Spastic Syndrome in a Holstein Bull: A Histologic Study

Abstract

Abstract.A 4-year-old Canadian holstein bull developed the spastic syndrome, an episodic but progressive disorder causing pelvic limb muscular spasms. A post-mortem study, including morphometry of skeletal muscles and teased peripheral nerve fibers of the pelvic limb, revealed mild type I1 skeletal muscle fiber atrophy and minimal, focal segmental demyelination with remyelination, and axonal degeneration in peripheral nerves. Such alterations are probably incidental or age-associated. Idiopathic muscular cramps is the most probable explanation of the clinical disease and is consistent with the absence of significant morphologic pathologic lesions. Materials and MethodsA Canadian holstein bull, originally imported in 1980 from Canada for artificial insemination use in the United Kingdom, began to show clinical signs when almost 4 years of age. A detailed clinical examination was done when the bull was 4 years 7 months of age, and daily visual inspections were continued until the bull was killed for necropsy 2 months later. Live weight immediately before death was 1,080 kg.The bull was killed by exsanguination following the simultaneous intravenous injection of xylazine (Bayer : Rompun) and etorphine hydrochloride/acepromazine maleate (C-Vet : Large Animal Immobilon). Upon necropsy, peripheral nerves and skeletal muscles identified were sampled from the left side of the carcass (Fig. 1). The brain and spinal cord, with attached complete spinal nerve roots of the left side at segments C7, L4-6, and S,, were fixed in phosphate-buffered, neutral, 10% formalin (BF). Other major organs and selected skeletal tissues were also sampled into BF.Lengths of identified peripheral nerves were dissected and suspended under tension in 2.5% glutaraldehyde in 0.1 M Sorensen's buffer at pH 7.4 and 4 C for 2 hours. Lengths were cut into 1.5 cm segments, and large diameter nerve segments were further subdivided along perineurial planes. Subsequent treatments were to provide isolated single nerve fibers, 1 pm plastic (araldite-embedded), and 5 pm or 10 pm paraffin wax sections.Nerve segments for plastic embedding and teased fiber preparations were removed from 2.5% glutaraldehyde after a further 1-2 hours and stored overnight in 0.1 M Sorensen's buffer. Nerve for teasing was post-fixed in Dalton's fluid" for 2 hours and for storing in araldite resin at -20 c.After thawing, isolated nerve fibers were prepared. l4 Fibers were progressively and unselectively teased by a single operator using straight No. 1 intestinal suture needles. Fifty to 70 individual fibers with at least three consecutive internodes were qualitatively assessed from each nerve. Measurements of internodal length and fiber diameter were made and the results expressed statistically and graphically. l6 Trimmed segments of Nn. femoralis, gluteus cranialis, and tibialis were post-fixed in 1% osmium tetroxide in 0.1 M Sorensen's buffer, routinely dehydrated, and embedded in araldite. Transverse and longitudinal sections were cut at 1 pm and stained with toluidine blue.Bl...

Bovine spastic syndrome: a review

“…Frauchiger and Hofmann 7 (1941) were also not able to observe histological changes in the CNS. Wells et al 13 reported (histo-)pathological lesions in a 4-year-old Canadian Holstein bull with a mild form of spastic syndrome (widespread arthroses among 16 31 Three (rather four) to seven years 1 Clinical signs Progressive hyperextension of the hindlimb(s) and contraction of the Achilles tendon caused by persistent spasms of certain muscles 16 Hyperextension of the hindlimb(s) caused by recurrent and reversible clonic and tonic muscular cramps 16 Affected areas of the body Hindlimb(s), unilateral or bilateral 16 Hindlimb(s), unilateral or bilateral; and with progression of the disease also back and neck muscles 16 Treatment Surgical treatment possible 16 52 Only symptomatic treatment possible 1 Similarities Clinical signs and affected areas of the body ► Unilateral or bilateral afection of the hindlimb(s) ► Oten an increased angle of the ankle joint ► Clinical signs appear only in rising, standing and moving animals (never in lying animals) ► No recovery of the clinical signs 16 53 other things; minimal changes in mixed and cutaneous peripheral nerves, sparse focal myelin degeneration, occasional ibres with intramyelinic bubbles in the lumbar and sacral dorsal roots; eosinophilic bodies in the nucleus gracilis). However, none of these indings were expected by the authors to account for the observed clinical signs.…”

Localization, morphology, and immunohistochemistry of spinal cord and dorsal root ganglion neurons that innervate the gastrocnemius and superficial digital flexor muscles in cattle

“…To our knowledge, this is the first investigation coupling the morphology and the function of Rexed's lamina IX in the lumbosacral region of the spinal cord of cattle. Results of this research could be useful for studying other bovine neuronal diseases involving the lumbosacral region of the spinal cord and its afferent pathways, such as spastic syndrome (standing disease) of adult cattle 20 or bovine spinal muscular atrophy. [21][22][23][24] We also investigated, by use of immunohistochemical procedures, substance P (SP), calcitonin generelated peptide (CGRP), galanin (GAL), and neuronal nuclear protein (NeuN) immunoreactivity of neurons.…”

Frameshift Variant in Novel Adenosine-A1-Receptor Homolog Associated With Bovine Spastic Syndrome/Late-Onset Bovine Spastic Paresis in Holstein Sires

“…Regarding LOC100848076, no animal models or human disease has been reported so far. In one BSS case report, demyelination was detected, which was later interpreted as a link to multiple sclerosis (Wells et al, 1987;Goeckmann et al, 2018). However, similar lesions were later identified also in Charolais cattle with progressive ataxia and American Brown Swiss with spinal demyelination (Thomsen et al, 2010;Duchesne et al, 2018).…”

“…So far, no functional pathway or genetic background was identified to enlighten its pathogenesis. Solely one pathological examination of a BSS-affected bull reports focal demyelination (Wells et al, 1987). In fact, for BSP, a decreased concentration of homovanillic acid in the cerebrospinal fluid was measured (De Ley and De Moor, 1975).…”