Equine Hyperthermia Part I

Summer is the primary season for many equine competitions, and intense exercise coupled with a high ambient temperature can quickly put horses in the danger zone for heat-related illness. Before going into greater detail, it is necessary to define some basic terms related to thermoregulation—or the regulation of body temperature. The normal rectal temperature of the horse ranges from 99 to 100.5°F. The horse's natural thermoregulatory mechanisms are capable of maintaining this normal body temperature except when overwhelmed by severe circumstances, such as disease or intense exercise in hot climates.

Hyperthermia (heatstroke) occurs when the core body temperature starts to rise because these regulatory systems can no longer effectively cool the horse. Heatstroke is a serious condition that can be fatal if not dealt with quickly. The most common clinical signs include an elevated respiratory rate of 40 to 50 breaths per minute (normal at rest is 8 to 16) that does not slow when at rest, a heart rate of 80 or more beats per minute (normal at rest is 36 to 44) that does not slow down after a few minutes of rest, a rectal temperature of over 103°F, lethargy, and/or profuse sweating or an absence of sweating altogether. Some horses may suffer from a condition called anhidrosis, a disorder where the horse does not sweat normally. These horses are especially prone to hyperthermia if not managed appropriately. The specific cause of anhidrosis is unknown; however, it is thought that there is a physiological defect at the level of the sweat gland that inhibits sweating. Your veterinarian can perform diagnostic tests that can confirm this condition if you suspect that your horse might be afflicted.

Hyperthermia most often occurs as a result of inadequate physical conditioning (poor fitness), extreme hot and humid conditions, a weakened thermoregulatory system, or a combination of the three. The heat index (HI), which is the temperature (in °F) plus humidity (%), gives a means of assessing the danger that extreme environmental conditions pose to horses performing intense exercise in such an environment. If the HI is less than 130 (e.g., 90°F and 20% relative humidity), then the horse's built-in cooling mechanisms are usually capable of dissipating the excess body heat generated during exercise. However, when the HI is greater than 150 (e.g., 100°F and 60% or higher relative humidity), the horse will probably need assistance in order to prevent heatstroke. Owners should proceed cautiously when, or seek alternatives to, exercising horses in situations where the HI is greater than 170 or the relative humidity is above 75% since these conditions severely diminish the effectiveness of the horse's thermoregulatory systems.

In order to maintain a normal body temperature, the horse must dissipate heat that is produced as a result of normal body processes (e.g., digestion and muscular exercise). There are four main mechanisms that allow for this: evaporation, conduction, convection, and radiation. Evaporation (sweating) is the most important cooling mechanism for the horse because it removes heat as water (sweat) changes from a liquid to a gas (water vapor). Conduction occurs when heat is transferred from a hotter object to a cooler object by direct contact, such as using an ice pack on a sprain. Convection is heat exchange that occurs when an air current moves over the skin to pick up heat and/or moisture from the skin and carry it away. Radiation occurs when infrared rays carry heat from a hotter object to a cooler object. The heat that we feel from the sun is an example of radiation. We will describe the practical significance of these mechanisms later in this guide when we discuss means of relieving heat stress.

References: Jason Turner and Sandra Barraza, New Mexico State University

Be Prepared for Hurricane Season

Now that we are into Hurricane Season and have experienced our first tropical storm of the year, it’s a good time for a reminder of  the many steps we can take to prepare our pets and farm animals for the season.  County and State Emergency Services, American Red Cross, and County Animal Response Teams across the state are is committed to helping residents with these preparations.

Please make sure your animals have been vaccinated for the most common disease concerns of this area.  Having vaccinations will not only be helpful if the were to need sheltering, but also if they were to get loose during or after a storm. Your veterinarian should be your first source for advice as to what is needed, but here is a list of what he or she may include for your horse as well as your pets: 

Dogs:     Distemper/Parvovirus combination, kennel cough, rabies, and

               heartworm prevention.

Cats:      Distemper/Upper Respiratory Viral Combination, rabies,

               Leukemia

Horses:  Influenza, Rhinopneumonitis, Eastern Equine Encephalomyelitis, tetanus, rabies, strangles, West Nile Virus, and a current (yearly) negative Coggins Test for Equine Infectious Anemia

In addition to having your animal vaccinated, here is a checklist of other items to consider and prepare for in your disaster plan:

1.     Keep a collar and tag on animals that should normally wear collars. Have a halter with your horse’s name on it and your phone number. Small tags similar to those for pets can be used.

2.     Identify several possible locations where you can take your animals, should you have to evacuate.

3.     Start a buddy system with someone in your neighborhood, so they will check on your animals during a disaster, in the event you aren’t home.

4.     In addition to your regular supply of animal food have at least a week’s supply on hand to be used during a disaster.

5.     You should have at least a week’s supply of water in storage at all times for your animals.

6.     Take several pictures of the animals and keep these pictures with your important insurance papers that you would take if you needed to evacuate.

7.     Talk to your vet before a disaster strikes to see if he/she has a disaster plan.

8.     Know where the animal shelters or animal rescue organizations are in your area.

Written by Eileen A. Coite

Prussic Acid Poisoning in Forages

Eve H. Honeycutt, Livestock Agent

Lenoir and Greene Counties

Adapted from an article by C. L. Rhykerd and K. D. Johnson, Purdue University

As you are gearing up for grazing a warm season pasture, you should keep be aware of what can happen to some of these warm season grasses under certain environmental and man-made conditions. 

Sudangrass, forage sorghums and sorghum-sudangrass crosses are the plants that can cause the most problems.  While these are summer forage crops, if they are left in a pasture during times of frost livestock can consume them and suffer from the prussic acid.  Death can result from prussic acid poisoning, most commonly when livestock have fed on plants that are either very young, stunted by drought or frosted.

Also present in the sorghums is a material called emulsion, which under certain conditions can react with other chemicals present to form prussic acid (also referred to as hydrocyanic acid). If plants are damaged, such as by freezing, chewing or trampling, the emulsion-dhurrin reaction is enhanced, freeing sufficiently larger quantities of poison (cyanide) to cause a potentially hazardous condition.

Prussic acid is extremely poisonous. A concentration greater than 0.1 percent of dry tissue is considered highly dangerous.

Signs of Prussic Acid Poisoning

The signs of prussic acid poisoning appear suddenly--i.e., within 15-20 minutes after animals consume the "tainted" forage. These visual symptoms include staggering, labored breathing, spasms and foaming at the mouth. Affected animals then often lie prostrate and thrash about. Treatment must be administered quickly to prevent death.

 Factors Affecting Prussic Acid Content In Plants

Species. The vegetative portion of all sorghums contains prussic acid. Generally, however, prussic acid content in sudangrass is about 40 percent less than in most other sorghums. As a group, the sorghum-sudangrass hybrids have more prussic acid than sudangrass. Crosses have now been developed, however, that contain extremely low quantities. As a precaution, plant those hybrids known to be lower in prussic acid.

Johnsongrass, shattercane and sorghum almum could contain dangerous levels of prussic acid, and may be hazardous in pure stands or as contaminants in sudangrass or sorghum-sudan cross pastures. Fence rows contaminated with these weedy species might also be hazardous. Plants of the Prunus genus, such as wild black cherry trees (P. serotina), chokecherry (P. virginiana) and pin-cherry (P. pennsylvanica) are potential problems and should be eliminated from grazing areas.

Pearl millet, another summer pasture crop, does not contain toxic levels of prussic acid.

Plant Parts:  In the sorghums, leaf blades normally contain higher prussic acid levels than leaf sheaths or stems, the heads are low in prussic acid, and the seeds contain none. Upper leaves have more prussic acid than older leaves. Tillers and branches ("suckers") have the highest levels, because they are mostly leaves and not stalk material.

Maturity. Highest prussic acid levels are reached before the boot stage. As plants mature, the stalks make up a greater proportion of the plant, causing prussic acid content in the total forage to decrease. However, the hazards associated with poisoning may decrease only slightly with age if animals selectively graze those plant parts that are high in prussic acid.

Drought. Severe drought is probably the most common cause of prussic acid poisoning. Drought-stricken plants are hazardous to feed because they are mostly leaves. Sorghum grazed or fed as green chop in the heart of a drought may retain high levels of this poison.

Freezing. Cold weather may kill only the tops of sorghum plants, leaving the lower portion alive. The unbound prussic acid in this forage does not decline until wilting begins. The forage is usually considered safe to pasture or feed as green chop 5-6 days after a killing frost. New shoots emerging from unkilled portions of the plant are apt to be high in prussic acid. Therefore, this forage should not be used until that new growth reaches a height of 2 feet.

Fertilizer. The excellent yield potentials of sudangrass, sorghum-sudangrass crosses and forage sorghums can only be attained by applying high rates of nitrogen fertilizer (e.g., 200 pounds per acre or more). However, if high N rates are applied to soils deficient in phosphorus and potassium, prussic acid levels usually increase.

Therefore, to reduce the hazard of prussic acid poisoning, maintain phosphorus and potassium levels according to soil test report recommendations. Also consider split-applying heavy N rates into 2-4 applications.

Herbicides. 2,4-D may cause prussic acid content to increase in forages. The effect may last several weeks.

 Safe Feeding of Potentially Hazardous Forages

Pasture. The risk of prussic acid poisoning can be reduced by feeding ground cereal grains to the animals before turning them out to graze. Carbohydrates in the grain tend to inhibit the emulsion from hydrolyzing dhurrin, which causes prussic acid formation.

Deaths on pasture are partially caused by the animal selectively grazing leaves and shoots. These plant parts may contain 2-25 times more prussic acid than stems. Animals may also avoid frost-damaged leaves and shoots, grazing instead the young suckers lower on the plant that could contain lethal levels of prussic acid. Therefore, if new shoots develop after a frost. the crop should not be grazed until this new growth is 2 feet tall.

In most cases, grain sorghum stubble can be safely pastured because cold weather is likely to have killed the plants before they are grazed However, the stubble should be observed carefully for dangerous suckers that may develop after the main stalks have been killed. Sorghum that has wilted and dried 5-6 days after being killed by frost is considered safe for grazing.

Hay. The prussic acid content of sorghum hay decreases as much as 75 percent while curing and is rarely hazardous when fed to livestock.

Treatment For Prussic Acid Poisoning

If large quantities of forage high in prussic acid are consumed rapidly, death can occur within a few minutes. However, the usual situation is that the animals consume smaller quantities of the forage over a longer period, causing first salivation, then a gradual increase in respiratory rate, followed by staggering, falling, severe convulsions and finally death within 45 minutes. Generally, animals that survive 2 hours after the onset of symptoms will recover.

Obviously, immediate treatment by a veterinarian is necessary to save the animals. Treatment includes administering sodium nitrite and sodium thiosulfate.

Poisoning caused by prussic acid is somewhat similar to nitrate poisoning. In fact, the treatment for prussic acid involves the inducement of a degree of nitrate poisoning (methemoglobinemia) by administering sodium nitrite. Simultaneous treatment with sodium thiosulfate converts the newly formed cyanmethemoglobin to thiocyanate and hemoglobin, which permits the blood to again transport oxygen normally.