Citrullinaemia
(Holstein/Friesian calves)
Affected calves are clinically normal at birth, become depressed by 24 hours, develop signs of neurological dysfunction by 48 hours. Typical clinical signs are seemingly aimless wandering, tongue protrusion, chewing on fixed objects, head pressing and ultimately collapse and death between the third and fifth day of life.
The mutation responsible for this defect was imported into Australia by a US-born bull whose descendants were selected for high EBVs for butter fat content of milk. The mutation is now relatively rare in the Australian Holstein herd due to selection against heterozygotes by AI centres.
Diagnosis
Clinical signs, histopathology, confirmation by DNA analysis.
Specimens required
See Collection of hair samples for DNA testing
(In order of preference)
Diagnosis of the disease
- 20 to 25 hairs, with roots attached, from the distal end of the tail.
- Whole brain in buffered formalin for histopathology.
Heterozygote detection
- 20 to 25 hairs, with roots attached, from the distal end of the tail.