Infectious causes of neurological conditions in ruminants

Question 1

Bovine viral diarrhoea

Answer 1

• Cattle
• Pestivirus (closely related to BDv)
• Teratogenic effects depend on gestational stage infected
• Cerebellar hypoplasia is most common neurological abnormality seen

Question 2

Border disease

Answer 2

• Sheep
• Pestivirus (closely related to BVDv)
• 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)

Question 3

Border disease: clinical signs

Answer 3

• 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
• “hairy little shakers”

Question 4

Border disease: treatment and control

Answer 4

• 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

Question 5

Listeriosis

Answer 5

• Listeria monocytogenes
• All ruminants affected but especially seen in sheep
• Various syndromes reported depending on where it colonises in the animal
• Will multiply at fridge temperature so unpasteurised cheese, etc can be a risk to those susceptible

Question 6

Listeriosis - syndromes reported

Answer 6

• 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)

Question 7

Listeriosis – how are animals infected?

Answer 7

• L.monocytogenes is ubiquitous in environment
• Typically associated with feeding poorly made/poorly stored silage
  – Silage that is poorly fermented or in aerobic pockets of otherwise well made silage
  – Silage pH 5.0-5.5 -> listeria multiplication
  – Silage pH < 4.5 -> inhibits multiplication
  – Baled silage might be higher risk than clamp silage -> lower density, poorer fermentation and risk of damage when wrapped
  – Soil contamination of silage increases risk (indicated by ash content >70mg/mg DM)
• Association with silage feeding -> seasonal occurrence
  – Especially sheep – commonly seen around lambing when silage is supplemented
• Bacteria is ingested and ‘accesses’ trigeminal nerves through abrasions of buccal mucosa or gum lesions
  – Ascending infection via trigeminal nerves to brainstem
  – Younger animals more commonly affected as have dental eruption going on

Question 8

Listeriosis: risk factors and herd/flock implications

Answer 8

• Despite ubiquity of L.monocytogenes only small proportion of animals develop clinical signs
• Risk factors include
  – Poor nutritional status
  – Suppressed immunity (e.g. pregnancy/parturition)
  – Sudden weather changes (typically dry to very wet)
• Cattle typically sporadic occurrence
• Sheep/goats often have flock outbreaks
  – Especially the abortive syndrome (can be up to 10% of flock affected)
  – Neurological syndrome averages ~2.5% flock affected but may be up to 35%

Question 9

Listeria: diagnosis

Answer 9

• 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

Question 10

Listeriosis ddx

Answer 10

Primary differential diagnoses:
- Pregnancy toxaemia (sheep) (but with twin lamb dz they won’t try to run away from you)
- Nervous ketosis (cattle)
- CCN (sheep and cattle)
- Scrapie (sheep/goats)
- Otitis media (sheep/goats/cattle)

Question 11

Listeriosis: initial stages clinical signs

Answer 11

• 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)

Question 12

Listeriosis: later stages clinical signs

Answer 12

• 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

Question 13

Listeriosis: final stages clinical signs

Answer 13

• Death due to respiratory failure within 2-4days for sheep/calves/goats or 1-2weeks for adult cattle

Question 14

Listeriosis: treatment

Answer 14

• 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? (used to reduce inflammation around the brain but evidence to support their use is fairly limited, but probably unlikely to cause a lot of harm. GCs might be of more benefit if think have cerebral oedema but will also result in a level of immunosuppression)
• Euthanasia is recumbent and non-responsive, as likelihood of response to tx at this stage is low

Question 15

Listeriosis: prevention

Answer 15

• Difficult as bacteria is ubiquitous
• Avoid feeding poorly fermented silage
• Remove lumps of mould from silage and some of the silage around that lump

Question 16

Listeriosis: public health implications

Answer 16

• 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)

Question 17

Louping ill

Answer 17

• Tick borne (Ixodes ricinus) flavivirus -> encephalitis
• Primarily sheep -> in particular rough hill grazing
• High mortality (up to 60%) in naïve animals
  5-10% in previously exposed animals
• Animals that survive retain immunity for life
• Definitive diagnosis = brain histology
• Rarely can be zoonotic either through tick bites or injury with contaminated equipment -> encephalitis
• Scotland see it a lot as lots of ticks

Question 18

Louping ill: clinical signs

Answer 18

• muscle tremors
• nibbling
• ataxia
• drooling
• death after 1-3 days

Question 19

Louping ill tx

Answer 19

• limited to supportive care

Question 20

Transmissible spongiform encephalopathies

Answer 20

• Prion diseases (cattle = BSE, sheep and goats = scrapie)
• Progressive, degenerative, ultimately fatal
• Slow to develop -> c/s typically seen in older animals
• Seen very infrequently now due to eradication programme and ongoing surveillance -> notifiable if suspected

Question 21

TSE: Clinical signs

Answer 21

• Circling, generalised ataxia, dull mentation
• Weight loss in spite of good appetite
• Scrapie in sheep also commonly associated with compulsive itching

Question 22

TSE: public health implications

Answer 22

• Serious public health issues in mid-90s -> BSE associations with CJD in people
• Specified risk material (SRM) not allowed in food chain

Question 23

Nervous coccidiosis

Answer 23

• Parasitic
• Neurological manifestation of Eimeria infection -> all domestic ruminants affected
• Thought to be due to neurotoxin
• Poor prognosis -> consider euthanasia
• Uncommon

Question 24

Nervous coccidiosis: clinical signs

Answer 24

• Typically enteric signs (haemorrhagic diarrhoea) precede neuro signs
• Clinical signs typical of cerebral disrders
  – Depression, ataxia -> recumbency, opisthotonos -> seizures -> death (1-5days after signs)
  – Whole body neurological signs

Question 25

Coenurus cerebralis (Gid)

Answer 25

• Localisation of C.cerebralis (tapeworm) 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
• Can be zoonotic (rare)
• Causes SOL in the brain, creating CS related to the area affected

Question 26

Coenurus cerebralis (Gid) : Clinical signs

Answer 26

• 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

Question 27

Coenurus cerebralis (Gid): prognosis

Answer 27

• poor
• death occurs after several months
• recommend euthanasia
• Albendazole will reduce the cyst size but no reports as to whether this improves the CS

Question 28

Coenurus cerebralis (Gid): tx

Answer 28

• can be attempted but prevention is better
• Anthelmintics (albendazole) -> reduces cyst size but clinical effect unknown
• Surgical removal or drainage of cysts

Question 29

Coenurus cerebralis (Gid): prevention

Answer 29

• Regular worming of dogs with praziquantel -> very effective control method
• Do not allow dogs to scavenge carcases of affected animals

Question 30

Tetanus

Answer 30

• All ruminants
• Clostridium tetani
• Soil dwelling spore-forming bacteria
• Spores are highly resistant and can remain in environment for years
• Following anaerobic incubation spores replicate and produce exotoxins
• Toxins enter body through puncture wounds
• Can also be through navel (neonates) or docking/ear tagging/dehorning sites

Question 31

Tetanus: clinical signs

Answer 31

All animals show similar clinical signs

• Initial muscle stiffness
• Inability to open mouth (‘lockjaw’) and drooling
• Anxious, alert expression -> pricked up ears, dilation of nares
• Constipation and difficulty urinating
• Tail held away from body
• Progresses to recumbency and convulsions + opisthotonos
• Death occurs due to respiratory arrest (ultimately diaphragm becomes affected and respiratory arrest is what causes death in most cases)
  – 5-10days in cattle
  – 3-4days in sheep

Question 32

Tetanus: tx

Answer 32

• Can be attempted
• Tetanus antitoxin
• Penicillin (double dose every 12-24hrs)
• Sedation if convulsions present
• Supportive care and nursing

Question 33

Tetanus: prognosis

Answer 33

• Prognosis is guarded to poor and recover is slow -. more mild/early cases have better prognosis
• Euthanasia needs to be considered (welfare grounds)

Question 34

Botulism

Answer 34

• All ruminants
• Clostridium botulinum
• Soil dwelling spore-forming bacteria
• Spores are highly resistant and can remain in environment for years
• During vegetative growth spores produce neurotoxins
• Toxins are typically ingested
  – Poorly made/stored forage
  – Contamination of forage with bird faeces
  – Poultry manure is implicated -> fertilisation of grazed pastures

Question 35

Botulism: clinical signs

Answer 35

• Cattle show flaccid paralysis (cf spastic paralysis with tetanus)
  – 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
  – Obvious muscle tremors
• Sheep initially present with muscle stiffness and ataxia
  – Progress to flaccid paralysis in later stages of disease

Question 36

Botulism: tx

Answer 36

• Prognosis is grave -> euthanasia recommended
• If recumbent prognosis is hopeless
• Treatment has been effective in foals
  – Early treatment with antitoxin (before recumbency)
  – Supportive care
  – Expensive

Question 37

Tetanus and botulism: prevention

Answer 37

• Minimise risk of exposure
• Ensure silage is made and stored well
• Do not feed poor quality or contaminated silage
• Do not spread chicken manure on fields used for feed
• Vaccinate with clostridial vaccines

Question 38

Brain abscesses

Answer 38

• Any ruminant -> young > old
• Haematogenous spread most common
• Direct spread from cranial injury or extension of adjacent lesions can also occur
• Space occupying lesions
• 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

Question 39

Spinal abscesses

Answer 39

• Any ruminant
• 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

Question 40

Visna

Answer 40

• Sheep, occasionally goats
• Neurological form of Maedi-visna disease
• Small ruminant lentivirus
• Very rare in UK (respiratory (Maedi) form usually seen)
• Common in America
• Disease is always fatal
• Euthanasia when diagnosed

Question 40

Visna: clinical signs

Answer 40

• 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

Question 41

Visna: diagnosis

Answer 41

• Serum ELISA is available for diagnosis
• Can be confirmed with brain histopathology

Question 42

Antibiotic choice for infectious neurological dz

Answer 42

• TMPS
• Amoxicillin
• Oxytetracycline
• Penicillin also appropriate for Clostridia and Listeria