Search

Summary: A 3‐year‐old Gypsy Vanner stallion was presented for evaluation of intermittent recumbency, muscle fasciculations, weakness, low head carriage, shifting of weight between the hindlimbs and an elevated tail head. History, physical examination and serum alpha tocopherol concentrations were suggestive of vitamin E deficiency and equine motor neuron disease (EMND). Sacrocaudalis dorsalis medialis muscle biopsy identified myositis secondary to sarcocystosis. Treatment with alpha tocopherol, ponazuril and sulfadiazine/pyrimethamine resulted in significant improvement in muscle weakness and body condition with resolution of sarcocystosis and inflammation on repeat muscle biopsy. This case illustrates the importance of muscle biopsy in horses with neuromuscular disease as concurrent diseases may be present that require specific treatment for a positive outcome. [ABSTRACT FROM AUTHOR]

In horses, immune-mediated muscle disorders can arise from an overzealous immune response to concurrent infections or potentially from an inherent immune response to host muscle antigens. Streptococcus equi ss. equi infection or vaccination can result in infarctive purpura hemorrhagica (IPH) in which vascular deposition of IgA-streptococcal M protein complexes produces ischemia and complete focal infarction of skeletal muscle and internal organs. In Quarter Horse–related breeds with immune-mediated myositis, an apparent abnormal immune response to muscle antigens results in upregulation of major histocompatibility complex class (MHC) I and II on muscle cell membranes, lymphocytic infiltration of lumbar and gluteal myofibers, and subsequent gross muscle atrophy. Rarely, an inflammatory event results in myositis with subsequent systemic calcinosis characterized by a pathognomonic hyperphosphatemia and high fatality rate. This review presents an overview of these immune-mediated myopathies and highlights clinical and pathological features as well as the suspected pathophysiology. [ABSTRACT FROM AUTHOR]

In the horse, the term occipitoatlantoaxial malformation ( OAAM) is used to describe a developmental defect in which the first cervical vertebra (atlas) resembles the base of the skull (occiput) and the second cervical vertebra (axis) resembles the atlas. Affected individuals demonstrate an abnormal posture and varying degrees of ataxia. The homeobox ( HOX) gene cluster is involved in the development of both the axial and appendicular skeleton. Hoxd3-null mice demonstrate a strikingly similar phenotype to Arabian foals with OAAM. Whole-genome sequencing was performed in an OAAM-affected horse ( OAAM1) and seven unaffected Arabian horses. Visual inspection of the raw reads within the region of HOXD3 identified a 2.7-kb deletion located 4.4 kb downstream of the end of HOXD4 and 8.2 kb upstream of the start of HOXD3. A genotyping assay revealed that both parents of OAAM1 were heterozygous for the deletion. Additional genotyping identified two of 162 heterozygote Arabians, and the deletion was not present in 371 horses of other breeds. Comparative genomics studies have revealed that this region is highly conserved across species and that the entire genomic region between Hoxd4 and Hoxd3 is transcribed in mice. Two additional Arabian foals diagnosed with OAAM ( OAAM 2 and 3) were genotyped and did not have the 2.7-kb deletion. Closer examination of the phenotype in these cases revealed notable variation. OAAM3 also had facial malformations and a patent ductus arteriosus, and the actual malformation at the craniocervical junction differed. Genetic heterogeneity may exist across the HOXD locus in Arabian foals with OAAM. [ABSTRACT FROM AUTHOR]

Reasons for performing study Although exertional rhabdomyolysis ( ER) is common in Arabian horses, there are no dedicated studies describing histopathological characteristics of muscle from Arabian horses with ER. Objectives To prospectively identify distinctive histopathological features of muscle from Arabian endurance horses with a history of ER (pro- ER) and to retrospectively determine their prevalence in archived samples from Arabian horses with exertional myopathies (retro- ER). Study design Prospective and retrospective histopathological description. Methods Middle gluteal muscle biopsies obtained from Arabian controls (n = 14), pro- ER (n = 13) as well as archived retro- ER (n = 25) muscle samples previously classified with type 2 polysaccharide storage myopathy (15/25), recurrent exertional rhabdomyolysis (7/25) and no pathology (3/25) were scored for histopathology and immunohistochemical staining of cytoskeletal proteins. Glutaraldehyde-fixed samples (2 pro- ER, one control) were processed for electron microscopy. Pro- ER and retro- ER groups were compared with controls using Mann-Whitney U and Fisher's exact tests. Results Centrally located myonuclei in mature myofibres were found in significantly more (P<0.05) pro- ER (12/13) and retro- ER (21/25) horses than controls (4/14). Degenerating myofibres were not evident in any biopsies. Retro- ER horses had amylase-resistant polysaccharide (6/25, P<0.05) and higher scores for cytoplasmic glycogen, rimmed vacuoles and rod-like bodies. A few control horses (3/14) and significantly (P<0.05) more pro- ER (12/13) and retro- ER (18/25) horses had disrupted myofibrillar alignment and large desmin and αβ-crystallin positive cytoplasmic aggregates. Prominent Z-disc degeneration and focal myofibrillar disruption with regional accumulation of β-glycogen particles were identified on electron microscopy of the 2 pro- ER samples. Conclusions In a subset of Arabian horses with intermittent episodes of exertional rhabdomyolysis, ectopic accumulation of cytoskeletal proteins and Z-disc degeneration bear a strong resemblance to a myofibrillar myopathy. While many of these horses were previously diagnosed with type 2 polysaccharide storage myopathy, pools of glycogen forming within disrupted myofibrils appeared to give the false appearance of a glycogen storage disorder. [ABSTRACT FROM AUTHOR]

Equine degenerative myeloencephalopathy (EDM) is characterized by a symmetric general proprioceptive ataxia in young horses, and is likely underdiagnosed for 2 reasons: first, clinical signs overlap those of cervical vertebral compressive myelopathy; second, histologic lesions—including axonal spheroids in specific tracts of the somatosensory and motor systems—may be subtle. The purpose of this study was (1) to utilize immunohistochemical (IHC) markers to trace axons in the spinocuneocerebellar, dorsal column–medial lemniscal, and dorsospinocerebellar tracts in healthy horses and (2) to determine the IHC staining characteristics of the neurons and degenerated axons along the somatosensory tracts in EDM-affected horses. Examination of brain, spinal cord, and nerves was performed on 2 age-matched control horses, 3 EDM-affected horses, and 2 age-matched disease-control horses via IHC for calbindin, vesicular glutamate transporter 2, parvalbumin, calretinin, glutamic acid decarboxylase, and glial fibrillary acidic protein. Primary afferent axons of the spinocuneocerebellar, dorsal column–medial lemniscal, and dorsospinocerebellar tracts were successfully traced with calretinin. Calretinin-positive cell bodies were identified in a subset of neurons in the dorsal root ganglia, suggesting that calretinin IHC could be used to trace axonal projections from these cell bodies. Calretinin-immunoreactive spheroids were present in EDM-affected horses within the nuclei cuneatus medialis, cuneatus lateralis, and thoracicus. Neurons within those nuclei were calretinin negative. Cell bodies of degenerated axons in EDM-affected horses are likely located in the dorsal root ganglia. These findings support the role of sensory axonal degeneration in the pathogenesis of EDM and provide a method to highlight tracts with axonal spheroids to aid in the diagnosis of this neurodegenerative disease. [ABSTRACT FROM AUTHOR]

Reasons for perfoming study Investigating the epidemiology of shivering in horses. Objectives The purpose of this study was to characterise the signalment, clinical signs and management factors associated with shivering (also known as shivers), a relatively rare, poorly defined movement disorder in horses. Study design Web-based case series survey and case-control study. Methods A Web-based survey was used to obtain information from owners, worldwide, who suspected that their horse had shivering. Survey respondents were asked to answer standardised questions and to provide a video of the horse. Authors reviewed the surveys and videos, and horses were diagnosed with shivering if they displayed normal forward walking, with difficulty during manual lifting of the hoof and backward walking due to hyperflexion or hyperextension of the pelvic limbs. Cases confirmed by video were designated 'confirmed shivering', while those with compatible clinical signs but lacking video confirmation were designated 'suspected shivering'. Owners of confirmed shivering horses were asked to provide information on 2 horses without signs of shivering (control group). Results Three hundred and five surveys and 70 videos were received; 27 horses were confirmed shivering (50 controls), 67 were suspected shivering and the rest had a variety of other movement disorders. Suspected shivering horses resembled confirmed shivering cases, except that the suspected shivering group contained fewer draught breeds and fewer horses with exercise intolerance. Confirmed shivering signs often began at <5 years of age and progressed in 74% of cases. Owner-reported additional clinical signs in confirmed cases included muscle twitching (85%), muscle atrophy (44%), reduced strength (33%) and exercise intolerance (33%). Shivering horses were significantly taller (confirmed shivering, mean ∼173 cm; control horses, ∼163 cm) with a higher male:female ratio (confirmed shivering, 3.2:1 vs. control, 1.7:1). No potential triggering factors or effective treatments were reported. Conclusions Shivering is a chronic, often gradually progressive movement disorder that usually begins before 7 years of age and has a higher prevalence in tall male horses. [ABSTRACT FROM AUTHOR]

Reasons for performing study Exertional rhabdomyolysis ( ER) is a reported syndrome in competing endurance horses; however, the prevalence and cause of ER in this population have not been defined. Objectives To determine the prevalence of ER in a sample of endurance racing horses and investigate factors, including relevant genetic defects, contributing to the occurrence of rhabdomyolysis in this group. Study design Prospective clinical study. Methods Riders of 101 horses participating in one of four 50-mile (80.5 km) distance races completed a comprehensive questionnaire regarding the medical history, management and performance of their horse. Serum creatine kinase activity ( CK) was measured before and 4 h after completion of exercise. Hair samples were analysed by PCR for the R309H mutation in the glycogen synthase gene ( GYS1) responsible for type 1 polysaccharide storage myopathy ( PSSM) and the C7360G mutation in the ryanodine receptor 1 ( RYR1) gene causing malignant hyperthermia ( MH). Results Samples were obtained from 68 Arabians, 20 half- Arabians and 13 horses of other breeds. Serum CK was above the resting reference interval (145-633 u/l) in 38 horses after racing (median 883 u/l, range 658-3739) but was compatible with values previously reported in apparently healthy endurance horses. Pathological ER was suspected to occur in 4 horses with serum CK activities exceeding 10,000 u/l 4 h after racing (median 84,825 u/l; range 10,846-381,790) including 3 Arabians and one half- Arabian horse. GYS1 and RYR1 mutations were not present in hair samples from any horses. Conclusions Exertional rhabdomyolysis occurred at a prevalence of 4.0% in a sample of horses participating in 50 mile distance events and all affected horses were Arabian or half- Arabian. The cause of ER in the endurance horse population remains unknown; however, ER in competing Arabian endurance horses is unlikely to be due to type 1 PSSM or MH. [ABSTRACT FROM AUTHOR]

Reasons for performing study To investigate and further characterise posture and movement characteristics during forward and backward walking in horses with shivering and acquired, bilateral stringhalt. Objectives To characterise the movement of horses with shivering (also known as shivers) in comparison with control horses and horses with acquired bilateral stringhalt. Study design Qualitative video analysis of gait in horses. Methods Owners' and authors' videos of horses with shivering or stringhalt and control horses walking forwards and backwards and manually lifting their limbs were examined subjectively to characterise hyperflexion, hyperextension and postural abnormalities of the hindlimbs. The pattern and timing of vertical displacement of a hindlimb over one stride unit was evaluated among control, shivering and stringhalt cases. Results Gait patterns of shivering cases were characterised as follows: shivering-hyperextension (- HE, n = 13), in which horses subjectively showed hyperextension when backing and lifting the limb; shivering-hyperflexion (- HF, n = 27), in which horses showed hindlimb hyperflexion and abduction during backward walking; and shivering-forward hyperflexion (- FHF, n = 4), which resembled shivering- HF but included intermittent hyperflexion and abduction with forward walking. Horses with shivering- HF, shivering- FHF and stringhalt (n = 7) had a prolonged swing phase duration compared with control horses and horses with shivering- HE during backward walking. With the swing phase of forward walking, horses with stringhalt had a rapid ascent to adducted hyperflexion of the hindlimb, compared with a rapid descent of the hindlimb after abducted hyperflexion in horses with shivering- FHF. Conclusions Shivering affects backward walking, with either HE or HF of hindlimbs, and can gradually progress to involve intermittent abducted hyperflexion during forward walking. Shivering- HF and shivering- FHF can look remarkably similar to acquired bilateral stringhalt during backward walking; however, stringhalt can be distinguished from shivering- HF by hyperflexion during forward walking and from shivering- FHF by an acute onset of a more consistent, rapidly ascending, hyperflexed, adducted hindlimb gait at a walk. [ABSTRACT FROM AUTHOR]