Congenital vitamin A and mineral deficiencies in a beef calf
Josepha DeLay, Mackenzie Littlejohn
Animal Health Laboratory, University of Guelph, Guelph, ON (DeLay), Kirkton Veterinary Clinical, Kirkton, ON (Littlejohn)
AHL Newsletter 2023;27(2):12.
A near-term beef calf was born prematurely and died a few hours after birth. This was the third premature delivery or late-gestation abortion in this herd of 55 cows over a span of 2 months. One premature calf survived until 3 days of age. Cows were routinely vaccinated against BVDV, viral respiratory pathogens, Leptospira spp, and neonatal enteric pathogens.
On postmortem examination, the calf was a normally formed male with features compatible with full gestational age. Multifocally over the entire body, hair was coated with clumps of soft, thick grey putty-like debris (Fig. 1). Patchy alopecia and hyperemia were present in skin in inguinal and axillary regions. Internal lesions were limited to blotchy red discoloration in lung. No other significant gross lesions were identified. Placenta was not available for evaluation. The calf had received colostrum by esophageal tube.
Skin lesions correlated microscopically with abundant orthokeratotic hyperkeratotic debris at the epidermal surface and concurrent follicular keratosis (Fig.2). Additional histologic lesions in the calf included fibrinosuppurative bronchopneumonia, funisitis (inflammation of the umbilical cord), and unilateral corneal ulcer with marginal granulation tissue. Inflammatory lesions in lung, umbilical cord, and cornea were compatible with an infectious, likely bacterial cause. Given the calf’s very young age (hours old), prenatal infection was considered likely, and association with placentitis was suspected. In comparison, cutaneous hyperkeratosis was a more long-standing lesion suggestive of a separate etiology, and raised concern of vitamin A deficiency as the cause. No fungi were detected in association with skin lesions in PAS-stained tissue sections.
Bacterial, viral, or protozoal pathogens were not detected in tissues by bacterial culture or PCR tests for BHV-1, BVDV, bovine adenovirus, Leptospira spp, and Neospora caninum. Suspected bacterial bronchopneumonia and funisitis were considered likely significant as the cause of the calf’s death, but a definitive etiology could not be confirmed.
Liver vitamin A level in this calf was extremely low (0.32 ppm; reference intervals 1.4-4.3 ppm / bovine fetus and 14.0-35.7 ppm / bovine neonate), supporting vitamin A deficiency as the cause for hyperkeratotic skin lesions. Fetuses and neonatal calves have low levels of vitamin A stored in liver compared with older animals, as transfer across the placenta is marginal. Hepatic stores of vitamin A are increased in neonates through ingestion of colostrum. This calf was also deficient in selenium and manganese, based on liver analyses.
Vitamin A is an essential nutrient in mammals. Provitamin compounds (carotenoids) are ingested from plant-based dietary sources, and conversion to an active form (retinol) occurs in intestinal epithelium, with subsequent storage in liver. Poor quality feed and forages produced under drought conditions have lower levels of vitamin A precursors, promoting deficiency. Deficiency of vitamin A adversely affects retinal function and vision, growth and maintenance of epithelial tissues (including skin), bone development, immune function, and reproductive function. In bovine fetuses and neonates, inadequate vitamin A levels most commonly result in neurologic signs including vision loss and ataxia, resulting from constriction of cranial nerves by defective remodeling of bones of the skull, and abnormal CSF production and flow. Cutaneous hyperkeratosis, as seen in this calf, is infrequently described in vitamin A-deficient neonates but has been documented in juvenile cattle. Vitamin A deficiency rarely occurs in isolation, and testing for other vitamins and minerals can reveal multiple micronutrient deficiencies, as in this case. Review of feeding management in this herd identified inconsistencies in vitamin-mineral supplementation of pregnant cows. The supplement was changed to one specific for late-gestation cows, and feeder space was doubled to improve cow access. The herd will continue to be monitored over the next gestational period. AHL
Figure 1. Abundant clumped putty-like debris (keratin) at skin surface over head of bovine neonate (arrows).
Figure 2. Massively thick layer of hyperkeratotic debris at epidermal surface of haired skin in a bovine neonate with vitamin A deficiency (red bracket). H&E stain.
References
1.Baldwin TJ, et al. Dermatopathy in juvenile Angus cattle due to vitamin A deficiency. J Vet Diagn Inv 2012;24(4):763-766.
2.Dewell G. Vitamin A deficiency in beef calves. Iowa State University Extension and Outreach publication, 2014. https://store.extension.iastate.edu/product/Vitamin-A-Deficiency-in-Beef-Calves
3.Hill BD, Holroyd, RG, Sullivan M. Clinical and pathological findings associated with congential hypovitaminosis A in extensively grazed beef cattle. Aust Vet J 2009;87(3):94-98.
4.McDowell LR. Vitamin A. In: Vitamins in Animal and Human Nutrition. Iowa State University Press, 2000:15-90.