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
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.