- Definition
- Pathophysiology
- Systems Affected
- Genetics
- Incidence/Prevalence
- Geographic Distribution
- Signalment
- Signs
- Causes
- Risk Factors
BASICS
Alloimmune-mediated destruction of a neonatal foal's erythrocytes, caused by ingesting maternally (colostral) derived anti-foal erythrocyte antibodies.
- Requires that a naive mare is sensitized to a new RBC antigenic sequence during blood transfusion or exposure to fetal RBCs that express the new antigenic sequence. Exposure may occur at parturition, or secondary to in utero disease such as placentitis
- During a subsequent pregnancy, the foal inherits the same stallion's RBC surface antigen
- At birth, the foal ingests antibody-rich colostrum and absorbs anti-foal RBC antibodies that cause destruction of RBCs
- Antibodies attach to the foal erythrocytes causing hemolysis and/or premature removal of damaged RBCs by the reticuloendothelial system
- Results in anemia
- Hemic/lymphatic/immune—intravascular and extravascular hemolysis leading to anemia, jaundice, and hemoglobinemia
- Renal/urologic—hemoglobinuria leading to pigment nephropathy, acute tubular necrosis, and acute kidney injury
- Cardiovascular—tachycardia from hypoxic anemia
- Nervous—hypoxic anemic shock causing weakness; hyperbilirubinemia causing basal ganglia dysfunction and seizures (kernicterus)
- Hepatic—liver failure development associated with high-volume blood transfusion
- There are many RBC surface antigen factors, and in theory any of these can be involved in NI development. However, Aa in the A system and Qa in the Q system represent the majority of cases
- In mules, the “donkey factor,” which is unique to all donkeys and not horses, is commonly involved
- Among Thoroughbreds and Standardbreds, the prevalence of disease is ≈1–2%
- In mule foals, the prevalence is as high as 10–25%
- Breed variability reflects the frequency of specific genes involved in erythrocyte antigenicity or blood groups found in each breed
- Most horse mares bred to donkey jacks are at high risk (see Risk Factors)
- The antigenic factors are not specific for, or limited to, any particular breed of horse
- Most mule pregnancies are incompatible regarding the blood group factor, “donkey factor,” in which donkeys express and horses do not
- Usually foals born to multiparous mares
- Most foals present during the first 4 days of life (mean range 0–8 days)
The severity of clinical signs varies depending on the magnitude and rate of hemolysis.
- Affected foals are generally healthy at birth and nurse appropriately
- Nonspecific signs such as lethargy begin within hours to days of colostral ingestion and immunoglobulin absorption. These signs may mimic other common neonatal disorders such as septicemia
- Icterus and generalized pallor soon develop
- Mare may have a history of producing jaundiced or NI-confirmed foals from previous pregnancies, especially if the same stallion had sired these foals
- Mare history of previous blood or other blood transfusion
- Lethargy, disinterest in suckling
- Tachypnea; tachycardia
- Pallor (acute stages) often progressing to jaundice
- Pigmenturia (hemoglobinuria)
- Recumbency
- Mild fever is often present
- Systemic signs of hypoxic insult and/or hyperbilirubinemia including colic, melena, and seizure activity (hypoxia; kernicterus)
Maternal production of anti-foal erythrocyte immunoglobulin from exposure of incompatible fetal blood.
- Mares lacking erythrocyte factors Aa and/or Qa are at greater risk (>90%) of producing antibodies to these blood types
- Donkey RBC antigen, “donkey factor”—the risk of an incompatible mating between a horse and a donkey (or the chance of a mare becoming sensitized to this antigen) is 100%. Because clinical NI in mule foals only occurs ≈8–10% of the time, it is suggested that many mule foals may have subclinical NI
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS