Large animal SC disease

Question 1

DDs for progressive cervical SC disease (C1-5 SCS) in the horse

Answer 1

1) Vertebral stenosis
2) EDM or neuroaxonal dystrophy
3) Equine protozoal myelitis
4) discopsondylitis
*neoplasia and IVDD rare in horse

Question 2

Name a congenital form of vertebral stenosis and which breed of horse is most affected?

Answer 2

Congenital occiopitoatlantoaxial malformation of Arabian breed (autosomal recessive)

An important diagnostic feature is the abnormal neck posture. The head and neck are more extended than normal and have a stiff appearance.

Question 3

Which factors predispose for vertebral stenosis in young athlete horses?

Answer 3

This disorder is multifactorial, which has all the features prominent in the racehorse industry: (1) selecting for the genes that foster rapid growth, (2) providing feed that is high in calcium and energy to encourage this rapid growth, and (3) placing these animals as soon as possible into a vigorous training program to make them winners as 2-year-old horses.

Question 4

Most common location of vertebral stenosis in young horses?

Answer 4

middle cervical vertebra from C3 to C6 and is caused by failure of the bone that surrounds the vertebral foramen to resorb sufficiently to enlarge the foramen enough to accommodate the growing spinal cord

Question 5

Radiographic features that suggest a vertebral stenosis?

Answer 5

1. A slight subluxation between vertebrae with increased flexion or dorsal angulation between adjacent vertebrae that is best seen between the bodies on either side of the intervertebral disc
2. A prominent caudal epiphysis that projects dorsally into the vertebral foramen
3. A caudal extension of the vertebral arch over the articulation

Question 6

How is the minimal sagittal diameter for equine vertebral stenosis determined and what are normal values?

Answer 6

The minimal sagittal diameter for the vertebral foramen of a vertebra is made by measuring the height of the vertebral foramen at its most narrow point. The minimal sagittal diameter ratio is determined by dividing this measurement of the minimal sagittal diameter of the foramen by the maximal sagittal diameter of the vertebral body, which is at the cranial aspect of the vertebral body. These measurements must be made perpendicular to the ventral surface of the vertebral foramen. A study in 1994 considered a ratio below 0.52 for C4 and C5 and below 0.56 for C6 and C7 to be abnormal.65 Greater ratio values are considered normal. Unfortunately, the value of these measurements is si

Question 7

Which measures can help to decrease the incidence of cervical vertebral stenosis of young horses?

Answer 7

This disorder may be prevented by slowing the rate of growth of foals by altering their diet and structuring a less vigorous training program while these horses are young, It may be hard to imagine a racehorse trainer recommending a restricted diet and less vigorous training program. Nonetheless, it will reduce the incidence of this disorder. A study was done on large breeding farms in Kentucky in which the foals were radiographed starting at 3 months of age. Radiographic changes were graded, and horses that were considered to be at risk for developing this cervical vertebral disorder were placed on a restricted diet and a restricted exercise program. These management changes resulted in a significant decrease in the incidence of this disorder on these farms.

Question 8

Primary lesion (pathogenesis) with EDM (equine degenerative myeloencephalopathy)

Answer 8

diffuse axonopathy throughout the white matter of the spinal cord that predominates in the superficial tracts of the dorsolateral and the ventral funiculi, but all portions are affected with the least lesions in the dorsal funiculi.
This axonopathy is accompanied by a secondary demyelination and astrogliosis.
In addition, loss of neuronal cell bodies and spheroid development (neuroaxonal dystrophy [NAD]) is extensive in the medullary lateral cuneate nuclei, with variable spheroid development in the medullary medial cuneate and gracilic nuclei, the nucleus of the dorsal38 spinocerebellar tract (nucleus thoracicus) in the spinal cord dorsal gray column, and olivary nuclei, reticular formation, and vestibular nuclei in the brainstem.
In addition, an accumulation of lipopigment occurs in the endothelial cells of capillaries in the spinal cord and the pigment epithelium and outer layers of the retina, similar to older horses with motor neuron disease.

Question 9

Proposed etiology of EDM?

Answer 9

Vitamin E defficiency

Question 10

What kind of disease will vitamin E deficiency cause in young compared to older horses?

Answer 10

Young horses: EDM (equine degenerative myeloencephalopathy)
Older horses: EMND (equine motor neuron disease)

Question 11

Histological difference between EDM (equine degenerative myeloencephalopathy) and ENAD (equine neuroaxonal dystrophy)

Answer 11

Similar onset (6-12 MO), numerous breeds affected, simmilar clinical signs (paraparesis and ataxia of pelvic limbs progressing to tetraparesis and ataxia of all limbs), also vitamin E defficiency as etiology

In horses with NAD there si only neuroaxonal dystrophy and it is associated with specific populations of neurons, and no microscopic lesions of axons are present in the white matter of the spinal cord or brainstem. The affected neuronal populations consistently include the medial and lateral cuneate and gracilic nuclei.

Question 12

Which vertebral bodies have the highest risc of developing discospondylitis in the horse?

Answer 12

caudal cervical vertebrae

Question 13

Which animal is the primary host in the life cycle of S. neurona? What about intermediate and abberant hosts?

Answer 13

opossum (which is why there is no disease in european horses, except if they travel)

Intermediate - accoon, striped skunk, and nine-banded armadillo

Aberrant - horse

Question 14

Life cycle of S. neurona?

Answer 14

merozoites encysted in muscle of intermediate host > ingested by the opossum, > invades the intestinal epithelium > Sexual reproduction > oocysts enter the intestinal lumen and sporulate to form sporocysts > sporocyst forms 4 sporozoites, > pass through feces into the external environment, > ngested by intermediate host > sporozoite invades intestinal epithelium and associated arterial endothelial cells the intermediate host > asexual reproduction by schizogony > production of merozoites > released into the bloodstream > migrate to the muscles > encyst > the intermediate host dies and the muscles are eaten by the opossum, the cycle is completed.

The horse becomes infected when it eats feed that has been contaminated by the feces of the opossum that contain infective sporozoites. These sporozoites are presumed to invade the intestinal epithelium. Where asexual reproduction occurs and how the organism reaches the CNS is unknown. Schizogony is seen in the CNS, but whether it also occurs in intestinal or other extraneural vascular endothelium is unknown. Merozoites have occasionally been found in CNS endothelial cells. Cysts have not been reported in the muscles of the horse, but these have not been adequately studied for this possibility. The assumption is that the CNS infection is usually hematogenous, with merozoites circulating free in the bloodstream or in infected lymphocytes.

Question 15

Which factors contribute to some horses infected w/ S. neurona developing clinical disease?

Answer 15

The few horses that develop lesions are believed to have been subject to some form of stress, such as transportation, training, showing, pregnancy, or some other change in their environment that might lead to stress-related immunosuppression.

Question 16

Signalment, onset and progression of EPM

Answer 16

Any age and breed of horse, but most commonly young adults 1-5 YO

Can be acute, subacude, chronic, quickly od slowlu progressive.

Usually assymmetric

Question 17

Most common sites lesions in horses w/ S. neurona?

Answer 17

SC > caudal brainstem > prosencephalon

Question 18

CSF findings in horses with EPM

Answer 18

CSF is often normal despite the presence of inflammation in the leptomeninges. Occasionally, mild elevations are noted in protein and lymphocytes and macrophages.

A polymerase chain reaction (PCR) test on CSF for the DNA of this organism will be positive only in the small percentage of horses in which the organism is present in the subarachnoid space. Therefore the PCR test is impractical.

Western blot immunoassay for antibodies in CSF is usually positive for horses with this disease, but false-positive results are common because obtaining a CSF sample from the lumbosacral subarachnoid space without some blood contamination is difficult. This test will be positive for the serum antibodies in CSF if the blood contamination is so small that CSF only contains eight red blood cells (RBCs) per cubic millimeter. This factor makes the interpretation of any antibodies in CSF using this procedure unreliable. Cisternal CSF is less likely to have blood contamination but general anesthesia is required to obtain CSF. More recently, an indirect fluorescent antibody test, which is quantitative for whole merozoites and very resistant to blood contamination, has been developed. CSF antibodies are produced intrathecally. Using the indirect fluorescent antibody test, a ratio of serum to CSF antibody titers can be obtained. The normal ratio is 100 to 1.

Many horses are infected and have serum antibodies, but only a very few have the disease and produce intrathecal antibodies!!!

Question 19

Therapy of EPM?

Answer 19

folate inhibitor drugs PO

The most common of these has been a combination of sulfadiazine and pyrimethamine.

Other considerations include ponazuril, diclazuril, toltrazuril, or nitazoxanide.

Intravenous dimethyl sulfoxide is often used to reduce the vasogenic edema in acutely affected horses.

Question 20

Outcomes in EPM?

Answer 20

Success of treatment depends on the severity and location of the lesions. Published results suggest that approximately 60% of horses with moderate to severe clinical signs will improve after treatment with any of the approved medications, and 10% to 20% will make a complete recovery.

Long-term therapy for 3 to 6 months may be necessary to prevent relapses.

Question 21

Name 2 DDs for an acute, non-progressive cervical myelopathy in the horse

Answer 21

1) FCEM - usually asymmetric
2) herpesvirus-1 myelopathy (rarely progress more than 2-3 days) - usually symmetric

Question 22

Pathologic mechanism of herpersvirus-1 in horses

Answer 22

Vasculitis of CNS (mostly spinal cord, rarely brainstem or prosencephalon, causes ischemic or haemmorhagic infarcts and thrombosis mostly of leptomeninges) and reproductive tract.
Sometimes also rhinopneumonitis.

(herpersvirus-4 more common cause of rinopneumonitis of foals)

Question 23

Diagnosis of herpesvirus-1 myelitis?

Answer 23

PCR of buffy coat or nasal secretions.

CSF usually only citoalbuminergic dissociation.

Question 24

Typical clinical picture of herpesvirus-1 myelitis in the horse?

Answer 24

T3 to L3 spinal cord segments plus urinary incontinence and mild tail and anal hypotonia is very characteristic of a mild to moderate infection with the equine herpesvirus-1 virus.

Question 25

Cause of scoliosis in horses and camelidae?

Answer 25

Parelaphostrongylus tenuis (meningeal worm) migration thru cervical spinal cord

Question 26

DDs for SC disease of young goats?

Answer 26

1) CAE (Caprine arteritis encephalitis) virus myelitis
2) Parelaphostrongylus tenuis myelitis
3) discospondylitis
4) vertebral malformation
5) copper deficiency (enzootic ataxia)
6) organophosphate intox

Question 27

DDs for chronic-progressive SC diseases of cows

Answer 27

1) discospondylitis/empyema (younger cows)
2) lymphoma (adult/older cows)
3) hepatic encephalomyelopathy (PSS)
4) rabies myelitis

Question 28

Lymphoma in cattle, 2 forms

Answer 28

1) enzootic form: BLV virus associated, usually older than 4 years
2) sporadic form: less common, usually cattle younger than 3 years

Question 29

2 specific microscopic changes of CNS in animals with hepatic encephalopathy?

Answer 29

1) Alzheimer astrocytes: change in the nuclei of the astrocytes that reflects their reaction to the increased levels of circulating ammonia and other metabolites not cleared by the liver

2) fluid accumulation within the myelin lamellae, causing a dilation of the myelin sheaths that is sometimes called polymicrocavitation (alls species except for the horse)

Question 30

Copper deficiency: relevant species and clinical picture?

Answer 30

Young pigs, sheep and goats
(ca. 3-6 MO)

rapidly progressive paraparesis and pelvic limb ataxia that can progress to paraplegia.