ABSTRACT
BACKGROUND: Snake envenomation is a cause of morbidity and mortality in domestic animals worldwide. The clinical features of crotalid snake (pit viper) envenomation are widely reported and well described in horses but elapid snake envenomation is poorly characterised. OBJECTIVES: To describe the presentation, clinical and laboratory findings, treatment and outcome of horses with a diagnosis of elapid snake envenomation in Australia. STUDY DESIGN: Retrospective case series. METHODS: Medical records of horses with a diagnosis of elapid snake envenomation (2006-2016) at several university and private veterinary practices were reviewed. Inclusion criteria comprised one or more of the following: 1) observed snakebite, 2) positive snake venom detection kit (SVDK) result, 3) appropriate clinical response to treatment with antivenom or 4) supportive post-mortem findings. RESULTS: Fifty-two cases met the inclusion criteria. Most cases (94%) demonstrated clinical signs of neurotoxicity, characterised by generalised neuromuscular weakness. Associated neurologic signs included staggering gait, muscle fasciculations, recumbency, mydriasis, ptosis and tongue paresis. Concurrent clinically important conditions included rhabdomyolysis (50%) and haemolysis (19%). Of 18 urine samples evaluated with a SVDK, only three (17%) were positive. Overall survival was favourable (86%) among 49 horses who received antivenom. Eighteen surviving horses (43%) required more than one vial of antivenom. MAIN LIMITATIONS: Possible cases within the searchable database were not included if horses died acutely or responded to symptomatic treatment without receiving antivenom. CONCLUSIONS: Elapid snake envenomation is primarily a syndrome of neuromuscular weakness. Supportive anamnesis or an obvious bite site is rarely encountered. In endemic areas, this diagnosis should be considered for horses with generalised neuromuscular weakness, altered mentation, rhabdomyolysis and/or haemolysis; especially during spring and summer months. Diagnostic suspicion is best confirmed by response to treatment with antivenom.
Subject(s)
Antivenins/therapeutic use , Elapidae , Horse Diseases/etiology , Snake Bites/veterinary , Snake Venoms/toxicity , Animals , Australia/epidemiology , Female , Horse Diseases/epidemiology , Horses , Male , Retrospective StudiesSubject(s)
Horses/physiology , Muscle, Skeletal/physiology , Physical Conditioning, Animal/physiology , Animal Welfare , Animals , Anti-Inflammatory Agents/adverse effects , Anti-Inflammatory Agents/pharmacology , Biomechanical Phenomena , Diuretics/pharmacology , Furosemide/pharmacology , Horses/genetics , Internationality , SportsABSTRACT
A 9-year-old Dutch Warmblood mare was presented with a history of abnormal behaviour and acute facial nerve paralysis on the left side. Clinical examination revealed a slight head tilt and a corneal ulcer of the left eye. The base of the left ear was warm and painful. Endoscopic examination of the left guttural pouch showed thickening of the proximal part of the stylohyoid bone. Computer tomography revealed a left-sided prominent bony enlargement of the middle and proximal part of the stylohyoid bone and the tympanic bulla, fusion of the temporrhoid joint, and osseous proliferation of the pars petrosa of the temporal bone. The diagnosis was confirmed postmortem. The literature concerning the anatomy, clinical signs, and therapy of temporrhoid osteoarthropathy is discussed.
Subject(s)
Bone Diseases/veterinary , Facial Nerve Diseases/veterinary , Facial Paralysis/veterinary , Horse Diseases/pathology , Animals , Bone Diseases/microbiology , Bone Diseases/pathology , Euthanasia, Animal , Facial Nerve Diseases/complications , Facial Nerve Diseases/pathology , Facial Paralysis/complications , Facial Paralysis/pathology , Female , Horse Diseases/microbiology , Horses , Keratitis/complications , Keratitis/pathology , Keratitis/veterinary , Staphylococcal Infections/complications , Staphylococcal Infections/pathology , Staphylococcal Infections/veterinary , Staphylococcus aureus/isolation & purification , Temporal Bone/pathology , Vestibulocochlear Nerve Diseases/pathology , Vestibulocochlear Nerve Diseases/veterinaryABSTRACT
Feeding a high-fat diet increases fat utilisation and may decrease glycogen utilisation resulting in a lower lactate production during moderate exercise. The effects of fat feeding on exercise- and lipid metabolism-associated blood variables were evaluated in 6 Standardbred horses during submaximal exercise. The horses were fed a high- (11.8% fat in total dietary dry matter) or a low-fat diet (1.5% fat) in a cross-over experiment with feeding periods of 4 weeks. At the end of each feeding period, the horses were subjected to a submaximal standardised stepwise exercise test on a treadmill. Blood samples were obtained prior to the start, during the last 10 s of each exercise step, and after recovery (40 min walking in hand). Pre-exercise test values for plasma lactate, pH, pCO2, ionised sodium, ionised potassium, ionised calcium, ionised chloride, glucose, nonesterified fatty acids and glycerol did not differ for the 2 diets. The pre-exercise concentration of triacylglycerols was significantly lower on the high- compared to the low-fat diet (mean +/- s.d. 0.17 +/- 0.06 and 0.23 +/- 0.08 mmol/l, respectively), whereas the concentrations of cholesterol (3.00 +/- 0.47 and 2.11 +/- 0.49 mmol/l, respectively), HDL cholesterol (1.80 +/- 0.18 and 1.35 +/- 0.27 mmol/l, respectively) and phospholipids (2.30 +/- 0.11 and 1.72 +/- 0.20 mmol/l, respectively) were significantly higher. There was significantly less plasma lactate accumulation during exercise when the horses were given the high-fat diet (P = 0.011). Horses on a low-fat diet had significantly different plasma lipid values when compared to being on a high-fat diet. The alterations in these values during and after moderate exercise were comparable for both diets. These results indicate that fat metabolism is significantly adapted on a high-fat diet; feeding such a diet may enhance potential performance by delaying lactate accumulation and thereby delaying the onset of fatigue.