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Large Animal Section: No. 4
DISEASES AFFECTING THE NERVOUS
SYSTEM IN CATTLE IN SOUTH(ERN) AFRICA
Please note:
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Several diseases may show a variety of clinical
signs and should therefore have been included in more than one table. For
the sake of brevity each disease has been tabulated only once.
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The diseases follow in more or less the following
order: congenital; infectious; toxic; nutritional; metabolic; and idiopathic
TABLE 1: PARESIS AND PARALYSIS
| DISEASE |
AETIOLOGY
and EPIDEMIOLOGY |
CLINICAL SIGNS |
NECROPSY FINDINGS
and DIAGNOSIS (D) |
| Botulism |
Clostridium
botulinum type C and D. Ingestion of preformed toxin in carcass material,
feed or water, often associated with pica |
Animals usually
mentally alert and watch surroundings but cannot respond. Stiff, clumsy
gait, lying down with paralysis and head resting on flank. Also protrusion
of tongue (uncommon), salivation, paralysis of tail |
No gross lesions;
± foreign bodies in rumen
D: history, clin.
findings, demonstration of toxin in serum, intestinal contents, water or
feed |
| The 'Downer cow' |
Primary causes
include calving paralysis (most common in heifers), toxic mastitis/metritis
and metabolic (milk fever - see elsewhere) with secondary ischemia of muscles
and nerves |
Calving paralysis:
onset of stiffness to paraplegia after delivery. Affected cow may dog-sit
and has paresis of pelvic limbs, flexor hyporeflexia with intact tail and
anal function |
Calving paralysis:
± haemorrhage and oedema in area of peripheral nerves
D: history |
| Rabies |
See
Table 3 |
| Diplodiosis |
Ingestion of
maize contaminated by Diplodia maydis. In cattle grazing on harvested
maize lands in winter |
Reluctancy to
move, ataxia, stiff-legged, high-stepping gait, falling often, paresis/paralysis,
constipation, salivation |
No gross lesions
D: history, histopath.
of CNS |
| Aspergillus
clavatus poisoning |
Ingestion of
sorghum beer residues or sprouted maize contaminated by A. clavatus |
Hypersensitivity,
tremors, ataxia, progressive paresis, paralysis, and constipation. Walking
with stiff-legged gait, taking short steps and show staggering and salivation |
± Greyish-white
areas in muscles of hindquarters
D: demonstration of
fungus, histopath. of spinal cord |
| Cardiac glycoside
poisoning |
Tulpe (Homeria
and Moraea spp.) and slangkoppe (Urginea spp.); non-cumulative
bufadienolides. May contaminate hay |
Hypersensitivity,
abn. gait, tremors or spasms, ataxia, post. paresis; diarrhoea; heart arrythmia’s |
± Lesions
of heart failure, ± leaves in rumen
D: histopath. of myocardium
not specific |
TABLE 2: SEIZURES/HYPERSENSITIVITY
| DISEASE |
AETIOLOGY
and EPIDEMIOLOGY |
CLINICAL SIGNS |
NECROPSY FINDINGS
and DIAGNOSIS (D) |
| Cerebral babesiosis |
Babesia bovis,
transmitted by Boophilus microplus |
Hyperaesthesia,
nystagmus, circling, head pressing, aggression, seizures, and paralysis.
Nervous signs may or may not accompany other signs of acute redwater |
Cherry-pink colour
of grey matter of cerebrum and cerebellum
D: demonstration of
parasites in brain smear |
| Heartwater |
Cowdria ruminantium,
transmitted by Amblyomma spp. |
May die suddenly
or, more commonly, show fever, hypersensitivity, ataxia, unsteady high-stepping
gait or standing with head down making chewing movements. Later falling,
lateral recumbency, paddling movements, seizures, opisthotonus, and death.
Diarrhoea in some breeds |
Necropsy may
be negative, usually fluid in body cavities, oedema of lungs and abomasal
folds and splenomegaly
D: demonstration of
organisms in brain smear |
| Nitrofuran poisoning |
Acute toxicity
in calves, occasionally in adult cattle; with recommended dosage or overdosing |
Inappetence,
hyperexcitability with incoordination, muscle twitching and convulsions.
Syndrome usually resolves when immediately removed from medication |
No gross lesions
D: history |
| Urea poisoning |
Ingestion of
excess in licks or feed, or animals not accustomed |
Short clinical
course. Initially show restlessness, hyperaesthesia or dullness, tremors
and twitching of muscles. Also colic, ataxia, blindness, violent struggling
and bellowing, and terminal tonic seizures elicitable by external stimuli |
No gross lesions,
or ± lung oedema and generalised congestion
D: analysis of feed
or licks, levels of ammonia in blood, serum, ruminal fluid, and urine |
| Prussic acid
poisoning ("geilsiekte") |
Ingestion of
plants containing cyanogetic glycosides |
Usually sudden
death, but may show dyspnoea, cyanosis accompanied by anxiety, salivation,
tremors, colic, convulsions, opisthotonos and rapid death |
Cherry red blood
at necropsy
D: necropsy, demonstration
of cyanide in plants or in rumen contents, liver and muscle |
| Organophos-phate
and carbamate poisoning |
Careless handling
of pesticides resulting in contamination of feed or dips, or malicious
poisoning |
Overstimulation
of parasympathetic system e.g. muscarinic: salivation, lacrimation,
colic, diarrhoea, miosis; later nicotinic: muscle fasciculation
and twitching, tremors, spasms, and hypertonicity causing stiff gait; CNS:
anxiety, restlessness, and depression |
No gross lesions
D: demonstration of
compound in suspected source and tissues (liver, fat, stomach content) |
| Chlorinated hydrocarbon
poisoning |
Careless handling
of pesticides resulting in contamination of feed or dips, or malicious
poisoning |
Initially animal
show apprehension, hypersensitivity or aggressiveness. Later fasciculation
and twitching of muscles, and generalized intermittent or continuous spasms
or seizures and death. May show ataxia and locomotor disturbances |
No gross lesions
D: demonstration of
compound in suspected source and tissues (liver, fat, stomach content) |
| Albizia
poisoning |
Pods of A.
versicolor and A. tanganyicensis; late winter or early spring |
Animals usually
found dead. Survivors show hypersensitivity, staggering gait and tetanic
seizures. Also wild expression in eyes, nystagmus and dyspnoea |
Often cyanotic
carcass; pods in rumen and seeds in reticulum
D: history, pods/seeds
in forestomachs |
| Annual ryegrass
toxicosis |
Ingestion of
ryegrass seedheads containing nematode (Anguina sp.) galls infected
by bacterium (Clavibacter sp.). Only reported from winter rainfall
area of Cape Province |
Usually not sudden
death. Excitability, muscular twitching, unsteady, high-stepping gait.
When handled or driven, epileptiform seizures with trembling, nystagmus
and frothing at the mouth |
Rapid rigor mortis,
no gross lesions
D: History, clin.
findings, demonstration of bacteria or nematodes in affected seed heads |
| Hypomagnesaemia |
Lactating dairy
cows on lush, well-fertilized pastures. DD: ammonified hay toxicity |
Usually acute
onset of iritability, hyperactivity, tremors, falling, recumbency and eventually
seizures. Subacute cases remain standing |
No gross lesions
D: clin. path. |
TABLE 3: CHANGES OF BEHAVIOUR/ ALTERED
STATE OF CONSCIOUSNESS
| DISEASE |
AETIOLOGY
and EPIDEMIOLOGY |
CLINICAL SIGNS |
NECROPSY FINDINGS
and DIAGNOSIS (D) |
Hydrocephalus/
hydranencep-haly |
Several causes
including in utero viral infections e.g. BVDV; or hypovitaminosis A (uncommon) |
Depression, lethargy,
head pressing, convulsions or paresis/paralysis, dullness, blindness and
weakness |
Doming of skull
and presence of hydrocephalus/hydranencephaly
D: necropsy, serology,
virus isolation |
| Malignant catarrhal
fever ("snotsiekte") |
Alcelaphine herpesvirus
1, occurring in 2 forms: wildebeest-derived and sheep-associated |
Multisystemic
disease: fever, nasal and ocular discharges, erosions of oral mucosa, panopthalmitis,
lymphadenopathy etc., and encephalitis with tremors, ataxia, depression,
wandering, aggression, and recumbency |
No gross lesions
of CNS
D: history, clin.
findings, pathology, virus isolation |
| Rabies |
Lyssavirus serotype
1; transmitted by the bite of diseased mammals e.g. yellow mongoose, suricates,
genets, wild felids, dogs |
Early signs include
separation from the herd, anorexia and docility or irritability. May develop
paralysis of tongue and jaw with salivation, bellowing, aggression, and
later, locomotory disturbances, tail paralysis, recumbency, paralysis,
seizures, and death |
No gross lesions
D: immunofluorescence
on brain (fixative 50% glycerosaline); histopathology lacks sensitivity |
| Sporadic bovine
encephalomye-litis (SBE) |
Chlamydia
psittaci, in calves |
Usually preceded
or concurrent with generalized infection. May show fever, depression, and
later stiffness, staggering, ataxia, circling and eventually falling with
seizures and paralysis |
± Serofibrinous
meningitis and ventriculitis
D: culture, demonstration
of organisms, pathology |
| Trombotic meningioence-phalitis
(TME) |
Haemophilus
somnus; most common in feedlot cattle 1-3 y old |
Sudden death
or fever, profound depression, reluctance to move, stiffness and knuckling
of the fetlocks initially. Later may show tremors, blindness, circling,
ataxia, paresis, paralysis, paddling, coma, and death |
Multiple infarcts
in grey and white matter of CNS
D: culture, pathology |
| Bacterial meningitis/
meningioventri-
culitis |
In neonatal calves,
often associated with another illness, e.g. enteritis, septisaemia; Pasteurella
spp., coliforms and Corynebacterium spp. |
Ataxia, paresis,
hyperaesthesia, or depression, wandering, star-gazing, paddling in lateral
recumbency, opisthotonus, nystagmus and seizures |
± Congestion
of meninges and lesions of concomitant disease
D: culture, pathology |
| Cerebral theileriosis
(turning sickness) |
Theileria
taurotragi, transmitted by Rhipicephalus appendiculatus; usually
in young cattle less than 3 y |
Sudden onset
of nervous signs including circling, head pressing, blindness, ataxia,
opisthotonos, and paralysis |
Congestion and
haemorrhages of meninges and brain, and malacic areas in brain
D: demonstration of
schizonts, pathology |
| Hepatic encephalopathy |
Seen in chronic
liver conditions e.g. chronic seneciosis |
Head pressing,
ataxia, seizures, blindness, coma and tenesmus |
Cirrhosis of
liver
D: pathology |
| Lead poisoning |
Often ingestion
of pieces of batteries from farm dumps or old car oil. DD: Ornithogalum
(chinkerinchee) toxicity |
Ataxia, depression,
seizures, hyperactivity, and twitching of the ears. May show salivation,
wandering, blindness, head pressing, opisthotonos, bellowing and constipation |
± Portions
of batteries in rumen
D: determine levels
in blood, liver, kidney, and rumen contents |
| Dipcadi
poisoning |
D. glaucum |
Animals walk
drunkenly with flexion of fetlocks and knuckling over, and show circling,
stumbling into trees, apathy, lying down with posterior paresis, and recumbency |
No gross lesions
D: history, clin.
findings, plant identification |
| Stootsiekte ("pushing
disease") |
Matricaria
nigellifolia |
Docility, apathy,
aimless wandering and pushing with the head against objects and incoordination
with scuffing of the feet and knocking on |
No gross lesions
D: history, clin.
findings, histopath. |
| Polioencephalo-malacia |
= cerebro-cortical
necrosis (CCN). Usually thiamine responsive, most common in feedlots. Also
with high dietary sulphate and following water deprivation |
Dullness, wandering,
staggering gait, opisthotonos, tremors, blindness, head-pressing, and later
recumbency with tonic-clonic convulsions, nystagmus, and opisthotonos |
Brain oedema,
± laminar necrosis of cerebrocortical grey matter
D: pathology, response
to treatment |
| Ketosis (nervous
acetonemia) |
High-yielding
cows in early lactation; single animals affected |
Sudden onset;
bizarre mental behaviour including chewing, licking of skin and objects,
bellowing, hyperaesthesia. Also walking in circles, head pushing, apparent
blindness |
Fatty degeneration
of liver
D: history, clin.
path |
| Hypocalcaemia
(milk fever) |
High-producing,
mature dairy cows usually within 3 days after calving |
Sudden onset
of tetany or tremor with excitement and depression, paralysis, and unable
to rise. Frequently they adopt a recumbent posture with head and neck turned
toward the flank. |
No gross lesions
D: history, clin.
path., response to treatment |
TABLE 4: MOVEMENT DISORDERS (GAIT, POSTURE,
ATAXIA OF HEAD AND LIMBS, AND VESTIBULAR DYSFUNCTION)
| DISEASE |
AETIOLOGY
and EPIDEMIOLOGY |
CLINICAL SIGNS |
NECROPSY FINDINGS
and DIAGNOSIS (D) |
| Listerial
meningio-
encephalitis |
Associated with
the feeding of silage |
Depression, head
tilt, circling, unilateral facial paralysis, dropped jaw, ataxia, recumbency,
and panophthalmitis |
No gross lesions
D: culture, histopath. |
| Tetanus |
Clostridium
tetani, associated with deep penetrating wounds |
Initially, increasing
muscle stiffness followed by tetanic spasms of muscles, and hyperaesthesia.
Also extended head, raised tail, slight abduction of legs, prolaps of 3rd
eyelid, stiffness, constipation, dullness, and depression |
No gross lesions
D: history, clin.
findings, culture, demonstration of toxin |
| Ionophore toxicity |
Acute:
3-7 d after feeding of rations containing high levels of ionophores (formulation
errors); chronic: 3 w or longer after feeding of poultry litter
containing ionophores usually maduramicin |
Sudden death
or lethargy and recumbency, and signs of heart failure. Some may show stiff
gait and tremors |
Lesions of heart
failure, ± mottling or pallor of myocardium in acute form; ±
dilation of myocardium in chronic form
D: feed analysis (confirmation
difficult in chronic case), history, pathology |
| Dipcadi
poisoning |
D. glaucum |
Walking drunkenly
with flexion of fetlocks, ± circling, ± pushing against objects,
posterior paresis |
No gross lesions
D: history, clin.
findings, plant identification |
| Melia
poisoning |
Melia decumbens,
in late winter and early spring following good winter rains |
Initially swaying,
unsteadiness and high-stepping gait. Later lying down and unable to rise,
tremors |
No gross lesions
D: history, clin.
findings |
| Kweek tremors |
Ingestion of
kweek grass (Cynodon dactylon) contaminated possibly by Claviceps
spp. |
Ataxia, tremors
and walking with stiff hind legs, taking short steps, lifting legs high
and frequently stumble and fall. Later, paresis progressing to paralysis
and recumbency |
No gross lesions
D: history, clin.
findings |
| Paspalum
staggers |
Cattle grazing
on seedheads of P. dilatatum (Dallis grass) infected with ergots
of Claviceps paspali |
Hypersensitivity,
tremors and incoordination, becoming more pronounced with exercise. May
show recumbency and paddling |
No gross lesions
D: history, clin.
findings |
| Maldronksiekte |
Solanum kwebense,
n & n-w Transvaal |
Signs elicited
when animals are disturbed, showing head tilt or rigid neck, star-gazing
and ataxia or falling, seizures and collapse with tremors after regaining
their feet |
Atrophy of cerebellum
D: history, pathology |
| White muscle
disease |
Selenium and/or
vitamin E deficiency |
May die suddenly
after exercise; stiffness, trembling, weakness, inability to stand, recumbency |
Pale streaks
in tongue and neck muscles (congenital), skeletal muscles and myocardium
(bil. simm.)
D: feed analysis,
histopath. of muscles |
Compiled by JJ vd Lugt; the lists were reviewed
by Drs PA Basson (Namibia), DJ Schneider (Stellenbosch), RD Last (Pietermaritzburg),
and T. Shakespeare (Pretoria)
For further information contact
VetPath Veterinary Pathologists
PO Box 8464, Pretoria 0001
Tel: (012) 529 8345/6
e-mail:
info@vetpath.co.za


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