Agreement of Temperatures Measured Using a Non-Contact Infrared Thermometer With a Rectal Digital Thermometer in Horses.

Evaluating the body temperature of horses is an essential tool for monitoring horse health and biosecurity in groups of horses. Temperatures of horses and foals are determined most often using rectal thermometry. Rectal thermometry has limitations that include safety considerations for horses and humans. Thus, we investigated the agreement between a noncontact infrared thermometer (NCIT) and a rectal digital thermometer in 142 horses and 34 foals. For each horse and foal, measurements using the NCIT were collected from the forehead (n = 2) or neck (n = 1) and with a rectal digital thermometer (n = 1). Although the NCIT demonstrated good reliability (i.e. repeatability of measurements), a large negative bias (nearly 2°F (-16.7°C) in adult horses and >3°F (-16.1°C) in foals) was observed between readings from the NCIT and the rectal thermometer in healthy horses. Although horses with febrile illness were not included in the study, our results indicate that the large and inconsistent bias observed with the NCIT indicates that these devices will not be a suitable substitute for rectal thermometry for obtaining valid estimates of core body temperature in horses.

Acute hepatic steatosis: a helpful diagnostic feature in metallic phosphide-poisoned horses.

Metal phosphides, particularly zinc and aluminum phosphide, occasionally poison horses and other equids following their use as rodenticides and insecticides. Grain-based aluminum phosphide baits are used to control rodents such as prairie dogs. The clinical course in intoxicated horses is short (<24-48 h), and animals may be found dead. Hepatic lesions caused by phosphine poisoning are not well described. Laboratory confirmation depends on detecting phosphine gas in gastric contents. Eight horses and a mule were exposed to zinc phosphide used to control prairie dogs on a Wyoming ranch. Three of 9 exposed equids developed some combination of sweating, ataxia, anxiety, and colic; 2 died acutely, and 1 recovered. A diagnosis of zinc phosphide was made by detecting phosphine in stomach contents from a horse and a mule. The liver was pale and swollen in the affected horse, which died after a clinical course of ~12 h. Other changes were generalized congestion and edema, pulmonary edema, and acute cerebrocortical edema. There was diffuse hepatocellular microvesicular steatosis. Similar histologic lesions were present in 7 equine livers from 2 previously published episodes of metallic phosphide poisoning. Older lesions (>24 h of clinical signs) had centrilobular hepatic necrosis with congestion and a mixture of microvesicular and macrovesicular steatosis. Phosphine poisoning should be considered in horses that die acutely and are found to have steatosis, either with or without hepatocellular necrosis.

Phosphine intoxication following oral exposure of horses to aluminum phosphide-treated feed.

CASE DESCRIPTION: 66 horses were potentially exposed to phosphine (a gas) 14 hours after being fed a pelleted ration treated with aluminum phosphide. CLINICAL FINDINGS: 28 horses had clinical signs of profuse sweating, tachycardia, tachypnea, pyrexia, ataxia, seizures, and widespread muscle tremors. Clinically relevant laboratory findings included hypoglycemia and high plasma concentrations of lactate and ammonia and activities of gamma-glutamyl transpeptidase, aspartate aminotransferase, and alkaline phosphatase. At least 4 horses had signs consistent with hepatic encephalopathy. Necropsy findings included petechial and ecchymotic hemorrhages in multiple organs, widespread vascular congestion, hepatic lipidosis, and neuronal necrosis in the brain. Phosphine was detected in the stomachs of the 3 horses tested. TREATMENT AND OUTCOME: On the farm, horses were treated with gastric lavage followed by administration of di-tri-octahedral smectite, atropine, fluids, and sedatives. Six horses were hospitalized, and lactated Ringer's solution and flunixin meglumine were administered IV. Additionally, 10% dextrose, corn syrup, and di-tri-octahedral smectite were administered PO. Twenty-seven horses died within 2 days after exposure. Two survivors (1 without clinical signs of toxicosis) made a complete recovery. CLINICAL RELEVANCE: Progression of clinical signs in affected horses in this report was rapid, with few treatment options available, leading to a high case fatality rate. Fumigation with aluminum phosphide is commonly performed to eliminate weevils and other insects from stored grains. When appropriate precautions are used during fumigation, risk to livestock is typically minimal.