Emily Brouwer

Animal Health Laboratory, University of Guelph, Guelph, ON. 

AHL Newsletter 2024;28(4):9.

In early September, a 4-month-old Holstein heifer presented to the referring veterinarian for euthanasia after suddenly developing neurological signs. This heifer had been examined and treated with meloxicam and florfenicol two days previously for suspected pneumonia, with no reported improvement. The morning of euthanasia, she was found down in lateral recumbency with opisthotonus. Her body temperature was 39°C. She was unable to maintain a sternal position, and it was noted that she had developed a mild ping over the right lateral abdomen in the region of the last ribs and the paralumbar fossa. She was euthanized and submitted to the AHL for postmortem examination. One other heifer in the same pen had died the day previously, and no postmortem examination was completed on her.

On external examination, the heifer was noted to be in good body condition and well hydrated. Internally, concentrated around the cerebellum and the ventral brainstem beneath the dura mater were sheets of yellow-tan, fibrinosuppurative exudate (Fig. 1). The lateral ventricles contained cloudy tan cerebrospinal fluid with flecks of fibrin. The exudate expanded the subdural space along the length of the spinal cord to the level of the lumbar spinal segments. The meningeal vessels were congested, and the leptomeninges were diffusely cloudy. Similar fibrinosuppurative exudate was present in the frontal sinuses. The tympanic bullae were clear.

Approximately 50 % of the right cranioventral lung was consolidated, dark pink-red and very firm. On cut section, there was moderate bronchiectasis and peribronchial fibrosis, and airway lumens contained purulent exudate. There were occasional pinpoint-2 mm diameter white nodules in the pulmonary parenchyma in the affected region. Few dense fibrous adhesions were identified between the pericardium and epicardial surface.

Microscopic examination confirmed the gross diagnosis of severe meningoencephalitis and myelitis, typical of a bacterial etiology. Bacterial culture of the brain isolated 2+ Pasteurella multocida in pure culture. Bacterial culture of the lungs isolated 2+ P. multocida, as well as 2+ Histophilus somni. In this case, it is possible that prior H. somni bacteremia led to CNS vascular damage which allowed for hematogenous spread of P. multocida to the brain and spinal cord. The lesions in the brain were not typical of infectious thromboembolic meningoencephalitis, but there was significant vascular injury noted in several sections of the spinal cord. Other mechanisms of direct invasion could be through the ears (though no lesions were noted) or through dehorning wounds.

The pulmonary lesions were chronic and typical of a bacterial etiology as well. The typical caseonecrotic lesions of Mycoplasma bovis were not present in these sections, but the PCR was positive for M. bovis with a cycle threshold of 25.48, and thus this organism was considered a contributor to the respiratory disease. Mycoplasma bovis has been reported in association with fibrinous meningitis in cattle as well, presumably related to otitis media, which was not present in this case.

Bacterial meningitis in ruminants is typically described in the context of neonates developing bacterial meningoencephalitis from bacteremia secondary to omphalitis or severe enteritis, often as a sequel to inadequate passive transfer of colostral antibodies. In addition, direct extension via otitis externa, skull fractures or sinusitis have been described. In cattle, most bacteria identified in meningitis cases are gram negative, and E. coli is significantly over-represented. This case involves an unusual presentation of bacterial meningitis in a young heifer, with various potential pathogeneses.  

Reference

1. Fecteau G, et al. Bacterial meningitis and encephalitis in ruminants. Veterinary Clinics: Food Animal Practice 2004;20(2):363-377.