How to Prevent the Leading Cause of Death in Neonatal Foals: Opinion

The leading cause of illness in neonatal foals upon admission in our clinic is bacterial infection (septicemia due predominantly to mixed infection with gram positive and gram negative organisms). The second leading cause of problems are related to birth asphyxia. These two conditions have been listed by Kentucky foal post mortem studies as the leading cause of death. This is despite a number of studies indicating passive transfer failure and low serum IgG are the cause of most of these neonatal deaths.

However, a number of people have begun to question that low IgG is the sole cause of this problems. Additionally, our efforts to raise IgG by various means seem to have not eliminated the problem of septicemia over the last 10-15 years. Well-conducted studies such as Balwin et al. (1991) have indicated that low IgG per se is not a health risk factor and several studies have indicated that foals with only 200 mg/dl IgG at 24 hours of age don’t get sick on some farms.

Leo Jeffcott (1974) demonstrated the indiscriminate active absorption of large molecules by the "open" gut shortly after birth. Unfortunately this avenue as a potential major route of exposure of the foal to pathogens has been overlooked. Specialized cells line the newborn gut and will non-specifically ingest various large molecular weight compounds (via pinocytosis) and not just immunoglobulin. Additionally, the lack of tight junctions between gut barrier cells allowed >70,000 MW molecules to freely pass into the lymphatics and circulate between cells. When these cells are used up, the gut assumes its normal structure and no further absorption of large molecules can take place.

Early on in foal medicine the umbilicus was considered the route of infection for most foals with septicemia and septic arthritis. Numerous studies have shown the umbilicus is not involved in the majority of foal septicemias. We developed the hypothesis that delayed gut closure and exposure to bacteria during udder seeking or due to delayed feeding or nursing and subsequent environmental licking or ingestion of bacteria by the newborn foal is the risk factor and source of bacteria for most septicemias in foals. Early administration or ingestion of colostrum may be associated with reduced illness in foals because of early (rapid) gut closure and prevention of absorption of bacteria across the gut wall. Thus a foal with high IgG could be a marker for wellbeing based on rapid and early feeding prior to bacterial access to the foal across the open gut. Additionally, this would explain healthy foals that stood and nursed vigorously but did not become ill despite low serum IgG. Delayed nursing and early exposure to pathogens (prior to any colostrum) are the key factors in risk of infection in this hypothesis.

This means that conditions that may be associated with delayed gut closure, such as neonatal maladjustment syndrome (birth hypoxic encephalopathy), prematurity, dystocia, musculoskeletal problems, weak at birth foals, twins, would have significant incidences of septicemia, which they certainly do. Good management for preventing infections are clean stalls, clean mares, factors that aid early ingestion of colostrum and short term post birth antibiotics in the newborn.

II. Method for Preventing Septicemia

1. Keep the mare in facilities in which foaling will take place to allow production of antibodies to pathogens within the area. Clean foaling stalls twice daily and disinfect stalls prior to use. Wash the mare before foaling.
2. Immediately following delivery prevent the foal from contacting the mare until steps C and D are completed.
3. Wash the mare after foaling with large volumes of soap and water to remove bacteria around the perineum, udder and rear quarters where the foal may lick during udder seeking. Dry the mare.
4. Milk the mares cleaned mammary gland of 2-4 oz of colostrum (preferably greater than 1060 specific gravity) and bottle feed the foal, prior to the foal rising, upon obtaining a suck reflex. Use colostrum from colostrum bank if necessary.
5. If the foal is weak, tube feed the foal within 1 hour of birth with 6-8 oz of colostrum or, if none available, use mare milk replacer or, if none available, use cow’s milk. In orphan foals continue feeding from a bottle or pan until 10% of body weight is fed. Feed when the foal is hungry.
6. In any foals without an observed birth and for foalings in an unclean area without the above precautions, I recommend veterinarians prescribe and begin antibiotic therapy within 8 hrs of birth and treat for 48 to 72 hours only. Longer treatment may produce antibiotic resistance and should be reserved for ill foals. The choice of antibiotic therapy will vary with the area. Post birth antibiotics have been a routine part of management on stud farms in the UK for the past 40 years and the incidence of sepsis is much lower than the United States.

For those of you concerned about aminoglycoside antibiotics in foals, monitor serum creatinine or urinalysis if you so desire. I find aminoglycosides safe in foals that are kept hydrated; that is most important. In a bright, alert foal receiving short-term antibiotics, this should be no trouble.
These are my opinions. Keep doing what works for you. If bacterial infections in neonates are a problem, consider these observations.