Neurological disease associated with degenerative axonopathy of neonatal Holstein‐Friesian calves

Pa, Harper; Pj, Healy

doi:10.1111/j.1751-0813.1989.tb09781.x

Cited by 20 publications

(17 citation statements)

References 9 publications

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“…This is a lethal neurological disease in neonatal Holstein-Friesian calves caused by a deficiency in the urea cycle enzyme, argininosuccinate synthetase, that converts potentially toxic ammonia to urea, resulting in extreme elevation of citrulline and ammonia in plasma. 29 Citrullinaemia was widely disseminated throughout the Australian Holstein-Friesian population following importation of semen of the Canadian Holstein-Friesian bull Linmack Kriss King (LKK) 34 and diagnosis is based on elevated levels of citrulline (1-3 mmol/L) by day 3 or on a DNA-based test to detect the C→T mutation at nucleotide 258 in the gene coding for argininosuccinate synthetase, converting Arg86 into a termination codon. Lesions include mild to moderate diffuse astroglial swelling in the cerebrocortical grey matter, and mild to severe hepatocellular hydropic degeneration (Figure 6b).…”

Section: Holstein-friesianmentioning

confidence: 99%

Neurological diseases of ruminant livestock in Australia. V: congenital neurogenetic disorders of cattle

Windsor

Kessell²,

Finnie

2011

Australian Veterinary Journal

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As part of a series on neurological disorders in ruminant livestock in Australia, this review focuses on the congenital neurogenic disorders of cattle. The genetic pressures that contribute to the emergence of congenital neurogenic disorders, as well as the methods of diagnosis, are discussed. Disorders reviewed are ordered by breed and include arthrogryposis multiplex, fawn calf syndrome, inherited congenital myoclonus and maple syrup urine disease.

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Section: Holstein-friesianmentioning

confidence: 99%

Neurological diseases of ruminant livestock in Australia. V: congenital neurogenetic disorders of cattle

Windsor

Kessell²,

Finnie

2011

Australian Veterinary Journal

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“…Similar syndromes are known in other breeds, including spinal dysmyelination of crossbred Brown Swiss calves, 3,4 degenerative axonopathy in Holstein‐Friesian calves, 2 weaver syndrome of Brown Swiss cattle, 5–10 and SMA in Brown Swiss, 11–13 horned Hereford, 14 Red Danish, 15 and Holstein Friesian calves 16 . These disorders are caused by genetic defects that lead to degenerative spinal cord disease.…”

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confidence: 68%

“…Several central nervous system (CNS) diseases in cattle have typical clinical features and are confined to specific breeds because of their genetic nature. Hereditary degenerative disorders of the CNS in calves include among others degenerative axonopathy, 2 spinal dysmyelination, 3,4 bovine progressive degenerative myeloencephalopathy (BPME or weaver syndrome), 5–10 and spinal muscular atrophy (SMA) 11–16 . The predominant clinical feature in the calf described here was moderate‐to‐severe spinal ataxia, leading to a tentative diagnosis of diffuse spinal cord disease with the most pronounced lesions in the segments between T3 and S3.…”

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confidence: 76%

Degenerative Axonopathy in a Tyrolean Grey Calf

Syring

Drögemüller

Oevermann

et al. 2010

Journal of Veterinary Internal Medicine

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A 2.5-month-old female Tyrolean Grey calf weighing 99 kg from a cow-calf herd in eastern Switzerland was referred to the Clinic for Ruminants at the Vetsuisse Faculty, University of Berne with a history of pelvic limb weakness. A complete clinical examination indicated that the calf was normally developed for its age and breed. It was alert and responsive, but had a nervous demeanor. Examination of the cardiovascular and respiratory systems disclosed no abnormalities, except for a high heart rate in the first days of the calf's stay at the clinic (136-160 bpm; normal, 60-100 bpm). Heart rate returned to normal within a few days, and tachycardia was attributed to stress upon arrival in a new environment. Respiratory rate and body temperature were normal. Appetite was present, and food prehension, mastication, and swallowing were normal. Examination of the digestive system was within normal limits, as was that of the urinary tract. The musculoskeletal system was normally developed except for slight muscular atrophy of the thighs. Palpable articulations were neither enlarged nor painful. Foot trim was adequate, and the claws had no abnormalities.Upon neurological examination, the calf's behavior was normal except for its markedly nervous reactions to manipulations. The calf often stood with a wide-based stance in the thoracic and pelvic limbs (Fig 1, Video S1). It showed mild ambulatory paraparesis with moderateto-severe ataxia of the pelvic limbs and a tendency to fall to both sides (Fig 2, Video S2). Postural reactions were normal in the thoracic limbs and decreased to absent in the pelvic limbs. Segmental spinal reflexes of the thoracic limbs were normal, but decreased in both pelvic limbs. The menace response was absent bilaterally, pupillary light reflexes and vision were normal. Other cranial nerves were normal. The cutaneus trunci response was absent. Tail tone was decreased, but anal tone, defecation, and urination were normal. Palpation of the spine was not painful.The main lesion was localized in the spinal cord from T3 to S3. At this point, differential diagnoses included degenerative, infectious, and inflammatory lesions, as well as a malformation of the spinal cord.A CBC a and a blood chemistry profile b were performed. No abnormalities were detected in the CBC, and the chemistry profile disclosed a slight increase in aspartate aminotransferase activity ( 1 A differential cell count was not performed. No changes in the animal's neurological status were observed during its stay at the clinic. On day 16 of hospitalization, general anesthesia was induced with xylazine, butorphanol, and ketamine, and maintained by inhalation of isoflurane vaporized in oxygen. Electromyography (EMG) c was performed on the right side of the body, including thoracic and pelvic limb muscles, as well as paraspinal and tail muscles. No spontaneous activity was detected. The calf was euthanized at the end of the EMG procedure with an overdose of pentobarbital. All procedures complied with the Swiss legislation on animal welfare...

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“…A diffuse axonopathy in 19 Holstein-Friesian calves was previously described. 2 Affected animals had severe clinical deficits and most were recumbent from birth. Neuropathological studies showed a diffuse axonopathy, most pronounced in the spinal cord, with degeneration extending into spinal roots.…”

Section: Discussionmentioning

confidence: 99%

Myelopathy in Holstein X Gir Calves in Brazil

Borges

Mendes

Luvizotto

et al. 2003

Veterinary Internal Medicne

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This case report contains clinical and pathologic features of a degenerative myelopathy in Holstein ϫ Gir crossbred calves in Brazil. The bilateral and symmetrical spinal cord white matter lesions were interpreted as a primary axonopathy that may be of the dying-back type.Key words: Axonopathy; Bovine; Degenerative myelopathy; Neurology T he central nervous system (CNS) is susceptible to a variety of insults, including infectious, toxicologic, and genetic disorders. Inherited disorders can be evident at birth or might not be apparent until later in the 1st year of life or beyond. Most neurological disorders are recognized in the dog and cat with fewer examples in farm animals. Case DescriptionAn abnormal pattern of locomotion progressing to tetraparesis was observed in calves of the Holstein ϫ Gir breed, some of which were presented to São Paulo State University Veterinary Hospital (Araça-tuba-Brazil). In the 1997 breeding season, the farm had 24 births, of which 7 calves (3 males and 4 females) were normal until 3 months when they suddenly showed an altered pattern of locomotion in the thoracic limbs. Fifteen to 22 days later, these animals were permanently recumbent and by 5 months of age had succumbed to complications of their recumbency (pneumonia, anaplasma, or babesia).All the affected calves were sired by a 4-year-old Holstein bull introduced in the 1996 breeding season, at which time he had no prior progeny. This bull was mated to Gir cows, producing Holstein ϫ Gir offspring. In the following year, this bull was used to breed 3 cows on a 2nd farm 10 miles from the 1st property; 1 of these 3 cows had a calf with the same disorder. We examined 5 animals over a period of 4 months, 3 of whom could walk when 1st presented to us and 2 of whom were recumbent. The 3 ambulatory calves were alert and responsive, could stand unaided, and walked with a distinct overreaching-floating action of the thoracic limbs. The pelvic limbs were slightly awkward and swayed slightly. All calves could see, had no head tremors, and did not have a basewide stance. Within days, the calves were unable to rise even when helped; respiratory complications developed, and they died after 1 to 3 months of hospitalization. Two other animals arrived at the hospital in recumbency, but the veterinarian who had examined them at the farm reported that the nature and evolution of neurological signs were the same. These animals became recumbent Botucatu, SP 18608000, Brasil; email: asborges@fmvz.unesp.br. Submitted February 25, 2003; Revised March 28, 2003; Accepted March 28, 2003. Copyright when 3 to 4 months old and died 2 to 10 weeks later of the same complications. These calves appeared bright and responsive but were recumbent and when lifted made no movements. The thoracic limbs appeared contracted with a fixed, flexed carpus bilaterally and were possibly atrophied.No hematological or biochemical abnormalities were present in the ambulatory calves and analysis of cerebrospinal fluid in 2 animals after cisternal puncture revealed no abno...

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Neurological disease associated with degenerative axonopathy of neonatal Holstein‐Friesian calves

Cited by 20 publications

References 9 publications

Neurological diseases of ruminant livestock in Australia. V: congenital neurogenetic disorders of cattle

Neurological diseases of ruminant livestock in Australia. V: congenital neurogenetic disorders of cattle

Degenerative Axonopathy in a Tyrolean Grey Calf

Myelopathy in Holstein X Gir Calves in Brazil

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