Etiology

• Gestational length in the mare is normally very variable, with the average being 334 days normal variation from 320-360 days.
• Gestation might be considered prolonged if >360-380 days.
• Nonetheless, prolonged gestation in the mare (unlike other species) very rarely results in fetal oversize and consequent dystocia   Reproduction: dystocia  .
• Causes of genuine prolonged gestation are unknown, but might (not proven) relate to arrest of fetal development during early pregnancy or a poor quality endometrium which has resulted in reduced supply of nutrients.

Often, a mare which an owner reports as being overdue is not: the covering/ovulation dates are unknown or incorrect. Do not be fooled into inducing these mares as the outcome will be disastrous.

Mares tend to be quite consistent within themselves in terms of gestational length, ie if a mare went 350 days last year she is likely to do so again and that is normal for her.

• In the majority of cases of prolonged gestation, even up to 400 days, the foal is not born because it is not ready to do so, and most are normal when they do eventually arrive.
• Male foals typically have a gestational length 2-3 days longer than female foals.

Pathologic prolonged gestation can occur with fescue toxicosis   Toxicity: fescue grass   in mares grazing on fescue grass.

• Tall fescue grass is frequently infected with the endophyteAcremonium coenophialum, which produces ergot.
• Alkaloids that cause severe adverse effects in pregnant mares and impair reproductive function and agalactia through stimulation of D2-dopamine receptors.

Pathophysiology

Pathologic prolonged gestation assocated with fescue toxicosis

• Endophyte toxins cause a decrease in serum prolactin and progesterone in broodmares.
• Mares which have fescue toxicosis fail to exhibit the normal late gestational surge in progestins.
• Maternal serum relaxin concentrations are also reduced in cases of fescue toxicosis.
• Foals exposed to ergopeptine alkaloids during late gestation have decreased plasma levels of immunoassayable progestins, cortisol, T4, and tri-iodothyronine (T3).
• Fetal cortisol is an important contributor to readiness for birth.
• Toxic disruption of the pathways for steroidogenesis and lactogenesis results in inhibition of the pathways which normally control parturition.
• Foal mortality is due to dysmaturity and hypoxia, resulting from poor placental blood flow.