Dominique Comeau 

Animal Health Laboratory, University of Guelph, Guelph, ON

AHL Newsletter 2023;27(3):9.

Three cattle from a group of approximately 20 Angus yearlings became ill with acute neurologic signs.  Clinical signs included central blindness, a hypermetric gait, teeth grinding, twitching ears and dehydration, as well as anorexia.  One of these animals was euthanized for a broken leg, and another showed signs of improvement with supportive therapy including selenium, thiamine, and penicillin, based on the top differential diagnoses of selenium deficiency, blackleg, and polioencephalomalacia.  The third animal demonstrated progressively worsening neurologic signs and was euthanized and submitted to the Animal Health Laboratory for postmortem.

On gross examination of the 15-month-old heifer, there were no lesions, excluding those associated with the method of euthanasia.  On histologic examination, there was multifocal vacuolation of the grey matter in the middle cortical lamina (Fig 1).  There were also hypereosinophilic shrunken (“red dead”) neurons, and frequent swollen glial cells in these affected areas, especially swollen astrocytes (Fig 2).  The endothelial cells of vessels in affected areas were plump and reactive.  These changes are all classic lesions of polioencephalomalacia.

A blood sample was submitted for testing of selenium levels.  The heavy metal screen found markedly elevated lead levels in the affected animal.  An extremely high lead level was confirmed by testing of the liver which had 17 ppm lead (normal reference level is less than 0.5 ppm).  On further review of the history, it was determined that there was a dilapidated car in the field the cows were grazing, with access to the car battery.

Polioencephalomalacia or cerebrocortical necrosis (CCN) is a common neurologic presentation in cattle.  It is most commonly associated with low levels of thiamine.  In adult cattle, this vitamin is produced by ruminal microbes.  Low levels of thiamine occur either due to lack of production due to alterations in ruminal microbes, or due to ingestion of plant enzymes or production of bacterial enzymes which break down thiamine.  A commonly-cited example of a plant with high levels of thiaminase is bracken fern. Alternatively, CCN can be caused by high intake of sulphur, which leads to production of abundant sulphide in the rumen which alters the ruminal microflora.  Increased dietary sulphur can come from water, feed additives, or forage.

Lead intoxication is one of the most common neurologic intoxications in cattle, but it is not always considered in cases of CCN.  Diagnosis is essential as specific chelating agents are needed for treatment, and animals with high levels of lead cannot enter the food chain due to the risk of human exposure.  The classical clinical signs are central blindness, ataxia, twitching of the ears and eyelids, and bruxism; however, these overlap extensively with the signs of CCN from other causes.  In subacute lead poisoning, gastrointestinal signs may predominate early in the course of disease, and include anorexia, ruminal stasis, and constipation.  Histologic lesions of cerebrocortical injury are not apparent in every case.  Inclusion bodies can often be seen in the kidney in subacute or chronic cases of lead toxicosis.  Common sources of exposure for cattle include old car or tractor batteries, lead paint, roofing materials, or contamination of foliage in areas exposure to industrial waste.  Young animals are more likely to consume these materials, and are more commonly affected. 

The remaining animals in this herd were tested for lead exposure.  Approximately 65 % of the animals had elevated lead levels in the blood.  This case is a reminder that lead toxicity remains an important differential in cases presenting as polioencephalomalacia if there is any history of possible exposure.   AHL 

Figure 1.  Vacuolation of the grey matter of the middle cortical lamina is evident on the right-hand side of the image.  This is characterized by clear (white) spaces within the background of the neuropil (pink). The tissue on the left-hand side of the image is unaffected.

Figure 2:  Higher magnificent view of an area of vacuolation showing swollen astrocytes (black arrow) and shrunken, dead neurons (white arrow).

Reference

1. Osweiler GO, et al. Epidemiology of lead poisoning in cattle– A five-year study in Iowa. Clin Toxicol 1973;6(3):367-376.