Peripheral neuropathy in twin calves.

Disorders of the peripheral nerves of domestic animals have been recorded in a number of dog breeds2-’.” and in a few cases of However, the majority have been of unknown etiology.1.2.6.8.11 Distal symmetrical polyneuropathies have been recognized in genetical, toxic, nutritional, and metabolic disorders in humansI4 and other animals.’’ The disease is attributed to the dying-back process, the concept of which is that distal regions of nerve fibers are affected primarily in case of the neuronal cyton’s trophic function impaired because the axon is dependent on the trophic influence of the nerve ce11.I3 This article describes morphological findings in twin calves that were affected with sporadically occurring distal symmetrical polyneuropathies. Animals used for this investigation were two male 5-monthold (No. 1) and 6-month-old (No. 2) Holsteins that were twins. A male 5-month-old Holstein without clinical neuromuscular disease was used for the control. Both cases were euthanized. Tissue blocks collected from the skeletal muscles of the whole body, the central and peripheral nervous systems, and visceral organs were fixed in 10% phosphate-buffered formalin and embedded in paraffin. Sections were stained with hematoxylin and eosin (HE). Selected sections from the central and peripheral nervous systems were stained with periodic acid-Schiff (PAS), Alcian blue, and Kluver-Barrera’s (KB) and Bielschwsky’s (modified by Hirano) methods. The peripheral nerves (P. brachialis, N . medianus, N. ulnaris, Nn. sacrales, N. ischiadicus, and N. tibialis) were immersion fixed in 4% paraformaldehyde in 0.5% phosphate buffer and post-fixed 1% osmium tetroxide. They were dehydrated and embedded in epoxy resin. The semithin sections ( 1 pm) were stained with toluidine blue. Teased fiber preparations of the peripheral nerves were also made. For histochemical examination, unfixed muscular tissues collected from calf No. 2 (Table 1) were divided into approximately 0.5 cm cubes and immersed in liquid nitrogen (180 C) for 15 seconds. Serial sections were cut transversely at 10 pm with a cryostat microtome at -20 C, stained with HE, and reacted for routine (pH 9.4) adenosine triphosphatase (ATPase) and modified (pH 4.3) ATPase. Clinically, calfNo. 1 showed abnormal gait with slow walking at 4 months of age. As the condition advanced, calf No. I presented progressive muscular weakness of both fore and hind legs, and dysstasia 3 days before necropsy. Calf No. 2 revealed protrusion of fetlock joints in both hind legs at 5 months of age. As the course was steadily progressive, calf No. 2 showed ataxia due to the motor disorder in the legs and inability to stand the day before necropsy (Fig. 1). According to the owner, these calves were raised by suckling for 3 weeks after birth and given commercial calf-pellets substituted for milk and dried grass during the following days. Other calves reared on the same food were clinically normal. Although their dam was a multiparous cow, these two calves were the first offspring provided with artificial insemination from the sire. This sire was evaluated as excellent and utilized with many dams; however, there was no information on whether other siblings from other dams presented the same symptoms. At necropsy, the skeletal muscles of both cases were slightly pale. The other organs and tissues were normal. Microscopically, lesions were confined to the peripheral nervous system and skeletal muscles. No abnormalities were seen in any spinal segmental nerve roots, nerve fiber tracts,