Colostrum. It's what's for dinner

 

The newborn foal is born without antibodies to enable it to fight disease.  Unlike other animals, the placenta is structured in such a way that antibodies from the mare’s blood cannot be transferred to the fetus.  While able to mount an immune response, it will be easily overwhelmed as there are no ready-made bullets in the gun to fire back.  Mother Nature’s answer: colostrum.

It’s all down to getting sufficient good quality colostrum onboard as soon as possible.

What is so magical about colostrum?  In addition to having higher concentrations than mare’s milk of proteins, fats and sugars, it contains immunoglobulins (Ig) derived from the mare aimed at pathogens the newborn foal is likely to encounter in the first period of extrauterine life.

Insufficient or failure of passive transfer (FPT) of maternal immunoglobulins, primarily IgG, to the neonatal foal predisposes the foal to potentially life-threatening illnesses.  Sufficient protection against these infectious diseases is attained when serum IgG concentrations in a newborn foal are above 800mg/dL. Partial FPT occurs when serum IgG concentrations are between 400 and 800 mg/dL, and failure of passive transfer occurs when serum IgG concentrations are less than 400 mg/dL after 24 hours post-partum. The frequency of FPT occurrence in newborn foals is between 3% and 20%, and several factors have been thought to influence the passive transfer of IgG.

These cut-off points are not random, rather they are the result of retrospective studies looking at populations of foals separated into sick and septic groups.  In one study of 87 Thoroughbred foals, FPT was found in 9/87 (10%)1.  Of these, 7/9 (78%) foals acquired infections requiring therapy. Twelve (14%) foals had partial FPT with 3 (25%) developing an infection requiring therapy. The remaining 66 (76%) foals considered to have adequate colostral transfer had only 2 (3%) develop infections. The failure of colostral IgG transfer was attributable to inadequate suckling or insufficient colostral IgG concentration.

Even with all care and attention, some foals remain at risk for FPT despite apparently consuming an adequate amount of colostrum within the ideal window of time (6-8 hours of life). Colostrum can be easily checked for quality by a Brix refractometer.  A reading of 23 or greater indicates excellent Ig content.  Despite this, absorption varies between neonates making it difficult to provide adequate Ig by oral intake alone in some cases.

Colostrum supplementation may be needed.  This can be stored colostrum if fresh is not available due to non-production or loss of the mare. Provision of colostrum to foals at risk from antibodies in the birth mare’s colostrum against the foal’s red blood cells (neonatal isoerythrolysis, NI) is another indication. Good quality colostrum can be frozen and maintain antibacterial properties up to two years.2 Stored colostrum has been shown to be perfectly adequate in raising Ig levels in the neonate.3 Do not microwave and avoid excessive heat during thawing. Refrigerate any excess for up to 12 hours. Ensure the colostrum is tested for antibodies that may cause NI.

What can be done when colostrum is not available from any source? In another study foals diagnosed with FPT received either 1 or 2 liters of equine plasma with 7000mg/dL protein content.  Treated foals did not contract severe disease, whereas 10% of affected and unsupplemented foals developed a sepsis score > 11, had a bacteriologically positive blood culture, or developed disease requiring hospitalization within the first 2 months of life. However, none of the nine foals with FPT that received plasma experienced severe disease. Where FPT was considered partial, foals displayed an increased susceptibility to severe disease (P < 0.001) when compared with normal foals.4

Achieving an adequate level of IgG in the foal is too important to miss. Check the serum IgG (the major Ig present in colostrum) levels of every foal within the first 24 hours.

 

1.    McGuire TC, Crawford TB, Hallowell AL et al. Failure of colostral immunoglobulin transfer as an explanation for most infections and deaths of neonatal foals. J Am Vet Med Assoc 1977;170:1302-1304.

2.    Honour P and Dolby JM. Bacteriostasis of Escherichia coli by milk. III. The activity and stability of early, transitional, and mature human milk collected locally. J Hyg (Lond) 1979;83:243-254.

3.    Nath LC, Anderson GA, Savage CJ et al. Use of stored equine colostrum for the treatment of foals perceived to be at risk for failure of transfer of passive immunity. J Am Vet Med Assoc 2010;236:1085-1090.

4.   Tyler-McGowan CM, Hodgson JL, Hodgson DR. Failure of passive transfer in foals: incidence and outcome on four studs in New South Wales. Austral Vet J 1997;75:56-59.

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