The strange case of the low-birth-weight calves

Several years ago, the Disease Investigation Unit at the Western College of Veterinary Medicine in Saskatoon was asked to investigate an unusual herd problem on a ranch near the end of calving season.

A large proportion of the heifers on this ranch had given birth to calves with birth weights of 30 to 40 pounds or less.

These calves appeared to be well-developed and full term. They had normal proportions and their hair and bottom incisors had erupted and therefore did not appear to be premature.

The affected low-birthweight calves were also weak and not vigorous. They were small and had poor muscle development and were quite thin with no body fat reserves.

Although most were born alive, many became sick and required treatment. A high proportion of the affected calves that became sick went on to die of respiratory disease.

Environmental stressors also obviously played a role in this outbreak and when weather conditions became inclement, a much higher proportion of these small calves did not survive. Calves that did survive the first few weeks of life remained small and stunted throughout the pre-weaning period.

The herd was well-managed and had a good nutrition and vaccination program

The investigation focused on four general areas that may have been responsible for this outbreak of low birth weights:

  • Genetic causes;
  • Nutritional factors;
  • Infectious causes;
  • Toxicological causes.

We were able to rule out genetic causes because of the number of bulls involved. It seemed highly unlikely that we would have a genetic problem arise this suddenly in such a large proportion of the herd.

It was also noted that a small group of heifers were purchased and came to the herd in late October. These heifers were bred at a different ranch and some of these heifers also gave birth to low-birthweight calves, which effectively rules out a genetic cause.

The ration was balanced by a nutritionist and there were regular feed tests performed on the ingredients. There was a well-planned trace mineral program and the heifers were in good body condition at the start of the winter feeding program.

It is highly unlikely that there was a major deficiency in protein, energy or trace minerals. Blood testing of calves and heifers showed some low levels of manganese in this herd in both normal and affected animals. Manganese is fairly abundant in pasture grasses and legumes, however, silages and cereal grains, especially corn are fairly poor sources of manganese.

However, the condition associated with manganese deficiency is usually associated with bone abnormalities and these were not present in this herd. The herd was well vaccinated, which lowers the likelihood of a number of infectious agents being causes such as the bovine viral diarrhea virus. Serological testing for the BVD virus and Neospora caninum was performed.

All of the heifers were negative for Neospora caninum antibodies.

BVD antibody levels were at a level that would be expected for a well-vaccinated herd. Unfortunately, pathological examinations of tissues from affected calves did not reveal any other infectious causes of disease.

The final potential cause of this problem to consider was the possibility of a toxin.

The heifers were fed a mill run pellet throughout the winter feeding period.

These types of pellets are often affected with high ergot levels. Ergot can cause blood vessel constriction and in severe cases can cause gangrene to occur in tails or ears causing frostbite-like lesions. Adults that are affected with ergot may also be lame. However, in several studies done at the Western College of Veterinary Medicine, adult animals can be fed fairly high levels of ergot without showing signs of gangrene or lameness.

We wondered if the blood vessel constriction occurred at the placental level, blood flow might be restricted to the placental tissue, which could cause low-birthweight calves.

One experimental study from the United States documented this in ewes fed ergot containing feeds.

There was some evidence of ergot in some of the feed samples obtained but at relatively moderate levels. The pellets that were fed in early gestation were no longer available for diagnostic testing.

Unfortunately, we were unable to conclusively find a cause of the low-birthweight calves in this herd. Potential infectious causes such as BVD and Neospora caninum were ruled out with diagnostic testing.

Low-birthweight calves have not been documented extensively in beef cattle and there are very few scientific references to a problem of this magnitude.

The theory of ergot potentially causing placental insufficiency made sense biologically, but could not be proven conclusively.

Many causes of low birthweights in humans are related to vascular problems during pregnancy in women.

Ergot toxicity could potentially cause a similar vascular problem, which would likely have a more severe effect in heifers where placental and uterine vasculature is developing for the first time.

Ergot testing is now readily available at our diagnostic laboratory and should certainly be considered when feeding purchased pelleted feeds, screenings and green feed this winter.

John Campbell is a professor in the department of Large Animal Clinical Sciences at the University of Saskatchewan’s Western College of Veterinary Medicine.

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