Immunoconversion against Sarcocystis neurona in normal and dexamethasone-treated horses challenged with S. neurona sporocysts.
Abstract: Equine protozoal myeloencephalitis is a common neurologic disease of horses in the Americas usually caused by Sarcocystis neurona. To date, the disease has not been induced in horses using characterized sporocysts from Didelphis virginiana, the definitive host. S. neurona sporocysts from 15 naturally infected opossums were fed to horses seronegative for antibodies against S. neurona. Eight horses were given 5x10(5) sporocysts daily for 7 days. Horses were examined for abnormal clinical signs, and blood and cerebrospinal fluid were harvested at intervals for 90 days after the first day of challenge and analyzed both qualitatively (western blot) and quantitatively (anti-17kDa) for anti-S. neurona IgG. Four of the challenged horses were given dexamethasone (0.1mg/kg orally once daily) for the duration of the experiment. All challenged horses immunoconverted against S. neurona in blood within 32 days of challenge and in CSF within 61 days. There was a trend (P = 0.057) for horses given dexamethasone to immunoconvert earlier than horses that were not immunosuppressed. Anti-17kDa was detected in the CSF of all challenged horses by day 61. This response was statistically greater at day 32 in horses given dexamethasone. Control horses remained seronegative throughout the period in which all challenged horses converted. One control horse immunoconverted in blood at day 75 and in CSF at day 89. Signs of neurologic disease were mild to equivocal in challenged horses. Horses given dexamethasone had more severe signs of limb weakness than did horses not given dexamethasone; however, we could not determine whether these signs were due to spinal cord disease or to effects of systemic illness. At necropsy, mild-moderate multifocal gliosis and neurophagia were found histologically in the spinal cords of 7/8 challenged horses. No organisms were seen either in routinely processed sections or by immunohistochemistry. Although neurologic disease comparable to naturally occurring equine protozoal myeloencephalitis (EPM) was not produced, we had clear evidence of an immune response to challenge both systemically and in the CNS. Broad immunosuppression with dexamethasone did not increase the severity of histologic changes in the CNS of challenged horses. Future work must focus on defining the factors that govern progression of inapparent S. neurona infection to EPM.
Publication Date: 2001-02-27 PubMed ID: 11223200DOI: 10.1016/s0304-4017(00)00420-9Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
- Blood
- Cerebrospinal Fluid
- Clinical Signs
- Corticosteroids
- Dexamethasone
- Diagnosis
- Disease Diagnosis
- Disease Etiology
- Equine Health
- Equine Protozoal Myeloencephalitis
- Histopathology
- Horses
- Immune Response
- Immunoglobulin G
- Immunohistochemistry
- Infection
- Necropsy
- Neurological Diseases
- Sarcocystis
- Veterinary Medicine
- Veterinary Research
Summary
This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.
This study looked into how horses responded to the Sarcocystis neurona parasite, both under normal conditions and under the influence of the immunosuppressive drug dexamethasone. It was found that all horses exposed to the parasite did build an immune response, with those given dexamethasone possibly exhibiting a faster response. The research is important as it helps develop understanding about equine protozoal myeloencephalitis – a neurological disease in horses common in North and South America.
Objective and Methods
- The research aimed to monitor immune response (immunoconversion) in horses against the parasite Sarcocystis neurona, the main cause of the equine protozoal myeloencephalitis (EPM) disease.
- The study used sporocysts (an infective life stage of the parasite) obtained from naturally infected opossums, the definitive host of S. neurona.
- Eight horses were fed sporocysts for seven days and then regularly examined for signs of illness.
- Both blood and cerebrospinal fluid (CSF) samples were collected from the horses over a 90-day period to monitor immune response through both qualitative (western blot) and quantitative (anti-17kDa) methods.
Using Dexamethasone
- Half of the challenged horses were given dexamethasone, an immunosuppressive drug, throughout the experiment. This was done to assess whether a suppressed immune system would affect the horse’s ability to defend against the parasite or impact the progression of potential disease symptoms.
Results
- All horses that were fed the sporocysts showed an immune response to the parasite within 32 days.
- The horses that were treated with dexamethasone appeared to immunoconvert earlier than those that were not, though this was not statistically significant (P = 0.057).
- The signs of neurological disease were mild to equivocal across all challenged horses, with those given dexamethasone displaying more severe signs of limb weakness.
- During the post-mortem examination, damage was seen in the spinal cords of the challenged horses; however, organisms were not visible in either routinely processed sections or via immunohistochemistry.
- Control horses remained seronegative throughout the period, although one eventually immunoconverted on day 75 in blood and day 89 in CSF.
Conclusion and Implications
- The immune responses observed occurred both systemically and within the Central Nervous System and indicate that a S. neurona infection had taken place.
- The study did not succeed in producing EPM-like neurological disease in the horses. It did, however, provide valuable insights into the progression from S. neurona infection to potential EPM disease in horses.
- The evidence gained could guide future research to refine the understanding of EPM and devise prevention or cure strategies.
Cite This Article
APA
Cutler TJ, MacKay RJ, Ginn PE, Gillis K, Tanhauser SM, LeRay EV, Dame JB, Greiner EC.
(2001).
Immunoconversion against Sarcocystis neurona in normal and dexamethasone-treated horses challenged with S. neurona sporocysts.
Vet Parasitol, 95(2-4), 197-210.
https://doi.org/10.1016/s0304-4017(00)00420-9 Publication
Researcher Affiliations
- Department of Pathobiology, PO Box 100880, College of Veterinary Medicine, University of Florida, Gainesville 32610, USA.
MeSH Terms
- Animals
- Antibodies, Protozoan / analysis
- Autopsy / veterinary
- Blotting, Western / veterinary
- Dexamethasone / pharmacology
- Encephalomyelitis / immunology
- Encephalomyelitis / veterinary
- Euthanasia / veterinary
- Horse Diseases / immunology
- Horses
- Immunoglobulin G / analysis
- Immunosuppressive Agents / pharmacology
- Molecular Weight
- Opossums / parasitology
- Polymerase Chain Reaction / veterinary
- Sarcocystosis / immunology
- Sarcocystosis / veterinary
Citations
This article has been cited 5 times.- Reed SM, Furr M, Howe DK, Johnson AL, MacKay RJ, Morrow JK, Pusterla N, Witonsky S. Equine Protozoal Myeloencephalitis: An Updated Consensus Statement with a Focus on Parasite Biology, Diagnosis, Treatment, and Prevention. J Vet Intern Med 2016 Mar-Apr;30(2):491-502.
- Dubey JP, Howe DK, Furr M, Saville WJ, Marsh AE, Reed SM, Grigg ME. An update on Sarcocystis neurona infections in animals and equine protozoal myeloencephalitis (EPM). Vet Parasitol 2015 Apr 15;209(1-2):1-42.
- Elsheikha HM, Murphy AJ, Mansfield LS. Phylogenetic congruence of Sarcocystis neurona Dubey et al., 1991 (Apicomplexa: Sarcocystidae) in the United States based on sequence analysis and restriction fragment length polymorphism (RFLP). Syst Parasitol 2005 Jul;61(3):191-202.
- Elsheikha HM, Rosenthal BM, Mansfield LS. Dexamethasone treatment induces susceptibility of outbred Webster mice to experimental infection with Besnoitia darlingi isolated from opossums (Didelphis virginiana). Parasitol Res 2005 Apr;95(6):413-9.
- Máca O, Kouba M, Langrová I, Panská L, Korpimäki E, González-Solís D. The Tengmalm's owl Aegolius funereus (Aves, Strigidae) as the definitive host of Sarcocystis funereus sp. nov. (Apicomplexa). Front Vet Sci 2024;11:1356549.
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