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1.
Berl Munch Tierarztl Wochenschr ; 125(11-12): 476-81, 2012.
Article in English | MEDLINE | ID: mdl-23227765

ABSTRACT

The objective of this study was to demonstrate that bovine neonatal pancytopenia (BNP) can be prevented when intake of maternal colostrum is prevented in a dairy farm with verified BNP cases. A group of 30 female calves was fed with a colostrum substitute instead of maternal colostrum (group A) whereas the control group of 30 female calves was fed with the colostrum of their own mothers (group B). The female calves were randomly assigned to groups A or B. All 60 calves were daily blood sampled in the first eleven days of life, afterwards up to the age of three weeks one blood sample was taken every other day. All blood samples were analyzed for thrombocyte and leucocyte counts. In addition, 113 calves of both sexes, which were born during the trial period, were blood sampled once at 6-10 days old. In group A, no BNP positive calf was verified. In group B, eight calves with a significant decrease of thrombocyte and leucocyte counts were observed. Only one of these eight calves had clinical signs consistent with BNP and the other seven calves were classified as subclinical BNP cases. Of the other 113 contemporary calves, eleven animals had clinical signs of BNP accompanied by a decrease of thrombocyte and leucocyte counts and four of these eleven calves died due to BNP. Our results revealed that replacement of maternal colostrum can prevent subclinical and clinical cases of BNP as well as losses due to BNP in a dairy herd with verified BNP-cases and in addition, that colostrum from these cows was the major risk factor for BNP in this dairy herd.


Subject(s)
Cattle Diseases/prevention & control , Colostrum , Immunologic Factors/administration & dosage , Pancytopenia/veterinary , Animals , Animals, Newborn , Cattle , Cattle Diseases/blood , Cattle Diseases/immunology , Female , Male , Pancytopenia/immunology , Pancytopenia/prevention & control
2.
Vet J ; 192(3): 520-2, 2012 Jun.
Article in English | MEDLINE | ID: mdl-21767967

ABSTRACT

A congenital unilateral cleft lip and jaw in association with campylognathia to the opposite side was identified in a family of Vorderwald×Montbéliarde cattle. Clinical examination, radiography and computed tomography revealed similar types and degrees of orofacial abnormality in three affected animals from different farms. Digital radiographs and computed tomography demonstrated absence of the rostral segment of the incisive bone in association with sigmoid curvature of the rostral lower jaw and campylognathia to the left side. All three affected animals could be traced back to a common ancestor, a Montbéliarde bull, who had sons and grandsons used for in-crossing in Vorderwald cattle. The affected animals were inbred on Montbéliarde sires, with inbreeding coefficients of 0.39% in one calf and 6.25% in two calves. Pedigree analysis supported the hypothesis of an autosomal recessive mode of inheritance.


Subject(s)
Cattle Diseases/congenital , Cleft Lip/veterinary , Jaw Abnormalities/veterinary , Animals , Cattle , Cattle Diseases/genetics , Cattle Diseases/pathology , Cleft Lip/genetics , Cleft Lip/pathology , Female , Jaw Abnormalities/genetics , Jaw Abnormalities/pathology , Male , Pedigree
3.
PLoS One ; 6(12): e28857, 2011.
Article in English | MEDLINE | ID: mdl-22174915

ABSTRACT

A dominantly inherited syndrome associated with hypopigmentation, heterochromia irides, colobomatous eyes and bilateral hearing loss has been ascertained in Fleckvieh cattle (German White Fleckvieh syndrome). This syndrome has been mapped to bovine chromosome (BTA) 22 using a genome-wide association study with the bovine high density single nucleotide polymorphism array. An R210I missense mutation has been identified within microphthalmia-associated transcription factor (MITF) as responsible for this syndrome. The mutation is located in the highly conserved basic region of the protein and causes a negative-dominant effect. SOX10 and PAX3 promoter binding site mutations in MITF could be ruled out as causative for the German White Fleckvieh syndrome. Molecular characterization of this newly detected bovine syndrome means a large animal model is now available for the Tietz syndrome in humans.


Subject(s)
Cattle Diseases/genetics , Deafness/veterinary , Genes, Dominant/genetics , Genetic Association Studies , Microphthalmia-Associated Transcription Factor/genetics , Mutation/genetics , Pigmentation/genetics , Amino Acid Sequence , Animals , Base Sequence , Cattle , Chromosome Mapping , Deafness/genetics , Exons/genetics , Female , Fundus Oculi , Gene Frequency/genetics , Genetic Predisposition to Disease , Genome/genetics , Germany , Male , Microphthalmia-Associated Transcription Factor/chemistry , Molecular Sequence Data , Pedigree , Phenotype
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