Enteric Bacteria (E. coli, Salmonella, Shigella, Campylobacter)

Question 1

Vibrio cholerae- main symptom? treatment?

Answer 1

copious watery diarrhea– oral rehydration (water, electrolytes)

Question 2

Vibrio cholerae- toxins, actions?

Answer 2

1) Ctx (“cholera toxin”): A+5B stucture, B binds cellular receptor and A is released into cell; increases adenylate cyclase activity, which increases cAMP and blocks Na+ reabsorption and triggers Cl- release => water flushed into intestinal lumen
2) toxin co-regulated pillus that adheres to intestinal epithelia

Question 3

Vibrio cholerae- where in the gut does it act?

Answer 3

small intestine

Question 4

common morphology of enteric bacteria

Answer 4

Gram negative rods (V. cholerae, Shigella, salmonella, E.coli)

Question 5

Vibrio cholerae: normal habitat; how infection occurs

Answer 5

normal habitat: coastal estuarine waters (assoc. with phytoplankton)
infection: contaminated food/water (esp when sewage systems are faulty), asymptomatic carriers (ie, Nepalese UN workers in Haiti 2010 earthquake relief)

Question 6

E. coli– normal habitat; how infections occur

Answer 6

many strains in gut; pathogenic strains may be in cows or other humans
- infection via fecal-oral contamination (esp manure, grey water irrigation of crops, food preparation, contaminated water)

Question 7

How are E. coli strains characterized?

Answer 7

O157:H7 O = O-antigen in LPS; H = flagellar antigen’s H protein

Question 8

4 strains of E. coli to know- where in the gut do they act?

Answer 8

small intestine- ETEC (enterotoxigenic), EPEC (enteropathogenic), EAEC (enteroaggregative)

large intestine- EHEC (enterohemorrhagic),

Question 9

ETEC- toxins/adhesions? key S/S?

Answer 9

Toxins: LT & ST, fimbriae & pili

S/S: traveler’s diarrhea (watery, copious)

Question 10

EPEC- toxins/adhesions? key S/S?

Answer 10

Toxins: none, effacement via intimin & a helical adhesive protein trigger diarrhea
S/S: watery/copious diarrhea

Question 11

EAEC- toxins/adhesions? key S/S?

Answer 11

Toxins: ST, alpha-hemolysin; fimbriae

S/S: water/copious diarrhea; I-comp patients; fimbriae aggregate in colonies

Question 12

EHEC- toxins/adhesions? key S/S?

Answer 12

Toxins: Shiga toxin or Shiga-like toxins (verocytotoxins); efface like EPEC
S/S: hemorrhagic colitis (nonfebrile bloody diarrhea), hemolytic uremia syndrome (more freq in kids)

Question 13

How do the ST & LT enterotoxins work? Naming? Which E. coli strains have which?

Answer 13

ST (heat stable)- increases cGMP
LT (heat labile): increases cAMP 
Those increases block electrolyte absorption, cause fluid excretion.
ST: in ETEC & EAEC
LT: in ETEC

Question 14

How does the Shiga toxin work? Where found?

Answer 14

Cleaves the 60s ribosomal subunit, preventing protein synthesis and thus killing cells.
Shigella & EHEC.

Question 15

Explain the hemorrhagic colitis of EHEC

Answer 15

Shiga toxin/verocytotoxins invades the mucosa, killing cells and causing structural damage in the large intestine which results in bloody diarrhea. NOT pussy (no leukocytes)

Question 16

3 key symptoms of hemolytic uremia- which enteric bacteria is it associated with?

Answer 16

EHEC

1) hemolytic anemia (lysed RBCs)
2) thrombocytopenia
3) kidney failure (damaged small vessels + lysed RBCs get caught in the glomeruli)

Question 17

Shigella- key S/S?

Answer 17

dysentery (bloody/pussy diarrhea, fever, abdominal pain); 30X/day (relatively infrequent compared to cholera)

Question 18

pathogenesis of Shigella

Answer 18

Invades the M cells of the epithelia, escapes phagosomes of macrophages and gets into the lamina propria, reinfects epithelial cells from underneath and rides cytoskeleton back to surface (cylic). In the process, M & epithelial cells die => ulcers, bleeding. Macrophage response causes inflammation=> neutrophils accumulate, causing pus.

Question 19

Treatment for Shigella

Answer 19

oral rehydration, no antibiotics

Question 20

How does Shigella infection occur?

Answer 20

contaminated f/w or contact with infected people; only need a few hundred cells for it to occur

Question 21

4 strains of Shigella

Answer 21

S. dysenteriae, sonnei, boydii, flexneri.

S. dysenteriae has the Shiga toxin, most common for disease.

Question 22

2 causes of dysentary

Answer 22

Shigella
Entamoeba histolytica (parasite!)

Question 23

3 causes of combo bloody/watery diarrhea

Answer 23

Salmonella, Campylobacter jejuni, Yersinia enterolitica

Question 24

Bloody/water diarrhea- which part of the intestine? S/S?

Answer 24

Ileum + colon (leads to tissue invasion); blood, water, pus, copious/liquidy diarrhea

Question 25

Key difference between E.coli/V.cholerae & Shigella/Salmonella infections

Answer 25

NO tissue invasion in E. coli/V. cholerae (no pus)

Question 26

Salmonella- natural habitats?

Answer 26

Chicken (eggs!), reptiles (pet turtles), cows, asymptomatic humans (typoid Mary)

Question 27

Typical S/S of Salmonella & atypical case

Answer 27

1) N/V/D nonsystemic gastroenteritis
2) Typhoid fever (systemic infectious)
Atypical: osteomyelitis in patients with sickle cell disease

Question 28

Pathogenesis of typhoidal salmonella & associated S/S

Answer 28

Infects via small intestine, then spreads via mesenteric LNs to blood stream. Multiplies in the macrophages of the liver, spleen, LNs, and bone marrow. Travels via bile to the gallbladder and then back to the small intestine.

In blood: causes septicemia, v v high fever => kidney/organ damage.
In gallbladder: cholecystitis, or asymptomatic carrier state
In small intestine: inflames/ulcerates Peyer’s patches, causes bloody diarrhea + perforations

Question 29

Treatments for Salmonella infection

Answer 29

Non-systemic: oral rehydration

Typhoidal: antibiotics required

Question 30

Campylobacter jejuni: Gram status? shape & culture features?

Answer 30

Gram negative. Seagull-shaped with 1 flagella.

Grows HOT! 42C with Co2-enriched medium

Question 31

Pathogenesis of Campylobacter & features of the IR

Answer 31

Invades mucosa of jejunum, ileum, colon. Produces endo, entero, cytotoxins.
Gastric juice secretion -> erosive lesions.
Complement cascade
Ab-dependent killing - > molecular mimicry can lead to Guillain Barre (CNS) and reactive arthritis (MSK)

Question 32

HLA risk factor for getting reactive arthritis from Campylobacter

Answer 32

HLA-B27+

Question 33

S/S of Campylobacter infection

Answer 33

Acute gastroenteririts, bloody diarrhea. 10d-4weeks of fever, malaise, crampy abdo pain.

Question 34

Campylobacter transmission

Answer 34

fecal-oral contact, unpasteurized milk, undercooked meat/poultry, close contact with infected animals (dogs/cats/pigs)

Question 35

Risk factors for Campylobacter

Answer 35

1) lack of gastric juices
2) complement deficiencies
3) Humoral deficiences (ie, hypo-gamma-globulinemia)

Question 36

Treatment for Campylobacter

Answer 36

Rehydration! Can give macrolides (though GI effects can be worse) or fluoroquinones