 16

Shigella

Back 16

S. dysenteriae = developing countries (severe)
S. sonnei = most common US, (mildest illness)
Infect humans only
Low infectious dose
Resistant to acid
Spread through sexual contact, direct contact, food water
Mostly seen in kids younger than 15
Endemic disease in male homosexuals
Mechanism = invade colonic mucoa, multiply intracellular and spread from cell to cell, leads to focal mucosal ulcers and inflammation.
Invasion located on large plasmid
Invasion associated with structural changes
Cytotoxin = only S. dystenteriae has Shiga toxin, an enzyme that irreversibly inactivates 60S ribosomal subunit synthesis
Disease is mild watery diarrhea to dysentery
Fecal sample will contain leukocytes
Culture will show lactose negative bacillus
Identify species by DNA probe/PCR
Therapy = antibiotics reduce duration illness and period of infectivity, AB resistance is common