Polioencephalomalacia in a calf

Polioencephalomalacia in a calf

History:  A 1 month-old Charolais cross was submitted for necropsy, from a herd where several were found acting “goofy” and walking in circles with foam and blood coming from their mouths. They died within 1 hour of symptoms. The calves were fed “wet cake” from an ethanol plant.

Gross Necropsy Findings:

The calf was in good body condition. There were no gross abnormalities. The brain did not fluoresce under UV light.


Brain, cerebrum: there is mild multifocal necrosis and degeneration of the superficial to middle laminar cortical neurons, characterized by cellular and nuclear pyknosis, hypereosinophilic, angular cell borders, and occasional rarefaction of the surrounding neuropli. There is multifocal hypertrophy of capillary endothelial cells, and a few macrophages in Virchow-Robbins spaces surrounding vessels.

Cerebrum, low power: The arrow marks the junction of the normal neuropil (lower left)from the rarefaction (upper right) indicating the abnormal neuropil

Cerebrum, higher power: A closer view shows the rarefaction (clear spaces) centerer around neurons in the superficial to middle lamina of neurons

Cerebrum, high power: The arrows indicate neurons undergoing necrosis, with eosinophilic cytoplasm, angular cell borders, and pyknotic nuclei. There is also few perivascular mononuclear cells (macrophages) around small blood vessels.

Morphologic Diagnosis:

Brain, cerebrum: Mild, multifocal laminar cortical necrosis and endothelial hypertrophy

Lab Results:

Listeria culture: Negative

Lead Toxicology: Liver =  24.67 ppm (toxic)/ Kidney = 99.29 ppm (toxic)


This is a case of lead toxicity causing laminar cortical necrosis or Polioencepahlomalacia in calf.  The mild lesions pose a contrast to the severity of clinical signs, probably as a function of the acute nature of the illness. The source of the lead was never discovered int his case.

Based on the history and described clinical signs initial differentials were thiamine deficiency (Wet Cake = distiller grain = high sulfur = thiamine deficiency), and listeriosis (unusual in a calf this young, but considered based on “circling” and multiple animals affected).  Listeria culture was negative, and based on the lead toxicology results thiamine deficiency is less likely.

Poliencephalomalacia in ruminants can be caused by thiamine deficiency (Bracken fern, Sulfur, grain overload), lead, and cyanide poisoning. It has also been described in salt poisoning in swine. In young animals PEM may cause acute death with only swelling of the brain or cerebral edema.


Maxie, M.G. and Youssef, S. Nervous System. Chapter 3 in Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals, 5th edition, M. Grant Maxie editor. 2007. Saunders, Elsevier.

About Brian

Anatomic Pathologist, VetPath Services, Stone Ridge, NY- musculoskeletal, oral/dental, and sinonasal diseases www.vetpathservices.com
This entry was posted in Necropsy Cases and tagged , , , . Bookmark the permalink.

Leave a Reply

Please log in using one of these methods to post your comment:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s