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| ==Pathogenesis== | | ==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. |
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| ===Feline neonatal isoerythrolysis=== | | ===Feline neonatal isoerythrolysis=== |
| [[Blood Groups - Cat|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. | | [[Blood Groups - Cat|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. |
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− | ===Equine neonatal isoerythrolysis===
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− | 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.
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| ==Clinical signs== | | ==Clinical signs== |
| ===Horses=== | | ===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. Death usually occurs if NI is not diagnosed and treated promptly. | + | 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. |
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| ===Cats=== | | ===Cats=== |
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| ==References== | | ==References== |
− | *Mair, T. S. (1998) '''Equine Medicine, Surgery and Reproduction''' ''Elsevier Health Sciences''
| + | 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''
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− | *Silvestre-Ferreira, A. C., Pastor, J. (2010) '''Feline Neonatal Isoerythrolysis and the Importance of Feline Blood Types''' ''Veterinary Medicine International Volume 2010''
| + | Norsworthy, G. D., Crystal, M., Grace, S. F. (2006) '''The Feline Patient''' ''Wiley-Blackwell'' |
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| + | 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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| [[Category:Materno-Fetal Immunity|E]] | | [[Category:Materno-Fetal Immunity|E]] |