CCN Advisory
The Department’s Regional Veterinary laboratories have diagnosed a number of cerebro-Cortical Necrosis (CCN) cases in ruminants in late June and the first week of July 2024.
CCN is a nervous disease in cattle, sheep, alpaca, and carnivores. Clinical signs include circling, blindness, incoordination, head pressing, recumbency, seizures, or even sudden death. Diagnosis is mostly based on clinical signs and a response to treatment, or the result of a post mortem examination.
A change in thiamine (Vitamin B1) status and high sulphur intake are amongst the potential causes of CCN.
Thiamine is mostly produced in the rumen; young animals in transition from milk to full rumen function are therefore most at risk. In adult ruminants conditions like grain overload can lead to overgrowth of thiaminase-producing bacteria causing significant reduction of rumen-derived thiamine. Also, the intake of thiaminase-rich plants like bracken fern have been discussed as potential causes.
High sulphur intake can occur via water, feed or forage. Both sulphites reacting with thiamine already present in the rumen, as well as an effect on cellular energy metabolism impacting the highly energy-dependent CNS are discussed as possible pathways of pathogenesis.
At post mortem examination brain swelling with flattening of gyri and cerebellar herniation into the foramen magnum can be visible. Fluorescence of the brain under UV light (Wood’s lamp) can be observed in affected animals. A final diagnosis is achieved by histopathology (an examination of the brain tissue under the microscope) where marked laminar necrosis in the cerebrum is present among other changes.
Treatment of the animal with Vitamin B1 can be successful in some cases. In cases of sulphur-induced CCN all sulphur sources should be removed.
Figure 1: Marked autofluorescence under ultraviolet light in a case of CCN in a calf. Photo: Rebecca Froehlich-Kelly
