Failure of Passive Transfer of Immunity
Failure of passive transfer (FPT) occurs when calves do not absorb sufficient immunoglobulins. Only small amounts of IgG and IgM to unknown antigens are made by the fetus, and they offer no protection against disease.
It has been estimated that approximately 31% of preweaning mortality events occurring in the first 3 weeks of life can be attributed to FPT.46 The problem in mixed-source calf-rearing properties is significantly worse.25 A high percentage (19.2% to 38%) of dairy calves are still found with significant FPT.44,45,47 There is some debate as to the serum IgG concentration that signifies FPT. Calves are generally defined as having FPT if the calf serum IgG concentration is less than 10 mg/mL when sampled between 24 and 48 hours of age.48 More recently it has been suggested that serum IgG concentration below 13.4 mg/mL constitutes FPT.43,49 Ensuring that every calf has adequate passive transfer is challenging, and rates of 10% probably indicate good management practices.43In on-farm monitoring programs for effectiveness of passive transfer, IgG levels are often inferred by measuring serum total protein. A serum protein below 5 g/dL (≈9 mg/mL IgG) will result in a 2.4 to 6 times greater risk of mortality up to 6 months of age.25,26,50,51 There is still an increase in relative risk of mortality when serum protein is between 5 and 5.5 g/ dL as compared to greater than 5.5 g/dL (13.4 mg/mL IgG), but it is not as marked, and the cost benefit of ensuring that all calves achieve a serum protein greater than 5.5 g/dL to prevent mortality is questionable. However, the growing body of evidence suggesting that other colostral factors are positively associated with feed conversion efficiency and lactation performance emphasizes the long-term benefits of actively feeding colostrum and not just the short-term immunological provision of IgG.
On any farm the baseline mortality will reflect management, nutrition, and the pathogens present. The risk of mortality associated with varying levels of passive transfer is independent of baseline mortality rate. Hence where the baseline mortality is high, adequate passive transfer will not prevent calves dying, but as serum immunoglobulin levels decrease below 13.4 g/L, the risk of mortality will increase relative to that herd's specific baseline mortality. It is important to recognize that most calves with total FPT will survive, especially where baseline mortality is low.25,52 The role of the passive transfer of immunity in preventing morbidity per se is well documented, but the effect of immunoglobulin levels on prevalence of specific disease syndromes varies. Epidemiological studies reflect the variation in management, environment and disease pathogens between properties, and the greater impact of other risk factors on disease incidence. Consequently, there are inconsistent results on the impact of adequate passive transfer on both main calfhood diseases—diarrhea and pneumonia—also reflecting study design and varying serum IgG levels used to define FPT.24,26,27,53-56 Studies on the risk of pneumonia generally demonstrate FPT as a risk factor, but the impact of FPT as a risk factor of diarrhea is less consistent. Often where a significant effect of IgG levels on the incidence of a specific disease has not been demonstrated, increasing the sample size to examine correlation with all calves treated with antibiotics, or all morbid calves within the study, has demonstrated a significant benefit of adequate passive transfer. The benefits of adequate passive transfer on disease incidence are likely to be long lasting, with evidence of ongoing prevention of postweaning disease, particularly feedlot pneumonia, although, again, not all studies demonstrate this effect.26,29,57
A better indication of the effect of passive transfer on disease appears to be consistent positive correlation demonstrated between adequate passive transfer and average daily weight gain both pre and post weaning.27-29,55,56,58 It is likely that much of the variation in weight gain is secondary to changes in the incidence of disease.26,57,58