Fescue Toxicosis: Part II

Week before last we discussed fescue toxicosis. Since then, you've tested your hay and pasture, and you've been advised that your hay is infected with endophyte. Your mare has been grazing it throughout her gestation, and she's entered her last leg of pregnancy. What can you do?Week before last we discussed fescue toxicosis. Since then, you've tested your hay and pasture, and you've been advised that your hay is infected with endophyte. Your mare has been grazing it throughout her gestation, and she's entered her last leg of pregnancy. What can you do?

Story originally posted by: Michael Lowder, DVM, MS

Week before last we discussed fescue toxicosis. Since then, you've tested your hay and pasture, and you've been advised that your hay is infected with endophyte. Your mare has been grazing it throughout her gestation, and she's entered her last leg of pregnancy. What can you do?

First, remove your mare from the affected pasture and notify your veterinarian. The veterinarian will decide if and when prophylactic medication should be administered. This is largely determined by the mare's stage of gestation.





The potential problems of fescue toxicosis include:
* Depressed levels of prolactin and progesterone
* Prolonged gestation
* Agalactia
* Abortion
* Thickened placental membranes
* Premature separation of the placenta
* Dystocia
* Placental retention

Fungal egopeptine alkaloids released from endophyte-infected fescue inhibits prolactin and progesterone (hormones) secretion in the pregnant mare. This hormonal alteration can have direct effect upon udder development, lactation, placentation, and parturition (foaling).

Prolactin is involved in the initiation of the birthing process. Without the prolactin signal, the mare's body does not recognize that it's time to foal. In cases of prolonged gestation, your veterinarian may need to induce parturition. This is not without complications, and the veterinarian must be present to assist in case of problems.

Progesterone is involved in the maintenance of pregnancy. Mares feeding upon infected hay may require frequent monitoring of progesterone concentrations. Supplemental progesterone administration to the end of gestation may be indicated in some mares.

Fescue toxicity is frequently associated with early fetal loss and embryonic absorption, however abortion and stillborn foals are a real possibility in mares that consume endophyte-infected fescue. Some mares do not show abnormal signs prior to aborting their foals. Abortion is the delivery of a dead or dying fetus before 290 days of gestation.

Agalactia (absence of milk at birth) is a major concern for the horse owner as the "first milk" contains colostrum. As mentioned in part one, the colostrum is essential for insuring that the foal receives the antibodies necessary for protection against disease. These antibodies provide immunity for the foal during the first two months of life.

Some mares will 'leak' milk for several days to weeks prior to birthing and not have any milk for the foal. A newborn foal needs approximately 8 oz of colostrum every hour for the first 8-10 hours of life (around 5 pints of colostrum). If the foal does not receive colostrum, your veterinarian will administer oral or intravenous plasma that will help the foal fight disease. Colostrum provided by a "colostrum bank" may be another alternative.

After immunity status is acceptable, a milk replacement or cow's milk + 20 grams/liter of glucose can be given to non-nursing foals (20-25% of the foal's weight).

Premature separation of the placenta results in the potential for neonatal asphyxia inside the uterus. The horseman will notice a red bag projecting from the vulva of the mare. Frequently, the mare is not straining. Prompt attention is essential.

Thickened placenta can be another potentially dangerous side-effect of fescue consumption as this often leads to retained fetal membranes. Retained placenta can have devastating results. Affected mares usually develop endotoxemia and subsequent laminitis. It is imperative that your veterinarian treats your mare within three to four hours of birthing.

Along with the prolonged gestation and thickened placenta, affected horses will frequently have a difficult birth (dystocia). Once active parturition commences, there is usually about a thirty-minute window to get the foal out alive. Correcting a dystocia is not for the novice horseman and should only be attempted by your veterinarian. The potential for serious injury to both person and horse is great.

What medication is commonly used to treat and manage mares affected with fescue toxicosis? Domperidone is the treatment of choice.

Domperidone is commonly used in horses (and their human counterparts as well) to treat lactation problems. Marketed under the trade name of Equi-Tox', this drug stimulates normal prolactin and progesterone production, therefore eliminating the problem of agalactia. However, it does not guarantee that the milk let down has any colostrial antibodies in it. Your foal's blood should be tested by your veterinarian.

Domperidone is given at 1 cc per 200 pounds of body weight by mouth once daily. The big question is when to administer the drug. This all depends upon the individual.

If the mare does not have any udder development, then I would suggest you give the medication about 10-14 days prior to the expected foaling date. In addition, I would give the medication for three to five days post foaling to ensure the mare is milking well.

If the mare has some udder development, then I would wait until about three days prior to foaling (use one of the commercial foaling test kits to help you determine when the mare is going to foal). Try not to use the drug too far in advance of foaling as you may stimulate milk letdown and loss of colostrum.

Fescue toxicosis is a costly disease of the equine industry, but it can be managed with success if the horseman is progressive in his management plan and is aware of the possible complications associated with consumption of endophye-infected tall fescue grass hay.

Read Part 1.


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