A case description of a herd outbreak of congenital chondrodystrophy and joint laxity in a seasonal calving dairy herd

Outbreaks of congenital chondrodystrophy and joint laxity have been described globally in cattle herds for over 20 years. Previous outbreaks have been characterised by calves that are born with a variety of clinical signs which include; disproportionate dwarfism, shortening of the long bones, distal joint laxity, domed crania, brachygnathia, spinal deformities and stillbirth (1). Although the exact aetiology of this condition is incompletely understood, it is taught to be the result of a maternal deficiency in key nutrients during the mid-gestation and is seen most often in beef herds. Epidemiological patterns highlight a number of precipitating risk factors during mid-gestation including; drought periods, feeding only grass silage and feeding silage low in manganese and/or zinc (1). The objective of this case description is to describe the epidemiological patterns observed in a herd outbreak that occurred in a seasonal calving dairy herd in Ireland. In this outbreak, 5 calves out of a total of 123 dairy cows (3.7%) were born affected by congenital chondrodystrophy and joint laxity between January and March 2024. Two affected calves were dwarfs with joint laxity ofn all four limbs, while the remaining 3 were normal in size but had joint laxity affecting all four limbs. All affected calves were born exclusively to heifers (i.e. primipara) and the total proportion of affected calves born to heifers was 17.2% (5/29). All affected calves were Holstein Friesian (HF) females due to the exclusive use of sexed semen in these heifers on the farm. Of the 5 affected calves, 3 calves were sired by one bull while 2 were sired by another bull indicating that a genetic aetiology related to the sire was less likely. Average birthweight of affected calves was 28.9 kg (SD = 2.8 kg) while average birthweight of unaffected HF females on this farm was 33.8 kg (SD = 3.1 kg). As all the dams were heifers, they were managed separately to the cows on the farm in terms of grazing and housing. These heifers were grazing from breeding in May to October at which point they were housed until calving. Commencement of housing corresponded to approximately 125-160 days of gestation for affected dams and during housing, they were fed a diet of grass silage exclusively. Trace element analysis of the grass silage fed showed high levels of iron, cobalt, selenium, aluminium and molybdenum but low levels of manganese (53.5 mg/kg of dry matter) and zinc (23.8 mg/kg of dry matter). Low levels of manganese and/or zinc have been associated with congenital chondrodystrophy and joint laxity in reports from similar grazing systems (2). In conclusion, outbreaks of congenital chondrodystrophy and joint laxity can occur in seasonal calving dairy systems due the nature of animals all being at a similar stage of gestation when a nutritional deficit occurs. Groups of in-calf heifers may be at increased risk especially if they are housed early and are maintained only on grass silage that is lower in either manganese or zinc.