Prematurity vs Dysmaturity

Not all foals are born equally developed. Some can be born premature with normal development, and others are born “on time” but incomplete development. This article will help explain the difference between Prematurity and Dysmaturity

Regardless of the species, when something goes wrong during the gestation period, a cascade of consequences may be seen after birth. Prematurity is pretty self-explanatory and means a baby that is born “early” or before a certain normal minimum date of gestation. Dysmaturity on the other hand, means any birth that appears clinically premature but with normal duration of gestation. There are also a few instances where babies can be born “postmature”, but these are much less common. The most accurate way of defining these foals is to categorize them together as examples of “gestational immaturity”.

What defines a gestationally immature foal? This is actually a very difficult question to answer because “normal” length of gestation is variable, and therefore “normal” is a very vague term in equine reproduction. Furthermore, foals that are born after shorter gestations can be normal, whereas those with “full-term” gestation can be dysmature, meaning that more than just time is involved in determining the quality of foal development.

Clinical Signs

Certain clinical signs have been identified to consistently present in premature or dysmature foals. In addition to meconium staining due to stress in utero, below are other signs associated with prematurity in foals:

Physical signs: small and low birthweight, domed forehead, silky haircoats, floppy ears and lips, minimal muscling and even “emaciated” appearance with generalized weakness, slow to stand and hyperextension of the fetlocks (dropped fetlocks), orange discoloration of the tongue and oral mucosa. Physical examination may also reveal low body temperature, respiratory distress with hypoventilation, and a persistently elevated heart rate.

Behavioural signs: Poor suckle reflex after birth or may develop dummy syndrome within 2 days.

Clinical Pathology: Reversed lymphocyte to neutrophil ratio (>2:1), lymphocytosis, neutropenia, low plasma cortisol despite normal-high ACTH (associated with adrenocortical insufficiency, Relative Adrenal Insufficiency or CIRCI), venous acidosis, hypoglycemia, hypoglobulinemia.

Developmental defects: Respiratory distress (low PaO2, high PaCO2, acidosis) due to poor lung capacitation and V/Q mismatch; low blood pressure; inefficient colostral immunoglobulin absorption and increased likelihood of failure of transfer of passive immunity (FTPI, previously known as “failure of passive transfer”); intestinal immaturity leading to dysmotility (meconium and fecal impactions) and dysbiosis.

Dysmature foals can present with the hallmarks of prematurity, but with variable severity, e.g., cortisol is not as low as a premature foal, but ACTH continues to increase after birth, or tendon laxity but normal haircoat. Therefore, dysmaturity may be difficult to recognize as only some parts of the foal may be immature, and the severity of the immaturity may vary by organ system.

Prevention

Fetal maturation in horses occurs later than in other species – starting around 300 days gestation, well into the last trimester. The adrenal gland grows dramatically in size and begins producing cholesterol-derived hormones (including cortisol) which starts the body’s cascade to maturation. Measurements of plasma spikes in cortisol levels found that they only occurred in the last few days before birth! Anything that disrupts the fetus’ access to nutrients, placental enzymes, or hormone metabolism, will inevitably delay the maturation of the foal.

In some instances, the cause of prematurity is evident: placental insufficiency, toxin exposure, infection or early placental separation, inappropriate exposure to oxytocin or prostaglandins, maternal illness, etc. In Saskatchewan, Canada, an “outbreak” of hypothyroidism in pregnant mares led to prolonged gestation and dysmaturity in foals. Tall fescue has also been associated with excessive gestational length and dysmaturity in foals. Unfortunately, many other instances of prematurity or dysmaturity seem to be a surprise to the breeder and attending veterinarian.

To further complicate the discussion, some maternal conditions may stress the fetus causing premature maturation of the HPA axis, e.g., placentitis, leading to a shortened gestation length, but producing a normal and fully developed foal.

The best advice offered is to avoid the known causes of dysmaturity, ensure good nutrition and avoid disease in mares. But despite our best efforts, dysmaturity in general, is unavoidable.

If you suspect that your foal or patient is suffering from dysmaturity, contact your veterinarian or CLASS for further guidance.