If a calf has failure of passive transfer (FPT) or dystocia, immune function can definitely be compromised. “FPT leads to absence or very low levels of serum antibody in the calf,” says Amelia Woolums, DVM, MVSc, Dipl. ACVIM, Dipl. ACVM, University of Georgia.
“And since serum antibody is also secreted back across epithelial surfaces, antibodies on the mucosal surfaces, which protect calves from respiratory and gastrointestinal infection, are also likely to be lower in calves with FPT. Thus, FPT calves are more susceptible to disease in the first days to weeks of life from lack of circulating antibody and because of suboptimal levels of antibody on mucosal surfaces.
When an immune cell identifies and kills an infectious agent, it becomes activated, and then it activates other immune cells. “Since lack of antibody decreases the efficiency of this process, calves with FPT may be slower to develop some cellular immune functions than if antibody was present,” explains Woolums.
However, notes Woolums, it has also been shown that calves with FPT will develop their own antibodies faster than calves with normal passive transfer when they are exposed to infection or vaccination. So while antibody provided by adequate passive transfer protects calves from infection by binding to infectious agents, which may amplify the activation of immune cells and speed development of immunity, it appears to slow the production of antibodies by the calf itself to infections or vaccinations.
Calves known to have FPT can be vaccinated as early as the first week of life. “When calves are vaccinated in the presence of low to moderate levels of maternal antibody, they appear to respond best if they are given a booster dose two to four weeks after the first dose,” Woolums says. “This is true even if modified live viral vaccines are given to calves, which can sometimes induce adequate immunity after only a single dose in adult cows.”
Read more about neonatal calf immunology here.