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Neuroblastoma in the Spinal Cord of an Aberdeen Angus Heifer Calf
Slowly progressive hindlimb ataxia in a 5 month-old calf. Not too common, and the differentials include intoxication, nutritional deficites, hereditary diseases etc. etc. The diagnosis after doing a lot of diagnostic workup is a rare disease: a neuroblastoma in the spinal cord. A very interesting patient with a guarded prognosis.

A 5-month-old, female, Aberdeen Angus heifer presented to the veterinary medical teaching hospital for evaluation of slowly progressive hindlimb ataxia.

The calf was clinically normal until 4 months of age, following routine pregnancy and delivery. Neurologic examination revealed marked symmetric spastic hindlimb paraparesis.

Thoracolumbar radiographs and cerebrospinal fluid (CSF) analysis were unremarkable.

A presumptive diagnosis of T3-L3 myelopathy was made, and neurologic status remained static for 3 months with broad-spectrum antibiotic and nonsteroidal anti-inflammatory therapy.

Additional diagnostic tests were refused, and a necropsy was performed following euthanasia.

A moderately well delineated, reddish-tan, soft mass 18 mm in diameter replaced 80% of the fourth lumbar spinal cord segment.

Histologic examination revealed two distinct features: undifferentiated, primitive, polygonal-to-round cells with typical morphologic characteristics of primitive neuroectoderm; and interspersed areas containing myelinated axons and cells with neuronal differentiation.

Immunohistochemical examination confirmed the presence of primitive neuroepithelium and cells with neuronal differentiation.

Source: H. Steinberg, S. F. Peek and K. M. Nelson (2006): Neuroblastoma with Neuronal Differentiation in the Spinal Cord in an Aberdeen Angus Heifer Calf. In: Vet Pathol 43:193-197 (2006)



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BOVINE

Zinc Deficiency-Like Syndrome in Fleckvieh Calvesmembers
Zinc deficiency-like (ZDL) syndrome is an inherited defect of Fleckvieh calves, with striking similarity to bovine hereditary zinc deficiency (BHZD). However, the causative mutation in a phospholipase D4 encoding gene (PLD4) shows no connection to zinc metabolism. The objectives of this study were to describe clinical signs, laboratory variables, and pathological findings of ZDL syndrome and their utility to differentiate ZDL from BHZD and infectious diseases with similar phenotype.

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