Radiological abnormalities of the cervicothoracic vertebrae in Warmblood horses with primary neck-related clinical signs versus controls.

Radiological observations at the cervicothoracic junction in horses with or without related clinical signs have not been comprehensively described. The aim was to evaluate the seventh cervical (C7) to second thoracic (T2) vertebrae in horses with neck-related clinical signs (neck pain and/or stiffness, neck-related forelimb lameness, or general proprioceptive [spinal] ataxia) and control horses. This prospective analytical cross-sectional study included 127 control horses and 96 cases, examined using standardized clinical and radiological protocols. Univariable logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (CI) to identify factors associated with radiological abnormalities. Severe modeling of the articular processes at C7-T1 was more likely in cases compared with controls, OR, 4.25; CI, 1.04-17.36; P = .04. Cases were more likely to have spondylolisthesis at C7-T1 than controls, OR, 3.61; CI, 1.75-7.44; P < .001. There was a lack of uniformity of disc space width at C6-C7, despite normal alignment of the vertebrae, in five (5.2%) cases and no control horses. Discospondylosis was seen in 9 (9.4%) horses at C7-T1 and 10 of 64 (15.6%) at T1-T2. The sagittal ratio for T1 was smaller for horses with neck-related forelimb lameness (P < .0002), neck pain/ stiffness (P = .04), or neurological cases (P < .001) than controls. The prevalence of radiological abnormalities at C7-T1 and T1-T2 highlights the importance of careful evaluation of the cervicothoracic junction in horses with neck-related signs.

Inflammatory and Immune-Mediated Myopathies, What Do We Know?

Inflammatory myopathies or myositis encompass diseases characterized by the presence of inflammatory cellular infiltrates, mainly polymorphonuclear cells and/or lymphocytes, in muscle. This is in contrast to most forms of muscle disease characterized by myodegeneration that results in macrophage infiltration. Inflammatory myopathies could have infectious or noninfectious causes. Noninfectious causes consist of primary (genetic, autoimmune) or acquired immune-mediated disease. Focal, multifocal or diffuse, acute or recurrent forms of disease can occur. This article will mainly review immune-mediated myopathies in horses. Myositis directly caused by infection such as Clostridium spp and others will not be discussed here.

Vestibular Disease.

The vestibular system (VS) is the primary specialized sensory system responsible for maintaining balance (equilibrium) and orientation of the eyes, neck, trunk, and limbs during rest and movement. Two important reflexes are responsible for maintaining balance: vestibulo-ocular and vestibulospinal reflexes. These reflexes involve peripheral and central components of the VS. Whether central or peripheral disease, most of the disorders of the VS result in ipsilateral neurologic deficits. A few uncommon exceptions present with contralateral signs to the site of the lesion. This article provides a brief review of functional anatomy, vestibular disease, clinical signs, and examples of disorders affecting the VS.

Dietary Caffeine Synergizes Adverse Peripheral and Central Responses to Anesthesia in Malignant Hyperthermia Susceptible Mice.

Ryanodine receptor (RYR) mutations confer stress-triggered malignant hyperthermia (MH) susceptibility. Dietary caffeine (CAF) is the most commonly consumed psychoactive compound by humans. CAF-triggered Ca2+ release and its influences on skeletal muscle contractility are widely used as experimental tools to study RYR function/dysfunction and diagnose MH susceptibility. We hypothesize that dietary CAF achieving blood levels measured in human plasma exacerbates the penetrance of RYR1 MH susceptibility mutations triggered by gaseous anesthetic, affecting both central and peripheral adverse responses. Heterozygous R163C-RYR1 (HET) MH susceptible mice are used to investigate the influences of dietary CAF on both peripheral and central responses before and after induction of halothane (HAL) maintenance anesthesia under experimental conditions that maintain normal core body temperature. HET mice receiving CAF (plasma CAF 893 ng/ml) have significantly shorter times to respiratory arrest compared with wild type, without altering blood chemistry or displaying hyperthermia or muscle rigor. Intraperitoneal bolus dantrolene before HAL prolongs time to respiratory arrest. A pilot electrographic study using subcutaneous electrodes reveals that dietary CAF does not alter baseline electroencephalogram (EEG) total power, but significantly shortens delay to isoelectric EEG, which precedes respiratory and cardiac arrest. CAF ± HAL are studied on RYR1 single-channel currents and HET myotubes to define molecular mechanisms of gene-by-environment synergism. Strong pharmacological synergism between CAF and HAL is demonstrated in both single-channel and myotube preparations. Central and peripheral nervous systems mediate adverse responses to HAL in a HET model of MH susceptibility exposed to dietary CAF, a modifiable lifestyle factor that may mitigate risks of acute and chronic diseases associated with RYR1 mutations. SIGNIFICANCE STATEMENT: Dietary caffeine at a human-relevant dose synergizes adverse peripheral and central responses to anesthesia in malignant hyperthermia susceptible mice. Synergism of these drugs can be attributed to their actions at ryanodine receptors.

The prevalence of temporal bone fractures is high in horses with severe temporohyoid osteoarthropathy.

Temporohyoid osteoarthropathy is a well-recognized cause of equine neurologic disease. Temporal bone fractures associated with temporohyoid osteoarthropathy have been recognized with CT, however, little information is available regarding these fractures. The aims of this retrospective analytical study were to assess the prevalence of these fractures and to describe the specific configurations and associated imaging and clinical features. Fracture of the temporal bone was identified with CT in 16 of 39 included horses. All fractures were unilateral, minimally displaced and extended through the temporal bone in a rostrodorsal to caudoventral orientation. Two fracture configurations were identified: in nine cases, the fracture extended the full width of the petrous pyramid into the cranial vault and in seven cases, the fracture only extended through the lateral part of the petrous temporal bone, not involving the cranial vault. Fusion of the temporohyoid joint was present in 13 of the 16 fracture cases. Quarter Horses were over-represented in the fractured population (14/16). All horses with fractures had ipsilateral neurologic deficits. Patient outcomes were not significantly different between temporohyoid osteoarthropathy horses with and without temporal bone fractures (P = 0.68). However, six of the nine patients with cranial vault involvement did not return to their previous use. Findings support previous studies indicating that temporal bones should be carefully assessed for concurrent fractures when temporohyoid osteoarthropathy is identified in CT images, especially when there is fusion of the temporohyoid joint. An improved awareness of specific fracture configurations will help with detection of these fractures.

An atypical presentation of multi-systemic B-cell lymphoma in a horse.

This report describes an unusual presentation of multicentric B-cell lymphoma with central and peripheral nerve involvement in a horse that was presented with acute onset, severe, multiple limb lameness, and muscle atrophy. This case highlights the importance of including neoplasia in the differential list in horses presenting for severe limb lameness associated with muscle atrophy, muscle fasciculations, and weakness.

Présentation atypique d'un lymphome à cellules B multisystémique chez un cheval. Ce rapport décrit la présentation inhabituelle d'un lymphome à cellules B multicentrique avec une implication du nerf central et périphérique chez un cheval qui avait été présenté avec une boiterie aiguë et grave de plusieurs membres et de l'atrophie musculaire. Ce cas souligne l'importance d'inclure la néoplasie dans la liste des diagnostics différentiels des chevaux présentés pour une boiterie grave d'un membre associée à l'atrophie musculaire, aux fasciculations musculaires et à la faiblesse.(Traduit par Isabelle Vallières).

Current dorsal myelographic column and dural diameter reduction rules do not apply at the cervicothoracic junction in horses.

Previously published myelographic studies do not report findings at the junction between the seventh cervical (C7) and first thoracic vertebrae (T1). Modern digital radiographic equipment allows improved visualization of C7-T1. Based on clinical experience, we hypothesized that 50% reduction of the dorsal myelographic column or 20% reduction of the dural diameter, criteria commonly used as a supportive finding for spinal cord compression in the cervical vertebral column, do not apply at C7-T1. A myelographic study was performed on 12 healthy, neurologically normal horses. Our hypothesis was confirmed; using established criteria eight of 12 horses would have been classified as having evidence of spinal cord compression at C7-T1. The dorsal myelographic column reduction at C7-T1 was 48 ± 12%, while the C6-C7 dorsal myelographic column reduction was 33 ± 17% (mean ± standard deviation) (P = 0.010). The dural diameter reduction at C7-T1 (22.0 ± 6.7%) was significantly greater than the dural diameter reduction at C6-C7 (13.2 ± 9.5%) (P = 0.0007). Further measurements and comparisons suggested that the apparent greater reduction of dorsal myelographic column and dural diameter at C7-T1 was due to larger intravertebral measurements at C7 rather than smaller intervertebral values at C7-T1. Based on these findings, alternative criteria should be used at C7-T1 when assessing clinical cases for cervical stenotic myelopathy. Reduction of the dorsal myelographic column by 60% or of the dural diameter by 30% would avoid high numbers of false positive myelographic cases at C7-T1.

Cardiovascular, respiratory and metabolic responses to apnea induced by atlanto-occipital intrathecal lidocaine injection in anesthetized horses.

OBJECTIVE: To determine physiologic responses to apnea-induced severe hypoxemia in anesthetized horses. STUDY DESIGN: Prospective experimental study. ANIMALS: Six university-owned horses with a median (range) body weight of 500 (220-510) kg and aged 13.5 (0.8-24.0) years scheduled for euthanasia. METHODS: Xylazine-midazolam-ketamine-anesthetized horses breathing room air spontaneously were instrumented with a facial artery catheter for pressure measurement and blood sampling, and were made apneic with atlanto-occipital intrathecal lidocaine (4 mg kg-1 ). Cardiopulmonary, biochemical and hematologic variables were recorded before (baseline) and every minute for 10 minutes after lidocaine injection. RESULTS: PaO2 values were: baseline, 55 mmHg (7.3 kPa); 1 minute, 28 mmHg (3.8 kPa); 2 minutes, 18 mmHg (2.4 kPa); 3 minutes, 15 mmHg (2.0 kPa), and 4-10 minutes, (8-11 mmHg (1.1-1.5 kPa). PaCO2 values were: baseline, 50 mmHg (6.7 kPa); 1 minute, 61 mmHg (8.1 kPa), and 2-10 minutes, 64-66 mmHg (8.5-8.8 kPa). Base excess values at baseline, 1 minute and 2-10 minutes were 5.3 mmol L-1 , 6.5 mmol L-1 and 7.0-8.1 mmol L-1 , respectively. Pulse rates at baseline, 1 minute and 2-7 minutes were 36, 53 and 54-85 beats minute-1 , respectively. Asystole occurred at 8 minutes. Pulse pressures were 50 mmHg at baseline and 1 minute, and 39 mmHg, 31 mmHg, 22 mmHg, 17 mmHg and 1-9 mmHg at 2, 3, 4, 5 and 6-10 minutes, respectively. Lactate was 0.9 mmol L-1 at baseline, progressively increasing to 1.7-2.4 mmol L-1 at 7-10 minutes. Packed cell volume increased after 7 minutes of apnea. There were no other major changes. CONCLUSIONS AND CLINICAL RELEVANCE: Apnea immediately exacerbated hypoxemia and hypercapnia and rapidly caused hemodynamic instability. Apnea in hypoxemic anesthetized horses is associated with a serious risk for progress to cardiovascular collapse.

PREVALENCE OF ANATOMICAL VARIATION OF THE SIXTH CERVICAL VERTEBRA AND ASSOCIATION WITH VERTEBRAL CANAL STENOSIS AND ARTICULAR PROCESS OSTEOARTHRITIS IN THE HORSE.

The sixth cervical vertebra (C6) has unique morphology due to a ventral extension from the transverse process known as the ventral lamina. Little information was found regarding the prevalence and clinical relevance of morphologic variations. Aims of this observational, retrospective study were to characterize C6 morphologic variations in a large sample of horses. Cervical radiographic studies of 100 horses were retrieved. Data recorded were signalment, clinical history, morphology of the C6 ventral lamina, presence of articular process osteoarthritis, and presence of static vertebral canal stenosis. Morphologic variations were found in C6 vertebrae for 24/100 horses, with symmetric absence of the ventral lamina in nine horses and asymmetric absence in 15. Anomalous C6 vertebrae were more common in Warmbloods, with 19/55 Warmbloods in the population being affected (P = 0.006). No association was found with sex. There was no significant difference in the mean of the intravertebral sagittal ratios between horses with normal or anomalous C6 vertebrae; however there was a significantly greater proportion of horses with anomalous C6 vertebrae that had an intravertebral sagittal ratio of less than 0.5 at C6 (P = 0.047). There was no association between the morphology of C6 and articular process osteoarthritis. Anomalous C6 vertebrae in our population were associated with a higher likelihood of cervical pain (P = 0.013). Authors propose that morphologic variations in the C6 ventral laminae could be linked to other developmental abnormalities such as vertebral canal stenosis, might affect regional biomechanics and should therefore be considered clinically relevant in horses. Future, controlled prospective studies are needed to test this theory.

Exploring the virome of diseased horses.

Metagenomics was used to characterize viral genomes in clinical specimens of horses with various organ-specific diseases of unknown aetiology. A novel parvovirus as well as a previously described hepacivirus closely related to human hepatitis C virus and equid herpesvirus 2 were identified in the cerebrospinal fluid of horses with neurological signs. Four co-infecting picobirnaviruses, including an unusual genome with fused RNA segments, and a divergent anellovirus were found in the plasma of two febrile horses. A novel cyclovirus genome was characterized from the nasal secretion of another febrile animal. Lastly, a small circular DNA genome with a Rep gene, from a virus we called kirkovirus, was identified in the liver and spleen of a horse with fatal idiopathic hepatopathy. This study expands the number of viruses found in horses, and characterizes their genomes to assist future epidemiological studies of their transmission and potential association with various equine diseases.

Atlanto-axial approach for cervical myelography in a Thoroughbred horse with complete fusion of the atlanto-occipital bones.

A 2-year-old Thoroughbred gelding with clinical signs localized to the first 6 spinal cord segments (C1 to C6) had complete fusion of the atlanto-occipital bones which precluded performing a routine myelogram. An ultrasound-assisted myelogram at the intervertebral space between the atlas and axis was successfully done and identified a marked extradural compressive myelopathy at the level of the atlas and axis, and axis and third cervical vertebrae.

Approche atlanto-axiale pour une myélographie cervicale chez un cheval Thoroughbred avec la fusion complète des os occipito-atloïdiens. Un hongre Thoroughbred âgé de 2 ans avec des signes cliniques localisés aux 6 premiers segments de la colonne vertébrale (C1 à C6) avait une fusion complète des os occipito-atloïdiens qui empêchait la réalisation d'un myélogramme de routine. Un myélogramme par échographie à l'espace intervertébral entre l'atlas et l'axis a été réalisé avec succès et a identifié une myélopathie extradurale compressive prononcée au niveau de l'atlas et de l'axis ainsi que de l'axis et de la troisième vertèbre cervicale.(Traduit par Isabelle Vallières).

Primary phenotypic features associated with caudal neck pathology in warmblood horses.

BACKGROUND: Detailed descriptions of clinical signs associated with radiological findings of the caudal cervical vertebral column are not available. OBJECTIVES/HYPOTHESES: Describe the clinical features associated with neck pain or stiffness, neck-related thoracic limb lameness, proprioceptive ataxia consistent with a cervicothoracic spinal cord or nerve lesion, and their frequency of occurrence compared with control horses. ANIMALS: A total of 223 Warmblood horses. METHODS: Case-control study. Controls and cases were recruited prospectively. All horses underwent predetermined lameness and neurologic examinations. The frequency of occurrence of each clinical feature was compared between cases and controls and relative risk (RR) were calculated. RESULTS: Ninety-six cases and 127 controls were included. Forty-seven (49%) of the cases were classified as neurologic, 31 (32.3%) had thoracic limb lameness, and 18 (18.7%) had neck stiffness or pain or both. Focal caudal cervical muscle atrophy (46, 47.9%), hypoesthesia (38, 39.6%), patchy sweating (16, 16.7%), hyperesthesia (11, 11.5%), and pain upon firm pressure applied over the caudal cervical articular process joints and transverse processes (58, 60.4%) were only observed in cases (P < .001). Sideways flexion of the neck was restricted in a higher proportion of cases (47/96, 49%) compared with controls (40/127, 31.8%; P = .009, RR 1.5). Hopping-type thoracic limb lameness was only observed in cases, (30, 31.6%). Deterioration in lameness after diagnostic anesthesia occurred in 13/31 (41.9%) cases. CONCLUSIONS AND CLINICAL IMPORTANCE: Systematic clinical evaluation using the methods described should enable clinical differentiation between horses with caudal cervical lesions and horses with other causes of gait abnormalities.

Juvenile idiopathic epilepsy in Egyptian Arabian foals, a potential animal model of self-limited epilepsy in children.

BACKGROUND: Juvenile idiopathic epilepsy (JIE) is categorized as a generalized epilepsy. Epilepsy classification entails electrocortical characterization and localization of epileptic discharges (ED) using electroencephalography (EEG). HYPOTHESIS/OBJECTIVES: Characterize epilepsy in Egyptian Arabian foals with JIE using EEG. ANIMALS: Sixty-nine foals (JIE, 48; controls, 21). METHODS: Retrospective study. Inclusion criteria consisted of Egyptian Arabian foals: (1) JIE group diagnosed based on witnessed or recorded seizures, and neurological and EEG findings, and (2) control group of healthy nonepileptic age-matched foals. Clinical data were obtained in 48 foals. Electroencephalography with photic stimulation was performed under standing sedation in 37 JIE foals and 21 controls. RESULTS: Abnormalities on EEG were found in 95% of epileptic foals (35 of 37) and in 3 of 21 control asymptomatic foals with affected siblings. Focal ED were detected predominantly in the central vertex with diffusion into the centroparietal or frontocentral regions (n = 35). Generalization of ED occurred in 14 JIE foals. Epileptic discharges commonly were seen during wakefulness (n = 27/37 JIE foals) and sedated sleep (n = 35/37 JIE foals; 3/21 controls). Photic stimulation triggered focal central ED in 15 of 21 JIE foals. CONCLUSIONS AND CLINICAL IMPORTANCE: Juvenile idiopathic epilepsy has a focal onset of ED at the central vertex with spread resulting in clinical generalized tonic-clonic seizures with facial motor activity and loss of consciousness. Electroencephalography with photic stimulation contributes to accurate phenotyping of epilepsy. Foals with this benign self-limiting disorder might serve as a naturally occurring animal model for self-limited epilepsy in children.

Congenital variants of the ventral laminae of the sixth and seventh cervical vertebrae are not associated with clinical signs or other radiological abnormalities of the cervicothoracic region in Warmblood horses.

BACKGROUND: There is controversy about the clinical relevance of congenital variants of the ventral laminae of the sixth (C6) and seventh (C7) cervical vertebrae and their relationship with other radiological abnormalities. OBJECTIVES: To document the prevalence of congenital variants of C6 and C7 and that of other radiological abnormalities from C6 to the second thoracic vertebra (T2). STUDY DESIGN: Cross-sectional. METHODS: The study included Warmblood horses ≥3 years of age undergoing clinical assessment at two referral institutions: 127 control horses and 96 cases (neurologic, neck pain or stiffness, or neck-related forelimb lameness). All horses underwent a standardised orthopaedic and neurologic examination. Lateral-lateral and lateral 45°-55° ventral-lateral dorsal (left to right and right to left) radiographic views of C5 to T2 were acquired and assessed blinded to the horse's clinical category using a predetermined grading system. RESULTS: The ventral profile of C7 was abnormal in 54 horses (24.2%). Cases were less likely to have congenital variants than control horses, p = 0.0002, relative risk (RR): 0.63 (95% confidence intervals [CIs]: 0.4, 1.0). There was no association between the presence of a congenital variant of C7 and the presence of modelling of the articular processes (APs) of C6-C7, C7-T1 or T1-T2. Cases were more likely to have severe modelling of the APs at C6-C7, p = 0.01, RR: 1.94, CI: 1.1, 3.5 and C7-T1, p = 0.04, RR: 1.97, CI: 1.2, 3.2 compared with control horses. MAIN LIMITATIONS: Radiographs were read by one assessor independently at each institution. CONCLUSIONS: There was no association between the presence of congenital variants of C7 and any other radiological findings. Congenital variants occurred less frequently in cases compared with control horses. There was no association between the presence or absence of a congenital variant and the type of case.

Parasympathetic tone activity, heart rate, and grimace scale in conscious horses of 3 breeds before, during, and after nociceptive mechanical stimulation.

BACKGROUND: Parasympathetic tone activity (PTA) in response to nociceptive stimulus in conscious non-sedated horses is unknown. OBJECTIVES: Study PTA, heart rate (HR), and horse grimace scale (HGS) at rest and during mechanical nociceptive stimulation. ANIMALS: Ninety healthy young adult horses (females, males): 30 each of Friesians, Quarter Horses, and Warmbloods. METHODS: Prospective control study. The study consisted of habituation to equipment (Day 1), baseline recordings (Days 2 and 3), and nociceptive testing applying mild pressure to the metacarpus (Day 4). Parasympathetic tone, HR, and HGS were recorded simultaneously on Days 2 to 4. Each study lasted 30 minutes and was done in triplicate at 3 different time points per day. RESULTS: Baseline PTA was not different among breeds. It decreased in Warmbloods and Quarter Horses during placement of the stimulus device without stimulation (P < .01). A significant decrease in PTA (P < .001) occurred during nociceptive stimulus (marked in Quarter Horses, intermediate in Warmbloods, and mild in Friesians). Heart rate and HGS increased significantly (P < .001) during the stimulus in all breeds but returned to baseline poststimulation. Friesians required higher pressure (P < .05) to elicit an aversive response to the stimulus. CONCLUSIONS: Horses' PTA, HR, and HGS change in response to a mild mechanical nociceptive stimulus with Friesians showing less variation. Stress induced a decrease in PTA in Quarter Horses and Warmbloods but not in Friesians. Friesians appeared to be more tolerant to pain based on PTA, HR, and HGS findings compared with other breeds.

Common and atypical presentations of Anaplasma phagocytophilum infection in equids with emphasis on neurologic and muscle disease.

BACKGROUND: Comprehensive descriptions of equids with granulocytic anaplasmosis (EGA) with neurologic or muscle disease and other atypical presentations are scarce in the literature. OBJECTIVE: Describe the clinical signs, laboratory findings, treatment, and outcome of equids with EGA with emphasis on neurologic and muscle disease. ANIMALS: Thirty-eight horses, 1 donkey. METHODS: Retrospective study. Equids with EGA were included. The electronic data base was searched from January 2000 to December 2022 using the words anaplasmosis, ehrlichiosis, granulocytic, and rickettsia. Signalment and clinical data were reviewed. Data were evaluated for normality using Shapiro-Wilk test. Parametric and nonparametric statistics were used for normally and non-normally distributed data. RESULTS: Common (41%) and other (59%) presentations were seen in horses ≥ 4 years of age (median, 14 years) with an overrepresentation of males (77%). Neurologic disease was common (41%), mainly presenting as diffuse symmetrical proprioceptive ataxia. Brain disease was less common manifesting as obtundation and cranial nerve deficits. Muscle disease was less common, with QH breeds with the variant causing myosin heavy chain myopathy (MYHM) having severe disease. Cavitary effusion, cardiomyopathy and disseminated intravascular coagulation (DIC) were uncommon. Clinical laboratory results varied depending on disease stage. Muscle enzyme activities were significantly higher in horses with muscle disease. Outcome was favorable with prompt tetracycline treatment. Death and long-term sequelae were not reported. CONCLUSIONS AND CLINICAL IMPORTANCE: Common and atypical presentations of EGA have a favorable outcome with prompt tetracycline treatment. Quarter horse breeds with muscle disease should be genotyped for MYHM.

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.

Clinicopathological and pedigree investigation of a novel spinocerebellar neurological disease in juvenile Quarter Horses in North America.

BACKGROUND: In 2020, a novel neurologic disease was observed in juvenile Quarter Horses (QHs) in North America. It was unknown if this was an aberrant manifestation of another previously described neurological disorder in foals, such as equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (eNAD/EDM). HYPOTHESIS/OBJECTIVES: To describe the clinical findings, outcomes, and postmortem changes with Equine Juvenile Spinocerebellar Ataxia (EJSCA), differentiate the disease from other similar neurological disorders, and determine a mode of inheritance. ANIMALS: Twelve neurologically affected QH foals and the dams. METHODS: Genomic DNA was isolated and pedigrees were manually constructed. RESULTS: All foals (n = 12/12) had a history of acute onset of neurological deficits with no history of trauma. Neurological deficits were characterized by asymmetrical spinal ataxia, with pelvic limbs more severely affected than thoracic limbs. Clinicopathological abnormalities included high serum activity of gamma-glutamyl transferase and hyperglycemia. All foals became recumbent (median, 3 days: [0-18 days]), which necessitated humane euthanasia (n = 11/12, 92%; the remaining case was found dead). Histological evaluation at postmortem revealed dilated myelin sheaths and digestion chambers within the spinal cord, most prominently in the dorsal spinocerebellar tracts. Pedigree analysis revealed a likely autosomal recessive mode of inheritance. CONCLUSIONS AND CLINICAL IMPORTANCE: EJSCA is a uniformly fatal, rapidly progressive, likely autosomal recessive neurological disease of QHs <1 month of age in North America that is etiologically distinct from other clinically similar neurological disorders. Once the causative variant for EJSCA is validated, carriers can be identified through genetic testing to inform breeding decisions.

Preliminary evaluation of hepatitis A virus cell receptor 1/kidney injury molecule 1 in healthy horses treated with phenylbutazone.

OBJECTIVES: To investigate if hepatitis A virus cell receptor 1/kidney injury molecule 1 (HAVCR1/KIM1) in urine is detectable concurrently with increases in serum creatinine concentrations in horses receiving a recommended dose of phenylbutazone (PBZ) for 7 days. DESIGN: Preliminary study. METHODS: Ten clinically healthy horses with normal physical examination and laboratory work were randomly assigned to PBZ or placebo groups (5 each). The PBZ group received PBZ at 4.4 mg/kg mixed with corn syrup orally every 12 hours. The placebo group received corn syrup orally every 12 hours. Both groups were treated for 7 days. Kidney ultrasonography was performed, and venous blood and urine samples were collected prior to commencement and at the end of treatment. Samples from 1 additional healthy horse, 3 horses with acute kidney failure, and 1 horse with chronic kidney failure were also evaluated. RESULTS: None of the 10 horses had detectable HAVCR1/KIM1 in urine at baseline. Serum creatinine concentrations in placebo group did not increase, and HAVCR1/KIM1 was undetectable in urine. At the end of treatment, 3 of 5 horses receiving PBZ developed increases in serum creatinine of >26.5 µmol/L (>0.3 mg/dL), and HAVCR1/KIM1 was detectable in urine, despite normal findings on kidney ultrasonography in all horses. CONCLUSIONS: HAVCR1/KIM1 is detectable in urine and is associated with increases in serum creatinine concentrations of >26.5 µmol/L in horses following treatment with PBZ for 7 consecutive days. Thus, HAVCR1/KIM1 might aid in the early detection of acute kidney injury in horses.

Effect of time and autologous serum addition on the analysis of cerebrospinal fluid in horses.

BACKGROUND: Cerebrospinal fluid (CSF) is highly labile and delayed processing might alter results of analysis. HYPOTHESIS/OBJECTIVES: To determine the effects of time and addition of autologous serum on cytological evaluation of CSF. ANIMALS: Ten client-owned adult horses requiring euthanasia. METHODS: Prospective study. Serum and CSF were collected from each horse before and within 10 minutes after euthanasia. CSF samples were divided into 15 aliquots (2 mL each); 1 aliquot was submitted for routine CSF analysis within 60 minutes of collection. Four drops of autologous serum were added to 7 of the aliquots, and stored at 4°C (serum group); the remaining 7 samples were stored unaltered at 4°C (control group). Total nucleated cell count (TNCC) and cell morphology score were done at T4, T8, T12, T24, T48, T72, and T96 hours after collection. Protein concentration was measured in the control group at T0 and T96 hours. RESULTS: The cell morphology scores were significantly different in the control group at T48 (median 2, range 0-4), T72 (2, 0-4), and T96 (3, 0-4) in comparison to T0 (1). No change was observed in the serum group. TNCC remained stable over time in both groups. No statistically significant difference in CSF protein concentration was found between T0 and T96. CONCLUSIONS AND CLINICAL IMPORTANCE: The addition of autologous serum to an aliquot of CSF sample before shipping improves the preservation of cell morphology up to 96 hours after collection.