Diseases affecting cattle

 

Home Up

Large Animal Section: No. 4

DISEASES AFFECTING THE NERVOUS SYSTEM IN CATTLE IN SOUTH(ERN) AFRICA

Please note:

  1. 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.
  2. 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

Home Up

For any animal pathology queries, please send e-mail to info@vetpath.co.za.
Questions or comments about the structure of this web site, please send e-mail to webmaster@vetpath.co.za.
Copyright © 2004 Bill Robb & Associates
Last modified: Friday June 25, 2004