Effects of a Supplement Containing Cannabidiol (CBD) on Sedation and Ataxia Scores and Health.

Supplements containing Cannabidiol (CBD) are available for horses, however, few studies have been published on their effects on behavior and health parameters. The purpose of this study was to determine if a daily oral supplement containing CBD would cause sedation, ataxia or alterations in other health parameters during administration for 56 days. Twenty clinically healthy adult Thoroughbred horses were housed in stalls. Before treatment was initiated, a complete physical examination, complete blood count (CBC) and biochemical panel were evaluated. In addition, horses were examined for sedation and ataxia using standard scoring systems. Horses were randomly divided into two treatment groups, treated (supplement pellets containing CBD as Hemp Extract, 150 mg) or control (supplement pellets without CBD). Horses were treated daily and sedation and ataxia scores were assigned by two masked observers once weekly for 56 days. Horses were monitored daily for clinical signs or adverse events and body weights were recorded weekly. A CBC and biochemical panel were repeated on days 28 and 56, two hours after administration of the supplement. The supplement was readily consumed by the horses and no adverse effects were seen over the treatment period. Sedation and ataxia scores ranged from zero to two for all horses during the weekly examinations and there was no statistical difference between treatment groups. There were no treatment effects on blood values, including indicators of anemia and blood proteins, liver enzymes, kidney values, electrolytes or calcium. Body weight significantly increased in all horses, by Day 56 compared to Day zero but no treatment by day effect was noted. The CBD supplement (150 mg) was readily consumed and safe and did not result in changes in mentation, gait, or other health parameters, and no adverse clinical signs were observed during 56 days of oral administration.

Dorsal laminectomy for treatment of cervical vertebral stenotic myelopathy in an alpaca.

CASE DESCRIPTION: An 11-year-old male breeding alpaca was evaluated for a 2-day history of lowered head carriage and lethargy. CLINICAL FINDINGS: On initial examination, the alpaca had signs of lethargy and lowered carriage of the head and neck, but no specific neurologic deficits. Medical management improved the clinical signs, but 8 months later, the alpaca developed acute, progressive general proprioceptive ataxia affecting all 4 limbs and was referred for further evaluation and treatment. Magnetic resonance imaging and CT identified disruption of the normal osseous architecture of C7 and T1. Medical management was attempted, but because of a lack of improvement, the patient underwent surgery 14 months after initial examination. TREATMENT AND OUTCOME: A dorsal laminectomy of C7 and T1 via a dorsal midline approach was performed, and the spinous processes of both vertebrae were removed prior to removal of the overlying lamina. Free dorsal expansion of the spinal cord was ensured by resection of the ligamentum flavum. Six months after surgery, the alpaca had returned to successful breeding with 7 hembra bred in the first year after surgery, producing 6 crias, and 4 crias in the second year. The patient was eventually euthanized 28 months after surgery because of neurologic deterioration but was still ambulatory at that time. CONCLUSIONS AND CLINICAL RELEVANCE: A good outcome with adequate alleviation of clinical signs and breeding soundness for > 2 years following dorsal laminectomy was achieved in this camelid patient. The surgical approach was similar to that in other species and was associated with mild postoperative morbidity. Veterinarians treating camelids should be aware of the initial clinical signs and treatment options for cervical vertebral stenotic myelopathy. In acute cases, the signs of reduced cervical mobility and pain on manipulation should prompt investigation including appropriate diagnostic imaging. Timely surgical intervention should be considered in patients that respond poorly to medical treatment to avoid irreversible spinal cord injury and optimize outcome.

Interference of an algal nutritional supplement with a urinary metabolic screening test for glycosaminoglycans in a dog suspected to have a storage disease.

The finding of excess urinary glycosaminoglycans (GAG) is the first step in the laboratory diagnosis of mucopolysaccharidosis (MPS). Urinary screening tests are based upon the binding of GAG to dimethylmethylene blue. Alternatively, paper spot tests using toluidine blue are used in human and veterinary laboratory medicine. Positive samples undergo GAG isolation for subsequent characterization. Here, we describe a 3-year-old English Cocker Spaniel with a positive urinary GAG test, but without other clinical signs of MPS. Urine samples were strongly positive with the dimethylmethylene blue test, and isolated GAG subjected to electrophoresis on cellulose acetate revealed a band co-migrating with dermatan sulfate. However, the isolated GAG were resistant to digestion with chondroitinase ABC, suggesting that the band did not represent dermatan sulfate. This was confirmed by mobility of the isolated GAG different from dermatan sulfate on agarose gel electrophoresis. MPS types VI and VII were excluded by enzyme assay. To test the hypothesis of a nutritional source, a healthy control dog was fed the same dog food as the index case. His urine showed a comparable abnormal GAG screening test and electrophoretic pattern. In addition, the analysis of an algal supplement present in the administered dog food showed a similar electrophoretic GAG pattern. The Cocker Spaniel was not available for further testing after withdrawal of the supplement. Algae contain highly sulfated fucans and galactans, and it appears that commercial dog food containing such algal, and possibly other, supplements can give rise to false-positive urinary MPS screening tests.

Thiamine deficiency in a cat: resolution of MRI abnormalities following thiamine supplementation.

Thiamine (vitamin B(1)) is an essential component of a number of metabolic pathways and thiamine deficiency results in a progressive encephalopathy in both humans and animals. Confirming thiamine deficiency is problematic and relies on demonstrating reduced red blood cells transketolase activity, or indirect methods including urinary organic acid analysis and dietary analysis. The characteristic and selective vulnerability of different brain regions in carnivores has been demonstrated by magnetic resonance (MR) imaging in the dog and cat as an aid to diagnosis. A 2-year-old, female, domestic shorthair cat was presented with an acute onset of seizures and ataxia. MR imaging was consistent with thiamine deficiency and supplementation resulted in a progressive clinical improvement. Repeated MR imaging 4 days after starting thiamine supplementation revealed near complete resolution of the MR abnormalities. Repeated MR imaging following appropriate therapy may be useful to further confirm thiamine deficiency.

[Feed-related selenium poisoning in swine]. / Fütterungsbedingte Selen-Vergiftung beim Schwein.

The following case report describes a selenium toxicosis in a pig-fattening farm of two finisher groups. The diseased animals partly showed ataxia and paresis or intense lameness in connection with band-like ablation of the epidermis at the coronary band. Some of them suffered from alopecia. Foot-and-mouth disease and swine vesicular disease were excluded by serological tests. Dissection revealed a multifocal bilateral symmetric poliomyelomalacia. Histological changes in the claws ranged from severe cell-decay in the germinative layer to distinctive decay of the stratum corneum. Due to damage of the claw epidermis the corium was partly exposed. Feed analysis revealed 100-fold increased selenium content in the finishing premix from the feed mill and as a result 20- to 60-fold increased selenium values in feed samples from the farm-made finisher mixture. Selenium concentration in the blood of diseased animals was 4- to 10-fold higher than normal values, which confirmed the tentative diagnosis of a selenium toxicosis.

Neurologic disease putatively associated with ingestion of Solanum viarum in goats.

Several Nubian-cross goats were evaluated because of chronic progressive neurologic disease. Physical and neurologic examination revealed signs consistent with diffuse cerebellar disease. Neurologic signs included generalized hyperresponsiveness, fine head tremors, wide-based posture, dysmetria, weakness, and horizontal nystagmus. No clinical improvement was noted after removing goats from affected enclosures. Histologic examination of cerebellar tissues revealed extensive vacuolation within the cytoplasm of Purkinje cells. The clinical and histologic lesions resembled closely findings that were associated with ingestion of Solanum spp in cattle and goats. Examination of enclosures revealed Solanum viarum (tropical soda apple) that had been heavily consumed by the goat herd. We hypothesized that ingestion of S. viarum caused the neurologic disorder.

Subclinical copper accumulation in llamas.

A 9-year-old, intact male llama with mild ataxia and generalized malaise of 1 month's duration was euthanized following clinical evaluation. Excessive liver copper concentrations were found in the llama and also in clinically normal herdmates. This case documents multiple animals with increased hepatic stores from standard diets and mineral supplements.

Suspected herbicide toxicosis in a dog.

An 8-year-old 38-kg spayed female Golden Retriever was admitted for vomiting, signs of abdominal pain on palpation, ataxia, anorexia, and generalized weakness of 2 days' duration. Ten hours prior to onset of clinical signs, the dog was found standing in and drinking from large pools of an accidentally spilled herbicide that contained an octanoic acid ester of bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) and an isooctyl ester of (2-methyl-4-chloro) phenoxyacetic acid (MCPA). Appendicular muscles were firm on palpation and persistent muscle contraction (myotonia > 1 minute duration) was found on muscle percussion, using a reflex hammer. Electrical activity indicative of myotonia was identified on electromyographic evaluation. With supportive treatment, the dog eventually recovered from suspected MCPA toxicosis. Although rare, MCPA toxicosis should be considered as a cause of acquired myotonia in dogs.

Lithium toxicosis in a cow.

A case of lithium toxicosis is described in a cow that had consumed grease. Clinical signs included increased salivation, ataxia, reduced consciousness, seizures and diarrhea. No treatment was instituted. The grease did not contain high concentrations of other heavy metals or minerals.

Ataxia and head tremor in an alpaca (Lama pacos)

An 18-month-old alpaca developed nervous signs, including swaying of the head and neck, a wide-based stance and hind-limb ataxia. No certain diagnosis was made but the animal recovered after successive treatment with amoxycillin, vitamin B1, ivermectin and copper oxide, followed by vitamin E and selenium. The differential diagnosis rationale of treatment is described.

A comparison of the sedative effects of three alpha 2-adrenoceptor agonists (romifidine, detomidine and xylazine) in the horse.

The sedative effects of a new alpha 2-adrenoceptor agonist, romifidine, were compared with those of xylazine and detomidine. Five horses were treated with two doses of romifidine (40 micrograms/kg body weight and 80 micrograms/kg body weight), two doses of detomidine (10 micrograms/kg body weight and 20 micrograms/kg body weight) and one dose of xylazine (1 mg/kg body weight) given by intravenous injection using a Latin-square design. The dose of 80 micrograms/kg romifidine appeared equipotent to 1 mg/kg xylazine and 20 micrograms/kg detomidine, although at these doses both xylazine and detomidine had a shorter action. Detomidine 20 micrograms/kg and xylazine both produced greater lowering of the head and a greater degree of ataxia than romifidine at either dose. Romifidine produced sedation similar to that of the other drug regimes. The effect upon imposed stimuli was similar.

Clinical, viral, and genetic evaluation of equine degenerative myeloencephalopathy in a family of Appaloosas.

A clinical, viral, hematologic , and genetic study was conducted over a 4-year period on a family of Appaloosas with high incidence of clinical ataxia and pathologic features of equine degenerative myeloencephalopathy. Marginal to deficient serum vitamin E (alpha-tocopherol) and blood selenium values were the only other consistent antemortem abnormalities in the affected horses. Members of this family were all descendants of a clinically normal mare and were raised in 3 separate environments with variable quality of feed. All horses had access to pasture grasses. Normal chromosomal karyotypes were found in 11 affected and/or related horses examined. Equine herpesvirus type 2 was isolated from 4 of the horses, but evidence for a role of this virus in the pathogenesis of the disease was not found. The role of antioxidant deficiency in the pathogenesis of neurologic dysfunction in this equine family and in others reported to be affected with equine degenerative myeloencephalopathy remains speculative.

Bobber: a cervical ataxic mutant in the domestic turkey responsive to sunlight.

Bobber is a genetic disorder in the domestic turkey that is usually expressed between two and four weeks of age. The condition is permanent and is characterized by ventrocaudad bending of the neck accompanied by a lateral pendulumlike motion of the head between the legs. Expressivity of the defect is variable and may be exhibited in some turkeys as a stargazing posture or a rapid clockwise twirling motion. When suspended by the legs in a head-down orientation, afflicted turkeys exhibit an inward turning of the neck and head toward the breast as opposed to an outward turning in normal turkeys. The disorder is inherited as a sex-linked recessive trait. The symbol bo is used for the gene. The defect can be corrected by exposure to intense light in the visible spectrum.

Incompatibility between lasalocid and chloramphenicol in broiler chicks after a long-term simultaneous administration.

Two growth experiments were conducted to evaluate in broiler chicks the compatibility between lasalocid medication in the feed (at 90 or 125 ppm) and a long-term administration of chloramphenicol either via the feed (500 ppm) or via the drinking water (500 mg/liter). The simultaneous administration of lasalocid and chloramphenicol generally caused severe growth depression, decreased feed intake and impaired feed conversion. Several chicks showed evident symptoms of intoxication, such as ataxia, leg weakness and paralysis. The development and frequency of these symptoms were dependent on the dosage of lasalocid and on the duration of the simultaneous administration. Biochemical examinations (Experiment 2) revealed in the affected chicks significant changes in several parameters, in particular a markedly increased activity of creatine kinase and GOT in the plasma. It confirmed that the observed leg weakness and paralysis were caused by myodegeneration.

Equine degenerative myeloencephalopathy: a vitamin E deficiency that may be familial.

Two horse farms, on which there was a high incidence of proven and suspected equine degenerative myeloencephalopathy (EDM), were studied. Symmetric ataxia and paresis, along with laryngeal adductor, cervicofacial, local cervical, and cutaneous trunci hyporeflexia, characterized the syndrome. Serum vitamin E concentration reflected a deficient state in affected and unaffected horses on both farms when compared with selected reference groups and with published values. A high incidence of the disease was evident in offspring of two particular sires on one farm. Vitamin E supplementation resulted in correction of the deficient state in most horses and was associated with a drastic reduction in the incidence of EDM on one farm from 40% to less than 10% the year following vitamin E supplementation. In addition, during the last year, the severity of signs in the few cases was dramatically reduced. This information substantiates the hypothesis that EDM is a vitamin E-responsive disorder of Equidae with a possible familial predisposition.

Cassia occidentalis toxicosis in growing pigs.

Approximately 70 feeder pigs developed ataxia and other signs of neuromuscular dysfunction. The ration fed the pigs was found to be contaminated with Cassia occidentalis seeds. Experimentally, other feeder pigs were fed this ration, and they developed ataxia and other signs of neuromuscular dysfunction within 6 to 8 weeks. In further experiments, feeder pigs fed diets containing 1%, 2%, or 4% ground cassia seeds also became intoxicated. Microscopically, diaphragmatic myopathy and pancreatic tissue necrosis were the principal pathologic findings.