Margaret Stalker, Gabriel Jantzi

Animal Health Laboratory, University of Guelph, Guelph, ON (Stalker), Metzger Veterinary Services (Jantzi)

AHL Newsletter 2021;25(2):9.

A one day-old cross-bred beef calf was submitted to the AHL for postmortem examination.  The calf came from a small herd of cross-bred and Hereford cows with a Simmental bull, with static genetics.  Of 20 currently calved this spring, 10 calves were clinically affected by a form of congenital dwarfism.

On postmortem examination, the calf was small statured (Fig. 1), with disproportionate shortening of all four limbs relative to the body and enlarged-appearing joints (Fig. 2).  No arthrogryposis or abnormalities of the head or spinal column were noted.  Histologic examination revealed reduced thickness of the physeal zones of hypertrophy and provisional calcification, with premature physeal closure in some joints, compatible with a chondrodystrophy.  Liver trace mineral analysis revealed a manganese level of 1.0 ug/g (reference interval 2-6 ug/g), and a zinc level of 140 ug/g (reference interval 24-100 ug/g).  PCR testing for BVDV was negative.

Differential diagnosis of congenital short stature in livestock includes genetic chondrodysplasia, nutritional chondrodysplasia, and chondrodysplasia due to exposure to plant toxins or toxic levels of vitamin A: 

• Genetic chondrodysplasia typically has a recessive inheritance so only a small number of animals are expected to be affected in the herd.  Affected animals are relatively uniform in their physical presentation with shortened long bones, enlarged joint epiphyses and often a domed head with brachygnathia inferior.
• Nutritional chondrodysplasia is associated with low liver zinc or manganese concentrations, although this may be a transient change if deficiency occurred for a finite period during gestation. This form of chondrodysplasia typically has a higher prevalence in the herd than expected for inherited forms of chondrodysplasia.  Affected animals may vary in the severity of dwarfism, and animals with mild cases may improve after birth.  Again, shortened long bones and enlarged epiphyses are typical, although the head abnormalities are not.  Histologic changes of genetic and nutritional chondrodysplasia are very similar, with alterations in thickness of the physes.
• Plant toxins are not typically a cause of chondrodysplasia in calves in Ontario.  The diagnosis of “acorn calves” has been used historically, although cases were found to be associated with a more general maternal nutritional deficiency (see above) rather than specific exposure to acorns. Maternal exposure to Veratrum californicum (white false hellebore) is the classical cause of congenital malformations including cranial and limb deformities in sheep and cattle in some areas of the world.  This plant species is not present in Ontario although a related species, Veratrum viride is present in Quebec.  Ingestion of wild lupines can also cause shortening and rotation of long bones and flexural contractures (“crooked-calf disease”); but again, wild lupines (Lupinus spp.) are not widespread in Ontario.
• Vitamin A toxicity due to supplemental injection of newborn calves has been associated with an unusual form of dwarfism with premature closure of the growth plates of the pelvic limbs resulting in a sloping back and small hindquarters, so-called “hyena disease”.

In this case, given the genetics of the herd, type of limb deformity and high prevalence, an underlying nutritional cause was suspected.  Evidence to support this however can be difficult to obtain.  The literature suggests this form of chondrodystrophy may be associated with a maternal deficiency of manganese or zinc during a critical stage of gestation for limb development.  This calf had liver manganese levels below the reference interval (RI), however the RIs were developed for adult animals, and calves are normally born with lower levels of liver manganese which increase over the first few weeks of life.  Interestingly, the literature states that some affected calves can be born with completely normal levels of liver trace minerals, possibly reflecting the earlier time period of the insult.

There is an association with grazing drought-affected pastures, or feeding silage/fermented forages to spring-calving cows during mid- to late-gestation, typically without dry feed or grain supplementation.  Although outright deficiency is possible in some diets, it has also been suggested that the bioavailability of manganese may be reduced in some ensiled forages, or that alterations in other minerals or factors may contribute to the necessary conditions to produce the long bone deformities.  In this case, this herd was being fed oat and pea silage, one of two cuts of sorghum, and a commercial beef premix.  Feed analysis of the silage and sorghum had mineral levels, including manganese and zinc, within the expected range on a dry matter basis.  The premix was initially fed free choice, then restricted to 100g/head/day and top-dressed.  Actual intake per cow is more difficult to assess.

The frequency of congenital defects such as this in Ontario cow-calf operations is unknown.  Gross postmortems to document deformities and further categorize these cases may yield useful information for producers, and may inform future discussions on optimizing mineral delivery to beef cows throughout pregnancy.  AHL

References

1. Dittmer KE, Thompson KG. Approach to investigating congenital skeletal abnormalities in livestock. Vet Pathol 2015;52:851-861.

2. Buskirk D. 2015. Prevent calf abnormalities by managing beef cow diets.  Michigan State University Extension.

3. Proulx JG, Ribble CS. 1992. Congenital joint laxity and dwarfism in a beef research herd. Can Vet J 33: 129-130.

Figure 1:  One day old beef calf with shortened limbs and enlarged joints (most apparent in the forelimbs).

Figure 2:  Sagittal sections of distal hind limbs: top limb is an age-matched Holstein calf for comparison; bottom limb is an affected beef calf showing the shortened tibia, thickened cortex and enlarged epiphyses.