Literature DB >> 16921889

Brachyspina syndrome in a Holstein calf.

Jorgen S Agerholm1, Fintan McEvoy, Jens Arnbjerg.   

Abstract

A stillborn premature Holstein calf was necropsied. The calf had severely reduced body weight and shortening of the vertebral column. The limbs appeared long and thin. Radiography and computer tomography scanning were performed, demonstrating malformation of the vertebral column. In addition, malformation of the kidneys, testicles, and heart was found at necropsy. Histologically, absence or incomplete development of intervertebral discs and complete or partial fusion of the epiphyses of adjacent vertebrae were found. In some areas, diaphyses of adjacent vertebrae were fused due to absence of epiphyses and intervertebral discs. Disturbed ossification of epiphyses in the appendicular skeleton was also present. The etiology of this syndrome was not identified. An inherited cause is possible due to a close relationship between the parents.

Entities:  

Mesh:

Year:  2006        PMID: 16921889     DOI: 10.1177/104063870601800421

Source DB:  PubMed          Journal:  J Vet Diagn Invest        ISSN: 1040-6387            Impact factor:   1.279


  10 in total

1.  A comprehensive biomedical variant catalogue based on whole genome sequences of 582 dogs and eight wolves.

Authors:  V Jagannathan; C Drögemüller; T Leeb
Journal:  Anim Genet       Date:  2019-09-05       Impact factor: 3.169

2.  First confirmed case of the bovine brachyspina syndrome in Canada.

Authors:  Jørgen S Agerholm; Josepha DeLay; Bryan Hicks; Merete Fredholm
Journal:  Can Vet J       Date:  2010-12       Impact factor: 1.008

3.  A 20 bp Duplication in Exon 2 of the Aristaless-Like Homeobox 4 Gene (ALX4) Is the Candidate Causative Mutation for Tibial Hemimelia Syndrome in Galloway Cattle.

Authors:  Bertram Brenig; Ekkehard Schütz; Michael Hardt; Petra Scheuermann; Markus Freick
Journal:  PLoS One       Date:  2015-06-15       Impact factor: 3.240

4.  Segmental spinal dysgenesis with caudal agenesis in a Holstein calf.

Authors:  Kaori Tokudome; Shuichi Ito; Tomoko Kato; Tohru Yanase; Tatsuo Kawarasaki; Yasuo Moritomo
Journal:  J Vet Med Sci       Date:  2016-12-13       Impact factor: 1.267

5.  Four novel candidate causal variants for deficient homozygous haplotypes in Holstein cattle.

Authors:  Irene M Häfliger; Mirjam Spengeler; Franz R Seefried; Cord Drögemüller
Journal:  Sci Rep       Date:  2022-03-31       Impact factor: 4.379

6.  A deletion in the bovine FANCI gene compromises fertility by causing fetal death and brachyspina.

Authors:  Carole Charlier; Jorgen Steen Agerholm; Wouter Coppieters; Peter Karlskov-Mortensen; Wanbo Li; Gerben de Jong; Corinne Fasquelle; Latifa Karim; Susanna Cirera; Nadine Cambisano; Naima Ahariz; Erik Mullaart; Michel Georges; Merete Fredholm
Journal:  PLoS One       Date:  2012-08-29       Impact factor: 3.240

7.  Identification of a nonsense mutation in CWC15 associated with decreased reproductive efficiency in Jersey cattle.

Authors:  Tad S Sonstegard; John B Cole; Paul M VanRaden; Curtis P Van Tassell; Daniel J Null; Steven G Schroeder; Derek Bickhart; Matthew C McClure
Journal:  PLoS One       Date:  2013-01-22       Impact factor: 3.240

8.  Familial occurrence of Danish and Dutch cases of the bovine brachyspina syndrome.

Authors:  Jørgen S Agerholm; Klaas Peperkamp
Journal:  BMC Vet Res       Date:  2007-05-08       Impact factor: 2.741

9.  Novel harmful recessive haplotypes identified for fertility traits in Nordic Holstein cattle.

Authors:  Goutam Sahana; Ulrik Sander Nielsen; Gert Pedersen Aamand; Mogens Sandø Lund; Bernt Guldbrandtsen
Journal:  PLoS One       Date:  2013-12-20       Impact factor: 3.240

10.  A 0.5-Mbp deletion on bovine chromosome 23 is a strong candidate for stillbirth in Nordic Red cattle.

Authors:  Goutam Sahana; Terhi Iso-Touru; Xiaoping Wu; Ulrik Sander Nielsen; Dirk-Jan de Koning; Mogens Sandø Lund; Johanna Vilkki; Bernt Guldbrandtsen
Journal:  Genet Sel Evol       Date:  2016-04-18       Impact factor: 4.297

  10 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.