A 23-year-old Thoroughbred gelding was referred for the evaluation of acute onset of ataxia and depression, and a 2-day history of fever. On physical examination, the gelding was profoundly depressed and 10-12% dehydrated. The horse appeared very unstable, with a wide-based stance in the hind limbs, severe symmetric ataxia in all 4 limbs, and proprioceptive deficits in both hind limbs. Nasogastric intubation produced 4 L of brown, fetid reflux, and rectal examination revealed mild small intestinal and cecal distention. Hematologic abnormalities included neutropenia with toxic change, compatible with acute inflammation and endotoxemia, and prolonged coagulation times. Serum biochemical abnormalities included prerenal azotemia. metabolic acidosis, and electrolyte abnormalities consistent with enteritis. Blood ammonia concentration was markedly increased (406 micromol/L; reference interval 4-49 micromol/L), however, serum bile acids concentration and hepatic enzyme activities were within reference intervals. Histopathologic examination of a liver biopsy revealed no abnormalities and results of tests for several infectious agents were negative. Clinical signs resolved with correction of the dehydration and electrolyte abnormalities and with antibiotic therapy. The horse was diagnosed with hyperammonemic neuropathy associated with gastrointestinal disease. In such cases, hyperammonemia is caused by increased production of ammonia by organisms in the gastrointestinal tract in combination with increased gut permeability that facilitates ammonia absorption.

This study was conducted to determine whether horses with naturally occurring, severe chronic recurrent airway obstruction (RAO) 1). have a greater resting energy expenditure (REE) than control horses, 2). suffer body mass depletion, and 3). have significantly decreased REE after bronchodilation and, therefore, also 4). whether increased work of breathing contributes to the cachexia seen in some horses with RAO. Six RAO horses and six control horses underwent indirect calorimetric measures of REE and pulmonary function testing using the esophageal balloon-pneumotachograph method before and after treatment with ipratropium bromide, a parasympatholytic bronchodilator agent, at 4-h intervals for a 24-h period. Body condition scoring was performed, and an estimate of fat mass was determined via B-mode ultrasonography. O(2) and CO(2) fractions, respiratory airflow, respiratory rate, and pleural pressure changes were recorded, and O(2) consumption, CO(2) production, REE, pulmonary resistance, dynamic elastance, and tidal volume were calculated. In addition, we performed lung function testing and calorimetry both before and after sedation in two control horses. RAO horses had significantly lower body condition scores (2.8 +/- 1.0 vs. 6.4 +/- 1.2) and significantly greater O(2) consumption than controls (4.93 +/- 1.30 vs. 2.93 +/- 0.70 ml.kg(-1).min(-1)). After bronchodilation, there was no significant difference in O(2) consumption between RAO horses and controls, although there remained evidence of residual airway obstruction. There was a strong correlation between O(2) consumption and indexes of airway obstruction. Xylazine sedation was not associated with changes in pulmonary function but did result in markedly decreased REE in controls.

A 9-year-old Arabian mare was evaluated for a 7-day history of malaise. Results of a CBC included a leukocyte concentration within the reference interval (8.4 x 10(3)/microL, reference interval 6.0-14.0 x 10(3)/microL) with an apparent degenerative left shift (segmented neutrophils 1.2 x 10(3)/microL, reference interval 2.5-7.5 x 10(3)/microL; hyposegmented neutrophils 1.8 x 10(3)/microL, reference interval 0.0-0.2 x 10(3)/microL). Serum clinical chemistry results included increased aspartate transaminase, alkaline phosphatase, and gamma-glutamyltransferase activities. A presumptive diagnosis of hepatitis or cholangiohepatitis was made. The horse was treated with antimicrobials and the malaise quickly resolved. However, in a recheck CBC on day 13, the apparent degenerative left shift remained. Further evaluation of the blood smear revealed many hyposegmented granulocytes with coarse mature chromatin and normal cytoplasmic features. On the basis of the microscopic examination, the horse was diagnosed with Pelger-Huët anomaly. The patient's offspring was subsequently also diagnosed with Pelger-Huët anomaly on the basis of blood film examination. Neutrophil, eosinophil, and basophil mean nuclear scores in both affected horses (mare, range 1.5-2.6; offspring, range 1.6-3.2) were lower than those in 2 unrelated Arabian horses (range, 2.8-5.0) and 5 non-Arabian control horses (range, 2.8-5.0). Results of immunophenotyping and phagocytosis/oxidative burst assays via flow cytometry showed no difference in the expression of myeloid-specific or adhesion molecules or in neutrophil function between affected and control horses. This is the second known report of equine Pelger-Huët anomaly, both of which affected Arabian horses.

This experiment was conducted to evaluate if consumption of endophyte-infected fescue alters digital circulation in the distal thoracic limb of the horse and to assess if soundness of the hooves of horses is affected by consumption of endophyte-infected fescue. Twelve American Quarter Horses (mean initial BW 459 ± 31 kg), 6 mares and 6 geldings, were used in this 90-d study that comprised high-endophyte (E+) and low-endophyte (E-) treatment groups. Fescue seed was integrated into the E+ diet at a rate sufficient to bring total ergovaline to 200 μg/kg, and endophyte-free fescue seed was incorporated into the E- diet from d 0 to 90. From d 30 to 60, native prairie hay was replaced with high- or low-endophyte fescue hay, bringing total dietary ergovaline to 280 μg/kg (E+) and 18 μg/kg (E-). From d 61 to 90, fescue seed was ground to decrease particle size. On d 0, 30, 60, and 90, Doppler ultrasonography and thermographic imaging were used to measure the diam. of the medial palmar artery, velocity of blood flow, and surface temperature of the hoof as indicators of digital circulation. Lameness examinations were conducted on the same days. There were no consistent treatment differences observed when evaluating measurements of digital circulation. On d 60, horses in the E+ treatment group showed increased hoof sensitivity in the left limb (P = 0.02). These horses tended to have increased hoof sensitivity when both thoracic limbs were averaged (P = 0.06), and they demonstrated increased lameness during longeing (P = 0.08). Data indicated that mares may have increased digital circulation, regardless of treatment, compared with geldings (P ≤ 0.05). Heavier horses also had greater arterial diam., velocity of blood flow, and hoof temperature than lighter BW horses (P ≤ 0.05) on d 30, 60, and 90 at time points that ranged from 90 to 180 min after feeding. Although horses consuming the E+ diet demonstrated increased lameness, especially on d 60, compared with horses consuming the E- diet, the measures of digital circulation did not support the hypothesis that digital circulation was reduced. Because of observed lameness issues, limiting the access of horses to endophyte-infected fescue may be prudent.

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