Large animal diseases Flashcards
DDs for progressive cervical SC disease (C1-5 SCS) in the horse
1) cervical vertebral stenotic myelopathy (CVSM) - leading cause of noninfectious ataxia in horses
2) EDM/neuroaxonal dystrophy (NAD)
3) Equine protozoal myelitis
4) discopsondylitis
*neoplasia and IVDD rare in horse
Name a congenital form of vertebral stenosis and which breed of horse is most affected?
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.
Which factors predispose for vertebral stenosis in young athlete horses?
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.
Most common location of vertebral stenosis in young horses?
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
Radiographic features that suggest a vertebral stenosis?
- 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
- A prominent caudal epiphysis that projects dorsally into the vertebral foramen
- A caudal extension of the vertebral arch over the articulation
How is the minimal sagittal diameter for equine vertebral stenosis determined and what are normal values?
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
Which measures can help to decrease the incidence of cervical vertebral stenosis of young horses?
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.
Primary lesion (pathogenesis) with EDM (equine degenerative myeloencephalopathy)
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.
Proposed etiology of EDM?
Vitamin E defficiency (dubious)
What kind of disease will vitamin E deficiency cause in young compared to older horses?
Young horses: EDM (equine degenerative myeloencephalopathy)
Older horses: EMND (equine motor neuron disease)
Histological difference between EDM (equine degenerative myeloencephalopathy) and eNAD (equine neuroaxonal dystrophy)
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.
Which vertebral bodies have the highest risc of developing discospondylitis in the horse?
caudal cervical vertebrae
Which animal is the primary host in the life cycle of S. neurona? What about intermediate and abberant hosts?
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
Life cycle of S. neurona?
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.
Which factors contribute to some horses infected w/ S. neurona developing clinical disease?
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.
Signalment, onset and progression of EPM
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
Most common sites lesions in horses w/ S. neurona?
SC > caudal brainstem > prosencephalon
CSF findings in horses with EPM
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!!!
Therapy of EPM?
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.
Outcomes in EPM?
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.
Name 2 DDs for an acute, non-progressive cervical myelopathy in the horse
1) FCEM - usually asymmetric
2) herpesvirus-1 myelopathy (rarely progress more than 2-3 days) - usually symmetric
Pathologic mechanism of herpersvirus-1 in horses
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)
Diagnosis of herpesvirus-1 myelitis?
PCR of buffy coat or nasal secretions.
CSF usually only citoalbuminergic dissociation.
Typical clinical picture of herpesvirus-1 myelitis in the horse?
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.
Cause of scoliosis in horses and camelidae?
Parelaphostrongylus tenuis (meningeal worm) migration thru cervical spinal cord
DDs for SC disease of young goats?
1) CAE (Caprine arteritis encephalitis) virus myelitis
2) Parelaphostrongylus tenuis myelitis
3) discospondylitis
4) vertebral malformation
5) copper deficiency (enzootic ataxia)
6) organophosphate intox
DDs for chronic-progressive SC diseases of cows
1) discospondylitis/empyema (younger cows)
2) lymphoma (adult/older cows)
3) hepatic encephalomyelopathy (PSS)
4) rabies myelitis
Lymphoma in cattle, 2 forms
1) enzootic form: BLV virus associated, usually older than 4 years
2) sporadic form: less common, usually cattle younger than 3 years
2 specific microscopic changes of CNS in animals with hepatic encephalopathy?
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)
Copper deficiency: relevant species and clinical picture?
Young pigs, sheep and goats
(ca. 3-6 MO)
rapidly progressive paraparesis and pelvic limb ataxia that can progress to paraplegia.
Which structures are particularly affected in equine degenerative myeloencephalopathy?
- dorsal spinocerebellar tract
- nuclei gracillis and cuneatus
Histologically, all animals had a diffuse degenerative myeloence
phalopathy, with degeneration of the neuronal processes of the white matter of all
spinal cord funiculi, especially in the dorsal spinocerebellar tract. Dystrophic axons were found at most spinal cord levels and were most severe in the nucleus of the dorsal
spinocerebellar tract, especially in the thoracic segments (T10 to T15). Axonal dystrophy
was also noted in the caudal medulla within the nucleus gracilis, medial cuneate nucleus and lateral (accessory) cuneate nucleus (LACN) and was most severe in the latter.
What is the difference between Equine Degenerative Myeloencephalopathy (EDM) and Equine Neuroaxonal Dystrophy (eNAD)
the current consensus is that the conditions have such striking clinical
and pathologic similarities that eNAD could be considered a localized form of EDM or
EDM a more diffuse form of eNAD.
The disease is classified
as eNAD if the histopathologic lesions were confined to the brainstem, specifically
within the lateral cuneate nucleus, medial cuneate, and gracilis nuclei whereas a diagnosis of EDM was assigned when axonal necrosis and demyelination extended into the dorsal and ventral spinocerebellar tracts and ventromedial funiculi of the cervicothoracic SC.
Typical signalment and presentation of a horse with eNAD/EDM
a young (<2 year-old) horse with symmetric
proprioceptive ataxia, abnormal basewide stance at rest and proprioceptive deficits in all limbs but some horses, particularly Warmbloods, are affected later in life and show behavior changes in addition to progressive ataxia.
What less common clinical signs (besides ataxia) can be exibited by horses with eNAD/EDM
- bilateral menace response with no apparent loss of vision
- hyporeflexia of the cervical, cervicofacial, laryngeal adductor (slap), and cuta
neoustrunci reflexes is described, - changes in behaviour (spookines, bad behaviour under the saddle), and obtunded mentation
- pigment retinopathy
Role of vitamin E in eNAD/EDM?
Unclear.
Although vitamin E deficiency has been reported in some cases of eNAD/EDM, low vitamin E levels are not present consistently in all cases. Serum vitamin E concentrations
were not significantly different between EDM-affected horses and control horses in many studies.
Both a genetic susceptibility and a temporal alpha tocopherol deficiency are required for the phenotype to develop in QHs.
Most common equine SC disease to cause tetra-ataxia
1) compression due to cervical vertebral stenotic myelopathy (CVSM),
2) inflammation due to infectious disease such as EPM, 3) neurodegenerative disease
(eNAD/EDM).
- Certain clinical signs heighten the degree of suspicion for these diseases; for example, a horse with neck pain is more likely to have CVSM, and a horse with asymmetrical ataxia or concurrent focal muscle atrophy is more likely to have EPM, unpredictable or aberrant
behavior is more commonly observed in horses with eNAD/EDM than those with
CVSM or EPM.
Role of phosphorylated neurofilament
heavy chain (pNfH) protein in the diagnosis of eNAD/EDM?
Serum pNfH > 1 ng/mL were significantly associated with eNAD/EDM, with only 12% sensitivity but 99% specificity.
CSF pNfH concentrations >3 ng/mL were
observed with either eNAD/EDM or CVCM.
A value of less than 1 ng/
mL (serum) and/or less than 3 ng/mL (CSF) did not exclude a diagnosis of eNAD/
EDM.
Therapy of eNAD/EDM?
Currently no effective therapies exist.
In families of horses in which eNAD/EDM has been diagnosed, supplementation of
pregnant broodmares and foals with alpha-tocopherol at 10 IU/kg PO once daily during
the last trimester (mares) and first 2 years of life (foals) is advisable.
Classification of CVSM?
Rooney types I-III
I - the vertebral column is fixed in flexed position at the site of malarticulation/malformation, which generally occurs at C2–C3, but has been observed at other sites (less common, present at birth)
II - symmetric overgrowth of both articular processes causing compression during flexion, most often in foals and weanlings and are generally found in the mid-cervical region
III - asymmetrical overgrowth of one articular process leading to compression of the SC either directly by bony proliferation or indirectly by associated soft tissue hypertrophy, most often seen in mature horses but can begin as early as 1 to 3 years of age. This lesion most often affects C5– C6 and C6–C.
Division based on broad categories of horses:
one is affecting young horses (suckling to 2 years) (Type I, which correlates with Rooney’s Type II) mostly Thoroughbreds and one is
affecting older horses of all breeds (Type II, which correlates with Rooney’s Type III).
DDs for GP tetra-ataxia and/or tetraparesis in a (young) horse?
1) CVSM,
2) equine protozoal myeloencephalitis (EPM),
3) trauma,
4) equine degenerative myeloencephalopathy
(EDM/eNAD),
5) equine herpesvirus 1 myeloencephalopathy.
Less common:
- rabies,
- viral encephalitides (Eastern, Western, Venezuelan, and West Nile),
- brain abscesses,
- vertebral neoplasia,
- hepatoencephalopathy
- vertebral fracture,
- discospondylitis,
- intervertebral disk protrusion,
- arachnoid diverticulum
- parasite migration,
- spinal hematomas
Congenital anomalies and malformations of the vertebral column which could cause compression of the cervical spinal cord are reported infrequently:
- occipitoatlantoaxial malformation,
- butterfly vertebrae, hemivertebrae, block vertebrae,
- atlantoaxial subluxation/ atlantoaxial instability
Five common radiographic findings in horses with CVSM?
1) “flare” of the caudal vertebral epiphysis of the vertebral body,
2) abnormal ossification of the articular processes
3) degenerative joint disease of the articular
processes,
4) malalignment between adjacent vertebrae,
5) extension of the dorsal laminae, and
Two causative agents of EPM?
Sarcocystis neurona
Nespora hughesi
*both protozoa from the phylum Apicomplexa,
the opossum is the definitive host, intermediate hosts are the skunk, raccoons, armadilos and cats. Horses are the inccidental (dead-end) host
How do horses get infected with the causative agents of EPM?
when they ingest food or water contaminated
with feces from an infected opossum (the definitive host where the sexual replication occurs in the GIT)
they cannot get infected from the intermediate hosts (sporozoite containing sporocysts), nir horizontally (and rarely vertically) between horses
Clinical signs that help differentiate EPM from other common neuro diseases?
- EPM - usually asymmetric with areas of focal muscle atrophy
- EMND (equine motor neuron disease) - may be confused because also focal severe muscle atrophy and limb weakness with fasciculations
- CVSM is usually symmetric, pelvic limbs more affected and no focal areas of muscle atrophy
- EHV-1 myeloencephalopathy (EHM) - usually a history of respiratory disease or abortion outbreak before neuro signs (usually acute, symmetric, pelvic limbs worse, blader distension, perineal/tail hypalgesia, tail/penile paralysis, fecal retention)
- EPM can mimic basically any neuro disease in the horse
Diagnosis of EPM
Immunological:
- positive serum/CSF antibodies are not enough (passive transfer of Ab thru BBB)
- Goldmann–Witmer coefficient (C-value) and the antigen-specific antibody index (AI) are tests of proportionality that assess whether there is a greater amount of pathogen-specific antibody in the CSF than would be present due to normal passive transfer across the BBB.
- IFAT can be used for detection of intrathecal production (UC Davies)
CSF PCR:
may complement the immunological methods, usually negative if therapy started before CSF tap
Postmortem:
organisms rarely visible (10-30% in H&E stains, 50% with IHC), typical patho findings: cuffing of blood vessels by mononuclear cells, necrosis of parenchyma with phagocytosis and gitter cell formation, astrocyte proliferation, and gemistocytes formation. Eosinophils are seen commonly, as are multinucleated cells, which may be giant in size.
Therapy of EPM?
1) Folate inhibitors: sulfadiazine and pyrimethamine (SDZ/PYR), PYR, 1 mg/kg, and SDZ, 20 mg/kg, SID PO at least 6 months has been considered the “standard” treatment.
2) Triazines: diclazuril and ponazuril (toltrazuril sulfone)
3) supportive tx: anti-inflammatory (eg. flunixine meglumine, corticosteroids, dimethyl sulfoxide), antioxidants (vitamin E), immunomodulators (levamisole)
*currently no effective vaccines
Easy, field diagnostic test for botulism in horses?
offer the affected equid 250 mL of concentrate; affected horses will generally take longer than
2 minutes to consume this amount, whereas normal counterparts could consume this
with ease, often in less than 1 minute
DDx for botulism in horses?
- white muscle disease
- HYPP (hyperkalemic periodic paralysis)
- hypocalcemia
- white snakeroot toxicity
- lead toxicity
- ionophore toxicity
- organophosphate toxicity
DDs for equine neonatal neurological disease?
1) neonatal encephalopathy (non-infectious causes):
- maladaption
- perinatal asphyxia
- metabolic abnormalities (sepsis, kernicterus, electrolytes, uremic encephalopathy)
2) bacterial meningoencephalitis
3) traumatic injury
4) developmental/congenital abnormalities (rare)
Negative prognostic factors for foals with neonatal encephalopathy (NE)?
- perinatal asphixia as cause of NE
- seizures
- SIRS, joint infections, or respiratory disease (aspiration pneumonia, meconium aspiration, and so forth)
- cerebral necrosis (high CSF protein, intracranial bleeding, increased ICP)
VCNA
Causes of hepatic encephalopathy in large animals?
1) Horses: acute hepatic necrosis (Theilers disease - post equine serum - Equine parvovirus-hepatitis)
2) Domestic large animals: pyrrolizidine alkaloid-containing plants, notably Senecio spp. and Crotalaria spp., occurs in any grazing animal
3) aflatoxicosis (horses, pigs)
4) iron overload (horses) - iron in groundwater, transfusion in neonatal foals
5) Tyzzer disease (Clostridium piliforme) - necrotic bacterial hepatitis in young ruminants
6) PSS (rare, described in all domestic species)
7) hepatic lipidosis (rarely causes HE)
*If one sign was put forward as the most common and typical early sign of hepatic encephalopathy in adult horses, it would be repetitive yawn
Clinical signs of hepatic encephalopathy in horsea?
- very often repeated yawning,
- leaving unchewed food in the mouth,
- head pressing,
- playing with water (sham-drinking),
- inspiratory stridor due to laryngeal paralysis (bilateral laryngeal paralysis)
Classification of equine arboviruses
1) Togaviridae family:
Eastern equine encephalitis virus [EEEV], Madariaga virus [MV], Western equine encephalitis virus [WEEV], and Venezuelan equine encephalitis virus [VEEV])
- only in Americas
2) Flaviviridae: West Nile Virus (WNV)
- Worldwide
Seroprevalence of the West Nile Virus (WNV) in Europa (and USA)?
<10%
What percentage of horses develops neurologic disease after infection with the WNV?
ca. 10% (in people < 1%)
After bitten by infected vectors (Culex and Aedes moscitos), horses clear the virus or develop short-lasting low viremias, may not show systemic signs, and only 10% develop neurologic disease.
Mosquitoes that feed on infected horses remain negative for WNV and do not transmit the virus to other horses.
Which clinical features of encephalomyelitis are consisten findings in WNV infection as compared to other viruses?
muscle fasciculations, tremors, and
behavioural changes (rapid transitions between hiperexcitable and quiet states).
Mortality rate in WNV neurologic disease, and what are negative prognostic factors?
25-40%
recumbancy
DDx for WNV encephalomyelitis
- Borna disease
- EHM: seasonal and can cause systemic signs
- rabies: not seasonal
most important ddx in europe - botulism
- EPM (USA)
- alphavirus encephalitis (EEE, WEE, VEE) - only in Americas
- CVSM
- EDM/eNAD
- hepatic encephalopathy
- parasite migration
- leukoencephalomnalacia
- intox
- polineuritis
Tests to diagnose WNV neuro disease
1) ELISA IgG: sensitive but not specific
2) plaque reduction neutralization
test (PRNT) - to confirm
3) MAC ELISA IgM: preffered in horses, can detect IgM 7 days post-infection, IgM do not rise with vaccination
4) RT-PCR from blood, CSF, nervous tissue
Risk factors for development of EHM with EHV-1 infection?
- Age >3 y, further increase in risk in mares over
20 y of age (66%) - Infection with D752 genotype
- Season: Late autumn, winter, spring
- Breed, sex
- Geographic region
- Vaccination against EHV-1 5 wk before event
- Crowding & mingling
- Past exposure
- Secondary fever several days following primary exposure
- Magnitude and duration of viremia
- Stress associated with weaning, transport,
introduction of new horses, secondary
infection, immune suppression - Pregnancy or foal at foot
- Keep in stable
- Presence of EHV-1 and/or a shedding horse
together with susceptible horses
Three clinical entities in EHV-1 infection?
Abortion - late term
Respiratory
Neurologic - EHM
*can also cause neonatal foal death and chorioretinopathy
Antemortem diagnostics of EHM?
(i) ruling out other neurologic conditions,
(ii) demonstrating xanthochromia and an elevated cerebrospinal fluid (CSF) protein concentration,
(iii) identifying or isolating EHV-1 from the respiratory tract, buffy-coat, or CSF (PCR)
(iv) demonstrating a fourfold increase in antibodies using serum neutralizing, complement fixation, or enzyme-linked immunosorbent assays performed on acute and convalescent serum from affected or in-contact horses 7 to 21 days apart (**many horses with EHM do not show this increase)
Which drugs are used to manage horses with EHM?
1) antivirals (valacyclovir and ganciclovir)
2) NSAIL
3) corticosteroids
4) heparin
5) aspirin
6) lidocain CRI (lowering endothelial
cell infection and lysis)
7) vitamin E
8) DMSO (anti-inflammatory)
Which skull bones fracture most often in horses and what kind of movement usually causes this injury?
Rearing or falling backwards (most often horses < 1 YO).
Basilar (basisphenoid and basioccipital) and temporal bone fractures are most common with rearing and generally in TBI.
Specific movement disorders in horses?
1) standing hyperflexion (pain, early onset of shivers, hyperactive reflex arc without the ability to relax the limb consciously) - normal forward and backward gaits
2) shivers (hyperflexion vs. hyperextension vs. forward hyperflexion)
3) stringhalt (pasture-associated vs idiopathic)
Neuro signs of different forms of shivers and stringhalt when walking forward or backward?
1) shivers-hyperextension - walk forward
normally but show exagerated extension of all four limbs when asked to walk backward.
2) shivers-hyperflexion have hyperflexion when walking backward and a normal
limb trajectory when walking forward.
3) shivers-forward hyperflexion have
consistent hyperflexion and abduction walking backward and intermittent hyperflexion
and abduction when walking forward.
1) Horses with pasture-associated stringhalt have hyperflexion consistently when walking backward and forward.
2) Traumatic and idiopathic forms of stringhalt may not show hindlimb hyperflexion when walking backward.
Pathological findings in horses with shivers?
selective distal axonal degeneration in cerebellar Purkinje cells
Which neural autoantibodies are increased in horses with “stiff horse syndrome”?
Anti GAD (glutamic
acid decarboxylase) antibodies
- it produces the active form of GABA in the central nervous system, have been identifiedinthe cerebrospinal fluid of confirmedcases
Diagnosis of PEM in calves?
1) serum thiamine levels (not reliable, < 50 nmol/L consistent with def., not always low)
2) necropsy/histopath: Bilateral and symmetric yellowish discoloration of the gray matter
will be observed grossly, histologically diffuse laminar necrosis of th cerebral cortex, neuronal necrosis, gliosis, neuronophagia, Wood lamp fluorescence of formalin fixed sections (ceroid lipofuscin)
3) MRI: T2W hyperintensisies of the cerebral cortex
Most common cause of brain abscess in calves?
Trueperella pyogenes
other described pathogens:
Fusobacterium necrophorum, Listeria monocytogenes, Bacteroides species, and
Candida
Most common causes of forebran disease of the adult ruminants?
1) metabolic derangements (acid/base + electrolyte imbalance, dehydration, ketosis)
2) toxic (ammonia, lead, salt, plants, urea …)
3) infectious (rare)
4) trauma
Which plant can cause cerebellar disease in cattle and goats?
- Solanum species (Americas)
- Locoweeds (Astragalus, Oxytropis, and Swainsona) worldwide
Grading systems for head shakers
Therapy of head shaking
1) nose net (75% relief in 25% horses)
2) gabapentin
3) carbamazepine + cyproheptadine
4) Sodium cromoglycate eye drops
5) surgery (caudal ablation of the infraorbital nerve via coil compression - 50% success rate in 57 horses but 26% relapsed with a median time of 9 months)
6) EquiPENS™ neuromodulation
7) Electroacupuncture
Which percentage of horses with head shaking presented for CT have idipathic trigeminal mediated head-shaking, and in what percentage is there a predisposing pathology found?
Although TNMH was the most common diagnosiswith 62 horses (60.2%) affected, in 22 horses (21.4%), a primary disease process was identified and treatment of the condition eliminated signs of head-shaking. Clinically relevant primary diseases included dental fracture, primary sinusitis, temporo-mandibular joint arthritis, nuchal bursitis, musculoskeletal pathologies, basisphenoidfracture, otitis externa and a mass affecting the infra-orbital nerve
Which minimal minimal sensory nerve conduction stimulus threshold (SNCT) can be used to differentiate healthy horses from those with trigeminal mediated head shaking?
Minimal SNCT ≤ 10 mA showed 100% specificity to distinguish TMHS from controls, but the sensitivity was only 41%.
Which diagnostic modality is best used to differentiate horses with idiopathic trigeminal mediated head shaking from those with secondary head shaking?
CT of the head
