Diseases of the spinal cord (7)
- Spinal trauma
- Spinal cord or vertebral abscessation
- Parasitic migration (Hypoderma bovis, Parelaphostrongylus tenuis in small & exotic ruminants).
- Spinal lymphoma
- Spinal form of rabies
- Spinal cord or vertebral malformations
- Occasionally spinal forms of Listeriosis, Hempophilus somnus (TME)
Most frequent diseases of the brain (7)
Neonatal bacterial meningoencephalitis
Cerebellar hypoplasia due to prenatal BVD infection
Thrombotic meningoencephalitis (TME) due to Haemophilus somnus
Rabies
Listeriosis
Polioencephalomalacia
Sporadic diseases of the brain (4)
Lead poisoning
Congenital brain and spinal cord anomalies
Brain and spinal abscesses
Organophosphate and chlorinated hydrocarbon poisonings
Bacterial meningoencephalomyelitis - presentin problem
Depression/weakness initially
Recumbency, stupor, hypersensitivity to touch later
Bacterial meningoencephalomyelitis - pathogenesis
Neonatal disease (FPT)
Omphalophlebitis/enteritis
Hematogenous spread of infection to the CNS
Suppurative exudative leptomeningitis of the brain/spinal cord, choroiditis & ependymitis
(agents = coliforms, strep, pasteurellae, mycoplasma)
Can also be due to Hemophilus agni in lambs, salmonella typhimurium , s. dublin, Actinobacillus equuli in foals
Bacterial meningoencephalomyelitis - clinical signs
Depression, semicoma, occasionally seizures reflect the effect on the cerebral cortex and RAS (reticuloactivating system of the thalamus, mid-brain and medulla)
Ataxia, nystagmus, head tremor, opisthotonos and paresis are frequent because exudate tend to accumulate in the cerebellomedullary region
HYPERESTHESIA (sensitivity to light touch) and hyperreflexia occur due to meningeal irritation and upper motor neuron release phenomena
Bacterial meningoencephalomyelitis - diagnosis
History(colostrum deprivation), fever, panophthalmitis, polyarthritis and other signs of systemic infection
Cerebrospinal fluid (CSF) analysis diagnostic if it contains high protein, high neutrophil count
Bacterial meningoencephalomyelitis - differentials (4)
Hydrocephalus
Cerebellar hypoplasia in newborn calves
Cerebral trauma/Cerebral anoxia at birth:
Vitamin A deficiency: Not common where green forage available throughout dam’s gestation Other congenital/hereditary brain disorders: (see Mayhew or path notes for possibilities)
Bacterial meningoencephalomyelitis - treatment
aggressive and early treatment with the appropriate antibiotic, supportive care (see lectures on neonatal colibacillosis)
Bacterial meningoencephalomyelitis - prognosis
prognosis is always guarded; recovered cases may develop secondary hydrocephalus from fibrinous exudate retarding CSF drainage from venous sinuses and the ventricles
Cerebellar Hypoplasia in newborn calves
Severe cases are in lateral recumbency showing extreme difficulty in trying to right
itself, opisthotonic head posture, very strong spastic limb movements and incoordinated head movements when stimulated; milder cases can stand and demonstrate base-wide stance, bilateral symmetrical truncal ataxia, hypermetria and head tremor i.e classic cerebellar dysfunction - Strength without control!
Additional features: abnormal at birth, normal demeanour, {good appetite, afebrile if no secondary infections or other brain defects), history of BVD infection in dam at about 185 days gestation, eye lesions, positive titre prior to colostrum ingestion
ependymitis
an inflammation of the ependymal tissue, the epithelial lining of the ventricles of the brain and of the canal of the spinal cord.
leptomeningitis
an inflammation of the arachnoid and pia mater layers of the meninges
Hydrocephalus - signs/diagnosis
Predominating signs are: Abnormal demeanour (varies from normal to slight
depression/lethargy or stupidity), bilateral cortical blindness, ventro -lateral bilateral
strabismus, normal gait unless intracranial pressure becomes critical
CSF analysis normal, skull may have domed shape
Rabies - presenting problem
Depends upon the phase and form of the infection
Classic case exhibits abnormal behaviour(1-3 days) followed by ascending paralysis,
and difficulty in eating and swallowing, terminating in death within 10 days (2-7 usual duration in farm animals)
Rabies - Pathogenesis
Bite of a carnivore
Incubation (2-8 weeks, but up to 6-12 months)
Replication in muscle
Spreads centripetally via nerves to the spinal cord/brain
Disseminates through CNS & effects limbic system (behavioural)
Cerntrifugal spread along nerves to organs (gut, skin, eyes, brown fat, salivary glands)
Variations in clinical signs occur
Rabies - clinical signs
Abnormalities in demenor
Agression/attack/sexual activity/alert/hypersensitive
Mandibular & pharyngeal/laryngeal paralysis - drooling & voice change
Ruminants & horses can be normal
slow onset of proprioceptive ataxia & paresis
Loss of sensation to the perineal area & pelvic limbs when motor activity is still present (unique)
Progressive ascending flaccid paralysis
Rabies - clinical diagnosis
history
Abnormal behavour
Sudden death
Unexplainable neurological signs of 7 days duration or less
Normal blood work & CSF changes typical of viral infection
Rabies - differential diagnosis for Abnormal Behaviour
Rabies
Lead poisoning: short course, cortical blindness and severe seizures Poliencephalomalacia: bilateral cortical blindness (rare in rabies)
TME (H. somnus): rapid course, fever
Metabolic diseases: (nervous ketosis, pregnancy toxaemia in ewes, hypocalcemia, hypomagnesemia){exclude thru P.E., appropriate laboratory tests}
Other toxicities: organophosphates and chlorinated hydrocarbons
Rabies - differential diagnosis for Clinical Presentation of Cranial Nerve deficits and Paresis
Listeriosis: Cranial nerve deficits usually unilateral (7 & 8), depression only
Brain Abscess: usually asymmetrical, CSF suppurative, duration often longer
Other encephalitides: TME, BMC fever, Buss disease (SBE -Chlamydia), Mycotic or parasitic infections
Rabies - differential diagnosis for signs of Spinal cord or Bilateral Peripheral nerve deficits
Trauma, spinal abscesses, parasitic myelitis, lymphoma, dystocia can damage the lumbosacral cord, cauda equina or peripheral nerves that may cause hyporeflexia and analgesia to the back legs and perineum. Physical exam, ancillary tests and time will rule in or out the diagnosis of rabies
Rabies - Treatment , Prognosis and Prevention
Rabies in N.Amer. is invariably fatal to farm animals; course may be prolonged by supportive therapy and corticosteroids sometimes
Vaccination is recommended for valuable animals; does not seem to be as effective as vaccination in dogs and cats
Thrombotic Meningoencephalitis (TME - H. Somnus - Presenting problem
If observed in early stages, depression, fever and stiffness present
more often, sudden death or recumbent comatose or semi-comatose animal is found
Thrombotic Meningoencephalitis (TME - H. Somnus - pathogenesis
H. Somnus activated due to stress –> septicaemia, multi-focal haemorrhagic infarction of the brain/spinal cord/myocardium/skeletal muscles. (serositis, arthritis, synovitis)
Stroke-like effect of CNS –> sudden loss of consciousness often. Neurologic deficits
Thrombotic Meningoencephalitis (TME - H. Somnus - Clinical signs
Standing? transient: depression , abnormal behaviour, partial or total blindness, bilateral stiffness and sometimes ataxia
-> sudden collapse
Not moribund or comatose? multi-focal and often asymmetric deficiencies eg. blindness
cranial nerves deficits, paralysis with medullary or spinal cord damage, spinal reflex deficits if LMN to a limb are damaged
Seizures rare; HYPERESTHESIA possible
Thrombotic Meningoencephalitis (TME - H. Somnus - diagnosis
history (6-12 month old entering feedlot in fall/early winter)
found dead or comatose, high temperatures
Retinal haemorrhages
CSF with suppurative inflammation
Gross post-mortem examination
Thrombotic Meningoencephalitis (TME - H. Somnus - differentials
Lead poisoning
Polioencephalomalacia
Listeriosis
Brain Abscess
Compare TME with brain abscesses
Can be a cause of sudden death, necropsy diagnosis necessary
More commonly slowly progressive, asymmetric thalamocortical dysfunction
(hemiparesis, hemianopsis, compulsive walking in circles)(see dd. for Listeria, Polio)
Thrombotic Meningoencephalitis (TME - H. Somnus - treatment & prognosis
Early treatment while the animal is standing is very important; once animal is down, it may survive but with a prolonged convalescent period which is economically impractical
Organism is very sensitive to oxytetracycline, penicillin G., colistin and novobiocin
Compare TME with lead poisoning
Lead Poisoning
Important because sudden death common
Prodromal signs more violent(mania), blindness bilateral
Severe violent seizures predominate terminally
CSF normal
Compare TME with polioencephalomalacia
Less acute onset, longer course, afebrile, rumen motile
Blindness always bilateral and cortical in origin, no focal cranial nerve deficits
Opisthotonos, HYPERESTHESIA and mild seizure activity common
CSF normal initially
Compare TME with listeriosis
course much longer, usually unilateral cranial nerve deficits with mild gait disturbance
CSF mononuclear pleocytosis, protein content mildly elevated
Compare TME with rabies
longer, more gradual course of ascending paresis and anaesthesia to limbs
CSF typically viral response (mononuclear, mild protein increase)
Listeriosis - presenting problem
Most common onset characterized by acute unilateral vestibular imbalance which causes a head tilt, nystagmus and movement in tight circles
Unilateral facial paralysis is also common but multiple cranial nerve deficits , depression and paresis may occur in severe cases
Listeriosis - pathogenesis
The meningoencephalitis of ruminants caused by Listeria monocytogenes is thought to occur by inoculation into the buccal mucosa through abrasion or when teeth erupt; entry to the brainstem, where it causes asymmetric multi-focal micro abscesses, seems to occur via the trigeminal nerve (although ascension to the CNS by other nerves or by bacteraemia has been documented)
Proliferation of the organism in spoiled silage(pH 5 or >) and stress are predisposing factors to clinical infection with this ubiquitous organism
Listeriosis - clinical signs
The degree of depression varies with the severity and acuteness of the lesions of the RAS of the brainstem; semi-coma is more common in lambs and kids
Cranial nerves 7 & 8 are most commonly affected, followed by pharyngeal and mandibular nerve dysfunction which reflects the variable multi-focal brain stem inflammation of Listeriosis; blindness due to optic neuritis or cerebritis is rare but exposure keratitis due to facial paralysis and occasionally panophthalmitis occurs
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• Gait deficits are often hemi-lateral and may be a mixture of vestibular and proprioceptive ataxia, and paresis; this again is dependent upon the distribution of the lesions in the brainstem
Listeriosis - diagnosis
History of exposure to spoiled silage helpful but can still occur in pastured animals;
Course of disease is 1-2 weeks in adult animal but often only 2-4 days in young
ruminants and sheep
CSF cytology is uniquely mononuclear for a bacterial infection; protein levels may
normal to moderately elevated
Listeriosis - differentials
rabies
Brain stem abscess or bacterial meningoencephalitis localized to the medulla
Polioencephalomalacia
Head trauma
Listeriosis - treatment & prognosis
Early treatment with chlortetracycline (l0mg/kg B.W. per day ) for at least 5 days may be effective; penicillin at dosage of 44,000 units/kg for 7 to 14 days has also been used
Animals with dysphagia will require fluid and nutritional support
The prognosis will vary with age group, species and severity of the signs; young
ruminants often succumb despite treatment
Compare Listeriosis with rabies
cranial nerve deficits bilateral, ascending anesthesia, shorter course in cattle, LMN paralysis vs UMN(Listeria)
Compare Listeriosis with Brain stem abscess or bacterial meningoencephalitis localized to medulla
most difficult diagnosis unless CSF examined which is typical of a suppurative inflammation
Compare Listeriosis with Polioencephalomalacia
no unilateral cranial nerve deficits, blindness always symmetrical and cortical in origin
CSF normal in early stages
Compare Listeriosis with head trauma
Fractures to petrous temporal bone, haemorrhage in cerebellomedullary angle may cause facial and vestibular deficits; P.E., X-ray and CSF may help in dx.
Polioencephalomalacia - presenting problem
In early stages (lasting 1-2 days), depression, bilateral blindness, tremors, hyperesthesia, head pressing, bilateral circling and ataxia with progression to lateral recumbency in severe cases
Polioencephalomalacia - pathogenesis
By mechanisms not fully defined, alterations in the rumen micro flora (usually in association with environmental changes and a high carbohydrate diet) produce thiaminases and thiamine analogues which affect the energy metabolism of the brain; the condition in ruminants is regarded as a thiamine-responsive disease rather than absolute thiamine deficiency as it occurs in monogastric species
the early stage causes a reversible cerebral cortical edema that will progress to an irreversible cortical necrosis (CCN) if not treated with thiamine soon enough
Polioencephalomalacia - clinical signs
depression/abnormal behaviour (thalmocortical dysfunction)
circling (adversive syndrome - rostral/thalamocortical lesions)
Blindness (cortical - occipital cortex) PLR in tact
CN - dorso-medial strabismus -> hemorrhage in the caudal collicular area (trochlear n); variable nystagmus due to pressure
Swelling -> cerebellar ataxia, opisthotonos, hyperesthesia and UMN paresis
Polioencephalomalacia - diagnosis
History of high carbohydrate diet or feed changes in feedlot lambs or cattle present
Response to treatment in early cases often diagnostic for the disease
Early cases usually afebrile; a motile rumen and bradycardia (due to increased cranial
pressure) often present
CSF normal in early stages
Polioencephalomalacia - differentials
Lead poisoning: shorter course, violent seizures, rumen static
Brain Abscess: asymmetric signs, CSF suppurative,
TME (H. Somnus): shorter course, more comatose initially, fever, CSF suppurative Listeriosis: not an important differential unless animal semi-comatose
Polioencephalomalacia - treatment
thiamine (every 3 hours 5x)
followed by oral thiamine
signs may improve
per acute –> die in 1-2 days despite treatment
opisthotonos
spasm of the muscles causing backward arching of the head, neck, and spine, as in severe tetanus, some kinds of meningitis, and strychnine poisoning.
Polioencephalomalacia - control & prevention
Thiamine supplementation
1.5 kg of roughage per 100 kg BW for ruminants on high carbohydrate diets
Diseases of the peripheral nervous system
- Traumatic: (as seen in horses), more prone to injection injuries
- Inflammatory: Occasionally otitis media/interna in calves
- Neuromuscular disorders: Spastic paresis(Elso heel), Spastic Syndrome, tetanus, botulism, organophosphate toxicity (including TOCP poisoning)
- Neoplasia: lymphoma (cauda equina infiltration), neurofibromatosis (occasional nerve root signs )