2017 ACVIM Forum Research Abstract Program

The foals of mares vaccinated with the initial series and revaccinated 4 to 6 weeks prior to parturition had significantly higher levels of ELISA WNV and EIV (clades 1 and 2) passively transferred antibodies 24 to 72 hours following parturition. The results of this study supports the importance and recommendation to vaccinate broodmares 4 to 6 weeks before foaling not only for their own protection, but most importantly to maximize concentrations of immunoglobulins in their colostrum to be passively transferred to their foals. The purpose of this pilot study was to determine if C-reactive protein (CRP) or serum amyloid A (SAA) increase with equine protozoal myeloencephalitis (EPM) compared to other neurologic diseases. Accurate antemortem EPM diagnosis requires evidence of intrathecal antibody production (e.g. serum:CSF SnSAG2, 4/3 titer ratio < 100). Some advocate the use of acute phase proteins in addition to serology, which alone results in substantial false positives. Serum and CSF CRP and SAA were measured in 25 cases of equine neurologic disease: EPM (10), cervical vertebral stenotic myelopathy (CVSM) (10), neuroborreliosis (2), equine motor neuron disease (1), degenerative myelopathy (1), and leukoencephalomalacia (1). Nine of 10 EPM cases had serum:CSF SnSAG2, 4/3 titer ratios ≤ 25. The untested EPM case was confirmed postmortem, as were 4 other EPM cases. Nine of the 10 CVSM cases were confirmed postmortem, and the other case had a positive myelogram and SNSAG2, 4/3 titer ratio of 200. The remaining cases were diagnosed on postmortem exam. Serum CRP was not elevated in any case. Serum SAA was only elevated in the two cases of neuroborreliosis (132 mg/L and 460 mg/L; reference 0-20 mg/L) suggesting SAA may aid its diagnosis, but further testing is warranted. Neither serum CRP nor SAA increased in cases of EPM or CVSM. Cerebrospinal fluid CRP and SAA also failed to differentiate cases of EPM (CRP median 3.35 mg/L, range 0.19-13.43 mg/L; SAA median 0.1 mg/L, range < 0.1-2.4 mg/L) from CVSM (CRP median 4.015 mg/L, range 0.16-9.62 mg/L; SAA median 0.62 mg/L, range < 0.1-2.91 mg/L). Recurrent exertional rhabdomyolysis (RER) affects 5-7% of racing Thoroughbreds, Standardbreds and potentially Quarter Horses, A genetic basis has been proposed but not substantiated. Dysregulation of sarcoplasmic reticulum calcium cycling has been suggested to cause RER. We hypothesized that calcium dysregulation in RER horses could be impacted by genes encoding newly discovered micropeptides such as sarcolipin (SLN), myoregulin (MRLN), DWORF and phospholamban (PLN) that modify the activity of sarcoplasmic reticulum calcium ATPase (SERCA). The purpose of this study was to determine; 1) gene expression of SLN, MRLN, DWORF and PLN in equine muscle, 2) the coding sequence of these micropeptides and 3) potential differences in their coding sequence between controls and RER Thoroughbreds, RER Standardbreds and RER Quarter Horses. Gene expression was determined in gluteal muscle from 11 horses using Next generation sequencing. Sanger sequencing of SLN, MRLN and DWORF was performed on DNA isolated from blood or muscle tissue of a minimum of 9 RER horses per gene and 9 control horses selected from the Neuromuscular Diagnostic Laboratory.