A retrospective study of 171 cases of equine meningoencephalomyelitis in the United States, 1996-2023

Abstract

Equine meningoencephalomyelitis is an important cause of morbidity and mortality and is associated with a wide variety of infectious etiologies. Because of the lack of large retrospective studies, the prevalence and incidence of these diseases are unknown. Here we describe 171 cases of meningoencephalomyelitis in horses submitted to the Section of Anatomic Pathology at the New York State Animal Health Diagnostic Center (Cornell University, Ithaca, NY, USA) from 1996-2023. Neuroinflammatory disease was identified in 5.4% of submitted horses with a wide breed, age, and sex distribution. A parasitic cause was identified in 32 (19%) cases, with protozoa in 18 (11%) cases and metazoa in 14 (8%) cases. A viral cause was identified in 31 (18%) cases, corresponding to infection by equid alphaherpesvirus 1 (EqAHV1; 12 of 31, 39%), eastern equine encephalitis virus (10 of 31; 32%), West Nile virus (5 of 31; 16%), and rabies virus (4 of 31; 13%), followed by 14 bacterial (8%) cases and 7 fungal (4%) cases. Of the remaining 87 of 171 (51%) cases, 20 (23%) had some histologic features, although not conclusive, of protozoal disease, and 8 (9%) of EqAHV1 infection. However, 59 (68%) cases did not have any neuropathologic changes that would support a definitive diagnosis. Although we found the expected causes of equine meningoencephalomyelitis in our study, the large number of cases with unknown etiologic diagnoses highlights the challenges of definitively proving causes of neuroinflammation in the horse and supports the need for improved ante- and postmortem testing.

Keywords: encephalitis; equine; infectious diseases; large case study; meningitis; myelitis; neuroinflammation.

Figure 1.

Distribution of 171 cases of equine meningoence-phalomyelitis. Unknown causes (87 of 171) were the most frequent, followed by viral (31 of 171), protozoal (18 of 171), metazoan (14 of 171), bacterial (14 of 171), and fungal (7 of 171).

Figures 2–7.

Equine CNS inflammatory disease. H&E. Figure 2. Metazoan meningoencephalitis. The meninges are expanded by lymphocytes, plasma cells, and macrophages in a case of Halicephalobus gingivalis infection. Figure 3. Metazoan meningoencephalitis. Within the neuroparenchyma are rhabditoid nematodes consistent with H. gingivalis associated with mixed inflammation. Figure 4. Metazoan myelitis. A large, track-like cavity is present in the spinal cord bordered by axonal spheroids, myelin vacuolation, hemorrhage, and gliosis. Figure 5. Metazoan myelitis. A large track of hemorrhage with abundant axonal spheroids, necrosis, and foamy macrophages. Figure 6. Protozoal encephalitis. Mild lymphoplasmacytic inflammation with gliosis. Figure 7. Protozoal encephalitis. Multinucleate cells admixed in dense inflammation.

Figures 8–13.

Equine CNS inflammatory disease. H&E. Figure 8. Eastern equine encephalitis virus (EEEV). Marked lymphohistiocytic inflammation admixed with marked gliosis, satellitosis, and neuronophagia. Figure 9. EEEV. Mixed inflammation dominated by neutrophils. Figure 10. West Nile virus encephalitis. Lymphoplasmacytic inflammation with marked gliosis and satellitosis. Figure 11. Rabies virus encephalitis. Lymphocyte-rich inflammation expanding perivascular spaces and extending into the parenchyma. Figure 12. Equid alphaherpesvirus 1 infection. A large, wedge-shaped area of hemorrhage extends from the white to gray matter. Inset: blood vessels are cuffed by a mild infiltrate of lymphocytes. Figure 13. Bacterial meningitis. The cerebellar meninges are expanded by large numbers of degenerate neutrophils.

Figures 14–19.

Equine CNS inflammatory disease. H&E. Figure 14. Fungal meningoencephalitis. The meninges and adjacent neuroparenchyma are massively expanded and infiltrated by large numbers of neutrophils admixed with hemorrhage and fibrin. Figure 15. Fungal encephalitis. Branched hypha (arrow) associated with neutrophilic vasculitis, encephalitis, and necrosis. Figure 16. Fungal meningitis. The meninges are expanded by pyogranulomatous inflammation with multinucleate giant cells and abundant yeast with thick capsules, consistent with Cryptococcus sp. Figure 17. Meningoencephalitis of unknown cause, protozoal infection suspected. Marked lymphoplasmacytic inflammation with necrosis and gliosis. Figure 18. Meningoencephalitis of unknown cause, possibly viral. Large perivascular cuffs of lymphocytes extending into the adjacent parenchyma. Figure 19. Meningitis of unknown cause. The meninges are expanded by a mixed population of lymphocytes, plasma cells, and macrophages.

Figure 20.

Distribution of suspected etiologies in cases of equine meningoencephalomyelitis of unknown cause. EPM = equine protozoal myeloencephalitis; EqAHV1 = equid alphaherpesvirus 1.