Encephalitozoonosis and nosematosis. Flashcards

(23 cards)

1
Q

microsporida is

A

Obligate intracellular protozoan parasites

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2
Q

What is the final host of Encephalitozoon cuniculi?

A

rabbit

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3
Q

location of Encephalitozoon cuniculi

A

Brain, kidneys

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4
Q

Encephalitozoon cuniculi - transmission

A

Through urine and transplacental transmission, ingestion of spores

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5
Q

Encephalitozoon cuniculi - life cycle

A

1) The infective form is a Resistant Spore, which can survive for a long time in environment.
2) FH eats spores through feces
3) The spore extrudes its polar tubule and infects the host cell in the intestines
4) The spore injects the infective sporoplasm into the eukaryotic host cell through the polar tubule
5) Inside the cell, the sporoplasm undergoes extensive multiplication either by binary fission or multiple fission (merogony or schizogony).
6) Sporogony produce the infective form (spore)

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6
Q

Encephalitozoon cuniculi - pathogenesis

A

A chronic, usually latent disease of rabbits characterised mainly by damage to the nervous system and kidneys, diarrhoea and respiratory symptoms (bronchitis, pneumonia or sinusitis).

ZOONOSIS!

3 main manifestations:
Neurological - central vestibular dysfunction (hearing dysfunction) –> head tilt, torticollis, tremor, circling, ataxia, nystagmus, seizures, asthenia, paresis, limb paralysis, urinary incontinence

Renal - chronic interstitial nephritis, polyuria/polydipsia, dehydration

Ocular - phacoclastic uveitis (lens trauma), uveitis, white intraocular lesions, cataract

Non-specific - anorexia, weight loss

Death

Multifocal depressions: granulomatous inflammation, scarring of renal interstitium
Organisms in pseudocyst: renal tubule epithelium, ruptures –> inflammation
Focal granulomas in brain

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7
Q

Encephalitozoon cuniculi - CS

A

Non-specific neurological signs

  • convulsions, tremors, head tilt - torticollis
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8
Q

Encephalitozoon cuniculi - DX

A

Light microscope, electron microscopy, IFA, PCR

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9
Q

Encephalitozoon cuniculi - TX

A
  • Fenbendazole (also in dogs)
  • Albendazole (also in dogs)
  • Pyrimethamine
  • Supportive
  • Surgery: remove lens of eye, enucleation
  • Humans: albendazole
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10
Q

Encephalitozoon cuniculi - prevention

A

Serological screening
Separation of seropositive animals
Screening of new animals
Preventive fenbendazole for rabbits at risk
Cleaning and disinfection
Personal hygiene

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11
Q

Encephalitozoon cuniculi - Encephalitozoonosis in dogs is an opportunistic infection, meaning it is only clinically manifested when:

A

immune system is weakened, or Transplacental infection

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12
Q

Encephalitozoon cuniculi - dx in dogs

A

Difficult as even healthy dogs can be antibodies
Clinical signs
Spores in urine
Post-mortem granulomas in tissues

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13
Q

Nosematosis is a disease of what species?

A

honey bees

  • Varimorpha ceranae (Nosema ceranae)
  • V. apis (N. apis)
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14
Q

What is the route of infection for Varimorpha ceranae?

A

fecal oral

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15
Q

What is the location of V. ceranae?

A

honey bee intestine

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16
Q

Encephalitozoon species

A

E. cuniculi
E. intestinalis
E. hellem
E. lacertae

17
Q

Describe the morphology of Varimorpha ceranae and V. apis:

A

Spores (difficult to distinguish)
V. ceranae: smaller spores, 20-23 polar filaments
V. apis: spores have 30-44 polar filaments

18
Q

Describe the life cycle of Varimorpha:

A

1) FH (bees) are infected by ingestion of food containing spores
2) Spores in midgut lumen —> spore germinate —> polar filaments everts and pierce midgut epithelial cell
3) Sporoplasm is injected to the cell’s cytoplasm
4) Merogony: sporoplasm develops into meront —> multiply by binary fission inside cytoplasm of midgut epithelial cell
5) Sporogony: Proliferative stage –> sporonts –> sporoblasts —> spore formation —> mature spores
6) infected cell ruptures; spores released into gut —> Spores released in feces

19
Q

What are the clinical symptoms of Nosematosis?

A

Enlarged abdomen of worker bees
Brown fecal marks on comb
Reduced brood production
Slow growth of colony
Unable to produce queen jelly
Production of mature larvae decreases
Stop caring for offspring and turn to foraging
Infected queen stop laying eggs
Shortened life span
Dysentery (V. apis)
100% mortality 10-14 days

20
Q

Describe the pathogenesis of Nosematosis?

A

Changes in sugar metabolism
Changes in hormone levels and pheromone production
Shortened life span
Change in flight activity
Reduced success in returning to hive stable
Loss of bees in colony
Faster conversion of honey bees to foraging - change in polyethism (division of labour)
Coexistence with other pathogens - increased mortality

21
Q

How do we diagnose Nosematosis?

A

Histopathology
Microscopy: light, TEM
Fluorescense microscopy
PCR
LAMP
Analysis of environmental DNA in honey

22
Q

How do we treat Nosematosis?

A

Oxytetracycline
Fumagillin
- side effects: digestive problems, decreased immune system

Natural: organic acids, polysaccharides, essential oils, microorganisms

23
Q

How can we prevent Nosematosis?

A

New queen bee
Control of other parasites
Avoid chronic exposure to pesticides or acaricides