Please select one of the following tests for further information:
Due to its autosomal recessive inheritance, BLAD affects animals carrying two copies of the mutated gene, solely. Heterozygous carriers do not show any clinical signs but can pass on the mutation and – when mated to a BLAD-carrier – can produce affected progenies.
Genetic testing of the causative mutation in the CD18 gene enables discrimination of BLAD-carriers from non-carriers and helps preventing breeding affected offspring.
A genetic test now facilitates the identification of carriers and fertility-impaired bulls at an early stage.
Genetic testing allows the reliably identification of carriers and avoidance of risk pairings.
Homozygous affected animals are either stillborn or usually die within the first 50 days of life when born alive. Clinical signs in affected animals are: stillbirth, low birth weights, tapered head shape and recurring bronchopneumonia.
In 2014, it became obvious that the mutation associated with the BH2 haplotype also occurs in the Fleckvieh breed.
Nowadays, BH2 genetic testing can be performed, in order to avoid risk pairings and in order to further reduce the frequency of the mutation in the cattle population.
A mutation in the SLC2A2 gene, which is responsible for the synthesis of a glucose transporter protein, was identified as the cause of the disease.
Based on these findings, genetic tests can now be used to implement systematic selection and mating in order to control the frequency of this mutation in the Fleckvieh population.
In homozygous state, the defect usually causes embryonic death within the first few weeks of gestation or results in stillbirth of the affected calf later on. Interestingly, bulls carrying the FH4 defect in heterozygous state have normal fertilization rates, similar to those of FH4-free bulls.
The FH4 status of an animal can be determined by genotyping. By doing so, it became possible to avoid risk pairings and to further reducing the frequency of the defect gene through moderate selection.
Due to the economic importance and its consequences concerning animal welfare, it is necessary rapidly reducing the frequency of this defect locus in the Fleckvieh cattle population.
FH5 genetic testing is a powerful tool for the determination of the defect locus in Fleckvieh and for taking it into account in breeding practice.
At an age of a few months, affected animals develop progressive signs of ataxia, paresis of the pelvic limb and deficits in proprioception.
Clinical signs of the disease deteriorate in the course of time and finally, severely affected animals become recumbent and may die from further complications. The genetic principle of this disease is now fully understood. Direct gene testing allows differentiating between homozygous healthy animals and heterozygous carriers of this disease.
Since SDM affected calves can not be cured, they are usually euthanized within the first weeks of life. The gene defect responsible for this autosomal recessive disease has recently been fully elucidated. Genetic testing of the underlying mutation allows clear distinction between homozygous healthy animals, heterozygous carriers of the disease, and homozygous affected animals.
The causal mutation has been identified which enables genetic testing for this disease.
By identifying the causative mutation, for some time, it has been possible to identify carriers of this disease and thereby to prevent risk mating and birth of affected calves.
DEB (Dystrophic Epidermolysis Bullosa) describes a heritable skin disease in the local cattle breeds Rotes Höhenvieh and Vorderwald cattle. The disease which is inherited in an autosomal recessive manner causes severe skin defects at the muzzle and the fetlocks. Due to an abnormal high fragility of the skin these lesions rapidly extend leading to further painful epidermal loss, ulcerations and dysungulation. There is no medical treatment for DEB in cattle and affected animals have to be euthanized to prevent them from further suffering.
A candidate causative mutation for this genetic disease has been identified and thus enables selection against the mutant allele.
Affected calves suffer from inflammatory lesions of face, eye region, sternum and extremities, as well as interdigital erosions and erosive / ulcerative lesions of the oral mucosa. Further clinical symptoms may be recurrent diarrhea and/or pneumonia, reduced growth rate, and poor general health. As a consequence, affected calves usually die with a few weeks up to a few months of age.
A nonsense mutation (p.W215X) in a phospholipase encoding gene (PLD4) was identified as candidate causal polymorphism. Genetic testing of this mutation allows for reliable differentiation of clinically normal carriers from ZDL-free animals.