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Abstract

Objective—To determine gene transcription for cytokines in nucleated cells in CSF of horses without neurologic signs or with cervical stenotic myelopathy (CSM), West Nile virus (WNV) encephalitis, equine protozoal myeloencephalitis (EPM), or spinal cord trauma.

Animals—41 horses (no neurologic signs [n = 12], CSM [8], WNV encephalitis [9], EPM [6], and spinal cord trauma [6]).

Procedures—Total RNA was extracted from nucleated cells and converted into cDNA. Gene expression was measured by use of real-time PCR assay and final quantitation via the comparative threshold cycle method.

Results—Cytokine genes expressed by nucleated cells of horses without neurologic signs comprised a balance between proinflammatory tumor necrosis factor-α (TNF-α), anti-inflammatory cytokines (interleukin [IL]-10 and transforming growth factor [TGF]-β), and Th1 mediators (interferon [IFN]-γ). Cells of horses with CSM mainly expressed genes for TNF-α, TGF-β, and IL-10. Cells of horses with WNV encephalitis mainly expressed genes for IL-6 and TGF-β. Cells of horses with EPM mainly had expression of genes for IL-6, IL-8, IL-10, TNF-α, IFN-γ, and TGF-β. Cells from horses with spinal cord trauma had expression mainly for IL-6; IFN-γ; TGF-β; and less frequently, IL-2, IL-10, and TNF-α. Interleukin-8 gene expression was only detected in CSF of horses with infectious diseases.

Conclusions and Clinical Relevance—Despite the small number of CSF samples for each group, results suggest distinct gene signatures expressed by nucleated cells in the CSF of horses without neurologic signs versus horses with inflammatory or traumatic neurologic disorders.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To describe cardiac lesions and identify risk factors associated with myocarditis and dilated cardiomyopathy (DCM) in beach-cast southern sea otters.

Animals—Free-ranging southern sea otters.

Procedure—Sea otters were necropsied at the Marine Wildlife Veterinary Care and Research Center from 1998 through 2001. Microscopic and gross necropsy findings were used to classify sea otters as myocarditis or DCM case otters or control otters. Univariate, multivariate, and spatial analytical techniques were used to evaluate associations among myocarditis; DCM; common sea otter pathogens; and potential infectious, toxic, and nutritional causes.

Results—Clusters of sea otters with myocarditis and DCM were identified in the southern aspect of the sea otter range from May to November 2000. Risk factors for myocarditis included age, good body condition, and exposure to domoic acid and Sarcocystis neurona. Myocarditis associated with domoic acid occurred predominantly in the southern part of the range, whereas myocarditis associated with S neurona occurred in the northern part of the range. Age and suspected previous exposure to domoic acid were identified as major risk factors for DCM. A sample of otters with DCM had significantly lower concentrations of myocardial L-carnitine than control and myocarditis case otters.

Conclusions and Clinical Relevance—Cardiac disease is an important cause of death in southern sea otters. Domoic acid toxicosis and infection with S neurona are likely to be 2 important causes of myocarditis in sea otters. Domoic acid–induced myocarditis appears to progress to DCM, and depletion of myocardial L-carnitine may play a key role in this pathogenesis. (Am J Vet Res 2005;66:289–299)

Full access
in American Journal of Veterinary Research

Abstract

Objective—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.

Sample Population—Test results of 428 serum and 355 CSF samples from 182 naturally exposed, experimentally infected, or vaccinated horses.

Procedure—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.

Results—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 ≤ 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.

Conclusions and Clinical Relevance—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.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To estimate risk of exposure and age at first exposure to Sarcocystis neurona and Neospora hughesi and time to maternal antibody decay in foals.

Animals—484 Thoroughbred and Warmblood foals from 4 farms in California.

Procedure—Serum was collected before and after colostrum ingestion and at 3-month intervals thereafter. Samples were tested by use of the indirect fluorescent antibody test; cutoff titers were ≥ 40 and ≥ 160 for S neurona and N hughesi, respectively.

Results—Risk of exposure to S neurona and N hughesi during the study were 8.2% and 3.1%, respectively. Annual rate of exposure was 3.1% for S neurona and 1.7% for N hughesi. There was a significant difference in the risk of exposure to S neurona among farms but not in the risk of exposure to N hughesi. Median age at first exposure was 1.2 years for S neurona and 0.8 years for N hughesi. Highest prevalence of antibodies against S neurona and N hughesi was 6% and 2.1%, respectively, at a mean age of 1.7 and 1.4 years, respectively. Median time to maternal antibody decay was 96 days for S neurona and 91 days for N hughesi. There were no clinical cases of equine protozoal myeloenchaphlitis (EPM).

Conclusions and Clinical Relevance—Exposure to S neurona and N hughesi was low in foals between birth and 2.5 years of age. Maternally acquired antibodies may cause false-positive results for 3 or 4 months after birth, and EPM was a rare clinical disease in horses ≤ 2.5 years of age. (Am J Vet Res 2004;65:1047–1052)

Full access
in American Journal of Veterinary Research

Abstract

Objectives

To identify Sarcocystis neurona-specific DNA sequences in the nuclear small subunit ribosomal RNA (nss-rRNA) gene that could be used to distinguish S neurona from other closely related protozoal parasites, and to evaluate a polymerase chain reaction (PCR) test, using broad based primers and a unique species-specific probe on CSF for detection of S neurona in equids.

Procedures

Sequencing of the nuclear small subunit ribosomal RNA gene from a new S neurona isolate (UCD 1) was performed. The sequence was compared with that of other closely related Sarcocystidae parasites. From this sequence, conserved DNA sequence primers were selected and an oligonucleotide probe was designed to hybridize with a unique region of the S neurona gene. For clinical evaluation, horses were considered test positive for S neurona infection on the basis of immunohistochemical detection of the parasites in the CNS.

Results

Sensitivity of this PCR and probe-based detection system was approximately 1 to 5 merozoites. Cerebrospinal fluid from 2 of 5 horses with histologic lesions consistent with equine protozoal myeloencephalitis were PCR- and probe-positive in a blind test of this procedure, and all uninfected horses were test negative.

Conclusion and Clinical Relevance

This PCR- based system is a useful method of confirming S neurona in CSF and has the advantage of facilitating detection of other apicomplexan protozoans that may be infective for horses. The usefulness of this test is limited by the presence of parasites free in the CSF of clinically affected horses. (Am J Vet Res 1996;57:975–981)

Free access
in American Journal of Veterinary Research

Abstract

Objective—To identify subclinical Babesia gibsoni infection in American Pit Bull Terriers from the southeastern United States and to determine the genetic sequence of parasite DNA isolated from these dogs.

Design—Case series.

Animals—33 American Pit Bull Terriers and 87 dogs of various other breeds.

Procedure—Blood smears were examined for microscopic evidence of the parasite, and DNA was extracted from blood samples and used in a polymerase chain reaction (PCR) assay designed to amplify the small subunit ribosomal RNA gene sequence of B gibsoni. Amplification products of the expected size were sequenced, and sequences were compared with published sequences for B gibsoni isolates. Hematocrit, platelet count, mean platelet volume, WBC count, and eosinophil count were compared between dogs with positive PCR assay results and dogs with negative results.

Results—Results of the PCR assay were positive for 18 of the 33 (55%) American Pit Bull Terriers, including all 10 dogs with microscopic evidence of parasitemia. Only 1 of these dogs was clinically ill at the time blood samples were collected. Results of microscopic evaluation of blood smears and of the PCR assay were negative for the 87 other dogs. Hematocrit and platelet count were significantly lower in dogs with positive PCR assay results than in dogs with negative results.

Conclusions and Clinical Relevance—Results suggest that American Pit Bull Terriers in the southeastern United States may be subclinically infected with B gibsoni. However, subclinical infection was not identified in dogs of other breeds from the same geographic area. (J Am Vet Med Assoc 2002;220: 325–329)

Full access
in Journal of the American Veterinary Medical Association

Summary:

Four dairy cows that had been successfully rebred following fetal Neospora infection and abortion were identified from 2 drylot dairies. All 4 cows had uncomplicated pregnancies with the birth of 5 full-term calves. The calves all had high precolostral serum IgG antibodies. The precolostral antibodies to Neospora sp as determined by indirect fluorescent antibody test ranged from 5,120 to 20,480, compared with maternal serum and colostral antibody titers from 320 to 1,280. Two calves had mild neurologic limb deficits. Three calves had mild nonsuppurative encephalomyelitis and Neospora organisms were found in the CNS of 3 calves. Findings indicate that repeat transplacental Neospora infections occur in cows. Additionally, calves born from cows with a history of Neospora fetal infection and abortion may have congenital Neospora infections and/or neurologic dysfunctions at birth. The Neospora indirect fluorescent antibody test appears to be a useful antemortem test for detection of calves exposed in utero to Neospora organisms.

Free access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To estimate the analytic sensitivity of microscopic detection of Toxoplasma gondii oocysts and the environmental loading of T gondii oocysts on the basis of prevalence of shedding by owned and unowned cats.

Design—Cross-sectional survey.

Sample Population—326 fecal samples from cats.

Procedures—Fecal samples were collected from cat shelters, veterinary clinics, cat-owning households, and outdoor locations and tested via ZnSO4 fecal flotation.

Results—Only 3 (0.9%) samples of feces from 326 cats in the Morro Bay area of California contained T gondii–like oocysts. On the basis of the estimated tonnage of cat feces deposited outdoors in this area, the annual burden in the environment was estimated to be 94 to 4,671 oocysts/m2 (9 to 434 oocysts/ft2).

Conclusions and Clinical Relevance—Despite the low prevalence and short duration of T gondii oocyst shedding by cats detected in the present and former surveys, the sheer numbers of oocysts shed by cats during initial infection could lead to substantial environmental contamination. Veterinarians may wish to make cat owners aware of the potential threats to human and wildlife health posed by cats permitted to defecate outdoors.

Full access
in Journal of the American Veterinary Medical Association

Objective—

To estimate the minimum rate of abortion attributable to infection with Neospora sp in selected California dairy herds.

Design—

Prospective study.

Animals—

Twenty-six dairy herds containing 19,708 cows were studied. Fourteen herds had a history of abortions attributable to neosporosis, and 12 were herds in which neosporosis had not been identified as a cause of abortions.

Procedure—

During a 1-year period, all available aborted fetuses were submitted to veterinary diagnostic laboratories to determine the cause of abortion. Reproductive records of cows that aborted were reviewed.

Results—

Neospora sp infection was the major cause of abortion identified (113/266 abortions, 42.5%). The majority (232/266, 87.2%) of the aborted fetuses were submitted from herds with a history of abortions attributable to neosporosis, and Neospora sp infection was identified as the causative agent in 101 of 232 (43.5%) of the abortions from these herds. Fewer aborted fetuses were submitted from the 12 herds that did not have a history of abortion attributable to Neospora sp; however, neosporosis was confirmed as a cause of abortion in 6 of these 12 herds and was identified as the causative agent in 12 of 34 (35.3%) abortions from these herds. The disease was widespread throughout the state (19/26 herds in our study). Available reproductive histories of cows that had abortions attributed to neosporosis were evaluated, and 4 cows were identified that twice aborted Neospora-in-fected fetuses.

Free access
in Journal of the American Veterinary Medical Association

Objective—

To determine whether heifers with naturally acquired congenital exposure to Neospora sp would transmit the infection to their offspring during gestation.

Design—

Prospective cohort study.

Animals—

Neonatal heifers on a dairy with a history of Neospora sp infections were selected for the study on the basis of their serum titers to Neospora sp, as determined by the use of indirect fluorescent antibody testing. Seropositive heifers (n = 25) had titers ≥ 1:5,120 and seronegative heifers (25) had titers ≤ 1:80. All heifers were raised and bred on the dairy, and samples were obtained from heifers and their calves at the time of calving.

Procedure—

Blood samples were tested for Neospora sp antibodies. Histologic evaluations, Neospora sp immunohistochemical examinations. and protozoal culturing were performed on samples obtained from selected offspring (second-generation calves).

Results—

Seropositive heifers gave birth to calves with titers ≥ 1:1,280 to Neospora sp. All offspring from seropositive heifers that were necropsied had evidence of Neospora sp infection. All seronegative heifers and their offspring had titers < 1:80 to Neospora sp.

Clinical Implications—

Congenitally acquired Neospora sp infection can persist in clinically normal heifers and be transmitted transplacentally to their offspring. Vertical transmission can be a way by which neosporosis is maintained in herds. (J Am Vet Med Assoc 1997;210:1169–1172)

Free access
in Journal of the American Veterinary Medical Association