Utilization of stress in the development of an equine model for equine protozoal myeloencephalitis

Saville, William J.; Stich, Roger W.; Reed, Stephen M.; Njoku, C. J.; Oglesbee, Michael; Wünschmann, Arno; Grover, Debra; Larew-Naugle, A.L; Staněk, Jan; Granstrom, David E.; Dubey, J. P.

doi:10.1016/s0304-4017(00)00421-0

Cited by 66 publications

(36 citation statements)

References 21 publications

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“…For experimental infection, nine horses that were seronegative for S. neurona were randomly assigned to three groups (a transport-stressed group, an acclimated group, and a group treated with dexamethosone after acclimation) prior to inoculation with S. neurona sporocysts from feral opossums, which is reported elsewhere (31). Briefly, these horses were shipped to the site of study and subjected to neurologic examinations by a masked observer on the day of arrival, at the time of inoculation, and biweekly thereafter.…”

Section: Horsesmentioning

confidence: 99%

“…All of these horses seroconverted and developed anti-S. neurona Ab titers in their CSF after sporocyst inoculation. Interestingly, the transport-stressed group had horses with the highest clinical scores but the fewest animals with histopathologic lesions in the CNS, while the dexamethasone-treated group had horses with lower clinical scores but a larger number of individual horses with lesions in the CNS (31). These results indicate that the severity of the clinical signs due to EPM was not associated with the severity of lesions in the CNS but, rather, was due at least in part to a factor other than parasite load.…”

mentioning

confidence: 96%

“…Previously, we reported on the association between stress and EPM and how this has been used to develop an experimental equine model for EPM (31). Three groups of horses were experimentally infected with S. neurona sporocysts from feral opossums either immediately upon arrival as a test of the effect of transport stress, after a 2-week acclimation period, or after dexamethasone treatment as a test of the effect of immunosuppression.…”

mentioning

confidence: 99%

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Reduced Levels of Nitric Oxide Metabolites in Cerebrospinal Fluid Are Associated with Equine Protozoal Myeloencephalitis

Njoku

Saville

Reed

et al. 2002

Clin Vaccine Immunol

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Equine protozoal myeloencephalitis (EPM) is a disease of horses that is primarily associated with infectionwith the apicomplexan Sarcocystis neurona. Infection with this parasite alone is not sufficient to induce the disease, and the mechanism of neuropathogenesis associated with EPM has not been reported. Nitric oxide (NO) functions as a neurotransmitter, a vasodilator, and an immune effector and is produced in response to several parasitic protozoa. The purpose of this work was to determine if the concentration of NO metabolites (NO x ؊ ) in the cerebrospinal fluid (CSF) is correlated with the development of EPM. CSF NO x ؊ levels were measured before and after transport-stressed, acclimated, or dexamethasone-treated horses (n ‫؍‬ 3 per group) were experimentally infected with S. neurona sporocysts. CSF NO x ؊ levels were also compared between horses that were diagnosed with EPM after natural infection with S. neurona and horses that did not have clinical signs of disease or that showed no evidence of infection with the parasite (n ‫؍‬ 105). Among the experimentally infected animals, the mean CSF NO x ؊ levels of the transport-stressed group, which had the most severe clinical signs, was reduced after infection, while these values were found to increase after infection in the remaining groups that had less severe signs of EPM. Under natural conditions, horses with EPM (n ‫؍‬ 65) had a lower mean CSF NO x ؊ concentration than clinically normal horses with antibodies (Abs) against S. neurona (n ‫؍‬ 15) in CSF, and horses that developed ataxia (n ‫؍‬ 81) had a significantly lower mean CSF NO x ؊ concentration than horses that did not have neurologic signs (n ‫؍‬ 24). In conclusion, lower CSF NO x ؊ levels were associated with clinical EPM, suggesting that measurement of CSF NO x ؊ levels could improve the accuracy of diagnostic tests that are based upon detection of S. neurona-specific Abs in CSF alone and that reduced NO levels could be causatively related to the development of EPM.

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Section: Horsesmentioning

confidence: 99%

mentioning

confidence: 96%

mentioning

confidence: 99%

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Reduced Levels of Nitric Oxide Metabolites in Cerebrospinal Fluid Are Associated with Equine Protozoal Myeloencephalitis

Njoku

Saville

Reed

et al. 2002

Clin Vaccine Immunol

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“…Alternatively, other authors have reported that clinical disease is less severe in horses given corticosteroids, due to abatement of associated inflammation. 11 In the present case, initial clinical neurologic signs began before corticosteroids were administered. It is impossible to know with certainty whether the initial clinical signs of the dog were truly related to protozoal infection.…”

mentioning

confidence: 99%

Sarcocystis neurona Encephalitis in a Dog

Cooley

Barr

Rejmanek³

2007

Vet Pathol

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Abstract. A 1.5-year-old male Feist dog was presented to a veterinarian for reluctance to stand on the hind legs. Treatment included dexamethasone and resulted in a favorable initial response, but posterior paresis returned and progressed to recumbency, hyperesthesia, and attempts to bite the owner. The dog was euthanized. The brain was negative for rabies by fluorescent antibody analysis. Multiple foci of encephalitis were found in the cerebrum and particularly in the cerebellum. Protozoa morphologically consistent with Sarcocystis sp. were identified at sites of intense inflammation and malacia. Additionally, multiple schizonts were identified in areas without inflammation. Immunohistochemistry using both polyclonal and monoclonal antibodies specific for Sarcocystis neurona was strongly positive. No reaction to polyclonal antisera for Toxoplasma gondii or Neospora caninum was found. Polymerase chain reaction confirmed that the protozoa were S. neurona. Additional aberrant hosts for S. neurona other than horses have been identified, but S. neurona encephalitis has not been documented previously in the dog.

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“…17 The current experimental model for causing clinical EPM in horses inoculated with S neurona involves transport stress, which results in a more rapid seroconversion and development of neurologic abnormalities than in horses not transport-stressed. 18 There has been a reported case of neosporosis causing encephalomyelitis and polyradiculoneuritis in an older mare with hyperadrenocorticism, and it was suggested that immune suppression associated with the pituitary adenoma was a significant factor in disease development. 6 A treatment protocol for EPM due to N hughesi has not been described.…”

mentioning

confidence: 99%

Equine Protozoal Myeloencephalitis Associated with Neosporosis in 3 Horses

Finno¹,

Aleman²,

Pusterla³

2007

J Vet Int Med

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A 24-year-old Appaloosa gelding was evaluated for a 2-month history of pelvic limb incoordination. The gelding had been administered phenylbutazone (2 mg/kg PO q12h) for 1 week before admission, and no improvement was apparent. Two months before presentation, the gelding had been vaccinated against Eastern and Western equine encephalitis (EEE, WEE), tetanus, influenza, West Nile virus (WNV), and rabies. Deworming was adequate, with oral dewormers rotated between ivermectin and pyrantel pamoate every 2 months. On admission, the gelding was tachycardic (52 beats per minute), normothermic (37uC, 99.0uF), and eupneic (16 breaths per minute). Muscling appeared symmetric; however, the gelding placed more weight on the right pelvic limb than on the left and the tail was held to the right side. A complete neurologic evaluation revealed asymmetric hypermetria, characterized by a grade 2 of 5 ataxia on the left thoracic and left pelvic limbs and a grade 3 of 5 ataxia on the right thoracic and right pelvic limbs. There were no cranial nerve deficits, and both tail tone and were normal. The gelding was observed to urinate and defecate normally.A CBC revealed a leukocytosis (14,000/mL; reference range, 5,000-11,600/mL) characterized by a mature neutrophilia (12,200/mL; reference range, 2,600-6,800/ mL). Serum biochemical abnormalities included hyperglycemia (124 mg/dL; reference range, 50-107 mg/dL). Findings of cervical radiographs revealed mild osteoarthrosis of the articular facets at C4-5 and C5-6. Lumbosacral cerebrospinal collection was performed, and clear cerebrospinal fluid (CSF) fluid was obtained and submitted for cytology, serology (immunoglobulin M [IgM] capture ELISA) for WNV, and indirect fluorescent antibody testing (IFAT) for equine protozoal myeloencephalitis (EPM) (Sarcocystis neurona and Neospora hughesi). The CSF total nucleated cell count (TNCC) was normal (1/mL; reference range, ,6/ mL) with the cell population consisting primarily of small mononuclear cells (70%), large mononuclear cells (17%), and neutrophils (13%). The CSF protein concentration was normal (47 mg/dL; reference range, 20-70 mg/dL). Red blood cell (RBC) concentration within the CSF was 8/mL. The IgM capture ELISA was negative for WNV. S neurona IFAT titers were negative in serum (,40) and CSF (,5), whereas the serum and CSF tested positive for N hughesi, with titers of 2,560 and 5, respectively. A diagnosis of EPM associated with N hughesi was made, and the gelding was started on a course of ponazuril (5 mg/kg PO q24h for 30 days) and phenylbutazone (2 mg/kg PO sid for 14 days).A repeat examination was performed after 30 days of treatment, and clinical improvement was noted, with the gelding graded as 1 of 5 ataxic on the thoracic limbs and grade 2 of 5 ataxic on the pelvic limbs. The right pelvic limb was slightly worse than the left pelvic limb, but otherwise the ataxia appeared relatively symmetric. Treatment with ponazuril was continued for another 30 days, and a repeat examination was performed after that time. The thoracic limb a...

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Utilization of stress in the development of an equine model for equine protozoal myeloencephalitis

Cited by 66 publications

References 21 publications

Reduced Levels of Nitric Oxide Metabolites in Cerebrospinal Fluid Are Associated with Equine Protozoal Myeloencephalitis

Reduced Levels of Nitric Oxide Metabolites in Cerebrospinal Fluid Are Associated with Equine Protozoal Myeloencephalitis

Sarcocystis neurona Encephalitis in a Dog

Equine Protozoal Myeloencephalitis Associated with Neosporosis in 3 Horses

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