Listeria Flashcards

1
Q

What are the 2 major species of Listeria of veterinary importance? What animals do they mostly affect?

A

L. monocytogenes
L. ivanovii

Ruminants (sheep)

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2
Q

What are the 2 major species of Listeria of veterinary importance?

A
  1. L. monocytogenes***
  2. L. ivanovii
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3
Q

How does Listeria stain? What morphologies do they undertake?

A

Gram positive

rod/bacilli

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4
Q

What respiration does Listeria undergo? Do they form spores?

A

facultative anaerobe

non-spore forming

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5
Q

How does Listeria respond to the catalase test?

A

catalase positive

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6
Q

Does Listeria have motile abilities? How is it tested?

A

yes - has flagella

tumbling motility and umbrella-shaped colony growth in a semi-solid motility media

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7
Q

What function do Listeria’s flagella have?

A

actin jet motility inside of host cell

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8
Q

How does Listeria grow on blood agar? In what 2 unique environments is Listeria able to grow in?

A

β-hemolytic

  1. resistant to high salt in environment
  2. able to grow at cold temperatures (4 degrees C)
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9
Q

What are the 14 different serotypes of Listeria based on? What 3 serotypes are the most virulent?

A

based on their different somatic (O) and flagella (H) antigens

  1. 1/2a = isolated from food
  2. 1/2b
  3. 4b = majority of human epidemics
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10
Q

What is the optimal agar for Listeria growth?

A

Mullen-Hinton agar enriched with 5% sheep blood

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11
Q

What are the 2 key issues with isolating Listeria on a culture media?

A
  1. requires an enriched media, since it is fastidious (β-hemolytic; ferments carbohydrates, producing acid and no gas)
  2. requires prolonged incubation time for the recovery of the stressed cells (at 4 degrees C for weeks; usually weakened or injured cells will not grow)
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12
Q

How are weak and injured Listeria isolated?

A
  1. put in 2 possible enrichment broth media: FDA BAM or ISO 11290
  2. after 4 hours selective agents, like acriflavin, nalidixic acid, and antifungal cycloheximide, are added to sample broth
  3. incubate FDA BAM for 48 hrs at 30 degrees C amd ISO 11290 for 24 hrs at 30 degrees C
  4. add full selective secondary-enrichment full concentration Fraser broth for 24 hrs
  5. spread plate on Listeria selective agar
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13
Q

What 3 Listeria adaptions make it really hardy?

A
  1. resistant to high salt in media
  2. survive and multiply on inanimate objects (silage through transition processes from one host to another)
  3. adapt to changing temperature and pH (able to multiply in a refrigerator)
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14
Q

What is the usual environment Listeria live in? Are they commensal? What temperature are they most commonly found at?

A
  • grow as saprophytes in soil and decaying vegetation in the environment (sewage, water, feed, food)
  • NO, they are a frank pathogen
  • abundant at colder temperatures in the EU and North America (< 4 degrees C)
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15
Q

What is Listeria’s host range like? What are they most common in?

A
  • DIVERSE - humans, mammals, birds, fish, insects
  • ruminants, mainly sheep —> seasonal outbreaks
  • sporadic in pigs and horses
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16
Q

What is Listeria considered in human disease?

A

well-recognized foodborne pathogen

17
Q

How does Listeria enter its host? How does this mainly happen in livestock and humans?

A

ingestion (orally)

  • LIVESTOCK: feeding of silage with high iron content, which is common in decaying plants
  • HUMANS: consumption of contaminated raw vegetables, meat, and milk
18
Q

What are the main 3 ways that Listeria exit their host?

A
  1. feces
  2. vaginal discharge (abortion)
  3. milk (mastitis)
19
Q

What 3 body structures contribute to Listeria’s virulence?

A
  1. flagella (1-5): motility, adhesion, invasion
  2. internalin (A, B, C): adhesion, invasion (like a drill)
  3. invasion-associated protein (iap): adhesion, invasion
20
Q

Can Listeria form biofilms?

A

YES

21
Q

What helps Listeria avoid host immune responses and treatment?

A

it is an intracellular pathogen that multiplies within tissue cells, monocytes, and macrophages, so it is able to hide from immune patrolling, antibodies, and antimicrobials

22
Q

What 2 enzymes factor into the virulence of Listeria?

A
  1. superoxide dismutase - protects against free radicals from host phagocytes
  2. phospholipase - pore-forming lysis on endocytic membrane of the host to free itself from lysosomes and get into the cytoplasm of host cells
23
Q

What 4 toxins contribute to Listeria’s virulence?

A
  1. β-hemolysin - pore-forming lysis on endocytic membrane of the host to free itself from lysosomes and get into the cytoplasm of host cells
  2. listeriolysin O - same as above
  3. listeriolysin S - kills competing gut microbiota
  4. actin-polymerizing protein (actA) - instructs host cell to deposit actin filaments on the end of Listeria that it is able to use to propel into nearby cells (zipper mechanism)
24
Q

What are 2 other bacteria that use the zipper mechanism of cell hopping?

A
  1. Rickettsia
  2. Yersinia pseudotuberculosis
25
Q

What 4 body barriers is Listeria able to enter?

A
  1. BBB
  2. placental barrier
  3. intestinal barrier
  4. cell membrane (lipid bilayer of cells)
26
Q

What are the 4 key steps to Listeria pathogenesis?

A
  1. attachment and adhesion to epithelial cells or macrophages
  2. intracellular invasion
  3. lysosomal escape and intracellular multiplication
  4. spread to other cells (zipper method, actin rocket)
27
Q

How is Listeria able to bind to epithelial cell surfaces?

A

surface protein on Listeria, internalin, binds to e-cadherin on the epithelial cell

28
Q

Why does the zipper/actin rocket method work so well for Listeria spread?

A

allows Listeria to propel from cell to cell without being exposed to antibodies, complement, and phagocytes

29
Q

What are the main 4 results of Listeriosis? What are 2 subclinical manifestations?

A
  1. febrile gastroenteritis
  2. septicemia/shock
  3. placentitis - abortion, still birth, neonatal sepsis/meningitis
  4. brainstem and cranial nerve dysfunction
  5. focal pyogranulomatous hematosplenitis
  6. enlarged lymph nodes
30
Q

What are the 2 major clinical manifestations of Listeriosis? What causes each?

A
  1. NEURAL - silage-fed sheep
  2. VISCERAL - septicemia
31
Q

What are the 3 major manifestations in neural listeriosis?

A
  1. microabscesses in brain
  2. ataxia, “circling disease”
  3. unilateral facial paralysis - head tilting to one side, unilateral ear dropping, tongue protrusion, salivation
32
Q

What are 7 results due to visceral listeriosis?

A
  1. gastroenteritis
  2. septicemia
  3. liver/spleen damage
  4. fetoplacental tropism (abortion)
  5. myocarditis
  6. osteomyelitis
  7. mastitis
33
Q

What is the prognosis of Listeriosis in humans?

A

grave —> L. monocytogenes is the 3rd leading cause of death from food-borne illnesses in the US

34
Q

What are 4 common treatments to Listeria infection?

A
  1. ampicillin
  2. chlortetracycline
  3. penicillin
  4. trimethoprim-sulphmethoxazole
    (not as resistant as ESKAPE)
35
Q

Why is it difficult to control Listeriosis infection?

A
  • hides within host cells
  • little is known about risk factors other than silage
  • vaccination is not widespread (LAV in Norway, killed vaccine in some others)
36
Q

How is Listeria infection controlled in humans?

A

food hygiene