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At least 73 records · Page 4Linked to original sources
PubMed1988

Pyrrolizidine alkaloid-induced liver disease in horses: an early diagnosis.

Nine adult horses were fed alfalfa hay cubes containing approximately 10% Senecio vulgaris until all horses had consumed approximately the same amount of toxic components of S vulgaris, pyrrolizidine alkaloids (PA). The amount of PA consumed was determined by the amount that induced clinical signs of PA toxicosis in 3 horses. The 6 other horses were given similar amounts per kilogram of body weight. An initial decrease of feed intake was observed when horses' diets were changed from alfalfa cubes to alfalfa/Senecio cubes, and feed intake was decreased further over 89 to 98 days. From 50 to 159 days, body weight decreased in all horses. Liver disease was induced in all 9 horses after they ate an average of 233 +/- 9.2 mg of PA/kg of body weight. Eight horses died or were euthanatized. Treatment with branched chain amino acids had no effect on mortality, but appeared to reduce neurologic problems. Clinical signs of PA-induced liver disease included ataxia, head pressing, and decreased feed intake. Other clinical signs of toxicosis were observed individual horses, but did not develop in most horses. Megalocytic hepatopathy developed. Liver abnormalities proceeded as PA was consumed and were severe in 8 of 9 horses before clinical signs of toxicosis appeared. Sulfobromophthalein sodium clearance did not decrease until PA-induced liver disease was advanced. Bile acid (BA) concentrations increased to greater than or equal to 50 mumol/L, in the 8 horses that died. One horse had hepatopathy and increased BA concentration, but survived. In this horse, BA concentration peaked at 33 mumol/L and then decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids, Branched-Chain↗
PubMed2006

[Depiction of the structure of the vitreous body in horses without ocular diseases and in horses with equine recurrent uveitis (ERU) using transmission electron microscopy].

Neither the ultrastructure of the vitreous body from horses without ocular diseases, nor the pathomorphological changes in the vitreous body associated with equine recurrent uveitis (ERU) have been described. However, the vitreous body plays an important role in the pathogenesis of ERU. Ten vitreous body samples obtained from 5 horses without ocular disease, and 38 vitreous body samples from horses with ERU (collected during vitrectomy) were examined by transmission electron microscopy. The vitreous body samples of horses without ocular diseases were characterized by a loose network of unbranched fibrils 10-12 nm in width. In the vitreous body samples of horses with ERU numerous dense bundles of fibrils, mononuclear inflammatory cells and necrotic cells represent the destruction of the vitreous fibrillar network. In this study, equine vitreous body ultrastructure was described for the first time. Thus, demonstrating ultramorphologically, the clinically apparent changes of the vitreous body associated with ERU.

Animals↗
PubMed2006

[Detection of leptospira in the vitreous body of horses without ocular diseases and of horses with equine recurrent uveitis (ERU) using transmission-electron microscopy].

Equine recurrent uveitis (ERU) is caused by persistent intraocular leptospira, which appear to use the vitreous body as a refuge. The detection of leptospira in the vitreous body of horses with spontaneous ERU by histological methods has not yet been described. Thirty eight vitreous body samples from 36 horses with ERU (collected during vitrectomy), and 10 vitreous body samples obtained from 5 horses without ocular disease (control group) were examined by transmission electron microscopy. Prior to sample collection, 2 ml of a leptospira culture suspension were injected into the vitreous body of 2 eyes enucleated from horses of the control group. The detection of leptospira in samples, experimentally inoculated with these bacteria was uncomplicated; in vitreous body samples from horses with spontaneous ERU the detection was successful in only a few cases (3/38). The morphologically varying envelope of leptospira in vitreous body samples of horses which developed ERU spontaneously suggests the existence of a bacterial masquerade in vivo.

Animals↗
PubMed1984

[Nutrition and skin diseases in the horse].

Skin diseases of the horse can be produced or enhanced through nutrient deficiency, intestinal formation of detrimental substances, photosensitizing compounds and by intake of allergenes. An exact case history regarding feeding is useful for evaluation of every skin abnormality.

Amino Acids, Essential↗
PubMed1977

Association of Australian arboviruses with nervous disease in horses.

An outbreak of Murray Valley encephalitis (MVE) occurred in New South Wales during the first five months of 1974. Specimens from 52 horses with nervous disease collected January to May 1974 were examined histopathological or virologically. Although MVE virus was not isolated, 13 horses had serological evidence of recent infection with MVE virus. Another 4 horses had evidence of recent infection with Ross River virus. Two animals had histological evidence of viral infection of the central nervous system. Attempts to experimentally infect 2 horses with a low dose of MVE virus were not successful by intravenous, intramuscular and subcutaneous routes.

Animals↗
PubMed1987

Evaluation and management of respiratory disease in the horse.

Respiratory disease is one of the commonest medical reasons for referring a horse to the Royal Veterinary College, with coughing the main presenting sign. Investigation requires the taking of a detailed history, clinical examination, the use of appropriate diagnostic aids and noting response to medication and management changes. On arrival the horse is stabled in a minimal dust environment, remaining there until discharge. The use of a dust-free box frequently produces a favourable response without the use of medication which in itself is diagnostic. The problem of a horse which is asymptomatic on discharge from the Royal Veterinary College and becomes symptomatic following the failure of its owner to implement advice given on changes in management is discussed.

Animals↗
PubMedDate not supplied

Investigation of the immediate analgesic effects of extracorporeal shock wave therapy for treatment of navicular disease in horses.

OBJECTIVES: To measure the acute analgesic properties of extracorporeal shock wave therapy (ESWT) in horses with navicular disease using objective ground reaction forces (GRF). STUDY DESIGN: Prospective study. ANIMALS: Nine client-owned horses with unilateral forelimb lameness caused by navicular disease. METHODS: Horses were trotted at 3 m/s over a force plate to record pre-treatment GRF of the lame and contra-lateral forelimbs. After ESWT of the lame limb, applied with a radial unit to each of the frog and heel bulb areas with 1500 pulses at 4 bar and 10 Hz, GRF measurements were repeated at 15 minutes and 24-hour intervals for 7 days. From the 5 trials recorded at each time, peak vertical force (PVF) was calculated and averaged. Data were compared between limbs and over time using a 2-way repeated-measures ANOVA. RESULTS: Mean (+/-SD) PVF was significantly different between lame (day 1; 4339+/-626 N) and contra-lateral (day 1; 5236+/-515 N) limbs pre-treatment (P<.05). After ESWT treatment, this difference remained unchanged at 15 minutes and from days 1 to 7. To confirm navicular disease, palmar digital analgesia significantly reduced the lameness (lame 5144+/-430 N; contralateral 5082+/-586 N; P>.05). CONCLUSIONS: Single ESWT treatment applied in this manner does not influence lameness in horses with navicular disease. CLINICAL RELEVANCE: Although many equine regulatory commissions currently ban the use of ESWT before competition, our results suggest that such regulations may be unfounded. Further research is required to determine the long-term analgesic properties of this frequently used treatment modality in equine athletes.

Analgesia↗
PubMed1980

Turnover of 131I-labelled albumin in horses with gastrointestinal disease.

Four horses with a history of chronic diarrhoea and weight loss were studied. Three of them revealed malabsorption, as indicated by decreased absorption of D(+)-xylose. Three patients had distinct hypoalbuminaemia, and 131I-albumin turnover rates of these three horses were increased, compared to two normal control horses. However, the increases were not very marked, probably because actual signs of enteric disease were few in the patients, all of which were studied during convalescence. It is suggested that the observed hypoalbuminaemia is due to a gastrointestinal protein loss during the chronic diarrhoeal disease.

Animals↗
PubMed2005

Systemic therapies for joint disease in horses.

Systemic therapies for joint disease may be prescribed when a single joint is involved or when multiple sites are affected. The precise therapeutic regimen recommended depends on the duration,cause, and site(s) of injury and is often an adjunct to intra-articular or supportive therapies. If the clinical signs of joint disease are acute and moderate in severity, nonsteroidal anti-inflammatory drugs are often administered to alleviate pain and inflammation. When aiming for more of a generalized maintenance or chondro-protective regimen, an alternative medication, such as hyaluronan,polysulfated glycosaminoglycan, or a nutraceutical will commonly be prescribed.

Animals↗