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.

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.

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.

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.

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.

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.

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.

Canine models of Charcot-Marie-Tooth: MTMR2, MPZ, and SH3TC2 variants in golden retrievers with congenital hypomyelinating polyneuropathy.

Congenital hypomyelinating polyneuropathy (HPN) restricted to the peripheral nervous system was reported in 1989 in two Golden Retriever (GR) littermates. Recently, four additional cases of congenital HPN in young, unrelated GRs were diagnosed via neurological examination, electrodiagnostic evaluation, and peripheral nerve pathology. Whole-genome sequencing was performed on all four GRs, and variants from each dog were compared to variants found across >1,000 other dogs, all presumably unaffected with HPN. Likely causative variants were identified for each HPN-affected GR. Two cases shared a homozygous splice donor site variant in MTMR2, with a stop codon introduced within six codons following the inclusion of the intron. One case had a heterozygous MPZ isoleucine to threonine substitution. The last case had a homozygous SH3TC2 nonsense variant predicted to truncate approximately one-half of the protein. Haplotype analysis using 524 GR established the novelty of the identified variants. Each variant occurs within genes that are associated with the human Charcot-Marie-Tooth (CMT) group of heterogeneous diseases, affecting the peripheral nervous system. Testing a large GR population (n = >200) did not identify any dogs with these variants. Although these variants are rare within the general GR population, breeders should be cautious to avoid propagating these alleles.

Red blood cell distribution width to platelet ratio in neonatal foals with sepsis.

BACKGROUND: Rapid and accurate markers to aid diagnosis of sepsis are needed in neonatal foals. The CBC variable red blood cell distribution width (RDW) to platelet ratio (RPR) is associated with inflammatory response and linked to poor outcomes of sepsis in human patients. HYPOTHESIS: Explore the correlation of RPR with sepsis in neonatal foals and evaluate RPR predictive and prognostic value. ANIMALS: Three hundred seventeen hospitalized neonatal foals ≤7 days of age that had a CBC and physical exam performed at admission between 2012 and 2021. METHODS: Retrospective case-control study. Clinical records were used to calculate sepsis scores and define groups. Red blood cell distribution width to platelet ratio was calculated and compared between groups (septic vs nonseptic) based on Kruskal-Wallis and Wilcoxon signed-rank tests. A multivariate logistic regression model to predict sepsis was created. The cutoff for RPR was obtained based on the maximal Youden Index. The Kaplan-Meier method and the log-rank test were used to estimate survival curves and compare survival rates based on RPR. RESULTS: Red blood cell distribution width to platelet ratio was significantly higher in septic foals (Median = 0.099, confidence interval [CI] [0.093; 0.108]) than in sick nonseptic (0.085, CI [0.083; 0.089]) and healthy foals (0.081, CI [0.077; 0.086]; P < .0001). Red blood cell distribution width to platelet ratio was able to predict sepsis with high accuracy (AUC = 82.1%). The optimal RPR cutoff for sepsis was 0.09. CONCLUSIONS AND CLINICAL IMPORTANCE: Red blood cell distribution width to platelet ratio calculation is practical, inexpensive, and based on CBC-derived data. Calculation of RPR along with CBC can aid in the diagnosis of sepsis and estimation of outcome.

Electroencephalographic evaluation under standing sedation using sublingual detomidine hydrochloride in Egyptian Arabian foals for investigation of epilepsy.

BACKGROUND: A standardized protocol for electroencephalography (EEG) under standing sedation for the investigation of epilepsy in foals is needed. HYPOTHESIS/OBJECTIVES: To evaluate a modified standardized EEG protocol under standing sedation using sublingual detomidine hydrochloride in Egyptian Arabian foals. ANIMALS: Nineteen foals (controls, 9; juvenile idiopathic epilepsy [JIE], 10). METHODS: Descriptive clinical study. Foals were classified as controls or epileptic based on history or witnessed seizures and neurological examination. Foals were sedated using sublingual detomidine hydrochloride at a dosage of 0.08 mg/kg to avoid stress associated with injectable sedation. Once foals appeared sedated with their heads low to the ground and with wide base stance (30 minutes), topical lidocaine hydrochloride was applied at the determined locations of EEG electrodes. Fifteen minutes were allowed for absorption and electrodes were placed, protected, and EEG recording performed. RESULTS: Level of sedation was considered excellent with no need of redosing. The EEG recording lasted from 27 to 51 minutes and provided interpretable data. Epileptic discharges (ED) were noted predominantly in the central-parietal region in 9 of 10 epileptic foals. Photic stimulation triggered ED in 7 of 10 epileptic foals and in none of the controls. Foals were not oversedated and recovered uneventfully. CONCLUSIONS AND CLINICAL IMPORTANCE: Sublingual detomidine hydrochloride is a safe, painless, simple, and effective method of sedation for EEG recording in foals. Sublingual sedation allowed the investigation of cerebral electrical activity during states of sleep and arousal, and during photic stimulation for the investigation of epilepsy in foals.

Evidence of intrathecally-derived antibodies against Toxoplasma gondii in horses suspected of neurological disease consistent with equine protozoal myeloencephalitis.

Among the recognized neurologic diseases in horses, equine protozoal myeloencephalitis (EPM) has been reported around the world and still presents challenges in diagnosis and treatment. Horses can present with clinical neurologic signs consistent with EPM while testing negative for the two main causative agents, Sarcocystis neurona or Neospora hughesi, and may still be clinically responsive to anti-parasitic drug therapy. This context led to our hypothesis that another protozoal parasite, Toxoplasma gondii, which is known to cause toxoplasmosis in other mammalian species, is a potential pathogen to cause neurologic disease in horses. To evaluate this hypothesis, serum and cerebrospinal fluid (CSF) were collected from 210 horses presenting with clinical signs compatible with EPM, and the indirect immunofluorescent antibody test (IFAT) was used to detect antibody titers for T. gondii, S. neurona, and N. hughesi. Additionally, the serum to CSF titer ratio was calculated for T. gondii, S. neurona, and N. hughesi infections, suggesting intrathecally-derived antibodies for each of the three agents if the serum:CSF ratio was ≤ 64. There were 133 (63.3%) horses positive for serum T. gondii antibodies using a cutoff titer of 160, and 31 (14.8%) positive for CSF T. gondii antibodies using a cutoff titer of 5. Overall, 21 (10.0%) of EPM-suspect horses had a serum:CSF ratio ≤ 64 for antibodies for T. gondii, while 43 (20.5%) and 8 (3.8%) horses had a serum to CSF ratio ≤ 64 for antibodies for S. neurona and N. hughesi, respectively. A total of 6 (2.9%) animals presented evidence of concurrent intrathecally-derived antibodies for T. gondii and at least one other apicomplexan parasite in this study. Signalment and clinical signs were not different across the groups aforementioned. These data provide evidence of intrathecal production of anti-T. gondii antibodies, indicative of T. gondii infection in the brain and/or spinal cord of horses with EPM-like disease.

Tolerability and pharmacokinetics of intravenous allopregnanolone with and without midazolam pretreatment in two healthy dogs.

The neurosteroid allopregnanolone (ALLO) is under investigation as a treatment for benzodiazepine-refractory status epilepticus (SE). Here, we assess the cardiopulmonary safety of intravenous ALLO by itself and after a clinically recommended dose of midazolam (MDZ) in two healthy adult beagles. Each dog received ALLO (1 mg/kg, IV), and after a washout period of 2 weeks, each dog was dosed with MDZ (0.2 mg/kg, IV) followed 10 minutes later by ALLO. Behavioral state, vital signs, arterial blood gases, blood chemistries, and plasma ALLO concentrations were monitored for up to 6 hours after dosing. The dogs appeared sleepy but were fully responsive after both treatments. No depression of mean arterial pressure or respiratory rate was noted. Blood gas measurements failed to show evidence of drug-induced acute respiratory acidosis. Estimated maximum plasma ALLO concentrations were in the range of 1500 to 3000 ng/ml. The results indicate that intravenous ALLO can be used safely to treat benzodiazepine-refractory SE, even when administered shortly after a benzodiazepine.

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.

Red cell distribution width values and red cell distribution width-to-platelet ratio in Thoroughbred foals in the first 24 hours of life.

OBJECTIVES: To report red cell distribution width (RDW) values, to calculate RDW-to-platelet ratio (RPR), and to investigate a possible correlation of RDW and RPR index values in neonatal foals classified as healthy or at risk based on clinical information from a population of foals up to 24 hours of life. DESIGN: Retrospective study conducted from records and CBCs of foals born between June and November from 2018 to 2020 foaling seasons. SETTING: Breeding farm. ANIMALS: Three hundred and nine neonatal full-term Thoroughbred foals. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Foals were evaluated by a veterinarian within 15 minutes after birth, and a blood sample was collected within 24 hours of life. Based on clinical information, 88 of 309 foals (28.4%) were considered at risk of perinatal disease, and 201 were healthy. Mean gestational age for the foals was 346.3 ± 9.7 days. RDW values did not differ between groups. Gestational length demonstrated to have a negative correlation with RDW (r = -0.156, P = 0.005) and mean corpuscular volume (r = -0.135, P = 0.01), indicating a link of these variables to foal maturity. RPR index was higher for at-risk (0.073 ± 0.018) than for healthy foals (0.068 ± 0.014, P = 0.01). CONCLUSION: RPR might be a promising early indicator of disease for the field triage of neonatal foals.

Prevalence of Genetic Mutations in Horses With Muscle Disease From a Neuromuscular Disease Laboratory.

Deleterious genetic variants are an important cause of skeletal muscle disease. Immunohistochemical evaluation of muscle biopsies is standard for the diagnosis of muscle disorders. The prevalence of alleles causing hyperkalemic periodic paralysis (HYPP), malignant hyperthermia (MH), polysaccharide storage myopathy 1 (PSSM1), glycogen branching enzyme deficiency (GBED), myotonia congenita (MC), and myosin heavy chain myopathy (MYHM) in horses with muscle disease is unknown. Archived slides processed for immunohistochemical analysis from 296 horses with muscle disease were reviewed blinded and clinical information obtained. DNA isolated from stored muscle samples from these horses were genotyped for disease variants. Histological findings were classified as myopathic in 192, neurogenic in 41, and normal in 63 horses. A third of the population had alleles that explained disease which constituted 45% of the horses with confirmed histological myopathic process. Four of six muscle disease alleles were identified only in Quarter horse breeds. The allele causing PSSM1 was detected in other breeds, and MC was not detected in these samples. The My allele, associated with susceptibility for MYHM, was the most common (62%) with homozygotes (16/27) presenting a more severe phenotype compared to heterozygotes (6/33). All cases with the MH allele were fatal upon triggering by anesthesia, stress or concurrent myopathy. Both, muscle histological and genetic analyses are essential in the investigation of muscle disease, since 10% of the horses with muscle disease and normal histology had a muscle disease causing genetic variant, and 63% of histologically confirmed muscle with alterations had no known genetic variants.

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.

Fish evacuation and emergency sheltering during wildfire disasters.

Wildfires are a serious and expanding threat in western North America, and wildfire encroachment on human populations leads to widespread evacuation and emergency housing operations for residents and their companion animals and livestock. Veterinarians are frequently part of wildfire response efforts and are called upon to assist in rescue, evacuation, and emergency housing operations as well as to provide medical care for evacuated animals. Although veterinarians are likely familiar with the principles of transporting and housing terrestrial animals, emergency response for aquatic companion animals presents unique logistic challenges. Veterinarians familiar with aquatic animal evacuation, housing, and care prior to a wildfire response can extend the scope of disaster recovery. This report offers general guidance for rescuing, evacuating, housing, and caring for aquatic animals in the wake of a wildfire.

Caecal microbiota in horses with trigeminal-mediated headshaking.

BACKGROUND: Trigeminal-mediated headshaking (TMHS) in horses is a form of neuropathic pain of undetermined cause that often results in euthanasia. The role of microbiota in TMHS has not been investigated in diseased horses. OBJECTIVE: To investigate if gastrointestinal microbiota in the cecum is different in horses with TMHS compared to a control population, during a summer season with clinical manifestations of disease. ANIMALS: Ten castrated horses: five with TMHS and five neurologically normal controls. METHODS: All horses were sourced from our institution and kept under the same husbandry and dietary conditions. All horses were fed orchard grass hay for 30 days and then were euthanized due to chronic untreatable conditions including TMHS and orthopedic disease (control group). Caecal samples for microbiota analysis were collected within 20 min after euthanasia. Sequencing was performed using an Illumina MiSeq platform and the microbiome was analyzed. RESULTS: The caecal microbiota of horses with TMHS was similar to control horses in terms of diversity but differed significantly with Methanocorpusculum spp. having higher abundance in horses with TMHS.  CONCLUSIONS AND CLINICAL IMPORTANCE: Methanocorpusculum spp. was more abundant in the cecum of horses with TMHS. However, its role in disease is unknown. Furthermore, it could also represent an incidental finding due to our small population size.

Gentamicin-induced sensorineural auditory loss in healthy adult horses.

BACKGROUND: Irreversible sensorineural auditory loss has been reported in humans treated with aminoglycosides but not in horses. OBJECTIVE: Investigate if auditory loss occurs in horses treated using the recommended IV daily dosage of gentamicin for 7 consecutive days. ANIMALS: Ten healthy adult horses (7-15 years; females and males, 5 each). METHODS: Prospective study. Physical and neurological examinations and renal function tests were performed. Gentamicin sulfate was administered at a dosage of 6.6 mg/kg via the jugular vein on alternating sides for 7 days. Gentamicin peak and trough concentrations were measured. Horses were sedated using detomidine hydrochloride IV to perform brainstem auditory evoked responses (BAER) before the first dose, immediately after the last dose, and 30 days after the last dose. Peaks latencies, amplitudes, and amplitude ratios were recorded. Data from the second and last BAER were compared to results at baseline. Bone conduction was performed to rule out conduction disorders. RESULTS: Seven horses had auditory loss: complete bilateral (N = 1), complete unilateral (N = 2), and partial unilateral (N = 4). Based on physical examination and BAER results, sensorineural auditory loss was suspected. Absent bone conduction ruled out a conduction disorder and further supported sensorineural auditory loss in horses with completely absent BAER. Auditory dysfunction was reversible in 4 of 7 horses. CONCLUSIONS AND CLINICAL IMPORTANCE: Gentamicin at recommended doses may cause sensorineural auditory loss in horses that might be irreversible. Follow-up studies are needed to investigate if other dosing protocols present a similar risk.