Neonatal Isoerythrolysis

Description

Neonatal isoerythrolysis is a disease of humans and domestic animals and has been observed in newborn cats, horses, pigs, cows and rarely in dogs. It is characterised by immune-mediated haemolytic anaemia due to ingestion of maternal colostral antibody directed against surface antigens on neonatal red blood cells. The maternal antibodies develop in response to exposure to specific foreign blood group antigens during previous pregnancies and unmatched transfusions.

Pathogenesis

Feline neonatal isoerythrolysis

Although feline neonatal isoerythrolysis (FNA) is rare, the mortality associated with it is high. Cats have two main blood types, type A and type B. Cats with type A red blood cell antigens have weak anti-B antibodies, and cats with type B red blood cell antigens have strong anti-A antibodies. FNI develops when type B blood mothers mate with type A tomcats. FNI affects the type A, kitten, born from a B blood type mother by receiving anti-A antibodies when it ingests maternal colostrum.

Equine neonatal isoerythrolysis

In foals, the condition results when a foal inherits red blood cell antigens (which the dam does not have) from its sire. Previous exposure of the mare to these antigens during a previous pregnancy or whole blood transfusion leads to the mare producing alloantibodies to the foal's red blood cells. At birth the foal ingests large numbers of antibodies in the colostrum, leading to severe haemolytic disease. During pregnancy however, the foal is unaffected because blood and antibodies are unable to cross the placenta.

Clinical signs

Horses

Affected foals appear clinically normal at birth, and clinical signs develop from several hours up to a week after ingestion of colostrum. Foals with NI usually become progressively weak, lethargic and depressed develop icterus, tachycardia and tachypnoea. Although the signs are not pathognomonic for NI, a foal displaying haemoglobinuria and icterus born to a multiparous mare should be strongly suspected to have the disease. If the foal becomes severely hypoxic, seizures may occur. Death usually occurs if NI is not diagnosed and treated promptly.

Cats

In a similar way to affected foals, kittens are born and nurse normally and clinical signs develop within a few hours or days. Signs may be variable and kittens may be found dead within a few hours of the onset of clinical signs. Affected kittens rarely survive the first week of life. Clinical signs may include failure to thrive, weakness, dark red/brown urine, icterus, and anaemia. Signs may vary in severity within a single litter; this is thought to be related to differences in colostral intake.

Affected kittens may separate themselves from the rest of the litter, stop nursing and appear weak. Other features of the disease may include necrosis and slouging of the tail tip and disseminated intravascular coagulation.

Diagnosis

To definitively diagnose the condition in horses, a minor cross-match is performed using the foal's red blood cells and the mare's serum. A positive agglutination indicates a diagnosis of NI. In cats, diagnosis is performed on the basis of clinical signs and blood typing of the queen and kitten. If FNI is suspected all kittens should be blood typed; this can be achieved using placental blood following delivery.

Treatment

Treatment in foals depends on rapid identification of sick foals and prevention of suckling the dam for 48-72 hours. If foals are less than 24 hours old at the time of diagnosis, it should be muzzled and fed supplemental milk. As the foal's intestine becomes impermeable to absorption of colostral antibodies by 24 hours of age, prevention of nursing until the foal is 30 hours of age should be sufficient. The mare should be milked every two hours during this period to ensure continued milk production. Separation of the mare and foal is not recommended as this may lead to unnecessary stress of the compromised foal.

A blood transfusion should be considered if the anaemia is severe (PCV less than 15%) or the foal is weak and shocked. The best donor of blood for transfusion is the dam, but this means that the serum containing the alloantibodies must be removed ('washing' of the red blood cells). This is achieved by mixing the mare's blood with saline and performing repeated centrifugation. If washed red blood cells from the mare are not available, blood from an acceptable blood-typed donor horse may be used.

Affected kittens should be removed from the queen for a period of 24 hours and fed milk replacer or fostered onto a lactating queen with blood type A. After this period, intestinal permeability to antibodies is greatly reduced and the kittens may be returned to the original queen. Supportive management of hypoglycaemia and hypothermia may be necessary. Severely affected kittens may require a blood transfusion, preferably with Oxyglobin if available. If this is not possible, washed type A blood is preferred.

Prevention

The disease in horses is prevented by ensuring that mares are blood-typed before being mated. Mares who are negative for the blood antigens known for causing disease (primarily Aa, Qa, Qc and Ua) can be matched to stallions who are also negative.

References

• Mair, T. S. (1998) Equine Medicine, Surgery and Reproduction Elsevier Health Sciences
• Norsworthy, G. D., Crystal, M., Grace, S. F. (2006) The Feline Patient Wiley-Blackwell