Neurological disease in ruminants 2 Flashcards
inherited
What is hydrocephalus?
in what breeds is it hereditary?
What is it normally seen with?
Brain ventricle distension with fluid
* Increased CSF production
* Obstruction of outflow
* Decreased CSF absorption
Hereditary:
* Holstein and Herefords (cattle)
* Suffolk (sheep)
Often seen alongside other congenital abnormalities
Neonates often still born – prognosis is often poor if born alive, but some may reach slaughter if mildly affected
inherited/infectious
Cerebellar hypoplasia and atrophy (cattle) is often secondary to what infectious condition?
in what breeds is it hereditory?
What are the clincical signs?
What is the prognosis?
- Commonly secondary to BVDv infection in utero (100-200 days gestation)
- hereditary: Hereford, Shorthorn, Ayrshire, Aberdeen Angus
- Clinical signs vary from recumbency and opisthotonos to generalised ataxia with hypermetric gait
- No treatment available
- Prognosis depends on severity of clinical signs
- Ultimately size of animal makes long term prognosis poor (dangerous to handle)
inherited
What is Spastic paresis (elso heel)?
what is the prognosis?
- Usually 1st seen from a few weeks old up to 6 months
- Very straight hocks, excess tone in gastrocnemius, ‘tin soldier’ gait, tail elevated –> usually one leg worse than other (or unilateral)
- In BB calves quadriceps femoris is affected –> usually bilateral
- Lameness becomes progressive until calf recumbent –> usually euthanised
- Treatment = partial tibial neurectomy
infectious
What disease does a Pestivirus (closely related to BVDv) cause in sheep?
What are the differnt types of this?
Border disease:
Teratogenic effects depend on gestational stage infected
* Very early pregnancy = foetal death
* 21-72 days gestation = persistently infected (PI) lambs
* Mid-pregnancy (60-80days) = variable teratogenic effects including neurological deformities
* Late pregnancy (>80days) = no effect (virus eliminated by foetus)
What are the clinical signs of border disease?
What is the treatment?
What is the control?
Clinical signs are seen at birth:
* Small with conformational abnormalities (short legs, short spine, domed head)
* Dry, hairy fleece (forms a ‘halo’ round body) –> not all breeds
* Neurological abnormalities –> most evident during movement
* Muscle tremors of large limb muscles or whole body
* Jerking/shaking movements
* Head bobbing
- No treatment available
- Most lambs will survive initially but do not thrive and are of increased risk of concurrent disease (e.g. pneumonia)
- Prevention/control is similar to BVD in cattle
- Identify and remove PI lambs
- Avoid buying in infected animals
- Vaccination is not available
What syndromes can listeria monocytogenes cause in sheep?
(affects all ruminants affected but especially seen in sheep)
- **Encephalitis/meningitis
- Abortion
- Keratoconjunctivitis/uveitis** (associated with ring/big bale feeders)
- Septicaemia (rare)
- Gastroenteritis (weaned lambs - rare)
- Spinal myelitis (rare)
- Mastitis (rare – public health risk)
How are animals infected with listeriosis?
What are the risk factors?
L. monocytogenes is ubiquitous in environment
Typically associated with feeding poorly made/poorly stored silage
- Association with silage feeding –> seasonal occurrence
- Especially sheep – commonly seen around lambing
- Bacteria is ingested and ‘accesses’ trigeminal nerves through abrasions of buccal mucosa or gum lesions
- Ascending infection via trigeminal nerves to brainstem
Risk factors include
* Poor nutritional status
* Suppressed immunity (e.g. pregnancy/parturition)
* Sudden weather changes (typically dry to very wet)
How is listeriosis diagnosed?
Clinical exam and history –> presumptive diagnosis
* Clinical signs similar for all species but disease progresses more quickly in smaller ruminants
* Ante-mortem confirmation not currently possible
* CSF = non-specific signs of inflammation/infection (raised neutrophils)
* Antibody titres not of diagnostic value because most ruminants are positive
* Diagnosis confirmed on post-mortem - Histopathology
What are the differential diagnoses for listeriosis?
Pregnancy toxaemia (sheep)
Nervous ketosis (cattle)
CCN (sheep and cattle)
Scrapie (sheep/goats)
Otitis media (sheep/goats/cattle)
What are the three stages of clinical signs of listeriosis?
Initial stages:
*Depressed, separate selves from flock
*When approached try to run away but are ataxic and fall easily
*Pyrexia >40 °C in very early stages (often normal by time c/signs seen)
Later stages:
*Progression to recumbency and severe depression (appear sedated) – rapid in sheep/goats
*Facial paralysis and hyperalgesia – drooling and flaccid tongue common
*Absent palpebral reflex may lead to exposure keratitis
Final stages:
*Death due to respiratory failure within 2-4days for sheep/calves/goats or 1-2weeks for adult cattle
What is the treatment for listeriosis?
- Early treatment needed for success
- Penicillin is drug of choice
- Double dose q12-24hrs for 10-14days
- Oxytetracycline reportedly effective in cattle but not so in sheep
- 10mg/kg q12hrs or 20mg/kg q24hrs IV for 10-14days
- Supportive care
- NSAIDs? Glucocorticoids?
What is the prevention and public health implications of listeriosis?
Prevention
* Difficult
* Avoid feeding poorly fermented silage
Public health implications
* Zoonotic
* Foodborne
* Unpasteurised milk/cheese
* Most contamination is through faecal contamination of milk, not from clinically affected animals
(L.monocytogenes can replicate at fridge temperatures (4 °C))
What causes louping ill?
What are the clincial signs?
- Tick borne (Ixodes ricinus) flavivirus –> encephalitis
- Primarily sheep –> in particular rough hill grazing
- High mortality (up to 60%) in naïve animals
- Muscle tremors, nibbling, ataxia, drooling, death after 1-3 days
- Animals that survive retain immunity for life
- Treatment limited to supportive care
zoonotic
What bacteria causes tetanus?
Where is this found?
How does it enter the body?
What are the clinicla signs?
What is the treatment?
- Clostridium tetani
- Soil dwelling spore-forming bacteria
- Toxins enter body through puncture wounds
Clincial signs:
* Initial muscle stiffness
* Inability to open mouth (‘lockjaw’) and drooling
* Anxious, alert expression –> pricked up ears, dilation of nares
* Progresses to recumbency and convulsions + opisthotonos
Treatment:
* Tetanus antitoxin
* Penicillin (double dose every 12-24hrs)
- Prognosis is guarded to poor and recover is slow
What bacteria causes botulism?
Where is this found?
How does it enter the body?
What are the clinical signs?
What is the treatment?
- Clostridium botulinum
- Soil dwelling spore-forming bacteria
- Toxins are typically ingested
Clinical signs:
* Cattle show flaccid paralysis
* Signs usually develop 3-17days after exposure but can be quicker
* Generalised weakness that progresses from the hindlimbs forwards to forelimbs, neck, head and throat
Sheep initially present with muscle stiffness and ataxia
Progress to flaccid paralysis in later stages of disease
Prognosis is grave –> euthanasia recommended
Can vacciante for prevention
What are the causes of brain abcesses?
What are the clinical signs?
What is the treatement?
- Haematogenous spread most common
- Direct spread from cranial injury or extension of adjacent lesions can also occur
- Clinical signs variable and relate to part of brain affected
- Treatment with antibiotics can be attempted but response often poor
- Antibiotic penetration of lesion is poor
- Definitive diagnosis is post-mortem exam
What are the causes of spinal abcesses?
What are the clinical signs?
What is the treatement?
- Haematogenous spread or direct spread from injury
- Iatrogenic injury related to IM injections common –> especially sheep
- Space occupying and compressive lesions
- May also have osteomyelitis
- Clinical signs variable and relate to location and size of abscess
- Treatment with antibiotics can be attempted but response often poor
- Antibiotic penetration of lesion is poor
- Definitive diagnosis is post-mortem exam
What neurological effects can meadi-visna cause in ruminants?
How is it diagnosed?
What is the prognosis?
- Very rare in UK (respiratory (Maedi) form usually seen)
- Slow onset signs relating to demyelinating encephalitis
- Progessive loss of condition and hindlimb ataxia —> eventually complete paralysis
- Circling, blindness, aimless wandering
- May have periods of normalcy
- Serum ELISA is available for diagnosis
- Can be confirmed with brain histopathology
- Disease is always fatal
- Euthanasia when diagnosed
Traumatic
Obturator nerve injury is Commonly related to calving (Large calves, Hip-locked calves)
What does it cause?
What is the treatment?
What is the prognosis?
- Hindlimb adductor muscle paralysis - ‘splits’
- Direct trauma to nerve or localised ischaemia secondary to pressure from calf
- Manage conservatively
- NSAIDs (for concurrent injuries)
- Deep bed
- Hobbles/shackles (maintain medial positioning of hindlimbs)
- Prognosis is good in most cases
- Full recovery can take several months
- Tearing/transection of nerve = poor prognosis
What are the clincial signs of sciatic nerver injury?
When does it occur?
What is the treatment?
what is the prognosis?
- Post-calving (typically dairy cows) and iatrogenic (typically calves and small ruminants)
- Difficulty standing
- Dropped hock with knuckled fetlock
- Bilateral or unilateral
- Characteristic leg position is diagnostic
- Treat conservatively
- NSAIDs
- Supportive care
- Prognosis = good
- Recumbency associated with poorer prognosis
- Recovery in a few days up to several weeks
What are the clincial signs of tibial nerve injury?
Sciatic runs caudal thigh and branches just before stifle
* Tibial branch –> caudal branch innervates hock extensors and digit flexors plus sensation to caudal distal hindlimb
* Peroneal (common fibular) branch –> cranial branch innervates hock flexors and digit extensors plus sensation to cranial distal hindlimb
- Injury to tibial nerve also presents with dropped hock but fetlock hyper-extended (cows walk on heels)
- Rare compared to sciatic injury
What causes femorla nerver injury in calves?
What are the signs?
What is the treatment?
- Calves injured during birth
- Associated with excessive traction - especially if hip-locked
- Calves are unable to extend stifle or bear weight on affected limb
- Bilaterally affected calves cannot stand (dog sit)
- Quadriceps femoris atrophies over approx. 10 days
- Patellar laxity also develops
- Treatment is conservative –> remember to ensure adequate nutrition
- Prognosis is dependent on severity of clinical signs
What are the cuases of brachial plexus injuries?
What are the clinical signs?
What is the treatment?
- Calves – birth injuries
- Associated with excessive traction on forelimbs - especially if cow goes down with calf half-way delivered
- Sheep – accidents (stuck in fence/gate) or harness injuries (rams)
- Inability to extend elbow, carpus or fetlock
- Dropped elbow, scuffed hoof, knuckled foot when resting
- Unable to bear weight on affected limb in severe cases
- Shoulder muscles atrophy
- Scapular spine becomes prominant
- Treatment is conservative
- Can splint forelimbs of calves to aid movement and prevent tendon contracture
What are the clincical signs of radial nerve innjuries?
What is the casue?
Occurs following prolonged lateral recumbency or traumatic injuries
Knuckling of carpus and fetlock but can still weightbear
Decreased sensation of antebrachium, metacarpus and foot
Conservative treatment
Prognosis depends on severity of injury
toxic
What is the presentation of lead toxicity?
- Acute form - tremors, staggering, blindness, twitching of face, neck and ears progresses to seizures and death in 12-24hrs
- Subacute form (more common) – GIT dysfunction (rumen atony, constipation followed by foul-smelling diarrhoea). Dull demeanour, blindness, muscle twitching (less severe than acute form). Sheep show neurological signs less often than cattle. Death occurs in 3-4days.
Have a look in the field as part of your exam - may find lead contamination (e.g. car batteries, pre-1960s paint tins)
What is the treatment of lead toxicity?
- Supportive care
- Sedate animals with severe neurological signs
- Provide IV fluid therapy
- Remove animal from source of lead
- Chelation therapy
- Calcium EDTA – 73mg/kg slow IV BID-TID for 3-5days
- SEs include renal and gastrointestinal toxicity
- Add thiamine (vit B1) at dose of 2mg/kg IM
What is the cause of hypernatremia in calves?
What are the clinical signs?
What is the treatment?
What is the prevention?
- Excessive sodium ingestion in absence of adequate water
- High sodium milk replacer with no water access
- Electrolyte solutions
- Cerebral oedema –> muscle tremors, seizures, ataxia, opisthotonos
- May just have high mortality with no obvious neuro signs
- Diagnosis
- Live calf = blood sample (Na > 160mEq/L)
- Dead calf = aqueous or vitreous humor. Can also send brain (fresh and fixed)
- Treatment
- Difficult –> consider euthanasia
- IV fluids –> formulate to match sodium concentration of calf and slowly reduce sodium concentration over several days
- Prevention –> ensure free water access and be careful with electrolytes (especially homemade)
What prion diseases cause neruological signs in cattle and sheep?
What are the signs?
Transmissible spongiform encepgalopathies:
Prion diseases (cattle = BSE, sheep and goats = scrapie)
Progressive, degenerative, ultimately fatal
Slow to develop –> c/s typically seen in older animals
Neurological signs typical of cerebral disease
* Circling, generalised ataxia, dull mentation
* Weight loss in spite of good appetite
* Scrapie in sheep also commonly associated with compulsive itching
Seen very infrequently now due to eradication programme and ongoing surveillance –> notifiable if suspected
What is nervous coccidiosis?
What are the clinical signs?
what is the prognosis?
- Neurological manifestation of Eimeria infection –> all domestic ruminants affected
- Thought to be due to neurotoxin
- Typically enteric signs (haemorrhagic diarrhoea) precede neuro signs
- Clinical signs typical of cerebral disrders
- Depression, ataxia –> recumbency, opisthotonos –> seizures –> death (1-5days after signs)
- Poor prognosis
What is Coneurus cerebralis (gid)?
What is it caused by?
What are the clinical signs?
What is the prognosis?
- Localisation of C.cerebralis in brain/spinal cord –> all domestic ruminants affected but primarily sheep
- Most often reported in growing sheep 6-18 months old
- C.cerebralis is intermediate stage of T.multiceps –> dogs and wild canids
- Acute stages sheep can exhibit irritation signs (e.g. salivation, frenzied running)
- Some die at this stage but majority progress to loss of function
- Clinical signs typical of area affected
- Cerebrum: e.g. blindness, ataxia, collapse, dull mentation, head pressing, circling
- Spinal cord: gradual development of paralysis
- Most common clinical sign = slowly developing unilateral blindness
- Compulsive circling also commonly seen
- Prognosis = poor –> death occurs after several months
Prevention is best
Regular worming of dogs with praziquantel –> very effective control method
Do not allow dogs to scavenge carcases of affected animals
