The 2011 and 2012 droughts that affected a large percentage of the United States have had some negative health and productivity impacts on the cow-calf herd.
In some areas reproduction has suffered due to excessive heat during breeding season, and in others lack of adequate forage and other feedstuffs for pregnant cattle is influencing dystocia in cows and heifers as well as weaker calves at birth.
“The birth of an unacceptable number of small, weak calves in a cow-calf herd can be due to a variety of causes, and in some situations multiple causes may be involved concurrently,” explains Amelia Woolums, DVM, PhD, MVSc, Dipl. ACVIM, Dipl. ACVM, University of Georgia.
“Evidence exists to support a role for inadequate dietary protein and/or energy fed to cows and heifers late in gestation, BVDV infection in the herd during gestation, selenium deficiency, fetal thyroid abnormalities (possibly due to selenium deficiency or iodine imbalance in the dam’s diet), and prenatal infection of calves with agents such as leptospira and adenovirus,” Woolums says.
Weak calf syndrome
Woolums notes that each of these possible causes of “weak calf syndrome” could theoretically impact the immune response of the young calf (see sidebar). “It is very likely that calves that are abnormally small and weak at birth due to any of these causes have suboptimal immune function.”
However, very little research has been done to specifically evaluate immune function in calves from herds with weak calf syndrome, so it is difficult to accurately characterize the nature and severity of immune dysfunction in affected calves. “It is likely that the specific effects, and the severity of the effects, depend on the specific cause or combination of causes,” Woolums says.
If weak calf syndrome is due to maternal dietary protein deficiency late in gestation, this may affect the ability of calves to absorb antibodies from colostrum. Research has shown that calves born to cows fed a diet low in crude protein (about 1 lb/day) in the last 100 days of gestation had very low serum IgG concentrations after colostrums ingestion, as compared to calves whose dams were fed a higher amount of crude protein (about 2 lbs/day).
This difference appeared to be due to decreased ability of calves from dams fed low protein diets to absorb immunoglobulin from colostrum they were fed, and not, in this case, due to lower concentrations of antibody in the colostrum of the cows (J An Sci 53:1174, 1981), Woolums explains.
“So small, weak calves born to cows fed a suboptimal amount of protein late in gestation could have a high rate of failure of passive antibody transfer from colostrum, due to decreased ability of these calves to absorb antibodies from colostrum.”
Woolums notes that although this is not proven in the context of weak calf syndrome, in other species, including humans, dietary protein deficiency is known to cause atrophy of the thymus and changes in production of hormones related to normal thymic function. “So it’s possible, though not yet proven, that dietary protein deficiency for cows and heifers in late gestation can cause dysfunction of T cells in weak, small calves that are born to such cows and heifers, due to impaired thymic function in the calves.”
Managing weak calves
Weak calves are already behind the 8-ball, and when you add into that failure of passive transfer from poor quantity or quality of colostrum, these calves may be set up for failure.
“Calves with failure of passive antibody transfer from colostrum are more likely to become sick or to die before weaning, and some studies have shown that such calves are more likely to become sick after weaning,” Woolums says. “Since a weak calf born to a dam who may have poor quality colostrum has a greater chance of experiencing failure of passive antibody transfer, the prognosis for normal healthy life is decreased, though it’s hard to put an exact percentage on that prognosis because of all the different variables that may be impacting immune function and health in small, weak calves.”
If deficiencies of dietary protein, energy, or selenium are contributing to an outbreak of weak calf syndrome, correcting these deficiencies may improve calf growth and immune function, relative to what will be possible for these calves if these deficiencies persist. “In young calves, reversal of nutrient deficiency can sometimes lead to reversal of related immune deficiency,” Woolums says. “However, as far as I know this has not been tested in the specific context of weak calf syndrome, and the benefit of correcting dietary deficiency will likely depend on the severity of the deficiency, and whether other factors (such as BVDV infection) are also involved.”
In the immediate postpartum period, one might consider feeding the calf with frozen colostrum or a colostrums replacer, if the dam’s colostrums quality is suspected to be deficient. “However, since some research suggests that calves born to cows fed a protein deficient diet cannot absorb immunoglobulins from colostrum as well as calves from cows fed a higher protein diet,” Woolums says.
Good old-fashioned animal husbandry such as warming weak, newborn calves may also help get them off to a better start. “Calves born to cows fed a diet low in protein have been shown to produce less heat than calves born to diets with higher amounts of protein in the immediate postpartum period (J An Sci 65:745, 1987), and this effect was more pronounced for smaller birthweight calves,” Woolums.
She adds that this suggests that calves born to cows fed suboptimal amounts of protein may not be able to generate body heat efficiently; they may thus benefit from being quickly dried and warmed so they don’t expend extra energy trying to warm themselves, and so they don’t become even weaker and perhaps die due to hypothermia.
Despite best efforts, sometimes these calves can’t overcome their deficiencies. “Certainly it’s logical that producers should try to ensure that small, weak calves take in an adequate amount of milk to support growth and immune function, but small weak calves often fail to thrive even with the best efforts of producers,” Woolums says. “So it may be that these calves have other as-yet-undetermined underlying physiologic, metabolic, or immunologic defects that impair their ability to survive.”
Japanese weak calf studies
A study of Japanese calves with weak calf syndrome indicated that affected calves had lower numbers of CD8 T cells and gamma delta T cells circulating in their bloodstream soon after birth, as compared to unaffected calves, and this difference persisted until the calves were at least 5 weeks old (J Vet Med Sci 65:793, 2003).
“Because CD8 and gamma delta T cells are involved in an effective immune response to a variety of infectious agents, these changes could be expected to impair immune function, but it is not known how severe or prolonged this effect is,” says Amelia Woolums, DVM, PhD, MVSc, Dipl. ACVIM, Dipl. ACVM.
In the study, a proportion of affected Japanese calves were found to have abnormalities of the thymus (not to be confused with the thyroid gland, which has also been found to be abnormal in some weak, small calves) at birth (J Vet Med Sci 70:1173, 2008). Because the thymus is the site of T cell maturation, abnormalities of the thymus may well lead to T cell abnormalities, “But more research is needed before we know how common thymic and/or T cell abnormalities are in North American herds with weak calf syndrome.”
Woolums adds that BVDV infection can cause changes in the thymus, so BVDV infection could lead to both thymic abnormalities and weak calf syndrome. However, in the Japanese research, the cows that gave birth to the small, weak calves with thymic abnormalities were not infected with BVDV, suggesting that other undetermined causes were involved.
Dystocia and weak calves
Dystocia can lead to hypoxia and acidosis, and calves with acidosis have been shown to be more likely to have failure of passive antibody transfer (FPT) from colostrum, apparently due to decreased ability of these calves to absorb antibodies, says Amelia Woolums, DVM, PhD, MVSc, Dipl. ACVIM, Dipl. ACVM.
“Of course hypoxia can also affect nervous system function, so calves experiencing dystocia have at least two reasons to develop FPT – they may be slow to move and ‘dumb’, because of decreased oxygen delivery to their central nervous system, so they may not be neurologically capable of getting up and nursing enough colostrum fast enough for timely absorption of antibodies.”
Also, they may not be able to absorb antibodies from the colostrum efficiently enough to support adequate passive antibody transfer, even if they do get some colostrum into their gastrointestinal tract. “That’s why it makes particular sense to administer colostrum to a calf born from a significant dystocia if the calf seems at all weak or slow at birth,” Woolums recommends. “Because such calves may not absorb antibodies efficiently, it also makes sense to give these calves a relatively larger volume of colostrum, within reason and the calf’s anatomic limits.”
For more information on managing dystocia calves, visit www.bovinevetonline.com and search for “dystocia calves”.