Agalactia, Dysgalactia, and Nutrition of the Postpartum Mare

Successful initiation and continuation of lactation in the postpartum mare depends on normal hormonal activity and a lack of any inhibitory influences on the mare. Impediments to adequate lactation include underlying systemic disease of the mare, pathology of the mammary gland, malnutrition, and diminished neonatal vigor reducing normal suckling activity.

1. Introduction

Lactation places considerable nutritional and physiological demands on the mare. The nursing mare must provide sufficient milk to allow the foal to achieve approximately 45% of its mature weight at weaning.¹  At the same time, to maintain a yearly foaling interval, the mare must be sufficiently recovered from the demands of gestation to allow rebreeding within the first month of lactation if so desired. Numerous management decisions and medical conditions can lead to either complete failure of lactation or insufficient milk production to meet the needs of the growing foal.

2. Anatomy, Physiology, and Endocrinology of Lactation

The equine mammary gland is composed of four separate functional gland units, two on either side of the inguinal midline. Each pair (collateral) is served by a single teat; however, each of these has two teat canals and cisterns, with separate duct and alveolar systems for each gland unit. Secretory epithelial cells line the alveoli, with myoepithelial cells encasing the alveoli. The alveoli empty milk into progressively larger ducts that converge into cisterns above the teats. Groups of alveoli cluster together to form lobules. In turn, these cluster together to form lobes, which is collectively known as a lobuloalveolar construct.

The mammary gland undergoes a cycle of growth and differentiation of tissue after every mating that results in a pregnancy. Growth of the mammary gland tissue continues to some degree into the lactation phase, with this being followed by a period of involution. In most species, growth of the lobuloalveolar tissue is stimulated by high levels of both estrogen and progesterone during pregnancy, with the latter inhibiting milk production.²

The mare differs from other species in that circulating progesterone levels are relatively low during the third trimester of gestation. Progesterone entering the maternal circulation from the fetoplacental unit is metabolized to the 5α-pregnanes.^3,4 The most bioactive metabolite is thought to be 5α- pregnane-3,20-dione, which is found in high concentration and has demonstrable affinity for the progesterone receptor.⁵ Estrogens are represented by the inactive equilin and equilenin during late pregnancy,⁶ with estradiol 17-β rising before parturition.^7,8

The trigger for initiation of lactation is thought to be the progestagen decrease and prolactin increase at the end of lactation. Prolactin has a major role in the initiation of lactation in the mare. Levels suddenly increase in the last days of gestation and peak at parturition,⁹ remaining elevated for up to 3 months postpartum.¹⁰ Prolactin is not required for the continuation of lactation once established,¹¹ even though suckling raises maternal prolactin concentrations.¹² Prolactin receptors are present in mammary tissue and increase in number during gestation and after parturition.

Lactation in the mare peaks 30 to 60 days postpartum. During this time, average daily production of 15 L per day in Thoroughbred mares and 12 to 13 L per day in Quarter Horse mares is achieved.^13,14 Therefore, daily consumption by the foal is in the range of 21% to 25% of body weight on average over this period.¹⁵

As the demand for milk by the foal decreases, the mammary gland undergoes a progressive involution. Weaning occurs at relatively high milk production, causing increased intramammary pressure due to accumulation of milk. This increased pressure along with suspected inhibitors in the milk further decreases production. Secretory tissue is subsequently replaced with connective and adipose tissue.²

3. Composition of Milk

Synthesis of milk within the mammary gland of the mare is similar to that in ruminants.¹⁶ Components are sourced from body reserves, feed materials, and de novo synthesis within the mammary gland epithelium. Throughout lactation, a slow decline occurs in energy, total solids, protein, ash, and minerals; however, lactose concentrations increase.¹⁷

Lactose is derived from glucose absorbed from the small intestine. Fatty acids are produced from acetate and 3-hydroxybutryrate sourced from carbohydrate digestion in the large intestine. Unsaturated C18 fatty acid is supplied either directly from the diet or from body reserves.¹⁸ Protein in milk is derived from the highly synthetic cells of the mammary epithelium. Most research has centered on the effects on the foal after variations in mare protein intake; however, research in mares has found that an increase in dietary crude protein up to 14% of the diet increased milk production.¹⁹

Compared with human and bovine milk, mare milk is of lower fat and hence energy content. Mare milk and human milk have a similar sugar content, whole protein, and electrolyte content, in contrast to the increased electrolyte content of cow’s milk, making that a less suitable replacement for mare milk.¹⁶

Antimicrobial defense in mare’s milk seems to be due mainly to the presence of lysozyme (as in human milk) and, to a lesser degree, to lactoferrin, which is preponderant in human milk.^20,21 A dynamic state of immunity exists during the prepartum and the immediate postpartum periods. Prepartum, colostral immunoglobulin accumulates in preparation for transfer of immunity to the neonatal foal. The mammary gland does not produce immunoglobulin G but instead concentrates it from the vascular supply. Lysozyme remains elevated in milk well after parturition, remaining active in the foal intestine and providing protection after cessation of macromolecule absorption. This elevated level of lysozyme may also protect the mammary gland against infection.²²

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