Equis ISSN 2398-2977

Immunology: neonatal isoerythrolysis

Contributor(s): Cody Coyne, Prof Derek Knottenbelt, Graham Munroe

Introduction

  • Cause: blood group incompatibility between foal and dam   →   a hemolytic syndrome mediated by absorbed colostral maternal antibody directed against antigens expressed as the foal's erythrocytes (alloantibodies).
  • Incidence: blood groups Aa and Qa are the most dangerous; newborn foals (<72-96 h) born to multiparous mares. A primiparous mare can produce an affected foal if she has been pre-sensitized by blood transfusion   Blood: transfusion  .
  • Signs: lethargy, pale mucous membranes, jaundice, intolerance to stress/exercise, sudden death.
  • Diagnosis: demonstrate alloantibodies against foal RBCs in dam's serum or colostrum.
  • Treatment: corticosteroids, supportive care, blood transfusions   Blood: transfusion   (rarely plasma phoresis).
  • Prophylaxis: withhold colostrum, administer oral donor colostrum, blood-type all breeding mares and stallions prior to mating, identify increasing alloantibodies in at-risk mares.
  • Prognosis: guarded to good, depending on dose of mare's colostrum ingested.

Pathogenesis

Etiology

  • Blood group incompatibility between foal and dam.
  • Many blood group antigens are not strongly immunogenic under normal conditions of exposure.
  • Blood group antigens Aa and Qa are highly immunogenic and the majority of cases are related to these equine blood types.
  • Mares negative for Aa and Qa are most at risk (19% Thoroughbreds, 17% Standardbreds).
  • Aa generated alloantibodies are potent hemolysins and usually   →    most severe clinical signs.

Predisposing factors

General
  • Multiparous mares.
  • Primiparous mares with early placental damage.

Specific

  • Any mare having received a prior sensitizing blood transfusion.

Pathophysiology

  • Hemolytic syndrome in newborn foals caused by blood group incompatibility between foal and dam.
  • Mediated by maternal antibodies, absorbed from colostrums that have binding avidity for antigens expressed by the foal erythrocytes.
  • Foal must inherit from sire and express an erythrocyte antigen that is not possessed by the mare. Blood group Aa is the most common.
  • The mare must become sensitized to the erythrocyte antigen and produce antibodies to it before it will appear in her colostrum.
  • There is some dispute regarding the sensitization mechanism:
    • Transplacental hemorrhage during previous pregnancy involving foal with the same incompatible blood factor, ie placental abnormalities, eg placentitis, or at parturition.
    • Prior sensitizing blood transfusion.
    • Transplacental contamination and sensitization in the current pregnancy (possible although an anamnestic response is generally necessary to generate pathogenic quantities of alloantibodies).
  • Horses lacking factor Ca frequently produce anti-Ca antibody which appears to confer some degree of protection against sensitization to other factors by causing a rapid elimination of foreign cells from the circulation.
  • After sensitization antibodies are concentrated in the colostrum during the latter part of gestation   →   ingestion by foal in first 24-48 h of life.
  • Immunoglobulins are absorbed   →   coat foal's erythrocytes   →   premature RBC removal from circulation by macrophages or lysed intravascularly via complement.
  • The amount and type of antibodies absorbed determines the speed of development and severity of subsequent clinical signs, eg Aa antibodies and mares sensitized in the previous pregnancy with the same antigen.

Timecourse

  • 24-72 h (rarely longer/slower).

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Finding E & McSloy A (2011) Neonatal isoerythrolysis and other immunological diseases of foals. UK Vet 16, 10-12 VetMedResource.
  • Boyle A G, Magdesian K G & Ruby R E (2005) Neonatal isoerythrolysis in horse foals and a mule foal: 18 cases (1988-2003). JAVMA 227 (8), 1276-1283 PubMed.
  • MacLeay J M (2001) Neonatal isoerythrolysis involving the Qc and Db antigens in a foal. JAVMA 219 (1), 79 PubMed.
  • Whiting J L et al (2000) Neonatal isoerythrolysis. Comp Cont Educ Pract Vet 22 (10), 968-975 VetMedResource.
  • Traub-Dargatz J L et al (1995) Neonatal isoerythrolysis in mule foals. JAVMA 206 (1), 67-70 PubMed.
  • McClure J J et al (1994) Characterization of a red blood cell antigen in donkeys and mules associated with neonatal isoerthyrolysis. Anim Genet 25 (2), 119-120 PubMed.
  • Zaruby J F et al (1992) Neonatal isoerythrolysis in a foal, involving anti-Pa alloantibody. Equine Vet J 24 (1), 71-73 PubMed.
  • Bailey E et al (1988) Equine neonatal isoerythrolysis - evidence for prevention by maternal antibodies to the Ca blood group antigen. Am J Vet Res 49 (8), 1218-1222 PubMed.
  • Becht J L et al (1985) Hematology, blood typing, and immunology of the neonatal foal. Vet Clin North Am Equine Pract (1), 91-116 PubMed.
  • Becht J L et al (1983) Evaluation of a series of testing procedures to predict neonatal isoerythrolysis in the foal. Cornell Vet 73 (4), 390-402 PubMed.
  • Becht J L et al (1983) Experimental production of neonatal isoerythrolysis in the foal. Cornell Vet 73 (4), 380-389 PubMed.
  • Bailey E (1982) Prevalence of anti-red blood cell antibodies in the serum and colostrum of mares and its relationship to neonatal isoerythrolysis. Am J Vet Res 43 (11), 1917-1921 PubMed.
  • Stormont C (1975) Neonatal isoerythrolysis in domestic animals - a comparative review. Adv Vet Sci Comp Med 19, 23-45 PubMed.
  • Osbaldiston G W et al (1969) Equine isoerythrolysis - clinical pathologic observations and transfusion of dam's red blood cells to her foal. Can J Comp Med 33 (4), 310-315 PubMed.

Other sources of information

  • Morris D D (1998) Diseases of the haemolymphatic system. In: Equine Internal Medicine. Eds: Reed S M & Bayly W M. W B Saunders. pp 564-566.
  • Vaala W A (1990) Neonatal anaemia. In: Equine Clinical Neonatology. Eds: Koterba A M, Drummond W H & Kosch P C. Lea & Febiger, USA. pp 571-588.


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