Diagnosis Of Equine Protozoal Myeloencephalitis Research Articles

A fresh look at the SarcoFluor antibody test for the detection of specific antibodies to Sarcocystis neurona for the diagnosis of equine protozoal myeloencephalitis

Equine protozoal myeloencephalitis (EPM) is a challenging disease to diagnose in horses with neurological signs. To optimize contemporary diagnostic testing, including the use of serum:CSF antibody ratios, the SarcoFluor antibody test for Sarcocystis neurona requires revalidation. The SarcoFluor, a previously validated immunofluorescent antibody test (IFAT) for the detection of antibodies specific to S. neurona in serum and cerebrospinal fluid (CSF) of naturally infected horses was analyzed using recent data and considering a serum:CSF antibody ratio threshold. Utilization of serum and CSF phosphorylated neurofilament heavy protein (pNfH) concentrations in support of an EPM diagnosis was also evaluated. 172 horses were divided into three groups: EPM-positive horses (EPM+, n=42), neurological non-EPM horses (n=74) confirmed with non-EPM neurological diseases (cervical vertebral compressive myelopathy, equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy), and control horses (control, n=56) without neurological signs and neurological abnormalities on histology. Logistic regression was used to compare EPM diagnostic regimens. Specifically, EPM+ horses were compared with neurological non-EPM horses showing neurological signs. To consider diagnostic utility, post-test probabilities were calculated by titer. When differentiating between EPM and other neurological diseases, the combination of serum and CSF SarcoFluor testing added more information to the model accuracy than either test alone. Using serum and CSF for pNfH in support of an EPM diagnosis did not identify cutoffs with statistically significant odds ratios but increased the overall model accuracy when used with the IFAT. Utilization of IFAT titers against S. neurona in serum and CSF result in a high post-test probability of detecting EPM+ horses in a clinical setting.

Molecular detection of Sarcocystis neurona in cerebrospinal fluid from 210 horses with suspected neurologic disease

An ante-mortem diagnosis of equine protozoal myeloencephalitis (EPM) is presently based on clinical presentation, immunodiagnostics performed on serum and cerebrospinal fluid (CSF), and ruling out other neurological disorders. Molecular techniques introduce a novel and promising approach for the detection of protozoal agents in CSF. Hypothesizing that real-time PCR (rtPCR) can be a useful complement to EPM diagnostics, 210 CSF samples from horses suspected of neurological disease with EPM included as a differential diagnosis were tested using rtPCR to detect Sarcocystis neurona DNA and immunodiagnostics targeting antibodies against the same pathogen, performed on serum and CSF samples. Molecular and immunological results were compared with respect to origin of the horse, time of the year, signalment, clinical signs and treatment history. Twenty-five horses tested positive in CSF for S. neurona by rtPCR only, while 30 horses had intrathecally-derived antibodies to S. neurona only (serum to CSF ratio ≤ 64 by indirect fluorescent antibody test - IFAT), and 13 horses tested rtPCR-positive in CSF with evidence of intrathecally-derived antibodies to S. neurona. Previous treatment for EPM was the only variable presenting statistical difference between the two testing modalities, highlighting that animals with history of anti-protozoal treatment were more likely to test positive solely in IFAT, while horses without treatment were more likely to test positive by rtPCR only. The results support the use of molecular diagnosis for EPM caused by S. neurona as a complement to immunodiagnostics. The use of rtPCR in CSF for the detection of S. neurona may improve the diagnostic work-up of neurologic disease suspected horses, especially in animals without previous anti-protozoal treatment.

Analysis of neurofilament concentration in healthy adult horses and utility in the diagnosis of equine protozoal myeloencephalitis and equine motor neuron disease

Neurofilaments (NFs) are structural proteins of neurons that are released in significant quantities in the cerebrospinal fluid and blood as a result of neuronal degeneration or axonal damage. Therefore, NFs have potential as biomarkers for neurologic disorders. Neural degeneration increases with age and has the potential to confound the utility of NFs as biomarkers in the diagnosis of neurologic disorders. We investigated this relationship in horses with and without neurological diagnosis. While controlling for horse type (draft, pleasure, and racing), we evaluated the relationship between serum heavy-chain phosphorylated neurofilaments (pNF-H) and age, sex, and serum vitamin E concentrations. Serum pNF-H concentrations increased by 0.002 ng/ml for each year increase in age. There were significant differences in the serum pNF-H concentration among the type of activity performed by the horse. The highest serum pNF-H concentration was found in horses performing heavy work activity (racehorse) and with lower serum pNF-H concentration found among light (pleasure riding) and moderate (draft) activity. There was no significant association between the pNF-H concentration and sex or vitamin E concentration. Serum pNF-H concentration was elevated among horses afflicted with EMND and EPM when compared with control horses without evidence of neurologic disorders. Accordingly, serum pNF-H concentration can serve as a useful biomarker to complement the existing diagnostic work-up of horses suspected of having EPM or EMND.

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

BackgroundAccurate 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.Hypothesis/ObjectivesThe 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.Animals25 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).MethodsSerum 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.ResultsSerum 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).ConclusionNeither SAA nor CRP in serum or CSF aid diagnosis of EPM.

Interobserver Variation in the Diagnosis of Neurologic Abnormalities in the Horse.

BackgroundThe diagnosis of equine protozoal myeloencephalitis (EPM) relies heavily on the clinical examination. The accurate identification of neurologic signs during a clinical examination is critical to the interpretation of laboratory results.ObjectiveTo investigate the level of agreement between board‐certified veterinary internists when performing neurologic examinations in horses.AnimalsNinety‐seven horses admitted to the Veterinary Teaching Hospital at The Ohio State University from December 1997 to June 1998.MethodsA prospective epidemiologic research design was used. Horses enrolled in the study were examined by the internist responsible for care of the horse, and later by an internist who was not aware of the presenting complaint or other patient history. Data were analyzed by descriptive statistics, and kappa (K) statistics were calculated to assess interobserver agreement.ResultsNinety‐seven horses were enrolled in the study. Overall, examiners, also referred to as observers, agreed that 60/97 (61.9%) were clinically abnormal, 21/97 (21.6%) were clinically normal, and the status of 16/97 (16.5%) of horses was contested. There was complete agreement among the examiners with regard to cranial nerve signs and involuntary movements. Disagreement involving severity of clinical signs occurred in 31 horses, and 25 of those horses (80.6%) were considered either normal or mildly affected by the primary observer. When examining the results of all paired clinical examinations for 11 different categories, there was wide variability in the results. When examiners rated the presence or absence of any neurologic abnormalities, lameness, or ataxia, the agreement among observers was either good or excellent for 80% of horses. When assessing truncal sway, the agreement among observers was good or excellent for 60% of the horses. When examining the horses for asymmetry of deficits, agreement was either good or excellent for 40% of the horses. Agreement among observers was excellent or good for only 20% of the horses when assessing muscle atrophy, spasticity (hypermetria), and overall assessment of the severity of neurologic abnormalities.Conclusions and Clinical ImportanceThis study underscores the subjectivity of the neurologic examination and demonstrates a reasonable level of agreement that may be achieved when different clinicians examine the same horse.

Diagnosis of Equine Protozoal Myeloencephalitis Using Indirect Fluorescent Antibody Testing and Enzyme-Linked Immunosorbent Assay Titer Ratios for Sarcocystis neurona and Neospora hughesi

The aim of this study was to compare two serologic tests used to support a diagnosis of equine protozoal myeloencephalitis (EPM). Serum and cerebrospinal fluid (CSF) samples were analyzed for antibodies to Sarcocystis neurona and Neospora hughesi by indirect fluorescent antibody testing (IFAT) and surface antigens of S. neurona and N. hughesi by enzyme-linked immunosorbent assay (ELISA). The samples originated from neurologic horses with confirmed and suspected EPM (nine S. neurona, three N. hughesi), from neurologic horses with confirmed neurologic diseases other than EPM (16 horses) and from healthy horses (10). The IFAT on CSF and ELISA titer ratios showed equal sensitivity in diagnosing EPM caused by S. neurona. The ELISA titer ratios showed slightly greater specificity in diagnosing EPM than the IFAT on CSF. Overall agreement between the IFAT on CSF and ELISA titer ratio was 90.9%. The IFAT on CSF and ELISA serum/CSF ratio are indicated to help support a laboratory diagnosis of EPM.

Accurate Antemortem Diagnosis of Equine Protozoal Myeloencephalitis (EPM) Based on Detecting Intrathecal Antibodies againstSarcocystis neuronaUsing the SnSAG2 and SnSAG4/3ELISAs

Recent work demonstrated the value of antigen-specific antibody indices (AI and C-value) to detect intrathecal antibody production against Sarcocystis neurona for antemortem diagnosis of equine protozoal myeloencephalitis (EPM). The study was conducted to assess whether the antigen-specific antibody indices can be reduced to a simple serum : cerebrospinal fluid (CSF) titer ratio to achieve accurate EPM diagnosis. Paired serum and CSF samples from 128 horses diagnosed by postmortem examination. The sample set included 44 EPM cases, 35 cervical-vertebral malformation (CVM) cases, 39 neurologic cases other than EPM or CVM, and 10 non-neurologic cases. Antibodies against S. neurona were measured in serum and CSF pairs using the SnSAG2 and SnSAG4/3 (SnSAG2, 4/3) ELISAs, and the ratio of each respective serum titer to CSF titer was determined. Likelihood ratios and diagnostic sensitivity and specificity were calculated based on serum titers, CSF titers, and serum : CSF titer ratios. Excellent diagnostic sensitivity and specificity was obtained from the SnSAG2, 4/3 serum : CSF titer ratio. Sensitivity and specificity of 93.2 and 81.1%, respectively, were achieved using a ratio cutoff of ≤100, whereas sensitivity and specificity were 86.4 and 95.9%, respectively, if a more rigorous cutoff of ≤50 was used. Antibody titers in CSF also provided good diagnostic accuracy. Serum antibody titers alone yielded much lower sensitivity and specificity. The study confirms the value of detecting intrathecal antibody production for antemortem diagnosis of EPM, and they further show that the antigen-specific antibody indices can be reduced in practice to a simple serum : CSF titer ratio.

Indirect Fluorescent Antibody Test and Surface Antigen ELISAs for Antemortem Diagnosis of Equine Protozoal Myeloencephalitis

Recent research suggests that serum : CSF titer ratios could provide the most accurate antemortem diagnosis of equine protozoal myeloencephalitis (EPM) caused by Sarcocystis neurona. The purpose of this study was to assess the utility of two commercially available tests, the indirect fluorescent antibody test (IFAT) and the surface antigen 2, 4/3 ELISA (SAG2, 4/3 ELISA), using archived paired serum and CSF samples. Samples were obtained from 4 types of clinical patients. Confirmed positive cases (n = 9 horses; 11 sample sets) had neurologic deficits and postmortem lesions consistent with EPM. Confirmed negative cases (n = 28) had variable clinical signs and postmortem lesions consistent with another disease. Suspected positive cases (n = 6) had neurologic deficits consistent with EPM, marked improvement after treatment, and exclusion of other diseases. Suspected negative cases (n = 14) had variable signs with a strong presumptive diagnosis of another disease. For each test, descriptive statistics were calculated using serum results alone, CSF results alone, and a serum : CSF titer ratio. Overall accuracy was highest for SAG2, 4/3 ELISA titer ratio at 0.97 (95% CI 0.88-0.99) with sensitivity = 0.88 (95% CI 0.66-0.97) and specificity = 1 (95% CI 0.92-1). IFAT CSF and titer ratio results also showed high accuracy at 0.88 (95% CI 0.77-0.94), but lower sensitivity = 0.65 (95% CI 0.41-0.83). Using serum results alone was least accurate for both test types. The more accurate methods, such as the SAG2, 4/3 ELISA serum : CSF titer ratio, should be utilized.

Evidence that inflammation associated with Sarcocystis neurona infection plays a role in clinical signs associated with equine protozoal myeloencephalitis

Sarcocystis neurona is a protozoal pathogen that causes equine protozoal myeloencephalitis (EPM). The commonly recognized neurologic signs that EPM causes are due to the pathological effects of the disease and can be due to infections of somatic and neural tissues by the asexual stages of S. neurona that cause cell dysfunction and death. A second component of EPM is the inflammatory host response to the parasitic insult. Inflammation may be as deleterious to the host as the initial insult. Anticoccidial drugs are necessary to treat the infectious aspect of EPM. An objective evaluation of treatment effect on protozoa is measured by a reduction in SnSAG 1, 5, and 6 antibodies. Recurrences of neurologic signs in horses that have diminishing antibody titers was controlled by levamisole HCl and indicate inflammation is a significant component of disease. There are no specific markers of inflammation due to S. neurona, therefore clinical exam was used to determine effectiveness of treatment. In a clinical field trial horses with a presumptive diagnosis of EPM based on veterinary clinical exam and the presence of serum antibodies against recombinant SAG’s 1, 5, and 6 by ELISA (> 1:16) were treated with 0.5 mg/kg decoquinate and 1 mg/ kg levamisole HCl PO for 10 days. A post-treatment clinical examination and antibody titer was determined. Horses that improved and then experienced recurrence of neurologic signs were treated with levamisole HCl PO until the horse resolved the clinical signs. Ninety-four percent of the EPM suspect horses resolved neurological signs within the 10 day treatment period based on clinical exam. Eighty-nine percent showed a reduction in antibody titers at 4-5 weeks and 97% showed a reduction in antibody titers by 12 weeks post treatment. Eleven percent of horses responded incompletely to decoquinate/ levamisole or responded completely but experienced recurrence from 7 to 14 days following treatment. Horses that experienced recurrence of signs responded to levamisole HCl and maintained the improvement after

Antibody Coefficients for the Diagnosis of Equine Protozoal Myeloencephalitis

Diagnosis of equine protozoal myeloencephalitis (EPM) remains a challenge for equine practitioners. Current utilized methods have inadequate sensitivity and specificity, because of a high number of false positive results. Evaluation of antibody indices to Sarcocystis neurona should provide high sensitivity and specificity for diagnosis of EPM. Archived samples from 29 clinical patients. Archived serum and cerebrospinal fluid (CSF) samples from clinical patients with either EPM (14) or cervical vertebral compressive myelopathy (CVM) (15) were examined and tested for anti-S. neurona antibodies by the SnSAG2 ELISA. The results were used to calculate the antibody index (AI) and C-value. Sensitivity and specificity were calculated, and the AI, C-value, immunoglobulin G (IgG) concentrations, and anti-S. neurona titers compared. In addition, negative CSF was spiked in varying concentrations with blood from a horse with a high anti-S. neurona titer, and the tests repeated. Results demonstrated that the IgG concentration, anti-S. neurona titer, AI, and C-value were significantly higher (P < .05) in horses with EPM than in those with CVM. Sensitivity and specificity of the AI was 71 and 100%, respectively, and that of the C-value was 86 and 100%, respectively. In addition, the AI and C-value from the samples spiked with S. neurona positive blood remained below 1 (eg, negative) in CSF with a red blood cell (RBC) count up to 10(5) RBC/μL. CONCLUSIONS/CLINICAL IMPORTANCE: Results of the study demonstrate the value of calculating the AI and C-value in the diagnosis of EPM in horses. In addition, the test is robust in the presence of blood contamination.

Utility of 2 Immunological Tests for Antemortem Diagnosis of Equine Protozoal Myeloencephalitis (Sarcocystis neurona Infection) in Naturally Occurring Cases

Antemortem diagnosis of equine protozoal myeloencephalitis (EPM) is challenging. Limited information is available regarding a commercial test (surface antigen 1 [SAG-1] ELISA). Performance of another commercial test (indirect fluorescent antibody test [IFAT]) using samples from an independent group has not been well described. The primary goal was to evaluate the SAG-1 ELISA and IFAT using naturally occurring EPM cases. A secondary goal was to obtain more information regarding clinical presentation. Hospital cases were admitted over 20 months and classified into 4 groups. Confirmed positive cases (n = 9) had asymmetric or multifocal neurologic deficits or both and postmortem lesions consistent with EPM. Confirmed negative cases (n = 17) had variable clinical signs and postmortem lesions consistent with another neurologic disease (or no lesions). Suspected positive cases (n = 10) had asymmetric or multifocal deficits or both, marked improvement after treatment for EPM, and other likely diseases excluded. Suspected negative cases (n = 29) had orthopedic disease and no neurologic deficits. Results of immunological testing (SAG-1 ELISA and IFAT on serum or cerebrospinal fluid [CSF] or both), neurologic examinations, CSF analyses, and postmortem examinations were analyzed retrospectively. SAG-1 ELISA sensitivity was 12.5% (95% CI, 1.6-38.4) and specificity was 97.1% (95% CI, 84.7-99.9) using serum. IFAT sensitivity was 94.4% (95% CI, 72.7-99.9) and specificity was 85.2% (95% CI, 66.3-95.8) using serum; sensitivity was 92.3% (95% CI, 64.0-99.8) and specificity was 89.7% (95% CI, 72.7-97.8) using CSF. Low sensitivity of the SAG-1 ELISA limited its usefulness for antemortem diagnosis of EPM in this patient population.

Indirect fluorescent antibody testing of cerebrospinal fluid for diagnosis of equine protozoal myeloencephalitis

To assess the use of CSF testing with an indirect fluorescent antibody test (IFAT) for diagnosis of equine protozoal myeloencephalitis (EPM) caused by Sarcocystis neurona. Test results of 428 serum and 355 CSF samples from 182 naturally exposed, experimentally infected, or vaccinated horses. EPM was diagnosed on the basis of histologic examination of the CNS. Probability distributions were fitted to serum IFAT results in the EPM+ and EPM-horses, and correlation between serum and CSF results was modeled. Pairs of serum-CSF titers were generated by simulation, and titer-specific likelihood ratios and post-test probabilities of EPM at various pretest probability values were estimated. Post-test probabilities were compared for use of a serum-CSF test combination, a serum test only, and a CSF test only. Post-test probabilities of EPM increased as IFAT serum and CSF titers increased. Post-test probability differences for use of a serum-CSF combination and a serum test only were < or = 19% in 95% of simulations. The largest increases occurred when serum titers were from 40 to 160 and pre-test probabilities were from 5% to 60%. In all simulations, the difference between pre- and post-test probabilities was greater for a CSF test only, compared with a serum test only. CSF testing after a serum test has limited usefulness in the diagnosis of EPM. A CSF test alone might be used when CSF is required for other procedures. Ruling out other causes of neurologic disease reduces the necessity of additional EPM testing.

Immunity, Pathophysiology, and Diagnosis of Equine Protozoal Myeloencephalitis

Our understanding of the pathophysiology of equine protozoal myeloencephalitis (EPM) remains incomplete, yet the development of clinical models, engineered mice, and molecular techniques have contributed markedly to our knowledge of this illness. Research confirms that the most important mediator of immunity to EPM is interferon-gamma, while the humoral immune system also contributes via inactivation of specific protozoal surface proteins. Diagnosis of EPM remains a clinical challenge, yet careful consideration of the clinical examination, coupled with ancillary diagnostic tests such as the cerebrospinal fluid evaluation, and various immunodiagnostic tests (Western blot, indirect fluorescent antibody) provide support for a clinical diagnosis.

Sensitivity and specificity of western blot testing of cerebrospinal fluid and serum for diagnosis of equine protozoal myeloencephalitis in horses with and without neurologic abnormalities.

To determine sensitivity and specificity of western blot testing (WBT) of CSF and serum for diagnosis of equine protozoal myeloencephalitis (EPM) in horses with and without neurologic abnormalities. Prospective investigation. 65 horses with and 169 horses without neurologic abnormalities. CSF and serum from horses submitted for necropsy were tested for Sarcocystis neurona-specific antibody with a WBT. Results of postmortem examination were used as the gold standard against which results of the WBT were compared. Sensitivity of WBT of CSF was 87% for horses with and 88% for horses without neurologic abnormalities. Specificity of WBT of CSF was 44% for horses with and 60% for horses without neurologic abnormalities. Regardless of whether horses did or did not have neurologic abnormalities, sensitivity and specificity of WBT of serum were not significantly different from values for WBT of CSF. Ninety-four horses without EPM had histologic evidence of slight CNS inflammation. The low specificity of WBT of CSF indicated that it is inappropriate to diagnose EPM on the basis of a positive test result alone because of the possibility of false-positive test results. The high sensitivity, however, means that a negative result is useful in ruling out EPM. There was no advantage in testing CSF versus serum in horses without neurologic abnormalities. Slight CNS inflammation was common in horses with and without S neurona-specific antibodies in the CSF and should not be considered an indication of CNS infection with S neurona.

Serologic prevalence of Sarcocystis neurona, Toxoplasma gondii, and Neospora caninum in horses in Brazil

Objective To determine serologic prevalence of Sarcocystis neurona, Toxoplasma gondii, and Neospora caninum in horses in Brazil. Design Prevalence survey. Animals 101 Thoroughbreds in Brazil. Procedure Blood samples were obtained from horses and tested for serum antibodies against S neurona by use of an immunoblot procedure with culture-derived S neurona merozoites as antigen, and for serum antibodies against T gondii and N caninum by use of a modified agglutination test with formalinpreserved tachyzoites and mercaptoethanol. Results Antibodies against S neurona and T gondii were detected in 36 and 16 of 101 horses, respectively. Cross-reactivity between antibodies against T gondii and S neurona was not detected. Antibodies against N caninum were not detected in any samples. Conclusions and Clinical Relevance The high prevalence of antibodies against S neurona detected in clinically normal horses emphasizes the importance of examining CSF for antibodies when establishing a diagnosis of equine protozoal myeloencephalitis. (J Am Vet Med Assoc 1999;215:970–972)

Seroprevalence of antibodies to Sarcocystis neurona in horses residing in Ohio

Objective To determine the seroprevalence of serum antibodies to Sarcocystis neurona in horses residing in Ohio. Design Prevalence survey. Sample Population Serum from samples from 1,056 horses. Serum was collected on every 36th sample submitted to the Ohio State Diagnostic Laboratory for testing for equine infectious anemia. Procedure Serum was frozen at −80 C and analyzed for antibodies to S neurona, using a western blot. Information regarding blood sample collection, age, breed, sex, and geographic location was recorded for each horse. Data were analyzed, using multivariable logistic regression. Results Horses of 37 breeds from 81 of Ohio's 88 counties were included in the study population. There were 481 females, 133 males, and 442 geldings ranging in age from 3 months to 27 years; &gt; 48% were &lt; 5.6 years old. More than 53% of samples were seropositive for antibodies to S neurona. A gender or breed effect on seroprevalence was not identified. There was a significant effect of age (P ≤ 0.0001; with older horses more likely to be affected), and of location (statistical and extension districts; P = 0.02 and P = 0.03, respectively) on seroprevalence. Location effects appeared to be correlated to the number of days with temperatures below freezing (P &lt; 0.05). Clinical Implications The high seroprevalence of antibodies to S neurona found in the sample population emphasizes the importance of examining CSF for S neurona-specific antibodies when establishing a diagnosis of equine protozoal myeloencephalitis. (J Am Vet Med Assoc 1997;210:519–524)

Seroprevalence of antibodies to Sarcocystis neurona in horses residing in a county of southeastern Pennsylvania

Objective To determine seroprevalence of Sarcocystis neurona-specific antibodies in a population of horses residing in Chester County, Pa. Design Prevalence survey. Sample Population 117 serum samples from selected members of a population of 580 Thoroughbred horses. Procedure Serum was analyzed for antibodies to Sarcocystic neurona, using a western blot. Information regarding age, sex, and housing of horse was obtained by questionnaire. Data were analyzed, using multivariable logistic regression. Results Seroprevalence was 45.3% (95% CI, 36.3 to 54.3%). A relationship was not found between seroprevalence and sex of horse. Seroprevalence was greater in older horses (logistic regression; P = 0.16). Clinical Implications High seroprevalence of antibodies to S neurona and the lack of neurologic deficits among horses sampled indicate that positive results of serologic examination alone are of limited value for diagnosis of equine protozoal myeloencephalitis. Clinical signs consistent with the disease are the most important consideration in accurate diagnosis. (J Am Vet Med Assoc 1997;210:517–518)

Seroprevalence of antibodies to Sarcocystis neurona in horses residing in Oregon

Objective To determine seroprevalence of antibodies to Sarcocystis neurona in neurologically normal horses residing in 4 regions of Oregon and to describe the effects of age, gender, breed, and housing on seroprevalence within each region. Design Prevalence survey. Sample Population Serum samples from 334 horses systematically selected by practicing veterinarians. Procedure Antibodies to S neurona were measured in sera, using a western blot. Information including age, gender, breed, housing, geographic location, and duration of residence was obtained for each horse. Data were analyzed, using descriptive statistics. Results 45% (149/334) of horses evaluated were seropositive for antibodies to S neurona with significant differences in the percentage of seropositive horses from different regions of the state. Seroprevalances of antibodies to S neurona in horses in regions I and II, west of the Cascade Range, were 65 and 60%, respectively; whereas seroprevalances in central and eastern Oregon, regions III and IV, were 43 and 22%, respectively. Seroprevalence consistently increased with age of horse for each region. Gender, breed, and housing were not associated with significant differences in seroprevalence of antibodies to S neurona in the overall sample population, or in comparisons of samples obtained from horses within a particular region, or among samples obtained from horses residing in different regions. Clinical Implications The high seroprevalence of antibodies to S neurona in neurologically normal horses indicates that analysis of serum alone would not be useful for definitive diagnosis of equine protozoal myeloencephalitis in horses in Oregon. (J Am Vet Med Assoc 1997;210:525–527)