A 500 lb. steer from a 30,000 head capacity feedlot was recognized as ill and pulled to a “sick pen”. The steer was from a pen of 45 head that had been on feed for approximately 45 days and appeared normal until recently. The steer was discovered on a routine daily pen check to be lethargic and reluctant to move. Twenty-four hours later he had become ataxic, appeared to be blind, symptoms attributed to a central nervous system disorder. Differentials included polio encephalomalacia, thromboembolic meningoencephalitis (TEME), pneumonia, coccidiosis, and rabies. The steer was treated, per protocol, with thiamine, corticosteroids, and antibiotics. He was found dead the next morning. The veterinarian performed a cursory necropsy and submitted samples to the Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) for laboratory testing. The brain was removed at necropsy and gross lesions were not observed at that time.
Heart, lung, trachea, liver, kidney, spleen, and brain were submitted for histologic examination. The brain samples had been selected in an unconventional manner yet did include cerebral cortex, brain stem, and cerebellum. At the midbrain subjacent to the cerebellum there was a large focus of leukocytic infiltration and perivascular infiltrates with necrosis. Other tissues were not remarkable. The histologic diagnosis was pyogranulomatous rhombencephalitis i.e. inflammation of the brain stem. The most common etiology of rhombencephalitis is Listeria monocytogenes, in cattle as well as humans. It is a zoonotic disease.
There is a high incidence of clinically normal, intestinal carriers of this bacterium. Rhombencephalitis in adult ruminants is the most frequently recognized clinical form. It is a recognized cause of abortions also. The reservoirs of infection are soil and the intestinal tracts of asymptomatic animals. Infected animals can shed L. monocytogenes in feces, milk, and uterine discharges. It is also found in aborted fetuses and occasionally in the nasal discharges and urine of symptomatic animals. Soil or fecal contamination results in its presence on plants and in silage. Most infections are acquired by ingestion, but Listeria can also spread by inhalation or direct contact. Venereal transmission might also be possible. Listeriosis is primarily a winter-spring disease of feedlot or housed ruminants. The less acidic pH of spoiled silage enhances multiplication of L monocytogenes. Outbreaks may occur around 10 days after feeding poor quality silage. Removal or change of silage in the ration often stops the spread of listeriosis, whereas feeding the same silage months later may result in new cases.
Precautions should be observed when collecting central nervous system (CNS) tissues for diagnostic examination because of the zoonotic potential of central nervous system infections. Submission of the entire intact head to TVMDL is a good way to manage the zoonotic risk of cases requiring examination of the brain.
For more information on TVMDL’s test catalog, visit tvmdl.tamu.edu.
REFERENCES
- thecattlesite.com/diseaseinfo/192/listeriosis/