Equis ISSN 2398-2977

Foal: failure of passive transfer (IgG)

Synonym(s): FPT

Contributor(s): Cody Coyne, Mark Holmes, Prof Derek Knottenbelt, Ruth Morgan, Graham Munroe, Vetstream Ltd

Introduction

  • Cause: partial or complete failure of passive transfer of immunoglobulins from dam to suckling foal via colostrum during the first 24 h of life    →   less than optimum serum IgG levels (<800 mg/dl).
  • Signs: failure to suck within the first few hours of life, non-specific signs of weakness within 24-48 h, the foal is immunocompromised and has an increased risk of contracting a variety of diseases; seen in up to 24% of normal Thoroughbreds, Standardbreds and Arabians. Infections develop within the first 2 weeks of life, eg neonatal septicemia.
  • Diagnosis: IgG analysis.
  • Treatment: administration of colostrum within 6-12 h of birth or alternatively, transfusion of fresh equine plasma. Treatment for subsequent infection or septicemia.
  • Prognosis: fair to guarded.
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Pathogenesis

Etiology

  • There is no placental transfer of immunoglobulins in the horse.
  • The foal has specialized small intestinal epithelial cells at birth that can absorb large protein molecules such as immunoglobulins. These cells are sloughed off within the first 24 h of life to be replaced with unspecialized epithelial cells.
  • Transfer of maternal immunoglobulins is therefore only possible during the first 24 h of life, decreasing in efficiency after 12 h.
  • Colostrum contains primarily IgG and IgG(T) plus smaller amounts of IgA and IgM; and cytokines, complement, and lactoferrin which provide local protection for the gastrointestinal tract and are important for the complete functioning of the foals immune system.
  • Failure of passive transfer of maternal immunoglobulins for whatever reason   →   an immunocompromised foal which has an increased risk of contracting infectious disease and even death.
  • Foals which fail to suckle by 3-6 h are usually partially immunocompromised; those which fail to suckle until after 12 h usually have complete failure of passive transfer of immunity.

Predisposing factors

General
  • Poor management +/or observation after delivery.
  • Foals born to mares >15 years old.
  • Poor mothering behavior in the mare, especially after prolonged/difficult delivery   Reproduction: foaling management  .
  • Premature lactation   →    reduced/absent colostrum at correct time   Mare: colostrum 01 - prepartum    Mare: colostrum 02 - prepartum  .
  • Agalactia in the mare, decreased immunoglobulins content of colostrum (specific gravity <1.060) or reduced colostrum formation, eg chronic debility during gestation, prolonged gestation, primiparous mare, premature delivery, sick/malnourished mare.
  • Foals delivered after prolonged gestation.
  • Congenital abnormality, eg cleft palate   Hard / soft palate: cleft  .
  • Inability of foal to stand and suckle within 3-6 h of birth for whatever reason, eg limb deformity   Musculoskeletal: angular deformity  ,   Musculoskeletal: flexural deformity  , premature/dysmature foals   Reproduction: prematurity / dysmaturity  .
  • Poor management in the immediate period postpartum, especially after a difficult or prolonged delivery   Reproduction: foaling management  .
  • Sick mare.

Specific

  • Death of the dam, eg after a difficult foaling    Reproduction: dystocia  or Caesarean section    Uterus: caesarean section  , before the foal has suckled.
  • Mares fed on endophyte-infected tall fescue grass/hay.
  • Stress-induced endogenous production of glucocorticoids may increase the rate of maturation of epithelial cells in the foal, thus speeding up the loss of absorptive epithelial cells required for absorption of immunoglobulins.

Pathophysiology

  • Because of the diffuse epitheliochorial placenta of the mare, maternal immunoglobulins are not transferred antenatally to the fetus. They must be transferred passively to the foal from colostrum. 
  • Failure of this passive transfer of immunoglobulins means that the foal does not obtain the IgG, IgA and IgM which are found in normal colostrum.
  • The ability of the foal to absorb immunoglobulins rapidly decreases and then ceases in the first 12 h after birth. This is thought to be due to maturation of absorptive epithelial cells which then become impermeable to macromolecules.
  • Once absorbed, immunoglobulins are catabolized so that by 1-2 months of age serum IgG has reached a low point even in normal foals, which can coincide with slow development of active immunity. This is a vulnerable time for the foal which can be compounded if insufficient passive transfer of immunoglobulins occurred at birth.
  • Inadequate/absent passive transfer of immunoglobulins results in low antibody levels in the foal which is therefore susceptible to infectious disease, debility and even death.
  • The commonest secondary disease is sepsis which may progress to generalized septicemia   Foal: neonatal septicemia syndrome  .

Timecourse

  • The foal is at risk from birth until its own immune system is mature enough to produce immunoglobulins, eg from around 6 weeks of age.
  • Mildly affected foals may survive with no adverse effects if kept in optimal conditions.

Epidemiology

  • All neonatal foals may be affected to a degree.

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.
  • Wong D Met al(2013)Evaluation of a point-of-care portable analyzer for measurement of plasma immunoglobulin G, total protein, and albumin concentrations in ill neonatal foals.JAVMA242(6), 812-819PubMed.
  • Riley Cet al(2012)Feasibility of infrared spectroscopy with pattern recognition techniques to identify a subpopulation of mares at risk of producing foals diagnosed with failure of transfer of passive immunity.Aus Vet J90(10), 387-391PubMed.
  • Hurcombe S D Aet al(2012)Serum protein concentrations as predictors of serum immunoglobulin G concentration in neonatal foals.J Vet Emerg & Crit Care22(5), 573-579PubMed.
  • Korosue K Het al(2012)Correlation of serum IgG concentration in foals and refractometry index of the dam's pre-and post-parturient colostrums: An assessment for failure of passive transfer in foals.J Vet Med Sci74(11), 1387-1395PubMed.
  • Palm Fet al(2011)Primary diagnosis, survival and long-term outcome in young horses with problems in the neonatal period.Pferdeheilkunde27(6), 695-700VetMedResource.
  • Hardefeldt L Yet al(2010)Incidence of transfusion reactions to commercial equien plasma.J Vet Emerg & Crit Care20 (4), 421-425PubMed.
  • Nath L Cet al(2010)Use of stored equine colostrum for the treatment of foals perceived to be at risk for failure of transfer of passive immunity.JAVMA236(10), 1085-1090PubMed.
  • Davis R & Giguere S (2005)Evaluation of five commercially available assays and measurement of serum total protein concentration via refractometry for the diagnosis of failure of passive transfer of immunity in foals.JAVMA227(10), 1640-1645PubMed.
  • Tyler-McGowan C M, Hodgson J L & Hodgson D R (1997)Failure of passive transfer in foals - incidence and outcome on four studs in New South Wales.Aust Vet J75(1), 56-59PubMed.
  • Raidal S L (1996)The incidence and consequences of failure of passive transfer of immunity on a thoroughbred breeding farm.Aust Vet J73(6), 201-206PubMed.
  • LeBlanc M M, Baldwin J L & Pritchard E L (1992)Factors that influence passive transfer of immunoglobulins in foals.JAVMA220, 197-183PubMed.
  • Bernoco M, Liu I K N, Ehlert Cet al(1987)Chemotactic and phagocytic function of peripheral blood polymorphonuclear leukocytes in newborn foals.J Repro Fert Supp35, 599-605PubMed.
  • Riggs M W (1987)Evaluation of foals for immune deficiency disorders.Vet Clin North Am Equine Pract3(3), 515-528PubMed.
  • Koterba A M, Brewer B & Drummond W H (1985)Preventions and control of infection.Vet Clin North Am1, 41-50PubMed.
  • Kruse-Elliot K & Wagner P C (1984)Failure of passive antibody transfer in the foal.Comp Cont Educ6, 702-707VetMedResource.
  • McGuire T Cet al(1977)Failure of colostral immunoglobulin transfer as an explanation for most infections and deaths of neonatal foals.JAVMA170, 1302PubMed.

Other sources of information

  • McClure J T, Miller J & DeLuca J L (2003)Comparison of Two ELISA Screening Tests and a Non-Commercial Glutaraldehyde Coagulation Screening Test for the Detection of Failure of Passive Transfer in Neonatal Foals.In:Proc 49th AAEP Convention.pp 301-305.
  • McClure J J (1993)The immune system.In:Equine Reproduction.Chapter 111. Eds: A O McKinnon & J L Voss. Philadelphia: Lea & Febiger, USA. pp 1003-1013.
  • White S (1989)The use of plasma in foals with failure of passive transfer and/or sepsis.In:Proceedings of the AAEP.pp 215-218.


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