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Immuno Bacteria > Bacteria of GI > Flashcards

Bacteria of GI Flashcards

1
Q

Listeria morphology? Growth range?

A 
Aerobic 
Gram +
Bacilli/Rod
Non-spore forming
1-45 degrees - storage and salt conditions of prepared foods/fridge
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2
Q

Explain Listeria’s pathogenesis

A

Ingest contaminated food
Enter and adhere to host (can survive bile salt and acid conditions)
Enter enterocytes or M cells of Peyer patches (ileum)
Low pH of phagosome activates listerolysin O + 2 different phospholipase C enzymes
Replicate in cytoplasm
ActA on one side of bacteria polymerize host actin so bacteria can move to the membrane
Pushes bacteria to uninfected cell, REPEAT

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3
Q

Which bacteria cause systemic infections?

A

Listeria

Salmonella

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4
Q

How does Listeria cause systemic infections?

A

After getting into enterocytes/M cells, it can polymerize the actin and push out of the intestinal lining -> entry into macrophage and SPREAD TO RETICULOENDOTHELIAL SYSTEM (spleen, liver, etc)

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5
Q

Listeria epidemiology? How can it be transferred?

A

Human disease (listeriosis) is sporadic

Unprocessed meats, unpasteurized milk, contaminated cheese, unwashed raw veggies

Feces of animals (mammals, birds, fish)

Can survive in fridge

HUMAN TO HUMAN via mother to child in utero (in 3rd trimester when cellular immunity is low)

Highest in eldery, neonates, pregnant women, transplant pts, AIDS, defects in CELLULAR immunity

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6
Q

How does listeriosis in neonates affect them?

A

Early onset in utero: abortion, stillbirth, premature

Granulomatosis infantiseptica = granuloma formation in multiple organs

Later onset (2-3 weeks after birth): meningitis or meningoencephalitis with septicemia

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7
Q

Clinical presentation of listeria in pregnant women?

A

Influenza with fever

Happens during 3rd trimester when cellular immunity is impaired

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8
Q

Clinical presentation of listeria in adults?

A

Healthy: mild flu-like sickness, acute, self-limited gastroenteritis

Compromised: meningitis, high mortality, significant neurologic sequelae

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9
Q

Lab dx of listeria?

A

Gram stain of CSF in meningitis pts (>10,000/ml)
Culture - cold enrichment (if its too hot, not as motile)
Biochemical tests
Serological tests (13 serotypes)
Pulsed gel electrophoresis

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10
Q

Treatment of listeriosis? Vaccine?

A

Gentamicin + penicillin or ampicillin

No vaccine!

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11
Q

Why is listeria hard to control? What steps to take?

A

Ubiquitous in environment, lots of animals, wide temp range
Naturally cephalosporin resistant
Avoid eating raw/partially cooked food, soft cheeses, unwashed raw veggies

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12
Q

Where is salmonella found?

A

soil, water, normal intestinal flora

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13
Q

What antigens can be found on salmonella?

A

H: flagellar protein antigen
K or Vi: capsular antigens for E. coli and S. typhi
O: LPS antigen

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14
Q

How many different salmonella serotypes?

A

> 2500 unique

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15
Q

Are all salmonella found in humans?

A

No, broad host range (mammals, birds, reptiles, rodents, etc

S. typhi and S. paratyphi are highly adapted to humans

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16
Q

How are Salmonella and Listeria similar? Different?

A

Similar:

  • Salmonella can resist stomach acid, attach and invade mucose of small intestine and invade into enterocytes/M cells of Peyer patches
  • Both cause systemic infections by replicating in macrophages and spreads through reticuloendothelial system - TYPHI (liver, spleen, blood, bone marrow)

Differences:
- Salmonella replicates within endocytic vacuoles (vs cytoplasm)

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17
Q

How does Salmonella cause gastroenteritis?

A

Serotypes OTHER than typhi and paratyphi!

  • Infection and replication induces inflammatory response
  • Disruption of enterocytes and malabsorption
  • Release of PGs, stimulation of cAMP and fluid secretion
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18
Q

How does Salmonella cause enteric or typhoid fever?

A

S. Typhi (humans, remember)

  • Same invasion and replication as in gastroenteritis
  • Typhi ALSO replicates in macrophages to enter reticuloendothelial system
  • Bacteremia causes fever and leads to localized infections like osteomyelitis, endocarditis, arthritis, or perforations of intestine
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19
Q

How is salmonella transmitted?

A

Enteric/Typhoid fever: human to human, fecal-oral
Gastroenteritis: Ingestion of contaminated food (poultry, eggs, dairy products, ground beef) ALSO feces from amphibians and reptiles

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20
Q

Outbreaks in children of Salmonella can occur with the introduction of _____

A

pet turtles

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21
Q

Clinical salmonella gastroenteritis?

A

Symptoms 6-48 hours after consumption of contaminated food and last for 2-7 days, self limiting

Fever, ab cramps, myalgias, headache, nausea, vomiting and nonbloody diarrhea

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22
Q

Clinical enteric fever?

A

10-14 days after ingestion; bacteremic phase (gradual fever, headache, anorexia, rose spots) followed by gastrointestinal symptoms

Colonization of gall bladder and reinfection of the intestines

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23
Q

Why is time a factor in diagnosing salmonella?

A

6 hours is a cut off point; is it an infection where the bacteria needed time to replicate or did the person consume contaminated preformed toxin which has quicker effects leading to intoxication?

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24
Q

ALL species of salmonella can cause bacteremia. True or false?

A

TRUE; Compromised hosts at risk for septicemia

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25
Q

Lab dx of salmonella?

A

Stool culture -> grow it in a medium that selects for salmonella vs normal flora

Lactose negative, motile, MAKES H2S!

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26
Q

How to treat salmonella?

A

Careful with food prep and storage, hand washing

- Ampicillin, trimethoprim-sulfamethoxazole OR ciprofloxacin for systemic infections

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27
Q

Is there a vaccine for Salmonella?

A

Yes, for travelers:

  • Live attenuated vaccine Ty21a, good for 5 years, 6 capsules every other day, booster at 4 years not rec for under 6 yo
  • Typhim = Vi polysaccharide capsule vaccine not rec for under 2 yo
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28
Q

Shigella characteristics?

A 
Gram neg
Non-motile
Doesn't ferment lactose
NO capsule
Low infectious dose, spread p2p, fec oral route
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29
Q

Where do shigella colonize and replicate?

A

Initially colonize in small intestines and invade M cells in Peyer patches.

Replicate intracellularly in the colon

30
Q

How does shigella get into cells to invade?

A

Inject type III effectors into cells to instruct the cytoskeleton to engulf them

“effectors” - IPA A, B, C and D - Invasion Protein Antigens

31
Q

How does replication of shigella compare to listeria and salmonella?

A

Similar to listeria:

  • gets into cell, lyses vacuole and replicates free in the cytoplasm
  • polymerize host actin to move to membrane and infect other cells
32
Q

How does shigella cause intense inflammation?

A

Induces apoptosis of phagocytic cells -> release IL-1beta -> severe inflammation

33
Q

What is shigella toxin?

A

Exported (NOT injected) by a type II secretory pathway
A:5B toxin
A: Cleaves 28S rRNA, disrupts protein synthesis and colonic epithelium dies, cells and mucus lost from large intestines
B: binding subunits that recognize host glycolipid GB3

34
Q

Reservoir for shigella?

A

Humans only!

35
Q

Shigellosis is predominant in ______

A

Children; considered a pediatric disease

60% in children less than 10yo

36
Q

Infection dose of shigella?

A

Low; 100-200 bacteria so p2p transmission through fec-oral is easy

37
Q

Clinical shigellosis?

A

Incubation after ingestion 1-3 days

  • cramps
  • straining to defecate
  • diarrhea
  • pus, blood, PMNs, mucus in stool

DYSENTERY: frequent passage of stool containing blood and mucous

38
Q

Lab dx similarity of shigella and salmonella? Difference?

A

Both lactose negative so appear as white colonies

Shigella is nonmotile, salmonella is motile
Shigella does NOT form H2S, salmonella does

39
Q

Treatment of shigella?

A

Mild infections usually self limiting

Antibiotics RESERVED FOR SEVERE ILLNESS. If gastroenteritis, let it flush out on its own. If enteric fever, TREAT because it can become systemic and colonize gallbladder.

Ampicillin, trimethoprim/sulfamethoxazole, ceftriaxone

ANtidiarrheal agents can make it worse -> more extensive cell death and inflammation

40
Q

EHEC is?

A

Enterohemorrhagic E. Coli

41
Q

EHEC infectious dose?

A

Low, p2p via fec-oral

42
Q

Toxic activity of EHEC can be neutralized with _____

A

Shiga antibodies (remember IPA invasion protein antigens antibodies)

43
Q

EHEC secrete shiga toxin. True or false?

A

True!

44
Q

Similarity and difference between EPEC and EHEC?

A

Same histopathology of attaching and effacing lesions

EHEC produce make shiga toxin, EPEC does NOT

45
Q

EHEC produce a distinct _______

A

histopathology of attaching and effacing lesions

46
Q

How does EHEC grow?

A

Inject protein called Tir, which embeds into host membrane, binds to bacterial outer membrane protein INTIMIN

Bacteria grow in place on top of pedestal and release Shiga toxin

47
Q

EHEC strains expressing ______ are more virulent

A

Stx-1 and Stx-2
Stx-1: shiga toxin
Stx-2: 60% homology to shiga toxin (A:5B)
*Shiga toxins are encoded in lysogenic bacteriophage in E. coli

48
Q

Shiga family toxins act by:

A

stimulating the expression of inflammatory cytokines

49
Q

EHEC is associated with __ and __ serotypes

A

O and H but is not a hard rule

50
Q

EHEC infections are associated with:

A

consumption of undercooked beef, other meat products, material contaminated in cattle feces, unpasteurized cider made from contaminated apples, spinach, sprouts

51
Q

Infectious dose of EHEC?

A

Low, 100-200 p2p fec-oral easy

52
Q

Clinical EHEC?

A

Range from mild uncomplicated diarrhea to hemorrhagic colitis (severe ab pain, bloody diarrhea 3-4 days after ingestion of contaminated food)

Vomiting in 50%, NO FEVER

Hemolytic Uremic Syndrome (HUS) in 5-10% of children

  • acute renal failure
  • thrombocytopenia
  • microangiopathic hemolytic anemia
53
Q

Lab dx of EHEC?

A

Differential ID based on the inability to ferment sorbitol (grow on sorbitol agar, EHEC can’t ferment so it will be colorless and normal, E. coli will be pink)

Look for serotypes associated with hemorrhagic colitis or HUS

Immunoassays to detect present of Stx-1 or Stx-2

54
Q

Treatment of EHEC?

A

Supportive care
Monitor HUS, development of microangiopathic complications
Careful cooking of food

Antibiotic therapy generally NOT beneficial
Antiperistaltic agents increase risk of systemic complications!

55
Q

Is antibiotic therapy useful for EHEC treatment? Why or why not?

A

NOT!
Does not alter length of illness
It increases shiga toxin release

56
Q

Campylobacter - systemic or not? Physical properties?

A

NOT systemic; pathogen that invades/inflammation/intoxicate

Gram negative
Comma shaped/rod, spiral
Microaerophilic, can grow at 42!
Motile - one or both poles

57
Q

Major isolates of campylobacter that cause human disease?

A

C. jejuni, upsalensis, coli and fetus

58
Q

Campylobacter pathology?

A
  1. ) Inflammation of jejunum, ileum and colon
  2. ) Infection associated with AUTOIMMUNE disorders
    - Guillain-Barre Syndrome (cross reactivity of some campylobacter LPS and neural gangliosides)
    - Reactive Arthritis
  3. ) Release toxin that stops cell division called CDT or CYTOLETHAL DISTENDING TOXIN
59
Q

How is campylobacter spread?

A

consumption of contamined food, particularly chicken

NOT/RARELY BY FOOD HANDLER

60
Q

Highest rates of campylobacter are when:

A

summer and early fall

61
Q

Domestic dogs are associated with which GI bacteria?

A

Campylobacter upsaliensis

62
Q

Acute enteritis is caused by which species of Campylobacter?

A

C. jejuni, coli, upsaliensis; incubation period of 1-7 days, onset of 2-4 days

63
Q

Why is campylobacter fetus particularly harmful?

A

Can cause systemic or extraintestinal infections and they are resistant to serum antibody and complement killing

64
Q

Lab dx of campylobacter?

A

DARTING motility in fresh fecal samples
S shaped organism in stool
Presence of RBC and WBC in stool
CULTURE IS DIFFICULT: slow growth, needs selective media since stool, microaerophilic environment, higher incubation temperatures

65
Q

Main treatment for campylobacter?

A

Fluid replacement as long as diarrhea lasts

66
Q

Helicobacter physical properties?

A

Gram neg
Curved rods
Multiple polar flagella (how does this compare to campylobacter?)
Microaerophilic

67
Q

Helicobacter colonization can be ______

A

lifelong

68
Q

Explain how helicobacter colonize gastric epithelium

A

They express urease, produces NH3 in front of them to survive acidic conditions, swim using flagella, adhere to gastric epithelium via LEWIS BLOOD-GROUP ANTIGENS and LAMININS

69
Q

What is the pH of gastric acid as you approach the cells?

A

pH 2 -> 4 -> 7 epithelial surface

70
Q

Production of peptic ulcers is strongly correlated with the possession of _____

A

2 genetic loci

  • VacA toxin
  • Loci that encodes many genes like:
  • –Type IV secretory system (specialized system) that injects CagA -> induces IL-8 release
  • — other genes that enhance IL-8 transcription in epithelial cells
  • — Type IV effectors that induce pedestal formation
71
Q

What is VacA and who makes it?

A 
Helicobacter
Multifunctional toxin 
- forms anion specific channels
- forms large vacuoles in cultured cells
- alter tight junctions
- induces gastric epithelial erosion in animal models

Immuno Bacteria (3 decks)

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