L5: Neuro Dz Of Ruminants Pt.1 (MacKay) Flashcards
Diencephalon =
Thalamus + Hypothalamus
Prosencephalon (forebrain) =
Telencephalon + Diencephalon
Symptoms of forebrain disease
- seizures
- dementia (head pressing, compulsive walking, excessive vocalization, teeth grinding, self-mutilation, hyperesthesia)
- blindness
- mental depression (obtunded)
- decorticate/decerebrate posturing
Hydrocephalus
Too much water in the ventricular system/CSF of the brain
Hydranencephaly
Replacement of brain parenchyma with water (usually in forebrain tissue)
Causes of Hydrocephalus/Hydranencephaly
1) Genetic:
- aqueductal stenosis due to neuropathic hydrocephalus in Angus
2) Acquired:
- fetal bluetongue, BVD infection
- fetal Akabane, Schmallenburg viruses
- Vit. A def. in the dam
- bacterial meningitis
CS of Hydrocephalus/Hydranencephaly
- classic forebrain signs (blind, wandering, dummies, seizures, lack of maternal bonding)
- generally stunted
- failure of passive transfer –> 2ary sepsis**
- domed forehead
Dx of Hydrocephalus/Hydranencephaly
- domed skull
- genetic testing
- cortical signs
- precolostral blood PCR, serology, virus isolation
- Ig quantification
- cross-sectional imaging
- necropsy
Infectious causes of neuro dz in ruminants
- Neonatal bovine suppurative meningitis*
- Thromboembolic meningoencephalitis (TEME)
- Sporadic bovine encephalitis (SBE, Buss disease)
- Brain abscess/pituitary abscess*
Meningitis most commonly affects what populations?
-neonates
Etiology of neonatal suppurative bovine meningitis (NSBM)
- hematogenous from gut, umbilicus
- direct from dehorning, tail docking, environment
- failure of passive transfer most common cause**
- most common pathogens assoc. with failure of passive transfer: E. Coli, Trueperella pyogenes, gram negs
- primary pathogens (not from FPT): Salmonella, mycoplasma
CS of neonatal suppurative bovine meningitis (NSBM)
- fever
- neck stiffness
- hyperethesia
- blind, seizures
- nystagmus, obtunded
- recumbent, coma
- sepsis signs (ie. Septic vasculitis)
- decerebrate
Dx of neonatal suppurative bovine meningitis (NSBM)
- CS
- plasma protein conc. (FPT)
- CSF tap: xanthrochromia, bacteria, neutrophilic pleocytosis (degenerate PMNs)
Tx of neonatal suppurative bovine meningitis (NSBM)
- euthanize
- dexamethasone
- abx (Ceftiofur 10 mg/kg IV q12hr, enrofloxacin)**
- hypertonic saline if opisthotonus
- blood/plasma for FPT
- anticonvulsant
- supportive
Telencephalon =
Cerebrum
CS of cerebral abscess
Asymmetric forebrain signs
CS of pituitary abscess/basilar empyema
- blindness
- obtundation, cranial nerves
Causes of brain/pituitary abscess
- adjacent infecton
- penetrating wound
- nose rings (pituitary)
Viral causes neuro dz in ruminants
Pseudorabies
Rabies
Malignant catharral fever
Bovine herpes encephalomyelitis
Pseudorabies (Mad Itch)
- caused by alpha herpesvirus
- pigs are carriers
- CS: fever, self-mutilation, pruritus, dementia, ataxia
- usually die within days*
- endemic in feral pigs in FL
- reportable dz
- > 95% mortality
Rabies virus, CS, forms
- Rhabdoviridae genus lyssavirus
- centripetal then centrifugal
- CS: fever, hypersalivation, can’t swallow, hydrophobia, metabolic acidosis, tenesmus, etc.
Forms:
- furious: forebrain, classic rabies
- dumb: brainstem, obtunded
- paralytic: spinal cord, polymyolitis
Dx of rabies
- mild mononuclear pleocytosis
- Negri bodies
- FA staining frozen sections
Prevention of rabies
- kill/quarantine suspects/exposed
- PEP for valuable animals (ie. Texas protocol)
- rabies vax
Malignant Catarrhal Fever
- y-herpesvirus
- sheep are carriers
- CS: fever, obtundation, aggression, ataxia, “white eye,” lymphadenopathy, diarrhea
- 95% mortality
Bovine Herpesvirus Encephalomyelitis
- alpha herpesvirus
- outbreaks in S. America
- fatal in calves
Transmissible Spongiform Encephalopathies (TSE)
BSE Scrapie CWD CJD Mink encephalopathy
CS and course of BSE
CS: forebrain signs esp. Apprehension, aggression, self mutilation; ataxia, m. Spasms, wt. loss
Clinical course = 1-6 mo. And fatal
Cause of BSE
Prions
- unique infectious protein that has no RNA or DNA
- has ability to transform normal PrPc proteins to abnormal form
- prions found in CNS, bone marrow, GI
BSE Surveillance
- rapid immunotests for PrPsc
- histology
- sample of obex (brain tissue under the cerebellum)
- IHC is official test
Scrapie
- affects sheep and goats (sheep > goats)
- distinct from BSE
- present in lymphoid tissues AND CNS (different from BSE)
- transmission: peri-natal, or between adults
- more common in black-faced sheep (can have PrPc gene polymorphism)
- endemic but rare
- similar CS as BSE
Scrapie eradication program
- genetic testing (blood samples)
- certification of negative herds
- live animal testing: 3rd eyelid, rectal biopsy
Nutritional/Toxic causes of neuro dz in ruminants**
- Salt poisoning/water intoxication*
- lead poisoning*
- polioencephalomalacia (thiamine)*
- polioenchephalomalacia (sulfur toxicity)*
- vit. A deficiency
- non-protein nitrogen toxicity
- = causes laminar cortical necrosis
- all have CS, but lead poisoning causes the most mania*
- more signs of colic in lead/salt poisoning than poliocephalomalacias*
Pathophys. of salt poisoning/water toxicity
- high salt or water deprivation
- high Na –> brain shrinking/hemorrhage
- water repletion –> brain swelling
- water toxicity by itself doesn’t cause CNS problems
- improperly mixed milk replacer is most common cause
> 50% mortality
CS of salt poisoning/water toxicity
Forebrain signs, then brainstem signs (opisthotonus, ataxia, limb weakness, coma) as brain swells up against calvarium and puts pressure on brainstem
GI signs: colic, d
Dx of salt poisoning/water toxicity
Hx High Na (>1 CSF: plasma ratio)
Tx of salt poisoning/water toxicity
IV 0.9% saline (can give IV saline and withhold milk), +/- 10-20 ml hypersaline/L
Monitor plasma Na
Aternative: small amounts of oral saline or milk slowly
Dexamethasone
CS of acute lead poisoning
- Hyperesthesia, bellowing, blindness
- twitching facial muscles
- progress to recumbency
- GI signs
- MANIA
CS of subacute/chronic lead poisoning
- blindness
- diarrhea
Dx of lead poisoning
- blood lead > 0.35 ppm
- urine ALA concentration
- tissue lead (post-mortem)
- CBC in subacute cases: polychromasia, basophilic stippling
Tx of lead poisoning
- Sedation (ie. Valium to prevent seizures)
- rumenotomy, MgSO4 (reduces bioavailability)
- EDTA chelation therapy
- thiamine (supports glucose metabolism in CNS)
- support
- fair prognosis w/ tx
Polioencephalomalacia: Thiamine deficiency
- can affect all ruminants/camelids (usually weanlings)
- sporadic outbreaks
- assoc. with overfeeding/roughage underfeeding/feed change/deworming
CS/Tx of thiamine deficiency
CS: bilateral dorsomedial strabismus***, star-gazing, seizures, wandering, etc.
Central vision can take a long time to recover**
Tx:
- thiamine 10-20 mg/kg slow IV, SC, IM BID-QID
- dexamethasone
- rumenal transfaunation
- support
Polioencephalomalacia: Sulfur Toxicity
- assoc. with feedlots, well water, distillers grain by-products**, molasses, anionic diets –> sulfur ingestion
- supportive tx only; can give thiamine
- sulfur is converted to H2S gas in the rumen –> eructation –> inhalation –> CNS toxin
Metabolic conditions that cause neuro dz in ruminNRA
Hepatoencephalopathy (protolaria ? Plant most common cause) Nervous Ketosis Electrolyte abnormalities Hypoglycemia Hypomagnesemia Early hypocalcemia
Nervous ketosis
- during early lactation
- ketonuric
- causes cerebral signs: licking, head-pressing
- tx: IV dextrose, oral propylene glycol, dexamethasone
