1. Ocular and cardiac malformations associated with maternal hypovitaminosis A in cattle
- Author
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Bonnin Jp, Fontaine Jj, Maillard R, Benoit-Valiergue H, and Yves Millemann
- Subjects
Heart Defects, Congenital ,medicine.medical_treatment ,biology.animal_breed ,Ice calving ,Physiology ,Cattle Diseases ,Physical examination ,Beef cattle ,Pregnancy ,Medicine ,Animals ,Eye Abnormalities ,Vitamin A ,General Veterinary ,biology ,medicine.diagnostic_test ,business.industry ,Vitamin A Deficiency ,Artificial insemination ,General Medicine ,medicine.disease ,Animal Feed ,Vitamin A deficiency ,Pregnancy Complications ,Animals, Newborn ,Hay ,Herd ,Cattle ,Female ,business ,Hereford cattle - Abstract
VITAMIN A deficiency in cattle usually occurs in France as outbreaks in beef cattle fed a ration with little green forage, especially when no mineral and vitamin supplement is provided. Clinical signs are mainly seen in male cattle (Paulsen and others 1989) and may vary: blindness, exophthalmia or dilatation of the pupil can occur, with good body condition and normal temperature (Meyus and others 2003). Convulsions, ataxia, stillbirths, poor growth and diarrhoea have also been associated with vitamin A deficiency (Divers and others 1986, Booth and others 1987, Paulsen and others 1989). This condition has also recently been associated with the birth to heifers of calves exhibiting ocular and cardiac abnormalities (Mason and others 2003). This short communication describes an ‘outbreak’ of marked ocular deformations in suckling calves, born to heifers or cows that were deficient in vitamin A. During November 2003, a small Charolais herd experienced the consecutive births of four animals presenting with ocular malformations and/or apparent blindness. The farm, in Burgundy, comprised 16 Charolais dams and approximately 200 ha of land on which cereals were grown. The calving period lasted from October 15 until the end of February each year and artificial insemination was never used, and heifers were presented to the bull at the end of February. The farmer rarely bought in animals, although he had replaced the bull one year previously. On average, a new bull was bought every three years. Animals at pasture also received hay; when indoors, they were fed maize silage, beet pulp pellets, and hay at night. Calves were fed alfalfa. Each year, new calves were sold in October. Deworming was based on the use of fenbendazole (Panacur; Intervet) once a year, at housing, although it had not yet taken place at the time of the investigation. Newborn calves remained with their dams. There was possible contact with two neighbouring farms: one dairy farm and one farm with suckling cows. The farm with the problems had a meadow without a neighbouring meadow, and one meadow with a double enclosure. All the animals had been housed, since November 1, in an old building that had been transformed into a free-housing stable. Cows and heifers were kept in separate houses but received the same feed. The bull was in an individual box. Any sick animals had been separated from others (since November 1) and placed in another building 200 m away. Two abortions had occurred in 2002. The initial hypotheses to explain the cases of blindness were bovine viral diarrhoea (BVD) virus in utero infection, hypovitaminosis A or an inherited condition, as has been described in Hereford cattle (Barkyoumb and Leipold 1984). As the offspring of two successive bulls were affected, the genetic hypothesis was dismissed. The farm was visited on November 22. The farmer reported that two or three sporadic cases of blindness had occurred several years previously. No clinical signs other than ocular signs were noticed, except for the abortions. A serological investigation for Brucella species, BVD virus, Chlamydia species and bovine respiratory syncytial virus had been carried out in 2002, without any positive result. There were no problems in the animals with regard to growth (good body condition), dermatology (coat quality) or balance (no ataxia). The four affected animals were a two-year-old heifer, which was blind without any visible ocular lesion, a one-yearold heifer with ocular malformations, an apparently blind four-month-old male calf and a three-week-old calf (calf 4) (Table 1). Another calf exhibiting ocular lesions had died the previous week. Their appetite and body conditions were not affected. The range of clinical signs can be seen in Fig 1. Other clinical signs included the absence of a menace reflex, but there was no observation of any dilated pupils or papilloedema. Complementary to the examination, investigation for antibodies to BVD virus and for BVD virus antigens was undertaken in the four affected animals as well as in their dams. All results were negative. Calf 4 was hospitalised in the Alfort National Veterinary School on December 1. Blood was sampled in order to verify its BVD virus status and to establish a biochemical ‘check-up’. A complete clinical examination was performed and the animal was monitored during the whole hospitalisation period. The same clinical signs of microphthalmos, blindness and gingival ulcerations were observed; the ulcers progressively recovered. In addition, tachycardia with a leftand rightsided heart murmur was present. The calf again tested negative for BVD antibodies and antigens in the blood. Also, viral cultures failed to isolate BVD virus. No major biochemical abnormalities were recorded. In parallel, a serological investigation for BVD and infectious bovine rhinotracheitis was undertaken on all 28 animals in the herd; all the animals were seronegative for both viruses. Calf 4 was euthanased on December 20. At postmortem examination, the following lesions were noted: microphthalmos, which was more severe in the left eye (Fig 2), hypogenesia of the optical nerves (especially the left one), abnormal liquid in ocular globes when cut (red in the left eye, brown in the right eye), bilateral retina atrophy, aphakia and the absence of vitreous body and anterior uvea. Examination of the heart showed a ventricular septal defect, right ventricular FIG 1: Ocular deformations seen in animals born to heifers or cows that were deficient in vitamin A. (a) Fully haired corneal dermoid on the right eye (heifer 2), (b) cutaneous proliferation on the left eyelids (heifer 2), and (c) right-sided microphthalmos (calf 4) (a) (b)
- Published
- 2007