Utility of C-reactive protein and serum amyloid A in the diagnosis of equine protozoal myeloencephalitis

BackgroundHypothesis/ObjectivesAccurate antemortem EPM diagnosis requires evidence of intrathecal antibody production. Some advocate the use of acute phase proteins in addition to serology, which alone results in substantial false positives. The purpose of this study was to determine if serum C-reactive protein (CRP) or serum amyloid A (SAA) concentrations were elevated in cases of equine protozoal myeloencephalitis (EPM) compared to other neurological diseases. AnimalsMethods25 clinical cases of equine neurological disease: EPM (10), cervical vertebral stenotic myelopathy (CVSM) (10), neuroborreliosis (2), equine motor neuron disease (1), degenerative myelopathy (1), and leukoencephalomalacia (1). Serum and CSF CRP and SAA were measured. Selection criteria included neurologic disease, antemortem diagnosis of EPM or CVSM, or postmortem diagnosis of EPM, CVSM, or other neurologic disease, and availability of serological results and archived samples for testing. ResultsConclusionSerum SAA and serum CRP levels were generally undetectable or low in horses with EPM (median CRP 0.1 mg/L, 0.1-14.4 mg/L; median SAA 0.1 mg/L, 0.1-6.11 mg/L) and CVSM (median CRP 0.1, 0.1-2.41 mg/L; median SAA 0.1mg/L, 0.1-13.88 mg/L). CSF CRP and SAA for horses with EPM (median CRP 3.35 mg/l, 0.19-13.43 mg/l; median SAA 0.1 mg/L, 0.1-2.4 mg/L) and CVSM (median CRP 4.015 mg/L, 0.16-9.62 mg/L; median SAA 0.62 mg/L, 0.1-2.91 mg/L) were also undetectable or low. Kruskal-Wallis test showed no statistically significant differences between serum CRP (P = .14), serum SAA (P = .79), spinal fluid CRP (P = .65), or spinal fluid SAA between horses with EPM and CVSM (P = .52). Neither SAA nor CRP in serum or CSF aid diagnosis of EPM.