Molecular heterogeneity for bovine α-mannosidosis: PCR based assays for detection of breed-specific mutations

tests, based on the polymerase chain reaction ( ), were developed for the detection of two breed-specific mutations responsible for the autosomal recessive disorder bovine α-mannosidosis. The tests involve separate amplification of two exons of the lysosomal α-mannosidase gene followed by restriction enzyme digestion of the amplicons. We demonstrate that one of the mutations, the 662G→A transition, is responsible for α-mannosidosis in Galloway cattle. The other mutation, the 961T→C transition, is uniquely associated with α-mannosidosis in Angus, Murray Grey and Brangus cattle from Australia. The 961T→C mutation was also detected in Red Angus cattle exported from Canada to Australia as embryos. All 39 animals classified as heterozygotes on the basis of biochemical assays were heterozygous for one of the two mutations. None of 102 animals classified as homozygous-normal on the basis of biochemical assays possessed the mutations. Our results indicate that the two breed-specific mutations may have arisen in Scotland and by the export of animals and germplasm disseminated to America, New Zealand and Australia.     

Reaction of Calves to Two Flooring Materials Offered Simultaneously in One Pen

Now that group housing is replacing individual crates, so that calves can lie, stand and walk on the pen floor, the quality of the floor for group-housed calves has become the focus of attention. The reaction of two groups of four calves to a double area of floor made from two materials (wooden slats and synthetic slats with a rubber coating) was examined round the clock for 5 days. The calves were switched between pens twice, and in each case the 5 day observation period was repeated. In all three phases all calves spent significantly more time ( P <0.01) lying on the wooden floor: on average 656 min day -1 compared with 294 min day -1 on the synthetic floor. The time spent in the standing/walking position on both floors, occurrence of slip incidents and self-maintenance behaviour did not differ significantly between floors. The observations on use of the pen floor for lying and for standing/walking in combination with feeding, plus observations on fouling of the floors with excreta suggest that future pen design could be functionally divided into lying and walking/eating areas.     

Evaluation of auditory evoked potentials to predict depth of anaesthesia during fentanyl/fluanisone−midazolam anaesthesia in rats

Objectives To assess a method for monitoring depth of anaesthesia using components of middle latency auditory evoked potential (AEP) waveforms during anaesthesia with fentanyl/fluanisone and midazolam. Study design Prospective observational study. Animals Five female Wistar rats weighing between 210 and 250 g. Methods Implanted electrodes were used to record AEPs in animals receiving five doses of anaesthetic. Recordings were made at 5 minutes post‐injection (deep anaesthesia; no pedal withdrawal response, PWR) and then at 25 minutes (light anaesthesia; strong PWR). Responses showed five characteristic peaks occurring at 11, 14, 23, 42 and 68 ms that were measured for latency of occurrence and peak amplitude. Results Auditory evoked potential peaks P14, N23 and P42 were increased significantly in latency with successive anaesthetic injections [avg. F(1,4) = 12.53, p < 0.001; avg. F(1,4) = 10.6, p < 0.001; avg. F(1,4) = 3.9, p = 0.02, respectively]. Peak N23 showed a significant reduction in latency during the 20 minute recovery period following both the first and second anaesthetic injections (t(3) = 7.52, p = 0.005; t(4) = 5.17, p = 0.007, respectively). Peak P42 occurred significantly earlier 20 minutes following the second anaesthetic injection (t(4) = 4.75, p = 0.009). The mean overall depth of anaesthesia assessed using PWR scores was significantly correlated with the mean latency of peak N23, such that as the strength of PWR increased, N23 occurred significantly earlier (r = ?0.99, p = 0.01). The amplitude difference between peaks N23 and P42 increased after the second and third drug administrations [avg. F(1,4) = 10.65, p = 0.031 and avg. F(1,4) = 11.24, p = 0.028, respectively]. Conclusion The characteristics of these peaks, and in particular latency of peak N23, may provide a useful tool for assessing depth of anaesthesia produced by this, and possibly other anaesthetic agents.     

The weakest link: medroxyprogesterone acetate in pig feed

Medroxyprogesterone acetate (MPA)-contaminated feed arrested the onset of farrowing, and induced post-lactational anoestrus in sows. Sixty percent of the sows developed cystic ovaries after weaning following exposure to pharmaceutical waste of MPA in glucose syrup. This waste ended up in acidified feed of by-products of a sow farm, and proved to be the cause of the disorders. Analysis by thin layer chromatography and Gas Chromatography/Mass Spectrometry of renal fat from 10 slaughter sows demonstrated residues of 2.5-8 ppb of MPA. Within the European Union use of MPA is illegal as growth promoter in production animals, and therefore MPA-exposed farms were placed under official control by the general inspection service. Clinical signs and diagnostic procedures of the initial case are presented and the role of the veterinary practitioner in detecting potential food safety hazards is discussed.     

Effect of dietary lipoic acid on metabolic hormones and acute-phase proteins during challenge with infectious bovine rhinotracheitis virus in cattle

OBJECTIVE: To determine the effect of dietary supplemental lipoic acid (LA) on serum concentrations of metabolic hormones and acute-phase proteins of steers challenged with infectious bovine rhinotracheitis virus (IBRV). ANIMALS: 32 steers. PROCEDURES: Steers were randomly assigned to 4 treatments: negative control (NC; no LA, no IBRV challenge), control (CON; no LA, IBRV challenge), 16 mg of LA/kg of body weight (BW)/d plus IBRV challenge (LA16), and 32 mg of LA/kg of BW/d plus IBRV challenge (LA32). Following a 21-day adaptation period, CON, LA16, and LA32 steers received IBRV (2 mL/nostril [day 0]); NC steers received saline (0.9% NaCl) solution. Blood samples, nasal swab specimens, BW, and rectal temperatures were obtained 0, 1, 3, 5, 7, 14, and 21 days after challenge. Serum was analyzed for concentrations of haptoglobin, amyloid-A, leptin, and anti-IBRV antibodies. RESULTS: Steers fed LA32 began gaining BW by day 7, whereas BW of CON and LA16 steers declined. Serum haptoglobin concentration of LA32 steers was lower than that of CON and LA16 steers on day 7. Serum neutralization titers for 30 of 32 steers were negative for anti-IBRV antibodies before challenge; however, all steers (including NCs) had antibodies on day 21. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that LA supplementation augmented certain aspects of the immune response; LA32 steers had a more rapid recovery from IBRV viral challenge than did others.     

Growth performance, carcass composition, quality, and enhancement treatment of fresh pork identified through deoxyribonucleic acid marker-assisted selection for the Rendement Napole gene

Progeny (n = 70) from unrelated, DNA tested, Rendement Napole carrier (RN-/rn+) Hampshire sires, and DNA tested, Rendement Napole normal (rn+/rn+) Yorkshire dams were genotyped for the segregating RN- allele via DNA marker-assisted methodology. Six slaughter groups ensued, with littermates all being represented within the same slaughter group. Boneless pork loins were removed from right carcass sides after a 48-h chill at 2 degrees C. The anterior portions of the loins were not enhanced, whereas the posterior sections were enhanced with a solution containing 0.5% sodium chloride and 0.5% sodium tripolyphosphate to 110% of their initial weight. Carcasses of carrier pigs had less (P < 0.05) 10th rib fat depth and a greater (P < 0.01) percentage carcass lean than carcasses of normal pigs. Postmortem LM pH of carrier pigs was lower (P < 0.002) at 3, 6, 12, and 24 h, and tended to be lower (P = 0.062) at 48 h compared with that of normal animals. Samples of LM from carrier pigs had greater (P < 0.01) glycolytic potential values, drip loss percentages, and a* values, and lower pH values at fabrication than LM from normal pigs. No genotype differences (P > 0.05) were found for LM lactate, L*, or b* values. Nonenhanced semimembranosus samples from carrier pigs exhibited greater (P < 0.05) purge loss percentages and L* values, and lower (P < 0.01) pH values than samples from normal pigs. Enhanced LM samples exhibited greater (P < 0.05) drip and purge loss percentages, greater pH, and lower L* values at fabrication, regardless of Napole status. These findings suggest that the Napole gene has a positive influence on carcass leanness but detrimental effects for lean quality, which were often further compounded when meat was subjected to enhancement treatment.     

Death of a horse infected experimentally with Anaplasma phagocytophilum

A 19-year-old horse that was one of a group of six horses infected experimentally with Anaplasma phagocytophilum for a study of the pathogenesis of equine granulocytic ehrlichiosis died suddenly two days after first showing clinical signs of disease. The clinical signs and laboratory findings observed before its death were similar to all those of the other infected horses, and to previous reports of this disease. A postmortem examination revealed widespread haemorrhaging in its internal organs, and vasculitis and thrombosis in the kidneys. These changes are consistent with disseminated intravascular coagulation, which has previously been reported in human beings infected with the presumably identical agent of human granulocytic ehrlichiosis.     

Pathology and Neurotoxicity in Dogs after Repeat Dose Exposure to a Serotonin 5-HT1B Inhibitor

AZD3783, a cationic amphiphilic drug and a potent inhibitor of the 5-hydroxytryptamine (5-HT_1B) receptor, was explored as a potential treatment for depression. To support clinical trials, repeat dose toxicity studies in rats and dogs were conducted. Here we report toxicity findings in dogs after dosing from 1 to 3 months. In the 1-month study, there were minimal neuronal vacuolation in the brain, a marked increase in liver enzymes accompanied by hepatocellular degeneration/necrosis and phospholipidosis (PLD), and PLD/cholecystitis in the gallbladder of animals dosed at 47 mg/kg/day. In the 3-month study, neurotoxicity resulted in euthanasia of one animal dosed at 30 mg/kg/day after 86 days. Extensive pathologic changes were seen in all animals in retina epithelium (inclusion bodies), brain (neuronal vacuolation, degeneration, or necrosis and nerve fiber degeneration), spinal ganglia (vacuolation, degeneration, or necrosis), as well as sciatic and optic nerves (degeneration). Pigment-laden macrophages were observed in the lung, kidney, liver, gallbladder, bone marrow, gastrointestinal tract, and lymphoid tissues. Also seen were vitrel and retinal hemorrhage in the eyes. A brain concentration and pathology study showed that the concentration of AZD3783 in the brain was approximately 4 times higher than in the plasma after 4 weeks of dosing, however, they were similar in all regions examined, and did not correlate with areas with pathologic findings. Our findings with AZD3783 in dogs have not been reported previously with other CNS compounds that effect through serotonergic pharmacology.