Equine Agalactia Study Guide

Overview and Clinical Importance

Agalactia refers to the complete absence of milk production in a postpartum mare. This condition represents a critical emergency in equine reproduction because foals are born immunologically naive (agammaglobulinemic) and depend entirely on colostrum ingestion within the first 12-24 hours of life for passive transfer of immunoglobulins. The absence of lactation puts the foal at immediate risk for failure of passive transfer (FPT), sepsis, and death.

Agalactia must be differentiated from failure of milk let-down (psychological inhibition of oxytocin release) and hypogalactia (insufficient milk production). While all three conditions compromise foal nutrition and immunity, their underlying pathophysiology and treatment differ significantly. On the NAVLE, agalactia is most commonly associated with fescue toxicosis in the southeastern United States.

Mammary Gland Anatomy and Lactation Physiology

Equine Udder Anatomy

The equine udder comprises one pair of mammae located in the inguinal region. Each mamma is drained by two independent mammary ductal trees, resulting in two orifices per teat. This anatomical arrangement differs from cattle (one ductal system per mamma) and represents an important consideration during intramammary treatment.

The mammary gland is organized into terminal duct lobular units (TDLUs) similar to the human breast. Each TDLU comprises lobules of milk-secreting alveoli supported by distinct zones of intralobular and interlobular collagenous stroma. The alveolar epithelium is bilayered with luminal secretory cells and basal myoepithelial cells that express alpha smooth muscle actin for milk ejection.

Hormonal Regulation of Lactation

Lactation is a complex process involving three main phases: mammogenesis (mammary development), lactogenesis (onset of milk secretion), and galactopoiesis (maintenance of milk production). The hypothalamic-pituitary axis plays a central role through regulation of prolactin secretion.

Etiology of Agalactia

Fescue Toxicosis: The Primary Cause of Equine Agalactia

Epidemiology and Pathophysiology

Tall fescue (Festuca arundinacea) is a cool-season perennial grass covering over 35 million acres in the eastern and central United States, with highest prevalence in the transition zone. Approximately 90% of tall fescue pastures are infected with the endophytic fungus Neotyphodium coenophialum (formerly Acremonium coenophialum).

The endophyte lives between plant cells and produces ergopeptine alkaloids, with ergovaline constituting approximately 90% of the toxic alkaloids. Ergovaline content greater than 200 ppb is considered toxic. The fungus provides drought resistance, pest tolerance, and improved persistence to the grass, which is why infected fescue is so prevalent.

Mechanism of Toxicity

Ergot alkaloids function as dopamine D2 receptor agonists. This produces three primary pathophysiological effects:

• Prolactin Suppression: Binding to D2 receptors on pituitary lactotrophs inhibits prolactin secretion, preventing mammary development and lactogenesis
• Vasoconstriction: Ergot alkaloids cause peripheral vasoconstriction, impairing uteroplacental blood flow and contributing to placental thickening
• Hormonal Disruption: Alterations in progesterone, estrogen, and relaxin concentrations disrupt normal preparturient hormonal changes

Clinical Signs of Fescue Toxicosis in Mares

Diagnosis

Clinical Assessment

Diagnosis of agalactia is based on clinical presentation and history. Key diagnostic steps include:

• Physical Examination of Udder: Agalactic mares have a slack, poorly developed udder that is NOT engorged with milk. This differs from failure of milk let-down where the udder is tense and full.
• History of Fescue Exposure: Determine if mare has grazed tall fescue pastures or been fed fescue hay in the last trimester. Geographic location in the transition zone is significant.
• Medication History: Check for pergolide administration (PPID treatment) that was not discontinued before foaling.
• Assess for Other Fescue Signs: Prolonged gestation (greater than 345 days), poor udder development approaching expected foaling date, lack of relaxation of pelvic ligaments.

Diagnostic Testing

Treatment

Dopamine Antagonist Therapy

Treatment of fescue-induced agalactia centers on dopamine D2 receptor antagonists to block the inhibitory effects of ergot alkaloids on prolactin secretion. These drugs competitively antagonize the dopamine receptors, restoring prolactin release and enabling lactation.

Domperidone Treatment Protocol (Equidone Gel)

• Timing: Start 10-15 days before expected foaling date (EFD = 340 days after breeding)
• Dose: 0.5 mg/lb (1.1 mg/kg) PO once daily
• Duration: Continue until 5 days post-foaling (longer if mare still not producing adequate milk)
• Adjust if dripping milk: If mare begins dripping colostrum prematurely, reduce or adjust dose
• Monitor IgG: ALL foals from domperidone-treated mares should have IgG tested - FPT may occur even without obvious milk dripping

Foal Management in Cases of Agalactia

Immediate Priorities

When a mare is agalactic, the foal is at immediate risk for failure of passive transfer (FPT) because it cannot obtain colostral immunoglobulins. Foals are born agammaglobulinemic (without circulating antibodies) due to the epitheliochorial placenta that prevents in utero antibody transfer. The foal has only a 12-24 hour window to absorb intact immunoglobulins across the intestinal epithelium before gut closure occurs.

Classification of Passive Transfer Status

Treatment of Foals with FPT

If foal is less than 12-18 hours old:

• Administer high-quality colostrum (donor colostrum or frozen-thawed colostrum with IgG greater than 3000 mg/dL)
• Dose: 250-300 mL every 1-2 hours for first 6 hours, total 1.5-2 L
• Can be given via bottle or nasogastric tube

If foal is greater than 18-24 hours old:

• Oral colostrum is ineffective due to gut closure
• Administer hyperimmune plasma IV (1-2 L for a 50 kg foal)
• Initial infusion rate: 0.5 mL/kg over 10-20 minutes, then 30 mL/kg/hr if no reaction
• Recheck IgG 12-24 hours post-transfusion

Lactation Induction in Nurse Mares

When agalactia cannot be resolved and a foster dam is needed, lactation can be induced in non-pregnant mares using hormonal protocols. This creates a nurse mare to provide nutrition and species-appropriate socialization for the orphan foal.

Standard Lactation Induction Protocol

• Days 1-7: Progesterone 150 mg + Estradiol 17-beta 50 mg IM once daily
• Day 7: Prostaglandin F2-alpha 5 mg IM (to cause luteolysis and progesterone decline)
• Days 1-10: Sulpiride 500 mg (1 mg/kg) IM twice daily OR Domperidone at twice standard dose
• Days 4-7: Begin milking 5-7 times daily when udder shows significant development
• Continue sulpiride for 30 days: After foal adoption, continue dopamine antagonist treatment for total of 30 days

Important: Induced lactation does NOT produce colostrum - the foal must receive colostrum from another source. Approximately 80% of treated mares will lactate successfully.

Prevention of Fescue Toxicosis

Pasture and Nutritional Management

• Remove mares from infected fescue: Remove pregnant mares from endophyte-infected tall fescue pastures 60-90 days before expected foaling date
• Test hay and pasture: Submit samples for ergovaline testing, especially during rapid growth periods (spring and fall)
• Dilute with legumes: Incorporate 20% or more legumes (clover, alfalfa) into fescue pastures to dilute toxin exposure
• Novel endophyte fescue: Consider replanting with novel endophyte fescue varieties that do not produce toxic alkaloids but retain plant hardiness
• Avoid seed heads: Ergovaline concentrates in seed heads - clip pastures or avoid grazing when seed heads mature

Pergolide Management in PPID Mares

Mares receiving pergolide for pituitary pars intermedia dysfunction (Cushing's disease) must have the medication discontinued 2-4 weeks before expected foaling to allow normal mammary development and lactation. Consider starting domperidone as pergolide is discontinued to counteract any residual dopaminergic effects.

Memory Aids for NAVLE

FESCUE = Foaling Emergency Syndrome Caused by Unknown Ergots

• Failure of udder development
• Extended gestation
• Separation of placenta (premature/red bag)
• Can't predict foaling (no waxing/milk calcium)
• Unviable or dysmature foal
• Ergovaline is the toxin

Dopamine Antagonists = "Don't Stop Prolactin" (DSP) - Domperidone, Sulpiride, Perphenazine block dopamine from stopping prolactin release