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Veterinary Bacteriology & Mycology > Moraxella & Francisella > Flashcards

Moraxella & Francisella Flashcards

1
Q

What is unique about Moraxella bovis structure?

A

appears as a Gram-negative diplococci —> not a true coccus, cells are rod-shaped around a penicillin disk

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2
Q

What respiration and fermentation does Moraxella bovis undergo?

A
  • strict aerobes
  • nonsaccharolytic: oxidizes sulfur and nitrogen (amino acids)
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3
Q

What infection does Moraxella bovis cause? What are the clinical signs?

A

infectious bovine keratoconjunctivitis (IBK, bovine pinkeye)

  • conjunctivitis
  • keratitis
  • corneal ulceration
  • more than 5% of herd infected
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4
Q

Where is Moraxella bovis commonly found? How is it transmitted? What is required for infection?

A

normal flora in upper respiratory tract

direct contact with fomites (grass), flies, dust

attachment to the eye and colonization

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5
Q

What are 5 predisposing factors to Moraxella bovis infection? How is infection commonly controlled?

A
  1. sunlight (UV) - irritation
  2. breed - non-hooded eyelids (Herefords)
  3. flies - transmission
  4. irritation - dust, grass
  5. prior infection

protect the eye from irritants (eye patches)

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6
Q

What cattle are more suscpetible to Moraxella infection?

A
  • less than 2 years old (lower immnuity)
  • those with non-hooded eyelids (Herefords)
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7
Q

What is a corneal pannus?

A

common presentation of Moraxella bovis infection - subepithelial fibrovascular tissue ingrowth occurs from the limbus onto the cornea, usually resulting from inflammation from chronic irritation

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8
Q

Moraxella bovis, pinkeye:

A

corneal opacity due to intraocular fluid pressure + bright red rim of pannus formation

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9
Q

Moraxella bovis, pinkeye:

A

ulcer in localized area of corneal opacity
- no pannus formation with shallow lesions

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10
Q

Moraxella bovis, pinkeye:

A

small corneal scar due to incomplete healing
- B = artifact from flash

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11
Q

What is a staphyloma?

A

secondary infection of Staphylococcus aureus in the resulting ulcer left from Moraxella bovis, resulting in a deep ulcer perforating through the aqueous humor

  • Staph. is common on skin and less fastidious, so it will be an opportunistic pathogen and commonly found in a culture with Moraxella
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12
Q

Moraxella bovis, pinkeye:

A

healing ulcer that has lost its red appearance

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13
Q

How does Moraxella bovis infection cause increased intraocular pressure? What does this result in?

A

impairs the drainage of aqueous humor —> glaucoma

damages the optic nerve due to increased pressure and chronic inflammation

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14
Q

Moraxella bovis, pinkeye:

A
  • secondary infection of the eye (endophthalmitis) with purulent inflammation and pus in the anterior chamber
  • pannus formation
  • white and irregular cornea
  • sight permanently lost due to scar formation, pus buildup, and glaucoma
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15
Q

What are the 2 major virulence factors of the virulent strains of Moraxella bovis?

A
  1. β-hemolysin - enhances lesion formation
  2. highly piliated - sticks to plate/eye
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16
Q

What are the 3 major effects of highly piliated strains of Moraxella bovis?

A
  1. cell adherence
  2. cytotoxicity
  3. enhances corneal pitting —> leaves holes upon detachement

(mutants without pili do not cause disease!)

17
Q

What are 4 other virulence factors Moraxella bovis contains?

A
  1. cytotoxin/hemolysin - RTX toxin
  2. cell detachment factor
  3. capsule - protective
  4. LOS - endotoxin that may act synergistically with other toxins
18
Q

What are the 5 steps to Moraxella bovis pathogenesis?

A
  1. bacteria adhere to corneal epithelial cells
  2. adherence factors and toxins cause pits or depressions on the cornea
  3. polymorphonuclear cells infiltrate lesion and causes inflammation, leading to conjunctivitis and serous discharge
  4. cornea becomes hazy, edematous, and opaque
  5. ulcers may develop and cause rupture of the anterior chamber
19
Q

What 3 aspects of immunity aid in Moraxella bovis protection?

A
  1. antibodies to pili are protective, but strain specific
  2. IgA highest in lacrimal secretions (may not prevent clinical disease)
  3. antibodies to toxins may reduce or prevent disease (pili and hemolysin both needed to cause disease)
20
Q

How long does it take for cattle to produce protective antibodies after given bacterins against Moraxella bovis?

A

4 weeks
- use a strain already isolated from the herd so the pili are antigenically identical

21
Q

How is Moraxella bovis infection prevented?

A

ANIMAL MANAGEMENT
- fly control via chemical insecticides, tags, sprays, dust bags
- manure/plant control
- eye patches

22
Q

How is Moraxella bovis infection diagnosed?

A

eye swab cultured immediately to blood agar
- remember: eye is not sterile, but Moraxella is not a part of the eye flora

Gram-negative diplococci
hemolytic
oxidase +
colonies pit agar

23
Q

What is the structure of Francisella tularensis like? What respiration does it undergo?

A
  • Gram-negative coccobacillus
  • stains bipolar with Giemsa stain —> tiny cells, hard to see
  • obligate aerobe
24
Q

What is required for Francisella tularensis growth on agar? What species has an exception?

A

cysteine (added to chocolate agar)
2-4 days for growth

F. novicida can grow on blood agar - less pathogenic, parent strain

25
Q

What disease does Francisella tularensis cause? How is it typically transmitted?

A

Tularemia predominantly in wild animals (+ cats and sheep)

  • ticks
  • deer flies
  • lice
  • water
  • handling infected carcasses
26
Q

What wild animals are most affected by tularemia? Domestic animals?

A

lagomorphs —> “rabbit fever”, rabbit hunters susceptible

cats and sheep (+ humans!) - dogs and cattle tend to be resistant

27
Q

Where are lesions due to tularemia most commonly found? What kind of pathogen is Francisella tularensis?

A

liver, spleen, lungs

facultative intracellular pathogen within phagocytes
(Category A select agent, BLS-3 pathogen)

28
Q

How does tularemia present in humans?

A
  • skin ulcer
  • swelling of closest lymph node
  • abrupt fever, headache, chills, body aches, and sore throat
  • nausea, vomiting, diarrhea = intestinal tularemia
  • chronic: sweats, fever, chills, weakness, weight loss
29
Q

What are the 5 subspecies of Francisella tularensis?

A
  1. TULARENSIS - type A, Tier 1 bioterrorism agent in North America, most virulent, associated with land
  2. HOLARCTICA - type B, worldwide (northern hemisphere), less virulent than type A, associated with water
  3. MEDIASTICA: less virulent, Asia
  4. NOVICIDA: less virulent, cysteine-independent, worldwide
  5. PHILOMIRAGIA - avirulent
30
Q

How does wildlife typically present with tularemia? Where does Francisella tularensis typically survive in the environment?

A

systemic disease with granulomatous lesions

in water and arthropods (tick) or as a biofilm

31
Q

What 2 virulence properties are important for Francisella tularensis?

A
  1. glycoprotein capsule
  2. LPS - NOT AN ENDOTOXIN; protective mechanism, O antigen does not cause inflammation
    - strains lacking O antigen are avirulent
32
Q

What is the result of Francisella tularnesis’ ability to invade phagocytic cells? What is required for survival in these cells?

A

allows it to survive intracellularyl, disseminate, and cause granulomatous lesions

pathogenicity island

33
Q

Why is Francisella tularensis considered an invisible pathogen?

A

host does not see it —> LPS is not a TL4 agonist, and by the time it causes a cytokine storm due to TLR-2 and the host is able to recognize it, infection has already presented

34
Q

Are compromising factors necessary for Francisella tularensis infection?

A

NO - frank pathogen

  • highly virulent by itself
  • exposure to infected animals and arthropod vectors leads to infection
35
Q

What form of immunity is necessary for Francisella tularensis protection? Why?

A

cellular immunity —> Th1 response (TNF-α, IFN-γ, IL-12) and T cell killing of infected cells

antibodies are unable to reach intracellular organisms, but may have protective potential prior to phagocytosis

36
Q

How is Francisella tularensis infection diagnosed?

A
  • cultured on cysteine-glucose-blood agar (F. novidica = blood agar) for 2-4 days in a BSL-3 lab
  • serology
  • PCR
  • FA
  • notifiable disease!

Veterinary Bacteriology & Mycology (47 decks)

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