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Food Animal Medicine & Surgery > Ruminant Neurological Diseases > Flashcards

Ruminant Neurological Diseases Flashcards

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1
Q

Diseases of the spinal cord (7)

A
  • 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)
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2
Q

Most frequent diseases of the brain (7)

A

Neonatal bacterial meningoencephalitis
Cerebellar hypoplasia due to prenatal BVD infection
Thrombotic meningoencephalitis (TME) due to Haemophilus somnus
Rabies
Listeriosis
Polioencephalomalacia

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3
Q

Sporadic diseases of the brain (4)

A

Lead poisoning
Congenital brain and spinal cord anomalies
Brain and spinal abscesses
Organophosphate and chlorinated hydrocarbon poisonings

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4
Q

Bacterial meningoencephalomyelitis - presentin problem

A

Depression/weakness initially

Recumbency, stupor, hypersensitivity to touch later

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5
Q

Bacterial meningoencephalomyelitis - pathogenesis

A

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

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6
Q

Bacterial meningoencephalomyelitis - clinical signs

A

 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

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7
Q

Bacterial meningoencephalomyelitis - diagnosis

A

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

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8
Q

Bacterial meningoencephalomyelitis - differentials (4)

A

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)

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9
Q

Bacterial meningoencephalomyelitis - treatment

A

 aggressive and early treatment with the appropriate antibiotic, supportive care (see lectures on neonatal colibacillosis)

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10
Q

Bacterial meningoencephalomyelitis - prognosis

A

 prognosis is always guarded; recovered cases may develop secondary hydrocephalus from fibrinous exudate retarding CSF drainage from venous sinuses and the ventricles

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11
Q

Cerebellar Hypoplasia in newborn calves

A

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

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12
Q

ependymitis

A

an inflammation of the ependymal tissue, the epithelial lining of the ventricles of the brain and of the canal of the spinal cord.

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13
Q

leptomeningitis

A

an inflammation of the arachnoid and pia mater layers of the meninges

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14
Q

Hydrocephalus - signs/diagnosis

A

 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

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15
Q

Rabies - presenting problem

A

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)

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16
Q

Rabies - Pathogenesis

A

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

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17
Q

Rabies - clinical signs

A

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

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18
Q

Rabies - clinical diagnosis

A

history
Abnormal behavour
Sudden death
Unexplainable neurological signs of 7 days duration or less
Normal blood work & CSF changes typical of viral infection

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19
Q

Rabies - differential diagnosis for Abnormal Behaviour

A

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

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20
Q

Rabies - differential diagnosis for Clinical Presentation of Cranial Nerve deficits and Paresis

A

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

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21
Q

Rabies - differential diagnosis for signs of Spinal cord or Bilateral Peripheral nerve deficits

A

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

22
Q

Rabies - Treatment , Prognosis and Prevention

A

 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

23
Q

Thrombotic Meningoencephalitis (TME - H. Somnus - Presenting problem

A

 If observed in early stages, depression, fever and stiffness present
 more often, sudden death or recumbent comatose or semi-comatose animal is found

24
Q

Thrombotic Meningoencephalitis (TME - H. Somnus - pathogenesis

A

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

25
Q

Thrombotic Meningoencephalitis (TME - H. Somnus - Clinical signs

A

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

26
Q

Thrombotic Meningoencephalitis (TME - H. Somnus - diagnosis

A

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

27
Q

Thrombotic Meningoencephalitis (TME - H. Somnus - differentials

A

Lead poisoning
Polioencephalomalacia
Listeriosis
Brain Abscess

28
Q

Compare TME with brain abscesses

A

 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)

29
Q

Thrombotic Meningoencephalitis (TME - H. Somnus - treatment & prognosis

A

 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

30
Q

Compare TME with lead poisoning

A

Lead Poisoning
 Important because sudden death common
 Prodromal signs more violent(mania), blindness bilateral
 Severe violent seizures predominate terminally
 CSF normal

31
Q

Compare TME with polioencephalomalacia

A

 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

32
Q

Compare TME with listeriosis

A

 course much longer, usually unilateral cranial nerve deficits with mild gait disturbance
 CSF mononuclear pleocytosis, protein content mildly elevated

33
Q

Compare TME with rabies

A

 longer, more gradual course of ascending paresis and anaesthesia to limbs
 CSF typically viral response (mononuclear, mild protein increase)

34
Q

Listeriosis - presenting problem

A

 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

35
Q

Listeriosis - pathogenesis

A

 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

36
Q

Listeriosis - clinical signs

A

 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
24
• 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

37
Q

Listeriosis - diagnosis

A

 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

38
Q

Listeriosis - differentials

A

rabies
Brain stem abscess or bacterial meningoencephalitis localized to the medulla
Polioencephalomalacia
Head trauma

39
Q

Listeriosis - treatment & prognosis

A

 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

40
Q

Compare Listeriosis with rabies

A

 cranial nerve deficits bilateral, ascending anesthesia, shorter course in cattle, LMN paralysis vs UMN(Listeria)

41
Q

Compare Listeriosis with Brain stem abscess or bacterial meningoencephalitis localized to medulla

A

most difficult diagnosis unless CSF examined which is typical of a suppurative inflammation

42
Q

Compare Listeriosis with Polioencephalomalacia

A

 no unilateral cranial nerve deficits, blindness always symmetrical and cortical in origin
 CSF normal in early stages

43
Q

Compare Listeriosis with head trauma

A

 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.

44
Q

Polioencephalomalacia - presenting problem

A

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

45
Q

Polioencephalomalacia - pathogenesis

A

 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

46
Q

Polioencephalomalacia - clinical signs

A

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

47
Q

Polioencephalomalacia - diagnosis

A

 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

48
Q

Polioencephalomalacia - differentials

A

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

49
Q

Polioencephalomalacia - treatment

A

thiamine (every 3 hours 5x)
followed by oral thiamine
signs may improve
per acute –> die in 1-2 days despite treatment

50
Q

opisthotonos

A

spasm of the muscles causing backward arching of the head, neck, and spine, as in severe tetanus, some kinds of meningitis, and strychnine poisoning.

51
Q

Polioencephalomalacia - control & prevention

A

Thiamine supplementation

1.5 kg of roughage per 100 kg BW for ruminants on high carbohydrate diets

52
Q

Diseases of the peripheral nervous system

A
  1. Traumatic: (as seen in horses), more prone to injection injuries
  2. Inflammatory: Occasionally otitis media/interna in calves
  3. Neuromuscular disorders: Spastic paresis(Elso heel), Spastic Syndrome, tetanus, botulism, organophosphate toxicity (including TOCP poisoning)
  4. Neoplasia: lymphoma (cauda equina infiltration), neurofibromatosis (occasional nerve root signs )

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