Neonatal Isoerythrolysis

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Also known as: Feline Neonatal Isoerythrolysis (FNI) — NI — Equine Neonatal Erythrolysis — ENI

Introduction

Neonatal isoerythrolysis is a disease of humans and domestic animals and has been most commonly observed in newborn cats and horses. Rarely it has also been described in other species following blood transfusions, vaccination or previous pregnancy. The disease is characterised by immune-mediated haemolytic anaemia due to ingestion of maternal colostral antibody directed against surface antigens on neonatal red blood cells. This leads to a type II hypersensitivity reaction causing extravascular and intravascular haemolysis during the first few days of life.

Pathogenesis

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. The Aa and Qa antigens are most strongly antigenic and 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 red blood cell 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. First foals are rarely affected, as a sensitization reaction (usually during an earlier pregnancy) is usually required.

Feline Neonatal Isoerythrolysis

Cats have three main blood types, type A, type B and type AB. Worldwide, the most common blood type in cats is type A and type A is dominant over type B. Queens with type B blood have high levels of naturally occurring alloantibodies to type A blood. Feline neonatal isoerythrolysis (FNI) develops when type B blood mothers mate with type A tomcats producing kittens with type A/B blood. The newborn kittens ingest maternal colostrum containing anti-A antibodies leading to the clinical signs of FNI.

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 and 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. Neurological abnormalities, such as somnolence or seizures, may also occur due to the phenomenon of kernicterus. Excessive amounts of unconjugated bilirubin are able to cross the blood-brain barrier in foals and lead to a bilirubin encphalopathy which can be permenent. Death usually occurs if NI is not diagnosed and treated promptly.

Cats

Although FNI is rare, the mortality associated with the disease is high. Purebred cats are more commonly affected than domestic shorthair cats. Similarly 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 are occasionally found dead within a few hours of the onset of clinical signs. Clinical signs may include failure to thrive, weakness, dark red/brown urine, icterus, and anaemia. Affected kittens may separate themselves from the rest of the litter, stop nursing and appear weak. Signs may vary in severity within a single litter; this is thought to be related to differences in colostral intake. Other features of the disease may include necrosis and sloughing of the tail tip and disseminated intravascular coagulation. Affected kittens rarely survive the first week of life.

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.

Treatment

Treatment in foals depends on rapid identification of sick foals and prevention of suckling the dam for 48-72 hours. If the foal is 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 B blood is preferred. Intraosseous administration of blood is recommended due to the small size of the patient.

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 can be matched to stallions who are also negative. Similarly in cats, the disease is easily prevented if blood typing of cats is peformed prior to breeding.


Neonatal Isoerythrolysis Learning Resources
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Equine Internal Medicine Q&A 09
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Neonatal Isoerythrolysis in cats publications

Neonatal Isoerythrolysis in horses publications


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

Silvestre-Ferreira, A. C., Pastor, J. (2010) Feline Neonatal Isoerythrolysis and the Importance of Feline Blood Types Veterinary Medicine International Volume 2010




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