Camelid - Neurologic Dz Flashcards

1
Q

What is the causative agent of parasitic myelopathy (a.k.a. ‘meningeal worm’) of camelids?

A

Parelaphostrongylus tenuis (nematode).

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2
Q

Describe the life cycle of P. tenuis.

A

Definitive host = white-tailed deer: adults living in subdural space and associated vessels lay eggs –> hatch in pulmonary capillaries –> L1 migrate to alveoli, coughed up and swallowed –> L1 passed in feces –> ingested by intermediate host = snails –> molt x 2 –> snails containing L3 ingested by definitive hosts or aberrant hosts e.g. camelids.

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3
Q

Describe the pathophysiology of P. tenuis infection in camelids.

A

in snails ingested by camelid –> migration to CNS parenchyma –> scattered foci of haemorrhagic necrosis and parenchymal loss –> CSx in ~40-50d.

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4
Q

List the neurologic deficits reported in camelids with parasitic myelopathy.

A
  • Typical CSx: wide-based hindlimb stance, hindlimb ataxia +/- progressing to recumbency; BAR.
  • Lesions vary: can see FL or lateralised deficits.
  • Atypical form: brain involvement –> acute-onset brain or vestibular signs including depression, seizures,
    circling, leaning, head tilt, and slow PLRs.
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5
Q

How do you diagnose parasitic myelopathy in a camelid anti-mortem?

A
  • CSF: eosinophilic pleocytosis with inc protein in most cases.
  • CBC: usually WNL +/- inc CK and AST.
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6
Q

At what time of year is parasitic myelopathy most frequently observed and in what age group of camelids?

A

Autumn and Winter (Oct to Mar).

Adults > young animals.

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7
Q

Describe the characteristic lesions of parasitic myelopathy observed on post-mortem of affected camelids.

A

Lesions of parasite migration: randomly distributed axonal degeneration that progresses to pannecrosis characterised by axon and axon sheath swelling, axon drop out, axonophagia, accumulation of gitter cells.
Lesions mainly in white matter.
Larvae rarely seen.

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8
Q

Outline the treatment of parasitic myelopathy in camelids.

A
  • Fenbendazole 50mg/kg PO for 5 days.
  • NSAIDs e.g. flunixin meglumine 1mg/kg q24-48h.
  • DMSO in severe cases.
  • Vitamin E and B (non-specific therapy).
  • IVF if required.
  • Physical therapy.
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9
Q

What is the prognosis for survival in cases of parasitic myelopathy of camelids?

A
  • Good if able to stand with assistance.
  • Poorer if recumbent.
  • Guarded with brain lesions.
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10
Q

What segment of the spinal cord is most frequently affected by trauma in camelids and was is the most common source of the trauma?

A
  • Cervical spinal cord.

- Fence-related injuries.

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11
Q

Describe clinical examination findings in a camelid with cervical trauma.

A
  • ‘Lump’ or ‘kink’ in neck (fibrosis, periosteal reaction).
  • Abnormal head and neck posture.
  • UMN/LMN deficits in FLs, UMN deficits in HLs.
  • May not see CSx after acute inflammation resolves due to wide spinal canal.
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12
Q

List treatment options for traumatic lesions of the cervical spinal cord in camelids?

A
  • Supportive care: NSAIDs, confinement.
  • Sx may be indicated in young, growing animals to stabilise vertebral canal –> aim to produce fusion between neighbouring vertebrae.
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13
Q

List possible aetiologies of otitis media in camelids.

A
  • Ascending infection up the eustachian tubes.
  • Extension of otitis interna.
  • Spinous ear ticks (Texas).
  • Most common bacteria isolated: Arcanobacter pyogenes, Staphylococcus app and Bacillus spp.
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14
Q

What abnormalities may be identified on neurologic examination of a camelid with otitis media?

A

Head tilt, facial nerve deficits (e.g. droopy ear, flaccid facial muscles, ptosis, inability to blink), circling, ataxia, nystagmus.

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15
Q

How do you diagnose otitis media in a camelid?

A
  • CT ideal.
  • Radiographs may be helpful if bony changes present.
  • CSF to rule out other causes of vestibular dz e.g. listeriosis; protein inc in 50% cases.
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16
Q

What is the frequency of occurrence and prognosis associated with listeriosis in camelids?

A
  • Not very common.

- Guarded px, with most failing to respond even to aggressive therapy.

17
Q

List the clinical signs of listeriosis in camelids.

A

Circling, ataxia, leaning to one side, nystagmus, recumbency, depression, seizures.

18
Q

What CSF changes are reported in cases of listeriosis in camelids?

A

Monocytosis, elevated protein and CK concentrations.

19
Q

Outline the components of aggressive therapy of a camelid with listeriosis.

A

IVFT, anti-inflammatories, thiamine, oxytetracycline (20mg/kg SID for 5d) or Na/K penicillin IV (80mg/kg q6h), nursing care.

20
Q

In what age group of camelids is meningitis or meningoencephalitis most frequently reported?

A

Neonates; secondary to sepsis.

21
Q

What organisms have been associated with meningitis in camelids?

A
  • Neonates: Listeria monocytogenes, Escherichia coli, Salmonella newport, Streptococcus bovis.
  • One reported of cryptococcal meningitis in an 8yo alpaca in Australia.
22
Q

Describe the typical CSF analysis findings in a cria with bacterial meningitis.

A

Leukocytosis, especially with suppurative inflammation.

23
Q

Describe clinical signs associated with meningitis in crias.

A
  • Vague and variable!
  • Weakness, depression, inability to stand or elevate the head, tremors, ataxia, opisthotonus and seizures.
  • Death in 100% reported cases.
24
Q

Outline the clinical signs and signalment of crias with vertebral abscessation.

A
  • HL ataxia, paresis or paralysis (thoracolumbar abscess)

- Reported in several crias under 6mo.

25
Q

Why are llamas more prone to heat stress than alpacas?

A

Both are poorly adapted to hot and humid climates, but llama breeders tend to barrel clip only vs alpaca breeders which completely shear.

26
Q

Describe presenting clinical signs in a camelid with heat stress.

A
  • Elevated body temperature >105F (may be up to 108F).
  • Respiratory distress.
  • Tachycardia.
  • Inability to rise (FLs weaker than HLs).
  • Check for CSx of underlying dz*
27
Q

List the common abnormalities identified on serum biochemistry of an alpaca with heat stress.

A
  • Elevated CK and AST.
  • Hypoproteinaemia despite haemoconcentration (cell damage).
  • Severe electrolyte imbalances esp hypokalaemia.
  • Metabolic acidosis.
28
Q

Outline therapy for a camelid with heatstress.

A
  • Completely shear the animal.
  • Hose with cold water; ice packs in inguinal and axillary regions.
  • Judicious fluid therapy: hypoalb + cell damage –> pulmonary oedema.
  • NSAIDs: analgesic (muscle pain) and anti-inflammatory.
  • Vitamin E: anti-oxidant.
29
Q

What is the aetiologic agent of Ryegrass Staggers in camelids?

A

Lolitrems = tremorogenic toxins produced by endophytes infecting ryegrass.

30
Q

What are the clinical signs of Ryegrass Staggers in camelids and the prognosis for complete recovery?

A
  • Head tremor +/- ataxia.

- Normally recover fully when removed from pasture but prolonged exposure may result in permanent damage.

31
Q

What agents induce polioencephalomalacia (PEM) in camelids?

A
  • Dietary change.
  • Excessive carbohydrate ingestion.
  • Amprolium overdosage (thiamine analogue).
  • Often unknown.
32
Q

What are the clinical signs of PEM in camelids?

A
  • Acute-onset blindness (cortical).
  • Depression.
  • Circling and head tremors.
  • Atypical presentation: charge walls, aggression.
33
Q

How is PEM treated in camelids?

A
  • Thiamine hydrochloride 10-15mg/kg q4h then daily for several days after resolution of signs.
  • Supportive and nursing care.
34
Q

Which viral encephalidites reported in other species can also occur in camelids?

A
  • Horses: EEE, WNV, EHV-1 (NB severe brain dz).
  • Sheep: ‘louping ill’ a.k.a. ovine encephalomyelitis.
  • Rabies.
35
Q

Can camelids be vaccinated against viral encephalidites?

A

No registered vaccines, however equine EEE, WNV and rabies results in production of neutralising antibodies.