Evidence of Toxoplasma gondii in horses suspected of EPM neurological disease

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Evidence of intrathecally-derived antibodies against Toxoplasma gondii in horses suspected of neurological disease consistent with equine protozoal myeloencephalitis
Vet Parasitol. 2023 Mar 29;318:109919.

Authors
Pedro N Bernardino 1 , Nicola Pusterla 1 , Patricia A Conrad 2 , Andrea E Packham 2 , Eva Tamez-Trevino 3 , Monica Aleman 1 , Kaitlyn James 4 , Woutrina A Smith 5
Affiliations

1 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, 1 Shields Avenue, Davis, CA 95616, USA.
2 Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, 1 Shields Avenue, Davis, CA 95616, USA.
3 William R. Pritchard Veterinary Medicine Teaching Hospital, Immunology/Virology Laboratory, 1 Garrod Drive, Davis, CA 95616, USA.
4 Department of Obstetrics, Gynecology and Reproductive Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
5 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, 1 Shields Avenue, Davis, CA 95616, USA. Electronic address: wasmith@ucdavis.edu.

Abstract

Among the recognized neurologic diseases in horses, equine protozoal myeloencephalitis (EPM) has been reported around the world and still presents challenges in diagnosis and treatment. Horses can present with clinical neurologic signs consistent with EPM while testing negative for the two main causative agents, Sarcocystis neurona or Neospora hughesi, and may still be clinically responsive to anti-parasitic drug therapy. This context led to our hypothesis that another protozoal parasite, Toxoplasma gondii, which is known to cause toxoplasmosis in other mammalian species, is a potential pathogen to cause neurologic disease in horses. To evaluate this hypothesis, serum and cerebrospinal fluid (CSF) were collected from 210 horses presenting with clinical signs compatible with EPM, and the indirect immunofluorescent antibody test (IFAT) was used to detect antibody titers for T. gondii, S. neurona, and N. hughesi. Additionally, the serum to CSF titer ratio was calculated for T. gondii, S. neurona, and N. hughesi infections, suggesting intrathecally-derived antibodies for each of the three agents if the serum:CSF ratio was ≤ 64. There were 133 (63.3%) horses positive for serum T. gondii antibodies using a cutoff titer of 160, and 31 (14.8%) positive for CSF T. gondii antibodies using a cutoff titer of 5. Overall, 21 (10.0%) of EPM-suspect horses had a serum:CSF ratio ≤ 64 for antibodies for T. gondii, while 43 (20.5%) and 8 (3.8%) horses had a serum to CSF ratio ≤ 64 for antibodies for S. neurona and N. hughesi, respectively. A total of 6 (2.9%) animals presented evidence of concurrent intrathecally-derived antibodies for T. gondii and at least one other apicomplexan parasite in this study. Signalment and clinical signs were not different across the groups aforementioned. These data provide evidence of intrathecal production of anti-T. gondii antibodies, indicative of T. gondii infection in the brain and/or spinal cord of horses with EPM-like disease.

Keywords: EPM; Neospora hughesi; Sarcocystis neurona; Toxoplasma gondii; Toxoplasmosis.