DeLahunta Chapter 11 - Large animal spijnal cord disease Flashcards
Slap test. Pathway.
Cuaneous brahcnes of cranial thoracic spinal nerves–> ipsilateral grey horn dorsal - INTERNEURONS–> then crosses opposite side via FASCISULUS PROPRIUS–> then GSE-LMN nucleus ambigus (contralateral of the slap) –> vagus–>recurent laryngeal nerve–> itristic muscle of larynx (clossing glottis oposite to the slap)
In what horse breed is there an inherited occipitoatlantoaxial malformation? How does this appear clinically, and how is it diagnosed? What gene is this associated with?
Arabian horses
Clinically the horses have a rigid neck that they struggle to move. Can show tetraparesis and ataxia, to recumbency if very bad. This can be diagnosed by palpation, or on radiographs
Associated with the HOXD3 gene
What are the main histopathological differences between equine neuroaxonal dystrophy and equine degenerative myeloencephalopathy? (https://onlinelibrary.wiley.com/doi/10.1111/jvim.16969) What are the typical clinical signs, and what vitamin is suspected to be involved
eNAD – bilaterally symmetrical axonal degeneration in brainstem and spinal cord grey nuclei (predominantly lateral cuneate with less involvement of medial cuneate and gracile nucleus of brainstem and thoracic spinal cord) characterised by axonal spheroids with or without vacuolation, chromatolysis, gliosis and lipofuscin pigment
EDM – grey matter lesions above AND spinal cord white matter degeneration, characterised by dilated myelin sheaths with scattered myelin laden macrophages (digestion chambers) or spheroids in ascending or descending (particularly dorsolateral and ventromedial) white matter tracts
Clinical signs: birth to 2 years, a progressive spastic paraparesis and pelvic limb ataxia that slowly progresses to the thoracic limbs. ENAD may occur in younger animals (6-12 months)
Vitamin E is suspected to be involved
What are the 2 main diagnostic methods for equine protozoal myeloencephalitis (EPM)? Is PCR considered a sensitive or specific diagnostic test? (https://pubmed.ncbi.nlm.nih.gov/33578198/)
Serum antibody levels (absolute values), serum to CSF antibody levels (SnSAG2/SnSAG4/3)
No PCR was not reliable in detecting cases
FROM BOOK:
PCR - maybe negative if protozoum not present
Western blot immunoassay - false positives if haemodilution (RBC <7 is ok)
IFA is the best in both serum cSF , normal should be 1:100 (CSF to serum), if it decreases hen diagnostic
What drug/combination of drugs can be used for the treatment of EPM in horses?
Toltrazuril, Diclazuril, ponauril, sulfadiazine/pyrimethamine
Regarding equine herpesvirus myeloencephalopathy
-What strain is predominantly responsible for neurological disease?
-What is the pathological mechanism by which the signs are caused, and why is this called a myeloencephalopathy rather than myeloencephalitis?
-What clinical signs may be seen?
How is this diagnosed? What CSF changes may be seen?
What strain is predominantly responsible for neurological disease? -> EHV-1
What is the pathological mechanism by which the signs are caused, and why is this called a myeloencephalopathy rather than myeloencephalitis? -> it predominantly causes a symmetric vasculitis and thrombosis as the virus affects endothelial cells. This leads to secondary ischaemic and haemorrhage causing the clinical signs.
What clinical signs may be seen? -> subtle pelvic limb ataxia to recumbency. Nasal and ocular discharge, limb oedema, anorexia, colic, may have mild cauda equine signs too. Pyrexia
How is this diagnosed? What CSF changes may be seen? -> PCR on nasal or blood sample. CSF changes include hypocellular, xanthochromic CSF
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What is the lifecycle of Parelaphostrongylus tenuis (including primary, secondary and aberrant hosts)?
L1 passed in faeces of the primary host, the white tailed deer. This enters the intermediate host, the slug or snail, and matures. This is then eaten by the deer. The worm migrates into the venous system of the head or vertebral column and lives here, releases L1 which migrate to the lungs and enter the gut
Aberrant host (small ruminant or camelid) consumes the L3 which penetrates the intestinal wall and migrates to the brain/spinal cord where it penetrates. This causes non-suppurative inflammation with eosinophils
Regarding CSF analysis and short term survival in camelids with suspected neurological disease: (https://onlinelibrary.wiley.com/doi/10.1111/jvim.16529)
What TNCC is associated with higher odds of survival?
Were Alpacas or Llamas more likely to survive when infected with Parelaphostrongylus tenuis?
- TNCC<3
-Alpacas
What toxicity can cause a sudden progressive ataxia and recumbency of all limbs in a group of feeder pigs? What pathological changes would you expect to see?
Selenium toxicity
Poliomyelomalacia, particularly of the ventral grey horns in the cervical and lumbar intumescence
Which region of the vertebral column is at a higher risk of developing discospondylitis in young foals?
CAUDAL CERVICAL
previously sepctic:
as a result of thrombophlebitis when born etc.
Aside from S. neurona, which other protozoa has been identified more recently that is less common but causes similar lesion in cases of Equine Protozoal Myelitis?
Neospora hughesi
True or False
In cases of Equine Protozoal Myelitis, lesions occur in both gray and white matter and are often symmetric in distribution.
asymmetric
Approximately, which percentage of EPM horses will have a complete recovery?
A)10 – 20%
b) 60 – 70%
c) None
d) 50%
10-20%
What is the aetiology of the Caprine Encephalitis Virus? Which are the 2 forms?
CAEV - Lentivirus < retrovirus (cousin to Maedi Visna)
Young goats: demyelinating leukoencephalitis
Old goats: mastitis, pneumonia, arthritis
Which clinical signs can cause Copper Deficiency in young sheep, goats and occasionally pigs? What is its histopath?
chronic progressive T3-L3 myelopathy (occasionally LMN)
Histopathologically it can be a dying back axonopathy with secondary demyelination and astrogliosis. Neuronal cell bodies from the brainstem, spinal cord grey column may undergo chromatolysis and eventually necrosis.
