Inherited forms of complement dysfunction or deficiency have not been reported in the horse. However, the foal is born with low serum complement activity, and colostrum is not a significant source of complement. Therefore, foals are transiently deficient in serum opsonic capacity, and rely on their own production of complement after birth. In sepsis, complement C3 components are rapidly consumed, which delays the physiological age-dependent increase observed in healthy foals.