References
Failure of passive transfer in foals
Abstract
Foals are born with a naive immune system, and rely upon the ingestion and absorption of immunoglobulins from the dam's colostrum to obtain passive immunity. Failure of passive transfer (FPT) is the most common immunodeficiency disorder in the horse and is associated with an increased risk of infectious disease and mortality. Routine screening is recommended, to allow early detection and treatment. Management of failure of passive transfer is dependent on the age of the foal at the time of diagnosis, but primarily involves intravenous plasma administration or the administration of colostrum (orally or via nasogastric intubation). Given the association between IgG concentration and clinical outcome, early detection and management of FPT are important in reducing morbidity and mortality in neonatal foals.
Failure of passive transfer (FPT) in neonatal foals is the most common immunodeficiency disorder in the horse, occurring in between 3–24% of newborn foals (Sellon, 2000; Giguère and Polkes, 2005). It is defined as the failure of the foal to ingest or absorb adequate immunoglobulin from colostrum, and is associated with an increased risk of infectious disease and mortality (McGuire et al, 1975; Sellon, 2000). Therefore detection and treatment of failure of passive transfer is important in reducing morbidity and mortality in neonatal foals.
Although a large proportion of immune system development occurs during gestation, the foal is considered immunologically naive at birth. Both IgM and IgG proteins are evident in fetal serum prior to 200 days gestation (Perryman and McGuire, 1980) and the fetus is capable of generating antigen-specific immune responses (Tallmadge, 2016). However, in utero the fetus is protected from exposure to pathogens, and it is rare for a primary immune response to occur prior to birth. Therefore, although the newborn foal is considered immunocompetent, meaning that it can initiate an immune response, it is immunologically naive as it has not yet been exposed to pathogens and developed the appropriate antigen-specific responses (Mealey and Long, 2018). In addition, the epitheliochorial structure of the equine placenta means that maternal immunoglobulins are unable to pass to the foal via the placenta and foals are essentially born agammaglobulinaemic. As a consequence, foals lack immediate immune protection following birth, and the ingestion and absorption of immunoglobulins in colostrum from the dam (Figure 1) is therefore critical (Giguère and Polkes, 2005). This passive immunity provides the foal with protection at birth, and should be sufficient to cover the foal for up to the first 3 months of life, at which point endogenous antibody production should reach protective levels.
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