Evidence that the agent of equine grass sickness may reach neurons by retrograde axonal transport.

This research tests the claim that the cause of equine grass sickness, a mysterious disease in horses, could be associated with neurons and transmitted by retrograde axonal transport. The results of the study suggested that the agent causing grass sickness does indeed impact the nervous system of horses, with the most severe changes observed in horses that had been experiencing symptoms for less than 12 hours.

Research Method

• The researchers collected serum from horses suffering from grass sickness and healthy horses as a control group.
• The collected sera were injected into the parotid salivary glands of ponies, which receive their sympathetic innervation from the cranial cervical ganglion on the same side of the body.
• The ponies’ health was monitored, but none of them displayed any local or systemic signs of illness.

Tissue Study

• After a week, several ganglia like the cranial cervical ganglia, stellate, and coeliaco-mesenteric ganglia were removed and analyzed histologically.
• Pathological changes were only found in the cranial cervical ganglion situated on the same side as where an injection of grass sickness serum had been administered.
• Out of five tested batches of serum from horses suffering acute grass sickness, four showed chromatolytic changes in neurons. This event indicates some form of cellular injury or stress to the neurons.

Observations and Findings

• The most severe neuron changes were found in horses which had been showing symptoms of grass sickness for less than 12 hours.
• Serum from a horse suffering chronically – for three weeks – did not show chromatolysis but did show an inflammatory infiltrate and neuronophagia, indicating neuron damage or death, suggesting that the diseases severity affects its interaction with the nervous system.
• When analyzing a batch of serum, the researchers separated it into two parts based on molecular weight. Only the part with components heavier than 30 kDa induced chromatolytic changes, indicating this could be an area of further investigation to identify the agent causing the disease.