Guide to Neurologic Diseases of

Cattle, Sheep and Horses

Dr. Jonathan Fox

Department of Veterinary Science
jfox7@uwyo.edu

Outline of lectures
Introduction
Neurologic disease by life-stage Diseases of the peri-parturient period (lecture 1)
Diseases
Di
off neonates
t (lecture
(l t
1)
Diseases of juveniles and adult (lecture 2)

Organization of the Nervous System

Central nervous system

Brain
Spinal cord
Peripheral nervous system
Nerves

Gray matter

White matter

Front of brain
Behavioral changes
Altered consciousness
Blind, circling
Spinal cord
Lameness
Weakness
Paralysis/recumbent
Nerve damage
Chewing
Prehension
Swallowing

Cerebellum
Incoordination
Tremor

Nerve damage
Lameness
Weakness

Neurologic Diseases of the

Periparturient Period

Ketosis of cows and ewes

These diseases
may occur in
Hypocalcemia of cows and ewes
combination, in
various forms
Hypomagnesemia of cows and ewes
Obturator nerve paralysis calving injury

What does periparturient mean?

Why is the periparturient period a time of
great physiologic stress to cows and sheep?

 What does periparturient mean?

Why is the periparturient period a time of
great physiologic stress to cows and sheep?
Rapid fetal growth last
6-8 weeks of pregnancy

Poor quality food

Fat and protein breakdown to

provide energy for growing fetus

Trauma

Parturition

Fat and protein breakdown to

provide energy for milk production
Abrupt change of pasture

Metabolic disease

Metabolic disease

Metabolic disease

Ketosis of ewes and cows 1.

AKA. twin-lamb disease, pregnancy toxemia in ewes
Species: Cattle (dairy>beef) usually high yielding dairy
cows. Sheep. The disease in sheep occurs typically up
to 6-weeks before lambing. In cows, the disease
typically occurs in the first few weeks after calving (up
until
til th
the point
i t off maximum
i
milk
ilk production
d ti around
d8
weeks of age).
Cause: Rapid breakdown of fat to maintain energy
balance in the face of rapidly growing fetus and reduced
ruminal capacity (ewes) or sudden increase in milk
production associated with low appetite post-parturition
(cows).

Ketosis symptoms 2.
Non-neurologic ketosis

Neurologic ketosis

Reduced appetite
Weight loss
Poor milk production
May be part of a subclinical
problem of low productivity
constant licking
also wandering, head
pressing, biting object in pen,
may appear blind, fine tremors

Diagnosis: History, clinical examination and testing for ketones in urine

(e.g. dip stick type tests are available). Sweet smell to breath (like
acetone) in some cases.

Treatment: Supply a carbohydrate source. Intra-venous glucose or

oral propylene glycol can be administered by a veterinarian. Optimize
nutrition.
Prevention: A case of ketosis may indicate the presence of a subclinical herd / flock problem. Ketosis is more common in thin or
overweight ewes and cows therefore good nutritional management is
important in disease prevention. Stress can precipitate ketosis e.g.
poor weather leading to reduced food intake.

Hypocalcemia of ewes and cows 1.

[aka. milk fever in cows]

Species: Cattle (dairy>beef) and sheep. The disease in sheep and

goats occurs typically up to 6-weeks before lambing. In dairy cows,
the disease typically occurs in the first few weeks after calving.
Cause: Disturbances of calcium homeostasis are nearly always
related to calcium mobilization for a rapidly growing fetus (ewes) or
for milk production (cows and mares).
Pathogenesis:
Low blood calcium interferes with the function of skeletal muscle.
Complicated cases may have disturbances of magnesium and
phosphorus.
Marginally low blood calcium in dairy cows will not result in
classical milk fever but may be associated with other problems
such as displaced abomasum (secondary to abnormal
gastrointestinal motility).

Hypocalcemia of ewes and cows 3: clinical findings

Symptoms: Ewes and cows have flaccid muscles (generalized weakness

progressing to recumbency). There may be neck flexure. Reduced
gastrointestinal motility may lead to bloat. There is no pyrexia.

Hypocalcemia of ewes and cows 4

Diagnosis: This is typically by history, clinical
examination and response to treatment. Serum calcium
concentration.
Treatment: Slow intra-venous or subcutaneous
calcium salts. Response to therapy is often dramatic.
Prevention:
Dietary manipulations in the peri-parturient period.
Good diet will reduce incidence, but not prevent all
cases. Consult a veterinary or animal nutritionist if
many cases.
Stress is an important predisposing factor in sheep
e.g. driving, change in diet, temporary absence of
food.

Hypomagnesemia in cattle and sheep 1.

Species: Cattle, sheep and goats.
Cause: Disturbances of magnesium
homeostasis. Magnesium intake not meeting
demand no significant magnesium storage
sites in body.
Symptoms: Ewes and cows typically show
excitability initially e.g. twitching, hypersensitive.
This progresses to prostration, paddling
convulsions and death. Many animals are found
dead. May occur in several animals
simultaneously, especially if after moving to
fresh pasture.

Hypomagnesemia 2: important differential

diagnosis for sudden death
Evidence of seizure activity prior to death: scuff marks on ground

Ecchymotic hemorrhages
are not specific

Vitreous Mg concentrations are

fairly stable post-mortem
Vitreal Mg in severe
hypomagnesemia
Sheep < 0.65 mmol/L for
up to 24 hours PM
Cattle < 0.55 mmol/L in
adult cows for up to 48
hours PM
Coy MC, Magnesium research. 17(2). 137-145. 2004

Hypomagnesemia in cattle and sheep 3.

Pathogenesis: Low blood Mg leads to low brain
magnesium interfering with electrical activity in the brain.
Many cases may have low calcium and / or phosphorus
which complicates diagnosis and treatment.
Diagnosis: History, clinical examination, response to
treatment and serum Mg, Ca, P analysis. Take a serum
sample before treatment incase animal fails to respond
respond.
Necropsy aqueous fluid magnesium concentrations.
Treatment: Magnesium and calcium injections should
be given by slow intra-venous injection.

Hypomagnesemia in cattle and sheep 4 prevention.

Consider testing other cows / ewes for
subclinical disease to determine extent of
problem
Pasture management heavily fertilized lush
pasture (K / N) significantly increase risk
Reduce exposure to other stressors e.g. weather
Nutritional management
Obtain advice from veterinarian / nutritionist
Improve nutrition hay, silage alone will help
Supplements magnesium oxide on food

Summary: Ketosis / hypocalcemia / hypomagnesemia

May be difficult to distinguish clinically and may co-exist Pretreatment blood samples
Green top tube
Gray top tube

Mg, Ca, Phosphorus

glucose, ketone bodies

Some veterinarians treat for all three conditions

simultanesoulyy
Mg, Ca, Phosphorus iv and sc
Glucose iv and / propylene glycol orally

Observe animals regularly at high risk periods

After moving to lush pasture for hypomagnesemia (cattle, sheep)
Prepartum and especially after driving for hypocalcemia (sheep)
Sheep ketosis condition scoring is a valuable tool for targeting
improved nutrition to pregnant ewes that are thin

Preventive measures can be implemented for all

conditions but will not prevent all cases

Obturator nerve paralysis 1.

Symptoms: reduced ability or inability to adduct (bring
to midline) one or both hind-limbs; affected animals are
at risk for doing splits. May present as a downer cow
therefore need to consider other causes of a downer cow
Cause: birthing injury usually assisted births in cows
Pathogenesis: the obturator nerve passes through the
pelvic (birth) canal and is prone to crush injuries during
parturition.

Obturator nerve paralysis 3

Complications

Swelling

Splits

Muscle tear (laceration)

Femoral neck fracture

Hip dislocation

Obturator nerve paralysis 4

Diagnosis: history, clinical signs, rule-out other causes
Treatment: Non-slip flooring, hobble to prevent
additional damage, if unable to stand role as frequently
as possible to prevent secondary muscle damage.
Prognosis is very poor if splits occur
Prevention:

body condition at calving

Nutrition
age at first calving
bull-breed
management of dystocia
non-slip flooring
hobble mildly affected animals

Diseases of Neonates
Bacterial meningoencephalitis
Cerebellar hypoplasia (congenital)
Swayback in lambs (congenital 8 weeks)

Bacterial Meningoencephalitis 1.
Species - Neonates of any mammalian species
Cause - A number of bacterial pathogens can
cause neonatal septicemia. Common isolates
are E.coli, Staphylococcus aureus,
St t
Streptococcus
sp. and
d Salmonella
S l
ll sp.
Symptoms Mild symptoms initially to severely
sick listless, unresponsive, prostrate,
hypoglycemia, hypo/hyperthermia, abnormal
posturing and head pressing

Bacterial Meningoencephalitis 2.
Head pressing

Abnormal posture severe opisthotonus

Unaware of environment

Bacterial Meningoencephalitis 3.
Pathogenesis
Bacteria gain entry to the body via a variety of routes such as
oral cavity and navel.
Maternally derived immunity is a big factor affecting the immunity
to neonatal bacterial infection.
Diagnosis - History, clinical findings, blood or meninges culture
poor.
Treatment Worth trying but prognosis is poor
Prevention

Cleanliness of birthing areas

Treat navels with antiseptic for confined calving / lambing.

Ensure adequate colostrum for each animal in first 12 hours of life.

Foals: consider having your veterinarian test serum IgG levels.

Maternal health and condition score is an important factor affecting

colostrum quantity and quality.

Cerebellar Hypoplasia in calves.

Cerebellar hypoplasia

Base-wide stance

Symptoms are typical for cerebellar disease

base-wide stance, ataxia, tremor on initiation of
movement
Cerebellar abiotrophy in an Arabian horse
http://www.youtube.com/watch?v=sj5RL3CmS34&NR=1

Swayback in lambs and kids (aka.

enzootic ataxia, hypocupremia) 1
Species: Lambs and kids, rarely in calves
Cause: Nutritional copper deficiency during last 3 months of
gestation and early post-natal life. Most commonly cases are
caused by a pasture copper deficiency. Some cases are caused by
excess molybdenum and sulfur in diet that interfere with copper
absorption.
Symptoms: Lambs are most often born with hind-limb weakness
p
cord
and ataxia ((incoordination)) that results from a defect of spinal
development (lack of myelination of axons). A delayed onset form of
the disease also occurs (enzootic ataxia) symptoms start at 3-4
weeks
Many parts of Wyoming are copper deficient
Many parts of Wyoming have high S in water
Some parts of WY have high Mb for example, Saratoga valley
Copper deficiency is also common in cattle usually manifests as
poor growth rates, poor coat quality, poor response to vaccines;
rarely manifests as swayback-like condition

Swayback in lambs and kids 2

Pathogenesis: Copper is an
essential metal. Copper deficiency
interferes with a number of
biochemical pathways that result
in CNS damage.
Diagnosis: Geographical area.
No history of trace element salt
li k S
lick.
Symptoms.
t
Li
Liver copper
levels on sacrificed animal.
Lesions in CNS include defects of
spinal cord.
Treatment: Copper
supplementation is not effective in
congenital swayback.

Swayback in lambs and kids 3

Prevention
In cases of true copper deficiency the pregnant ewe
should receive copper supplementation in the last 3 months
of pregnancy. Can be by injection, mineral lick or ruminal
copper oxide capsules.
Sheep are generally very sensitive to copper toxicity
toxicity, and
susceptibility varies dramatically between breeds.
Dietary supplementation may be of mixed value if there is
a secondary copper deficiency due to high molybdenum or
sulfur. Understanding underlying cause of Swayback is
important.

Questions
Where is the main location of calcium storage in the
body?
Does hypocalemia in ewes normally manifest before or
after lambing?
Why does ketosis in sheep generally occur before
g, and in dairyy cows after calving?
g
lambing,
Name one way in which you can limit the risk of
hypomagnesemia in cows.
Name two ways in which you can limit the risk of
obturator nerve damage during parturition in cows
Why do you think that you should not provide cattle trace
element licks to sheep?

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