Poisoning in the feed room
Although rare, feed-associated poisoning in horses occurs, sometimes with fatal consequences.
Now that cooler weather has come back and pasture grass is becoming scarce, it's time for owners to increase the amounts of hay, grain and processed feeds given to their horses. Usually, this means simply buying feed from a local mill or feed store, stacking the bags in the feed room and hay in the barn and putting carefully measured amounts into each horse's feed pan. And that's exactly what happens just about every day.
Occasionally, however, an owner will pour feed into a pan and put hay into a rack—and inadvertently begin the process of poisoning and possibly killing a horse.
While feed-associated poisonings are relatively rare, they still occur, and often with serious consequences. Multiple animals in one location usually are affected. Severe and often permanent pathology or death can occur, and the economic and psychological loss can be great.
Sometimes, it's easy to uncover the source of the poisoning, while other times it's nearly impossible. In late 1997, the Arizona Veterinary Diagnostic Laboratory Newsletter contained a report of eight horses that died at a training facility within a 36-hour period.1 The horses were fed only alfalfa hay, and their water was from a well that also was used for the household, although no other animals or people on the farm were affected. The particular toxin in that reported case—monensin—was eventually identified from stomach contents, but the source of the poisoning was never uncovered.
It's beneficial to periodically review the clinical signs and causes of feed-associated poisonings in horses because these scenarios are possible. Moreover, long-term poisonings often present with vague clinical signs and problems that often are hard to diagnose or are easily confused with other conditions.
This type of intoxication involves specific feed additives used as growth-promoting agents in cattle and as coccidiostats in poultry and other birds. The major drugs in this category are monensin, lasolacid, laidlomycin, narasin and salinomycin.2
Monensin (Rumensin—Elanco) is produced as an additive for pelleted or bulk feeds for ruminants. The problem, however, is that horses are extremely sensitive to ionophore poisoning. The LD50 for monensin in horses is 2 to 3 mg/kg, whereas cattle and poultry can tolerate much higher levels without issue (cattle LD50 = 20 to 34 mg/kg; poultry LD50 = 90 to 200 mg/kg). Ionophores become a problem when higher-than-acceptable concentrations are found in horse feed, and this typically occurs when horses come into contact with poultry or cattle feed or because there's a problem with contamination at the feed mill.2
The drugs in the ionophore class inhibit sodium and potassium ion transport across cell membranes. Mitochondrial failure, decreased ATP activity and decreased calcium ion availability eventually lead to muscle fiber hypercontractility, cellular necrosis and, eventually, total system failure and death. Clinical signs can occur within 12 to 24 hours after consuming an acutely toxic dose. Chronic low-level ingestion may prolong the onset of clinical signs for days or weeks and will lessen their severity.2
Horses that are acutely poisoned may experience colic, intermittent sweating, ataxia, muscle weakness, tachycardia, myoglobinuria, polyuria followed by oliguria, respiratory distress and recumbency. Death is possible less than 24 hours after ingestion. Horses surviving the initial intoxication, or horses with chronic exposure, may show progressive signs of congestive heart failure due to irreparable cardiac muscle damage, as well as poor growth and poor weight gain. A number of cases of sudden death in the weeks or months after intoxication have been reported.2
Because of the primary action of these drugs, cases of ionophore poisoning usually appear as damage to the myocardium, skeletal muscle and kidneys. Hematologically, increases in creatine phosphokinase, lactate dehydrogenase, serum glutamic oxaloacetic transaminase and alkaline phosphatase activities, as well as increased blood urea nitrogen and creatinine concentrations, can occur. Calcium and potassium concentrations may be slightly decreased, but, generally, there are few major blood concentration alterations at the early stages of this condition.2
Similarly, few gross postmortem lesions are present in horses that die less than 24 to 36 hours after acute poisoning. Even horses that have been chronically exposed show only subtle lesions. Pale streaking of skeletal and cardiac muscle can be noted along with ascites, hydrothorax, hydropericardium and pulmonary congestion. Ionophore poisoning is diagnosed by identifying ionophore content in the stomach. Thin-layer chromatography is used to make this identification and can be used to link ionophores to feed products.2
No specific treatment for ionophore poisoning is known, but supportive care includes oral administration of activated charcoal in acute cases to block intestinal absorption. Although treatment success is rare, aggressive fluid therapy supports cardiac and kidney function, and correction of electrolyte abnormalities with supplemental potassium is advised.2
Because most ionophore poisonings involve contaminated or poorly mixed feeds, it's imperative that horse owners deal with reputable feed companies and that quality assurance programs be in place and enforced in all mills that produce equine nutritional products. There is thought to be a fungus-produced ionophore that can cause toxicosis in pastured horses if weather conditions are favorable. Most of these cases have been in cool, wet weather, and research is ongoing to determine the exact source of this particular toxin.
Wet-weather conditions also are associated with another potentially deadly feed-associated condition in horses. Mycotoxins are poisons produced by molds in living and stored plant materials such as grains and hay. These toxins are heat- and chemical-stable, so once feed materials are contaminated, it's nearly impossible to remove this toxic threat. Adding to the problem: Most molds in equine feeds don't affect palatability, so horses readily consume the contaminated feeds.
Three mycotoxins—aflatoxin, vomitoxin (also referred to as deoxynivalenol or DON) and fumonisin—have been recognized by the U.S. Food and Drug Administration as being so potentially damaging to horses that there are regulatory and advisory limits for them in horse feeds. While all these mycotoxins can potentially produce medical problems, fumonisin is of particular importance because it's the cause of equine leukoencephalomalacia (ELEM), or moldy corn poisoning.
ELEM is caused by Fusarium moniliforme, a fungus that tends to grow best on corn that's stressed during the growing season. Thus, excessively wet or dry conditions favor ELEM development. Just as the case with ionophore poisoning, horses are especially sensitive to fumonisin toxin and can show signs of poisoning after exposure to concentrations as low as five parts per million.
Clinical signs of ELEM are incoordination and dullness or reduced response to stimuli. Affected horses can then progress to aimless wandering, circling, head pressing, blindness, recumbency and paralysis. Extensive deterioration of the cerebral cortex produces this array of neurologic signs, and most horses with ELEM die, usually in the first 24 to 48 hours.
Some horses affected by ELEM develop liver disease rather than neurologic issues. These horses show weight loss, edema, unthriftiness and hemorrhage. Blood work will show increased bilirubin concentrations and increased serum hepatic enzyme activities such as gamma-glutamyltransferase and bile acids. If this liver damage becomes chronic, the result is a horse in poor condition that loses weight, even though it's generally fed more than an adequate diet.
Treatment for ELEM is supportive, with some horses being maintained in slings throughout the recumbency period. If these horses are not permitted to lie down, they seem to respond better, and numerous support systems (e.g., The Becker Sling—Häst, hast.net/rescue-equipment.htm; UC Davis Large Animal Lift—Large Animal Life Enterprises, largeanimallift.com) have been developed to help with these cases. Still, many horses that survive ELEM develop long-term neurologic problems.
Avoiding mycotoxin seems to be the best plan, but it's also the most difficult approach. Rapid and accurate detection tests are available and can be done (in fact, many companies already use these systems) to help identify and avoid loads of grain that are contaminated with mycotoxins. These tests are expensive and represent a "major investment," according to Jeff Katelan of Pennfield Feeds. "Our No. 1 priority is to have a top-notch quality-control process."
Pennfield Feeds relies on these highly effective, rapid-detection chemical tests to identify and eliminate tainted ingredients before they enter the various processing plants. Various companies also use buffered mold inhibitors. These products are sprayed onto the corn kernels to reduce the possibility of mold growth. Companies committed to purchasing high-quality, safely produced grains tend to produce high-quality feeds that have been checked for molds and other contaminants before they arrive on a farm. That said, there is no substitute for owner vigilance. Each bag of grain and flake of hay should be inspected—both visually and by smell.
What veterinarians can do
Veterinarians can help educate clients about potential problems with contaminated or toxic feeds. Good knowledge of clinical signs of these conditions is also important because cases of unthrifty, weak or unusually thin horses (despite normal to increased feeding) should be investigated, and it's wise to keep chronic poisoning cases high in your index of suspicion.
Dr. Marcella is an equine practitioner in Canton, Ga.
1. Diagnostic update: equine. Ariz Vet Diagnostic Lab Newsletter 1997;2(4):2.
2. Ionophore poisoning in horses. Ariz Vet Diagnostic Lab Newsletter 1997;2(4):1-2.