Multifocal polioencephalomyelomalacia in Simmental calves with elevated tissue aluminum and decreased tissue copper and manganese.

A spectrum of related malacic disorders called Simmental multifocal symmetrical encephalopathy have been reported in Simmental and Simmental crossbred cattle in Canada, Australia, and New Zealand. The cause of this condition is unknown. We describe multifocal polioencephalomyelomalacia in Simmental calves reared in Oregon, USA, with morphologic lesions similar to those described in Simmental multifocal symmetrical encephalopathy. These calves also had elevated tissue concentrations of aluminum and deficient hepatic copper and manganese concentrations, which may be related to this condition. Four 7-month-old bull calves from a herd of 135 Simmental cows developed paresis, ataxia, and knuckling over of both hind limbs that progressed over a 2-month period to inability to rise. During the previous 2 years, 3 calves similarly affected died. Affected calves remained bright and alert and maintained the ability to suckle. Antibiotic therapy was not beneficial, and complete blood count and serum chemistry profiles were normal in the 3 calves evaluated. Two of the calves were presented to the Oregon State Veterinary Diagnostic Laboratory for postmortem examination. Significant lesions were limited to the central nervous system, with secondary mild symmetrical atrophy of the rear limb muscles. Grossly, oblong to circular foci of malacia of various sizes (up to 1 cm diameter) were seen throughout the gray matter of the brain. Similar gross lesions were within the gray matter of the lumbar spinal cord in 1 of the calves. Microscopically, these lesions were cavitated and were composed almost entirely of necrotic debris (Fig. 1). Scattered viable neuroglial cells were within these foci but neurons were not observed. Microgliosis, astrocytosis (including gemistocytes), active neuronal necrosis, ischemic neuronal changes, and vasculitis were not observed. Vessels were prominent within the lesions, principally because of hypertrophy of endothelial nuclei. Neurofibrillary tangles and/or extensive demyelination were not observed in multiple Bodainand Luxol fast blue-stained histologic sections. The histopathologic changes were markedly uniform throughout the affected foci. The distribution of brain lesions was essentially identical in the 2 affected calves. The gray matter lesions of the brain involved numerous nuclei but invariably extended beyond nuclear boundaries. Individual lesions often involved more than 1 nucleus with some extension into the adjacent white