Elapid snake envenomation in horses: 52 cases (2006-2016).

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.

Effects of polymyxin-B on TNF-α production in equine whole blood stimulated with three different bacterial toxins.

Polymyxin-B is used to treat equine systemic inflammation. Bacterial toxins other than lipopolysaccharide (LPS) contribute to systemic inflammation but the effects of polymyxin-B on these are poorly defined. Whole blood aliquots from six healthy horses diluted 1:1 with RPMI were incubated for 21 hr with 1 µg/ml of LPS, lipoteichoic acid (LTA) or peptidoglycan (PGN) in the presence of increasing concentrations of polymyxin-B (10-3000 µg/ml). A murine L929 fibroblast bioassay was used to measure TNF-α activity. Polymyxin-B significantly inhibited the effects of all three bacterial toxins. Analysis of variance showed the IC50 value for polymyxin-B for TNF-α inhibition caused by LTA (11.19 ± 2.89 µg/ml polymyxin-B) was significantly lower (p = .009) than the values for LPS (46.48 ± 9.93 µg/ml) and PGN (54.44 ± 8.97 µg/ml). There was no significant difference in IC50 values between LPS and PGN (p > .05). Maximum inhibition of TNF-α was 77.4%, 73.0% and 82.7% for LPS, PGN and LTA, respectively and was not significantly different between toxins. At the two highest concentrations of polymyxin-B, TNF-α began to increase. These data suggest that polymyxin-B may inhibit the effects of bacterial toxins other than LPS and might be a more potent inhibitor of LTA than LPS or PGN.

Sequential plasma lactate concentrations as prognostic indicators in adult equine emergencies.

BACKGROUND: Sequential lactate concentration ([LAC]) measurements have prognostic value in that hospitalized humans and neonatal foals that have a delayed return to normolactatemia have greater morbidity and case fatality rate. HYPOTHESIS: Prognosis for survival is decreased in horses with a delayed return to normal [LAC]. ANIMALS: Two hundred and fifty adult horses presented for emergency evaluation excepting horses evaluated because of only ophthalmologic conditions, superficial wounds, and septic synovitis without systemic involvement. METHODS: Prospective observational study. [LAC] was measured at admission and then at 6, 12, 24, 48, and 72 hours after admission. The change in [LAC] over time ([LAC]deltaT) was calculated from changes in [LAC] between sampling points. RESULTS: Median [LAC] was significantly (P < .001) higher at admission in nonsurvivors (4.10 mmol/L [range, 0.60-18.20 mmol/L]) when compared with survivors (1.30 mmol/L [range, 0.30-13.90 mmol/L]) and this difference remained at all subsequent time points. The odds ratio for nonsurvival increased from 1.29 (95% confidence interval 1.17-1.43) at admission to 49.90 (6.47-384) at 72 hours after admission for every 1 mmol/L increase in [LAC]. [LAC]deltaT was initially positive in all horses but became negative and significantly lower in nonsurvivors for the time periods between 24-72 hours (- 0.47, P = .001) and 48-72 hours (- 0.07, P = .032) when compared with survivors (0.00 at both time periods) consistent with lactate accumulation in nonsurvivors. CONCLUSIONS AND CLINICAL IMPORTANCE: These results indicate that lactate metabolism is impaired in critically ill horses and [LAC]deltaT can be a useful prognostic indicator in horses.

Hyperhydration prior to a simulated second day of the 3-day moderate intensity equestrian competition does not cause arterial hypoxemia in Thoroughbred horses.

Dehydration and the associated impairment of cardiovascular and thermoregulatory function comprise major veterinary problems in horses performing prolonged exercise, particularly under hot and humid conditions. For these reasons, there is considerable interest in using pre-exercise hyperhydration to help maintain blood volume in the face of the excessive fluid loss associated with sweat production during prolonged exertion. However, recently it was reported that pre-exercise hyperhydration causes arterial hypoxemia in horses performing moderate intensity exercise simulating the second day of an equestrian 3-day event competition (E3DEC) which may adversely affect performance (Sosa Leon et al. in Equine Vet J Suppl 34:425-429, 2002). These findings are contrary to data from horses performing short-term maximal exertion, wherein hyperhydration did not affect arterial O2 tension/saturation. Thus, our objective in the present study was to examine the impact of pre-exercise hyperhydration on arterial oxygenation of Thoroughbred horses performing an exercise test simulating the second day of an E3DEC. Control and hyperhydration studies were carried out on seven healthy Thoroughbred horses in random order, 7 days apart. In the control study, horses received no medications. In the hyperhydration experiments, nasogastric administration of NaCl (0.425 g/kg) 5 h pre-exercise induced a plasma volume expansion of 10.9% at the initiation of exercise. This methodology for inducing hypervolemia was different from that of Sosa Leon et al. (2002). Blood-gas tensions/pH as well as plasma protein, hemoglobin and blood lactate concentrations were measured pre-exercise and during the exercise test. Our data revealed that pre-exercise hyperhydration neither adversely affected arterial O2 tension nor hemoglobin-O2 saturation at any time during the exercise test simulating the second day of an E3DEC. Further, it was observed that arterial blood CO2 tension, pH, and blood lactate concentrations also were not affected by pre-exercise hyperhydration. However, hemodilution in hyperhydrated horses caused an attenuation of the expansion in the arterial to mixed-venous blood O2 content gradient during phases B and D of the exercise protocol, which was likely offset by an increase in cardiac output. It is concluded that pre-exercise hyperhydration of horses induced in the manner described above is not detrimental to arterial oxygenation of horses performing an exercise test simulating the second day of an E3DEC.

Pre-exercise hypervolaemia is not detrimental to arterial oxygenation of horses performing a prolonged exercise protocol simulating the second day of a 3-day equestrian event.

REASONS FOR PERFORMING STUDY: Hyperhydration, prior to prolonged moderate-intensity exercise simulating the 2nd day of a 3-day equestrian event (E3DEC), may induce arterial hypoxaemia detrimental to performance. OBJECTIVES: Because moderate-intensity exercise does not induce arterial hypoxaemia in healthy horses, the effects of pre-exercise hypervolaemia on arterial oxygenation were examined during a prolonged exercise protocol. METHODS: Blood-gas studies were carried out on 7 healthy, exercise-trained Thoroughbred horses in control and hyperhydration experiments. The study conformed to a randomised crossover design. The sequence of treatments was randomised for each horse and 7 days were allowed between studies. Hyperhydration was induced by administering 0.425 g/kg bwt NaCl via nasogastric tube followed by free access to water. The exercise protocol was carried out on a treadmill set at a 3% uphill grade and consisted of walking at 2 m/sec for 2 min, trotting for 10 min at 3.7 m/sec, galloping for 2 min at 14 m/sec (which elicited maximal heart rate), trotting for 20 min at 3.7 m/sec, walking for 10 min at 1.8 m/sec, cantering for 8 min at 9.2 m/sec, trotting for 1 min at 5 m/sec and walking for 5 min at 2 m/sec. RESULTS: NaCl administration induced a significant mean +/- s.e. 15.5 +/- 1.1% increase in plasma volume as indicated by a significant reduction in plasma protein concentration. In either treatment, whereas arterial hypoxaemia was not observed during periods of submaximal exercise, short-term maximal exertion caused significant arterial hypoxaemia, desaturation of haemoglobin, hypercapnoea, and acidosis in both treatments. However, the magnitude of exercise-induced arterial hypoxaemia, desaturation of haemoglobin, hypercapnoea, and acidosis in both treatments remained similar, and statistically significant differences between treatments could not be demonstrated. CONCLUSIONS: It was concluded that significant pre-exercise expansion of plasma volume by this method does not adversely affect the arterial oxygenation of horses performing a prolonged exercise protocol simulating the 2nd day of an E3DEC.

Prevalence of Neospora antibodies in beef cattle in New Zealand.

AIM: To estimate the prevalence of Neospora infection in a sample of New Zealand beef cattle. METHODS: The prevalence of Neospora caninum infection in New Zealand beef cattle was estimated by collecting blood at slaughter from 499 beef cattle from 40 different farms at 2 slaughter plants in the North Island and 1 in the lower South Island . Sera were tested using an ELISA against Neospora tachyzoite antigen. RESULTS: The prevalence of seropositive cattle was 2.5% (n=120), 3.6% (n=166) and 2.3% (n=213) at the plants surveyed, the overall prevalence being 2.8%. The serologically positive cattle came from 9 farms, 3 of which had more than 1 positive animal. The highest prevalence recorded amongst animals from 1 farm was 4/13 (31%), in a group of young steers. CONCLUSION: Neosporosis appears to be present at a lower level in the New Zealand beef cattle population than in the New Zealand dairy cattle population. Nevertheless, from the high seroprevalence evident amongst young cattle on 1 farm, we suggest that Neospora may be a cause of infertility in beef cattle in this country.