In 1921, someone took note that there were a lot of calves suffering from intestinal coccidiosis that also had nervous signs. Once this link was made, the disease was dubbed nervous coccidiosis. Though the incidence in Canada has not been established, it has been calculated as many as 10,000 calves die annually from this disease in the United States.
Nervous coccidiosis can occur at any time of the year, but in Canada it is primarily a fall and early winter disease, coinciding with the arrival of calves at feedlots.
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In every calf showing nervous signs within a few months of feedlot arrival, nervous coccidiosis should be considered as a cause.
Most producers are familiar with intestinal coccidiosis that causes diarrhea.
Coccidial organisms invade the mucosal cells that line the intestine and disrupt fluid transport. The result is watery feces.
Affected calves have soiled hindquarters and may strain to pass their feces. Some veterinarians describe the tail posture as a “pump handle tail.”
As more coccidial organisms invade, more mucosal cells are damaged. It is not unusual for clots of blood to be seen in the feces. In severe cases, manure can change into a bloody fluid containing clumps of sloughed mucosal cells.
Severely affected calves can die from dehydration. Others are weakened so much they succumb to secondary infections such as pneumonia. Most just suffer from diarrhea and poor growth. Coccidiosis can reduce profits considerably.
Nervous signs can be seen in up to 30 percent of calves with clinical signs of intestinal coccidiosis. The first symptom is usually muscle inco-ordination. The calves seem unbalanced and have difficulty walking. Next, there is muscle twitching and loss of balance, which can progress to seizures.
Convulsing calves may collapse on their sides, have rigid legs, jerky eye movements, snapping eyelids and irregular breathing. Some will bellow and appear blind. Most calves return to normal between seizures, but stress or handling can trigger the onset of another one. Calves that have seizures are likely to die.
The clinical signs of nervous coccidiosis resemble all other ailments that affect the cerebral cortex, which is the outer layer of the brain. These include polioencephalomalacia (thiamine deficiency), lead poisoning, listeriosis and hemophilus septicemia , better known as ITEME, to name just a few.
On post-mortem examination, there are no brain lesions with coccidiosis. This makes it difficult to understand how coccidiosis causes the nervous symptoms.
One suggestion is that damage to the intestinal tract caused by coccidia, coupled with the stressors common in feedlots, results in a loss of minerals such as magnesium and calcium. Support for this idea comes from the fact that magnesium, calcium, dextrose solutions and sulfamethazine can be used successfully to treat coccidiosis.
Other researchers believe there is a toxin involved. When serum samples from calves with nervous coccidiosis are injected into mice, the nervous signs can be reproduced.
Death rates from nervous coccidiosis are high, ranging from 72 to 90 percent. Treatment must begin as early as possible for any chance of recovery for the calf.
Producers can prevent nervous coccidiosis if they control intestinal coccidiosis. That means reducing stress, maintaining optimal hygiene and feeding coccidiostats to all incoming cattle.
