ANATOMY AND PHYSIOLOGY

The equine udder consists of two flattened, cone-shaped glands, each terminating in a short, laterally flattened teat. Each gland contains distinct lactiferous duct systems, organized into lobes and lobules that are incompletely separated from one another by fascial trabeculae extending into the gland from the medial and lateral suspensory ligaments. The cranial lactiferous duct system is the largest. Each teat has two or three orifices, each connecting to its own lactiferous duct system within the gland. The orifice leads to a streak canal that connects to a cistern within the teat. Each teat cistern opens into a gland cistern above the teat in the lactogenic portion of the gland.^2,3 The small size of the teat orifices and the separate lactiferous duct systems associated with each gland complicate intramammary therapy in cases of mastitis.

During the first gestation the mare’s udder changes from two small inguinal skin folds with teats into recognizable mammary glands under the influence of the gestational hormones. Estrogen promotes mammary gland duct development; progesterone facilitates proliferation of the lactogenic epithelial cells and organization of clumps of these cells into mammary alveoli.

The decline in estrogen and progesterone late in gestation is associated with increased prolactin release from the anterior pituitary during the last week of gestation.^1,4,5 It is thought that prolactin release is made possible by suppression of prolactin-inhibiting factor from the hypothalamus. Dopamine is likely the prolactin-inhibiting factor in mares and other animals.¹ Thyrotropin-releasing hormone (TRH) may function as a prolactin-releasing factor.⁴ A rise in prolactin is associated with final development of the mammary gland and the onset of lactogenesis. In addition to prolactin, adrenal corticosteroids, insulin, growth hormone, glucagon, and thyroid hormones play a role in mammary gland development and lactogenesis, although their exact functions in mares are poorly understood.⁴

During nursing, milk ejection occurs as myoepithelial cells surrounding the mammary alveoli contract in response to oxytocin released from the posterior pituitary. Oxytocin is synthesized in the hypothalamus and stored in secretory vesicles within the hypothalamic oxytocin neurons. It is released from nerve terminals in the posterior pituitary. Hypothalamic oxytocin neurons are also stimulated to release oxytocin in response to vaginal stimulation, which occurs during parturition.⁵

Abnormal endocrine stimulation may lead to functional lactational abnormalities such as agalactia, hypogalactia, galactorrhea, precocious lactation, premature lactation, or eclampsia.

AGALACTIA

Agalactia must be differentiated from failure of milk letdown. The udder is slack and not engorged with milk in agalactic mares. On the other hand, some maiden mares with tender edematous mammary glands or nervous mares are reluctant to relax and allow nursing and thus retain milk in the glandular alveoli. Phenothiazine tranquilizers and warm towel massages of the udder are helpful in these mares.^6,7 In addition to their calming effect, phenothiazine tranquilizers stimulate release of prolactin and may augment lactation. Oxytocin (10–20 units) has also been used to help stimulate milk letdown once mares are relaxed.⁸

Agalactia at parturition may actually be delayed onset of lactation. This condition has been described in some maiden and multiparous mares that had small udders and only honey-like mammary secretions.⁶ Many of these mares start lactating within a day or two but some may have decreased milk output. Phenothiazine tranquilizers, udder massage with hot packs, and repeated stripping of secretions from the udder may help speed the onset of lactation. TRH (2.0 mg SC, twice a day for 5 days) has been used successfully in some affected mares.⁹

Agalactia in mares without udder development is typical of fescue toxicity.^6,7,10 Fescue toxicity occurs frequently when pregnant mares are fed fescue infected with the endophyte fungus Acremonium coenophialum. This fungus produces a toxin (thought to be an ergot alkaloid) that suppresses prolactin release.¹¹ Prolactin levels return to normal by 2 to 3 weeks after the toxin is removed.¹¹ The endophyte is spread through fescue seeds. A similar syndrome is seen in mares that ingest Claviceps purpura (ergot).¹² Fescue toxicity is most significant during the last 90 days of gestation in mares. In addition to agalactia, affected mares may experience prolonged gestation and thickened placentas, which are associated with neonatal asphyxia. Mares grazing infected fescue may also experience reduced fertility.¹³ The mares experiencing prolonged gestation frequently have a history of udder development at their expected due date, but the udder involutes and they are agalactic by the time of delivery.

Treatment of fescue-induced agalactia has been aimed at overcoming suppression of the release of prolactin and possibly TRH. TRH, as well as phenothiazine tranquilizers, has been used as described in some cases.¹⁴ More recently, the use of the dopamine receptor antagonist perphenazine (0.3 mg/kg PO twice a day) has been popular for treating fescue-related agalactia.¹⁵ However, some mares experience severe side effects when treated with this drug, including sweating, colic, hyperesthesia, ataxia, and posterior paresis.^16,17 The dose of perphenazine should be calculated based on the patient’s weight, and treatment must be carefully monitored and suspended if adverse effects become evident. The selective DA₂ dopamine receptor antagonist domperidone (1.1 mg/kg PO once a day) prevents the signs of fescue toxicosis without adverse side effects.¹⁷

Prevention of fescue toxicosis rather than treatment should be the primary objective. The current recommendations include the following: (1) maintain mares on nonfescue pasture when practical; (2) dilute the toxin by overseeding pastures with a palatable legume every 2 years so that 20% of the forage is a legume; (3) kill the infected fescue with herbicides and tillage and reseed with noninfected endophyte-resistant strains of fescue that are not allowed to develop seed heads for at least 2 years; and (4) remove mares from fescue during the last 90 days of gestation and provide nonfescue forage or hay.⁷ Prevention of toxicosis may also improve fertility, neonatal survival, and foal growth in addition to eliminating agalactia.

Agalactia may be encountered in mares that have established lactation but prematurely cease milk production. Insufficient energy intake to support lactation must be considered, especially in mares that have experienced excessive weight loss during lactation. If the ration is adequate, the stress of pain or disease must be ruled out as the cause of cessation of lactation. Attempts to reinitiate lactation are unsatisfactory.⁶