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

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1
Q

Vibrio cholerae- main symptom? treatment?

A

copious watery diarrhea– oral rehydration (water, electrolytes)

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2
Q

Vibrio cholerae- toxins, actions?

A

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

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3
Q

Vibrio cholerae- where in the gut does it act?

A

small intestine

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4
Q

common morphology of enteric bacteria

A

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

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5
Q

Vibrio cholerae: normal habitat; how infection occurs

A

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)

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6
Q

E. coli– normal habitat; how infections occur

A

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)

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7
Q

How are E. coli strains characterized?

A

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

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8
Q

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

A

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

large intestine- EHEC (enterohemorrhagic),

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9
Q

ETEC- toxins/adhesions? key S/S?

A

Toxins: LT & ST, fimbriae & pili

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

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10
Q

EPEC- toxins/adhesions? key S/S?

A

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

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11
Q

EAEC- toxins/adhesions? key S/S?

A

Toxins: ST, alpha-hemolysin; fimbriae

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

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12
Q

EHEC- toxins/adhesions? key S/S?

A

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)

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13
Q

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

A
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
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14
Q

How does the Shiga toxin work? Where found?

A

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

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15
Q

Explain the hemorrhagic colitis of EHEC

A

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)

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16
Q

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

A

EHEC

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

17
Q

Shigella- key S/S?

A

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

18
Q

pathogenesis of Shigella

A

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.

19
Q

Treatment for Shigella

A

oral rehydration, no antibiotics

20
Q

How does Shigella infection occur?

A

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

21
Q

4 strains of Shigella

A

S. dysenteriae, sonnei, boydii, flexneri.

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

22
Q

2 causes of dysentary

A
Shigella
Entamoeba histolytica (parasite!)
23
Q

3 causes of combo bloody/watery diarrhea

A

Salmonella, Campylobacter jejuni, Yersinia enterolitica

24
Q

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

A

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

25
Q

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

A

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

26
Q

Salmonella- natural habitats?

A

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

27
Q

Typical S/S of Salmonella & atypical case

A

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

28
Q

Pathogenesis of typhoidal salmonella & associated S/S

A

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

29
Q

Treatments for Salmonella infection

A

Non-systemic: oral rehydration

Typhoidal: antibiotics required

30
Q

Campylobacter jejuni: Gram status? shape & culture features?

A

Gram negative. Seagull-shaped with 1 flagella.

Grows HOT! 42C with Co2-enriched medium

31
Q

Pathogenesis of Campylobacter & features of the IR

A

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)

32
Q

HLA risk factor for getting reactive arthritis from Campylobacter

A

HLA-B27+

33
Q

S/S of Campylobacter infection

A

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

34
Q

Campylobacter transmission

A

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

35
Q

Risk factors for Campylobacter

A

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

36
Q

Treatment for Campylobacter

A

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