Housing system may affect behavior and growth performance of Jersey heifer calves.

Social pressure is increasing to adopt alternative housing and management practices that allow farm animals more opportunity to exercise and demonstrate social behavior. The present study investigated the effect of pair housing on the behavior and growth performance of Jersey heifer calves. Forty female Jersey calves were allocated to individual or pair housing at birth and monitored for 9 wk. Calves were provided with a single hutch, and those allocated to the pair housing treatment were provided a pen enclosure twice the size of individually housed calves and only one hutch was provided per pair. All calves were fed milk replacer via bucket twice per day (1.89 L/feeding first 7 d; 2.27 L/feeding until weaned) and had ad libitum access to grain and water. Gradual weaning commenced on d 49 by reducing the calves' milk allowance to one feeding per day, and weaning occurred on d 56. Grain consumption was monitored daily and calves were weighed weekly. Direct behavioral observations were conducted twice per week. Calves housed in pairs tended to have greater average daily gain compared with calves housed individually (0.63 vs. 0.59 ± 0.02 kg/d, respectively). Pair housing also increased final body weight compared with individual housing (64.9 vs. 61.7 ± 0.59 kg, respectively). During observation periods, calves housed individually spent more time engaging in nonnutritive sucking than calves housed in pairs (21.5 vs. 8.15 ± 0.03% of total observations). Calves housed in pairs were observed cross sucking 13.5% of the time during observational periods. Although housing Jersey calves in pairs may increase measures of growth performance, future research should aim to reduce cross-sucking behavior within the Jersey breed through alternative feeding systems or environmental enrichment.

Neurotoxicity of ethyl methacrylate in rats.

Ethyl methacrylate (ethyl 2-methyl-2-propenoate, EMA) has been implicated in the development of neurologic impairment following occupational exposure. The potential of EMA to produce neurotoxicity was investigated in adult male Sprague-Dawley rats in two experiments. In the first experiment, animals were administered 100, 200, 400, or 800 mg/kg by daily intraperitoneal (i.p.) injections for 60 d. Control rats received daily i.p. injections of 1 ml saline/kg. Clinical observations, spontaneous motor activity, and performance in the Morris water maze were assessed. Alterations in clinical parameters in the higher dose groups included lethargy, impaired breathing, decreased weight gain, and increased mortality. Alterations in motor activity were observed at 100 mg/kg, a dose that did not cause alterations in clinical parameters, body weight gain, or mortality. There was also a dose-dependent impairment in performance in the Morris water maze. In the second experiment, animals were administered EMA in drinking water at concentrations of 0.1, 0.2, or 0.5% for 60 d. Control rats were administered tap water. Animals were perfused at the termination of exposure and samples of brain, spinal cord, and sciatic nerve were prepared for histological examination. Spongiform alterations were observed in fiber tracts of the forebrain, brainstem, and spinal cord. Clusters of axonal swellings were scattered throughout the dorsal, ventral, and lateral columns of the spinal cord, and typically involved internodal segments of two or three neighboring axons. Shrunken axons with separated myelin lamellae and large axons with thinner than normal myelin sheaths were apparent in the sciatic nerve. The patterns of alterations in the white matter of the spinal cord and the sciatic nerve are consistent with myelinopathy, but additional experiments are necessary to confirm whether oligodendroglia and Schwann cells are the primary sites of injury. In addition to the alterations associated with myelin, there was a decrease in the density of neurons in the ventral horn of the spinal cord. While the observed effects of EMA on the nervous system of rats are consistent with neurologic symptoms of workers exposed to EMA, additional experiments are necessary to determine if the level and route of exposures associated with occupational use produce these impairments in experimental animals.