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Unlike most cases of eosinophilic meningitis, this dog was a very young female and of a small breed, vital signs remained normal throughout, and there was an extremely rapid and stable resolution of most neurological signs when the COX-2 inhibitor was withdrawn and glucocorticosteroid treatment was instituted. We believe that our experience with a recent canine neurological case will be of interest to readers as it highlights the possibility that drugs may be a cause of the syndromes associated with aseptic meningitis and encephalitis in dogs, as in people. [Extracted from the article]

CASE HISTORY AND CLINICAL FINDINGS: On 9 January 2014 (Day 0) a mare from a stud farm in the Waikato region presented with urinary incontinence without pyrexia. Over the following 33 days 15 mares were clinically affected with neurological signs. All but one mare had a foal at foot. The most commonly observed clinical signs were hind limb paresis and ataxia. In some cases recumbency occurred very early in the course of disease and seven mares were subject to euthanasia for humane reasons. LABORATORY FINDINGS: Equid herpesvirus (EHV) type 1 was detected using PCR in various tissues collected post mortem from two mares with neurological signs. DNA sequencing data from the DNA polymerase gene of the virus showed a nucleotide transition at position 2254, a mutation encoding amino acid D752that is highly associated with the neuropathogenic genotype of EHV-1. In total 12/15 mares were confirmed positive for EHV-1 on PCR. Results from a virus neutralisation test and ELISA on paired serum samples, and PCR on whole blood and nasal swabs, indicated that of four paddocks in a high-risk area where a cluster of cases had occurred, 20/21 (95%) horses were likely to have been exposed or were confirmed infected with EHV-1. Subsequent to the outbreak two mares aborted, one at 9 months and one at 10 months of gestation. The cause of abortion was confirmed as EHV-1 with the same genotype as that involved in the outbreak. DIAGNOSIS: Equine herpesvirus myeloencephalopathy. CLINICAL RELEVANCE: The outbreak described shows the considerable impact that can occur in outbreaks of equine herpesvirus myeloencephalopathy in New Zealand. Early biosecurity controls not only reduced the effect on the farm but mitigated the potential for the virus to spread to other horse enterprises. [ABSTRACT FROM PUBLISHER]

AIM: To ascertain whether resistance was present inParascaris equorumto the macrocyclic lactone anthelmintic ivermectin, using faecal egg count reduction tests. METHODS: Thirty-nine foals aged between 11 and 28 weeks on three Thoroughbred stud farms (Farms A; n=20, B; n=5 and C; n=14) were treated with ivermectin (Day 0) and faecal egg counts (FEC) were monitored before and for 21 (Farms A and B) or 14 (Farm C) days after treatment. On Farms A and B, the foals were treated with a macrocyclic lactone/benzimidazole/praziquantel combination on Day 21 and FEC assessed on Day 35. The three farms were all in the Manawatu region in the southern half of New Zealand's North Island. RESULTS: Of the 39 foals, 15 were not sheddingP. equorumeggs on the day they were treated with ivermectin, but all 15 did so post-treatment. The FEC on Farms A and B showed no evidence of a reduction at any time between Day 7 and 21; egg output increased steadily over this period. Following combination treatment FEC were reduced by 94% on farm A and 100% on Farm B. On Farm C, there was a 69% reduction inP. equorumFEC on Day 14. Twelve of the 14 foals on Farm C were shedding strongylid eggs on Day 0 and on Day 14 FEC were reduced by 84%. CONCLUSIONS: Without comparison to untreated control animals, these results do not allow a reliable estimation of the exact level of efficacy of ivermectin againstP. equorum, but they nevertheless show that, within the farms studied, ivermectin no longer achieved a complete kill of egg-laying adults and that foals treated with this drug may continue to shed considerable numbers of eggs after treatment. The results also indicate that ivermectin had sub-optimal efficacy against strongylid nematodes on one of the farms. [ABSTRACT FROM PUBLISHER]

Familial episodic ataxia of lambs is a congenital transient autosomal dominant disorder of newborn lambs, with varying expressivity. Affected lambs show episodes of an asymmetric ataxic gait, base-wide extensor hypertonia of the thoracic limbs and flexor hypertonia of the pelvic limbs. The aim of the study was to determine the genetic variant causing familial episodic ataxia in lambs. Using whole genome sequencing of two half-sib affected lambs, their sire, and their two normal dams, a heterozygous C>T transition at OAR10:77593415 (Oar_v3.1) in exon 1 of the fibroblast growth factor 14 (FGF14) gene (c.46C>T) was identified. The c.46C>T transition resulted in a premature stop codon at position 16 of the 247 amino acid FGF14 protein (p.Q16*). PCR and Sanger sequencing was used to genotype an additional 20 clinically affected animals, demonstrating all lambs carried the c.46C>T variant but 1 clinically more severely affected inbred lamb was homozygous (TT). A further 11 unrelated normal ewes were positionally sequenced, none of which had the variant, while in 18 lambs of unknown status born over 2 years of breeding trials six lambs were found to have the c.46C>T variant, likely clinically unidentified heterozygotes due to the variable expressivity, while 12 did not. In conclusion, familial episodic ataxia of lambs is potentially associated with a c.46C>T variant in the FGF14 gene. Further research is required into the mechanism behind the apparent recovery of lambs.

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., (© 2014 EVJ Ltd.)

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., (© 2014 EVJ Ltd.)

Trauma is a common cause of death in neonatal New Zealand sea lion pups, and subadult male sea lions have been observed picking up and violently shaking some pups. In humans, axonal injury is a common result of traumatic brain injury, and can be due to direct trauma to axons or to ischaemic damage secondary to trauma. 'Shaken baby syndrome', which has been described in human infants, is characterised by retinal and intracranial subdural haemorrhages, and has been associated with axonal injury to the brain, spinal cord and optic nerve. This study identifies mechanisms of traumatic brain injury in New Zealand sea lion pups, including impact injuries and shaking-type injuries, and identifies gross lesions of head trauma in 22/36 sea lion pups found dead at a breeding site in the Auckland Islands. Despite the high frequency of such gross lesions, only three of the pups had died of traumatic brain injury. Observational studies confirmed that shaking of pups occurred, but none were shown to die as a direct result of these shaking events. Axonal injury was evaluated in all 36 pup brains using β-amyloid precursor protein immunohistochemistry. Immunoreactive axons were present in the brains of all pups examined including seven with vascular axonal injury and two with diffuse axonal injury, but the severity and pattern of injury was not reliably associated with death due to traumatic brain injury. No dead pups had the typical combination of gross lesions and immunohistochemical findings that would conform to descriptions of 'shaken baby syndrome'. Axonal injury was present in the optic nerves of most pups, irrespective of cause of death, but was associated with ischaemia rather than trauma., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Intestinal motility disorders are an important problem in horses and donkeys and this study was carried out in order to evaluate the enteric neurons in animals with and without intestinal disease. Surplus intestinal tissue samples were collected from 28 horses undergoing exploratory laparotomy for colic. In addition, surplus intestinal samples from 17 control horses were collected immediately following humane destruction for clinical conditions not relating to the intestinal tract. Similar samples were also collected during routine post-mortem examinations from 12 aged donkeys; six animals were humanely destroyed for conditions related to the intestinal tract, while the remaining six were humanely destroyed for other reasons including dental and orthopaedic diseases. Tissue samples were fixed in formalin and immunohistochemical labelling was performed targeting the enteric neurons using a polyclonal antibody specific for the neuronal marker PGP 9.5. The distribution and density of neuronal networks were assessed qualitatively and semiquantitatively. There was strong PGP 9.5 expression in both the horse and donkey samples and labelling was detected throughout the tissue sections. In both species, PGP 9.5-immunoreactive nerve fibres were detected in all layers of the intestinal tract, both in large and small intestinal samples. Networks of enteric neurons were present in the donkey with a similar distribution to that seen in the horse. There was no demonstrable difference in enteric neuronal density and distribution in the groups of animals with intestinal disease compared with those without, apart from two (out of 28) horses with intestinal disease that showed a marked reduction in PGP 9.5 immunoreactivity. Apart from these two animals, this total cohort analysis differs from some previously observed findings in horses with intestinal disease and may therefore reflect the different pathophysiological processes occurring in varying intestinal conditions resulting in colic both in the donkey and the horse., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Pasture-associated stringhalt is an acquired equine disease characterized by peripheral neuropathy and hyperflexion of the pelvic limbs. The disease occurs most commonly during periods of drought in horses grazing pastures heavily contaminated by Hypochaeris radicata. We hypothesized that stringhalt is caused by neurotoxins elaborated by H. radicata in response to the stress of drought conditions. Supernates were collected from H. radicata that were stressed (or not) by immersion in copper chloride solution, then extracted with ethyl acetate and dried. Dilutions of extracts from stressed (SE) and control, unstressed (UE) plants were incubated with myelinating spinal cord cultures (MSCC) established from fetal Swiss mice, and with spinal ganglion cultures (SGC) and dermal fibroblast cultures derived from neonatal mouse tissues. Cytotoxicity in culture monolayers was evaluated both morphologically by microscopy and by release of lactate dehydrogenase activity into culture supernates. Three different SGC preparations were exposed to a single H. radicata extract and single preparations of fibroblasts and MSCC were exposed to three different extracts. Repin, a plant-derived sesquiterpene lactone neurotoxin, was included as a positive control. Significant dose-dependent cytotoxicity was seen within 24 h in all three culture types when incubated with SE or repin. Complete morphologic destruction of culture monolayers was induced by the highest concentrations tested of SE (100 μg/mL) and repin (30 μg/mL). Cytotoxic effect of SE was significantly greater than that of UE for all three cell types and was not due to copper contamination of the extract. This study has identified a cytotoxic activity in leaf exudates of H. radicata that was upregulated by the model stressor, copper chloride., (Copyright © 2013. Published by Elsevier Ltd.)

Aim: To investigate the effects of lolitrem B intoxication on renal K(+) secretion in response to increased tubular flow rates., Methods: Results are derived from a repeated measure pilot study of seven horses fed non-perennial ryegrass feed for a week prior to exposing them to perennial ryegrass seed and hay that contained an average of 2 ppm lolitrem B. At the end of the control and treatment period frusemide (1 mg/kg I/V) was administered and serial fractional excretion of K(+)(FEK(+)) and fractional excretion of Na(+)(FENa(+)) calculated. Baseline concentration of aldosterone in plasma, serum K(+)concentration and feed K(+) concentration were also compared., Results: Key findings included a reduced change in FEK(+) from 0 to 15 minutes in response to frusemide administration (p=0.022, Wilcoxon signed-rank test) and a reduced baseline concentration of aldosterone in plasma (p=0.022, Wilcoxon signed-rank test) during the treatment period compared with the control., Conclusions: Results suggest that lolitrem B intoxication reduced flow-mediated K(+) secretion and interfered with aldosterone production or secretion. However, further investigation is required to validate these findings and to further elucidate the underlying pathophysiology., Clinical Relevance: Lolitrem B intoxication in horses may cause disruption to electrolyte handling in addition to neurological deficits.

Reasons for Performing Study: Perennial ryegrass staggers is purported to be a common neurological mycotoxicosis of horses but the case description lacks detail and evidence., Objective: To describe the clinical syndrome of lolitrem B intoxication in horses, limiting tests to those that are applicable to clinical practice, and to assess the potential value of enzyme-linked immunosorbent assay (ELISA) tests for lolitrem B in horse body fluids., Methods: Seven horses in 2 separate groups were fed perennial ryegrass seed and hay containing 2 ppm lolitrem B. Paired data were collected prior to and after 2 weeks exposure to lolitrem B, including video-documented neurological examination and clinical examination., Results: All horses developed a variable degree of tremor and ataxia when exposed to lolitrem B. Tremor depended on the level of activity and included a subtle, rapid tremor of the eyeball. Ataxia was exaggerated by blindfolding and primarily involved a truncal sway and irregular, but predictable, limb placements. No change was detected in urine lolitrem B levels and, although plasma lolitrem B increased during the treatment period, levels did not correlate with the severity of clinical signs displayed. Limb swelling, heel lesions and serous nasal discharge were also observed in horses most severely intoxicated., Conclusions: The clinical effects of lolitrem B intoxication in horses primarily involve action-related tremors and symmetrical vestibular ataxia. Ergovaline may have caused the limb swelling, heel lesions and serous nasal discharge. Plasma ELISA for lolitrem B may be of diagnostic use in the future., Potential Relevance: This study provides a clearer appreciation of the clinical signs and variability of perennial ryegrass intoxication in horses., (© 2011 EVJ Ltd.)

Reasons for Performing Study: The generation and maintenance of intestinal motility patterns involve the complex interactions of several components including the gastrointestinal pacemaker cells (interstitial cells of Cajal, ICC). Central to ICC function is the generation of rhythmic pacemaker currents, namely slow waves, which represent the rate limiting step for intestinal smooth muscle contractions. Currently, intracellular slow wave activity has not been demonstrated in the equine colon., Objectives: To characterise the in vitro myoelectrical activity of the equine pelvic flexure using intracellular recording techniques., Methods: Intestinal samples were collected immediately following euthanasia from 14 normal horses. One millimetre thick tissue sections were pinned and superfused with warmed, oxygenated Krebs solution. Intracellular recordings were made from smooth muscle cells close to the submucosal border of the circular muscle layer. The L-type Ca(2+) channel blocker nifedipine was added to the superfusion fluid in 9 experiments while the Na(+) channel blocker tetrodotoxin was added to the superfusion fluid in 4 experiments. The data were recorded and stored using an acquisition system and a software package used to analyse the recordings., Results: In 10 of the 14 horses, electrical events consistent with slow wave patterns were recorded from individual smooth muscle cells. Surprisingly, adding nifedipine to the superfusion fluid abolished all electrical activity. In contrast, tetrodotoxin had no apparent effect on the electrical activity., Conclusions: Assuming that the electrical events were slow waves, the blockade by nifedipine suggests significant and potentially important differences in the ionic mechanisms responsible for slow waves in the different regions of the equine intestinal tract, which deserve further evaluation., (© 2011 EVJ Ltd.)

Background: Episodic collapse in horses has equine welfare and human safety implications. There are, however, no published case series describing this syndrome., Objectives: To characterize the cause and outcomes for horses referred for investigation of episodic collapse., Animals: Twenty-five horses referred for investigation of single or multiple episodes of collapse., Methods: Retrospective study. Clinical records from the Dick Vet Equine Hospital, University of Edinburgh from November 1995 to July 2009 were searched using the following keywords: collapse, collapsing, fall, syncope. Collapse was defined as an incident in which the horse lost postural tone with or without progression to recumbency and with or without loss of consciousness. Long-term follow-up information was obtained by telephone conversation with the owner., Results: A final diagnosis was reached in 11 cases, namely cardiac arrhythmia (4), right-sided heart failure (1), hypoglycemia (2), generalized seizures (2), and sleep disorder (2). A presumptive diagnosis was reached in 8 cases, namely neurocardiogenic syncope (5), exercise-induced pulmonary hemorrhage (2), and generalized seizures (1). No diagnosis was reached in 6 cases despite comprehensive investigations. Three horses were euthanized at presentation. Treatment was attempted in 9 horses with 6 cases having successful outcome before discharge. Follow-up information was available for 14 of 19 horses discharged from the hospital. Only 1 of these horses was observed to collapse after discharge., Conclusions and Clinical Importance: Definitive diagnosis was more likely to be reached in cases with multiple episodes of collapse. Horses in which 1 episode of collapse occurred did not necessarily collapse again., (Copyright © 2010 by the American College of Veterinary Internal Medicine.)

Previous immunohistochemical studies targeting the receptor tyrosine kinase (c-Kit) have demonstrated an apparent reduction in the number of gastrointestinal pacemaker cells--the interstitial cells of Cajal (ICC)--in horses with intestinal motility disorders. This study compared the level of transcription of the c-kit gene encoding this receptor in horses with and without such motility disorders. Transcription levels of this gene were also compared to the density of ICC immunohistochemically positive for the c-Kit antigen. Intestinal samples were collected from 18 horses with intestinal disease and from 15 control animals. Following gene extraction and identification, real-time quantitative analysis of c-kit and a control gene, ACTB (β-actin), was carried out on all samples and the density of the c-Kit-positive ICC compared. There was a significant reduction in c-Kit immunoreactivity in the ICC of horses with large intestinal obstructive disorders relative to controls but no significant difference in the transcription of the c-kit gene between normal and affected animals. Further studies will be required to elucidate the mechanisms regulating c-Kit expression and to assess the pathophysiological significance of these findings., (Copyright © 2009 Elsevier Ltd. All rights reserved.)

Evaluation of horses for eye problems and for suspected impairment of visual acuity often requires a thorough neuroophthalmic examination to be conducted. Along with a full ophthalmic evaluation, the results of such an examination should indicate the likely site of any lesion(s) accounting for blindness, miosis, mydriasis, anisocoria, Horner's syndrome, strabismus, facial paralysis and facial spasm, nystagmus and other signs of vestibular disease, and cerebellar disorders, that may be present. Such a thorough examination with guidance for correct interpretation of findings is given here.

Intestinal tissue samples were collected during routine post-mortem examinations from 12 aged donkeys. Six animals were euthanised due to impaction of the pelvic flexure of the large colon, while the remaining six were euthanised for non-enteric reasons such as dental or orthopaedic disease. Immunohistochemical labelling was performed to demonstrate the gastrointestinal pacemaker cells, the interstitial cells of Cajal (ICC), with polyclonal c-Kit antibodies. The distribution and density of the cellular networks were assessed qualitatively and semi-quantitatively. ICC networks are present in the donkey, with distribution similar to that of the horse, and they remain strongly immunoreactive in the older animal. There was no difference in the density and distribution of ICC in animals with or without intestinal disease., (Copyright 2009 Elsevier Ltd. All rights reserved.)

Reasons for Performing Study: A glycogen synthase (GYS1) mutation has been described in horses with histopathological evidence of polysaccharide storage myopathy (PSSM) in the USA. It is unknown whether the same mutation is present in horses from the UK., Objectives: To determine whether the GYS1 mutation occurs in UK horses with histopathological evidence of PSSM and exertional rhabdomyolysis., Hypothesis: The R309H GYS1 mutation is present in a variety of UK horse breeds and that the mutation is commonly associated with exertional rhabdomyolysis., Methods: DNA was extracted from 47 muscle or blood samples from UK horses with histories of exertional rhabdomyolysis in which muscle biopsy diagnosis had been pursued. The proportions of GYS1 mutation positive cases were compared among histopathologically defined groups. In addition, breeds that carried the GYS1 mutation were identified from a total of 37 grade 2 (amylase-resistant) PSSM cases., Results: Of 47 horses with exertional rhabdomyolysis in which a muscle biopsy diagnosis was pursued, 10 (21%) carried the GYS1 mutation. The mutation was only found in horses with grade 2 PSSM (i.e. not in horses with normal, idiopathic myopathy or grade 1 PSSM biopsy samples). In total, the GYS1 mutation was found in 24/37 (65%) of grade 2 PSSM cases. A variety of breeds, including Quarter Horse, Appaloosa, Warmblood, Connemara-cross, Cob, Polo Pony and Thoroughbred cross carried the mutation., Conclusions: The GYS1 mutation is an important cause of exertional rhabdomyolysis of UK horse breeds but does not account for all forms of PSSM., Potential Relevance: Genotyping is recommended in cases of exertional rhabdomyolysis, prior to or in combination with, muscle biopsy. However a significant proportion of horses with histopathological evidence of PSSM and/or exertional rhabdomyolysis have different diseases.

Neurectomy of the deep branch of the right lateral plantar nerve was performed on a single healthy mature horse. Six weeks after surgery, the horse was subjected to euthanasia and both hind suspensory ligaments harvested. The cross sectional area of the muscular part of the proximal part of the suspensory ligament was measured and assessed for morphological abnormalities in a blinded fashion. There was a clear difference in cross sectional area of the muscular part between treated and control ligament and there was profound neurogenic atrophy of the muscular fibres in the treated ligament.

Reasons for Performing Study: Recurrent laryngeal neuropathy (RLN) is a common and debilitating peripheral nerve disease of horses, but it remains unclear if this disease is a mono- or polyneuropathy. An understanding of the distribution of the neuropathological lesions in RLN affected horses is fundamental to studying the aetiology of this very significant disease of tall horses., Objective: To determine whether RLN should be classified as a mono- or polyneuropathy., Methods: Multiple long peripheral nerves and their innervated muscles were examined systematically in 3 clinically affected RLN horses, Results: Severe lesions were evident in the left as well as right recurrent laryngeal nerves in all horses, both distally and, in one case, also proximally. No primary axonal lesions were evident in other nerves nor were changes found in their innervated muscles., Conclusions: RLN is not a polyneuropathy but should be classified as a bilateral mononeuropathy., Potential Relevance: Genetic and local factors specifically affecting the recurrent laryngeal nerves in RLN-affected horses should now be investigated further.

Objective: To evaluate the effect of intermittent oral administration of ponazuril on immunoconversion against Sarcocystis neurona in horses inoculated intragastrically with S neurona sporocysts., Animals: 20 healthy horses that were seronegative for S neurona-specific IgG., Procedures: 5 control horses were neither inoculated with sporocysts nor treated. Other horses (5 horses/group) each received 612,500 S neurona sporocysts via nasogastric tube (day 0) and were not treated or were administered ponazuril (20 mg/kg, PO) every 7 days (beginning on day 5) or every 14 days (beginning on day 12) for 12 weeks. Blood and CSF samples were collected on day - 1 and then every 14 days after challenge for western blot assessment of immunoconversion. Clinical signs of equine protozoal myeloencephalitis (EPM) were monitored, and tissues were examined histologically after euthanasia., Results: Sera from all challenged horses yielded positive western blot results within 56 days. Immunoconversion in CSF was detected in only 2 of 5 horses that were treated weekly; all other challenged horses immunoconverted within 84 days. Weekly administration of ponazuril significantly reduced the antibody response against the S neurona 17-kd antigen in CSF. Neurologic signs consistent with EPM did not develop in any group; likewise, histologic examination of CNS tissue did not reveal protozoa or consistent degenerative or inflammatory changes., Conclusions and Clinical Relevance: Administration of ponazuril every 7 days, but not every 14 days, significantly decreased intrathecal anti-S neurona antibody responses in horses inoculated with S neurona sporocysts. Protocols involving intermittent administration of ponazuril may have application in prevention of EPM.

Cervical vertebral malformation is one of the most common causes of ataxia in horses. The most important factor in the diagnosis of cervical vertebral malformation is the identification of cervical vertebral canal stenosis, but published data for minimum sagittal diameter ratios in adult horses are only available for C4-C7 intravertebral sites. Intra- and intervertebral sagittal diameter ratios at C2-C7 were evaluated in 26 ataxic horses, for which a complete clinical and neuropathological evaluation was undertaken. Eight of these horses were diagnosed with cervical vertebral malformation. In these horses the majority of compressive lesions were intervertebral. The mean sagittal diameter ratios of horses with cervical vertebral malformation were significantly smaller than those of horses without cervical vertebral malformation, and for an individual horse in our study, the site with the smallest intervertebral sagittal diameter ratio was always the site at which the spinal cord was compressed. Mean sagittal diameter ratio intravertebral site measurements of horses with cervical vertebral malformation were smaller than those of horses without cervical vertebral malformation; however, the site of compression could not be predicted from the data. For our dataset, horses with a sagittal diameter ratio of < or = 0.485 at any inter- or intravertebral site could be correctly classified as having cervical vertebral malformation, and sagittal diameter ratio measurements were an effective tool to identify at least one site of compression in an individual case.

Reasons for Performing Study: Equine ataxia is routinely evaluated subjectively by clinicians; however, objective measurements of the movement and coordination of ataxic horses have not been reported., Objectives: To document the movement pattern of ataxic horses and compare the results to the movement of neurologically sound horses with, and without, sedation., Methods: Seventeen ataxic horses were evaluated walking and trotting on a treadmill using a 3D high speed video system. From the horizontal movement of hoof markers the autocorrelation function (ACF) of the left forelimb and the cross correlation function (CCF) between the left forelimb and other 3 limbs (CCF foreleft/hindright [flhr], foreleft/ hindleft [flhl], foreleft/foreright [flfr]) was calculated. This resulted in a value of motion cycle consistency. The results were compared to data of 17 neurologically normal horses with, and without, sedation with detomidine. For statistical analysis the t test for independent samples was used., Results: Comparing normal (NO) and ataxic (AT) horses at the walk, highly significant differences for the ACF and for all the CCFs were documented. At the trot, ACF and CCFs flhr and flfr were significantly different in the NO and AT groups. Comparing sedated and ataxic horses, only the CCF flfr at walk and at trot were significantly different., Conclusion and Potential Relevance: Ataxia is best documented and examined at the walk. At trot pendulum effect may make coordination easier for horses. The results of this study serve as basic data for evaluating questionably ataxic horses.

Aim: To identify the interstitial cells of Cajal in the porcine ileum for the first time immunohistochemically and to examine the electrical properties of intestinal smooth muscle in the same region., Methods: In vitro intracellular microelectrode recordings were made from smooth muscle cells in cross-sectional preparations from abattoir-derived healthy porcine ileum. Immunohistochemical labelling of interstitial cells of Cajal was performed using an anti-Kit antibody., Results: Slow waves were recorded in the circular muscle layer of all ileal preparations. The mean resting membrane potential of smooth muscle cells was -61.0 +/- 1.3 mV. Slow waves had a mean amplitude of 8.5 +/- 0.5 mV, a frequency of 9.9 +/- 0.1 cycles per minute and a duration of 5.6 +/- 0.1 s. A waxing and waning pattern of slow wave activity was occasionally observed. In addition, higher frequency spiking activity associated with contractions was observed in some recordings. The L-type calcium channel blocker nifedipine abolished both the spiking activity and the contractions, but had no significant effect on slow wave characteristics. Current-injection manipulation of the resting membrane potential had no effect on slow wave amplitude, frequency or duration. Kit-immunoreactive interstitial cells of Cajal were identified in the ileal samples and were present in the region of the myenteric plexus and in the circular and longitudinal muscle layers., Conclusion: This study recorded slow waves in vitro and demonstrated immunohistochemically the presence of interstitial cells of Cajal in the normal porcine ileum. This study forms a basis for future physiological and pathophysiological comparative studies of intestinal motility.

Reasons for Performing Study: Equine motor neuron disease (EMND) was diagnosed in 3 horses maintained on lush, grass-based pasture. This contrasted with North American studies which identified limited or no access to green herbage as an important risk factor for EMND., Hypothesis: Grazing horses that have an apparently adequate intake of pasture herbage to meet normal equine vitamin E requirements can develop EMND., Methods: Owners of 32 European horses diagnosed with EMND completed a questionnaire regarding intrinsic, managemental, nutritional and environmental factors that could potentially be risk factors for EMND, and also regarding clinical signs, treatments and case outcome. Plasma/serum vitamin E data for these horses were supplied by the veterinarians. No control population was studied., Results: Thirteen of 32 horses (termed the 'grazing' group) had part- or full-time access to grass-based pasture at the onset of EMND (median duration at pasture 12 h/day, range 3-24 h). Five of these horses were at pasture for at least 235 h/day at the onset of EMND, 2 of which were at pasture for at least 23.5 h/day throughout the year. Despite grazing, all these horses had a low vitamin E status. The remaining 19 horses resembled those cases reported from North America, in that they had no or limited access to pasture., Conclusions and Potential Relevance: A diagnosis of EMND should not be discounted on the basis that a horse has access, even full-time, to lush grass-based pasture. Inadequate vitamin E intake was probably not the sole cause of either the EMND or the low vitamin E status in the grazing horses; the latter was probably the result of abnormal bioavailability or excessive utilisation of vitamin E.

Reasons for Performing Study: Radiography is a very important aspect of equine stifle imaging. The precise radiographic anatomy of the soft tissue structures of the equine stifle has not been described previously., Objective: To describe the anatomical relationship between sites of attachment of soft tissue structures of the equine stifle and their locations on standard radiographic views., Methods: The sites of bony attachments of the tendons, ligaments and fibrous portion of the joint capsules of equine stifles were determined by gross dissection. These sites of attachment were transposed onto one set of bones deprived of soft tissue and mapped using radiopaque markers. This specimen was then radiographed in the standard radiographic projections (lateromedial, caudocranial and caudal 60 degrees lateral-craniomedial oblique) to determine the position of the attachment sites on the radiographs., Results: Two radiographic maps were drawn per radiographic projection, one for the attachment sites of the ligaments and tendons and one for the attachment sites of the joint capsules., Conclusions and Potential Relevance: The radiographic maps of the precise position of the soft tissue attachments of the tendons, ligaments and joint capsules of the equine stifle should assist interpretation of equine stifle radiographs.

Four at-risk Highland ponies on the same premises all retained their fetal membranes in the same breeding season. The ponies were treated with a combination of oxytocin, infusion and distension of the allantochorionic sac with fluid, gentle traction in one case, and supportive therapy. The possible causes of the condition were investigated with clinicopathological tests and analyses of the herbage for its species composition and fungal contamination. No obvious possible causative abnormalities were identified apart from a low total serum calcium level in one case. No fescue grass was found and no pathogenic fungi were detected.

This paper describes the histopathological and immunohistochemical changes in the central, autonomic and enteric nervous systems in a well-documented case of equine dysautonomia (ED), after the animal had recovered without significant residual clinical signs. Evidence of neuronal degeneration, such as neuronal chromatolysis, glial scars or a decrease in density of neurons, was not observed in the midbrain, pons, medulla oblongata or spinal cord, including the nuclei of cranial nerves III, V, VII, X and XII. In addition, no evidence of muscle denervation or re-innervation, such as group atrophy of clusters of cells or grouping of cells of similar size in the triceps muscle, was observed. These findings support the hypothesis that the chromatolytic motor neurons may not progress to cell death in ED. The autonomic ganglia showed evidence of previous neuronal loss. In the myenteric and submucosal plexuses of the ileum there was significant loss of enteric neurons. However, in the ileum, a continuous network of interstitial cells of Cajal (ICC) was observed by means of immunohistochemical techniques. It is possible that recovery without significant residual clinical signs was associated with lack of damage to, or more likely recovery of, the ICC, which have a pacemaker function in the intestinal tract.

Reasons for Performing Study: The gastrointestinal pacemaker cells, the interstitial cells of Cajal (ICC), have been implicated in several human gastrointestinal dysmotility syndromes. Recently, the involvement of these cells in equine gastrointestinal diseases has been investigated in cases of equine grass sickness where a significant reduction in ICC density was observed., Objective: To investigate ICC density in equine obstructive gastrointestinal disorders using immunohistochemical labelling methods., Methods: Intestinal samples were analysed from 44 horses undergoing exploratory surgery for colic and from 11 control animals subjected to euthanasia for conditions not related to the gastrointestinal tract. Immunohistochemical labelling of ICC was carried out using an anti-c-Kit antibody. Two independent observers assessed ICC density using a semiquantitative grading system., Results: There was a significant reduction in ICC density in horses with large colon disorders compared to the controls (P<0.01). Horses with strangulating lesions of the small intestine showed no difference when compared to the controls., Conclusions: There was a reduction in ICC density in horses with large intestinal disorders., Potential Relevance: The reduction in ICC density may be associated with the clinical findings as well as recurrent colic episodes observed in a number of these cases. This immunohistochemical study provides a basis for future functional electrophysiological investigations to determine the precise effect of ICC reduction on equine intestinal motility.

Reasons for Performing Study: Disorders of the equine sphenopalatine sinus, including empyema and neoplasia, have been reported to cause damage to cranial nerves II and V. However, the clinical anatomy of these sinuses is not well described in horses., Objective: To examine the anatomy of the sphenopalatine sinuses in a range of equidae and, in particular, to examine the relationship of these sinuses to adjacent major nerves and vessels., Methods: The anatomy of the sphenoidal and palatine paranasal sinuses was examined in 16 equidae, primarily using transverse skull sections. Relevant structures were documented and photographed., Results: There was much variation between individual horses in sphenopalatine sinus anatomy. The sphenoidal sinuses were small in young horses and appeared to become larger and more complex with age. Variation was present in the extent that the sphenopalatine sinus extended into the basisphenoid bone. The septum dividing left and right sphenoidal sinuses was frequently not midline, but was intact in all cases. The sphenoidal and palatine sinuses communicated in most horses. In such cases, what could accurately be termed the (combined) sphenopalatine sinuses usually drained directly into the caudal maxillary sinuses. Additionally, in 5 out of 16 cases, some compartments of the sphenoidal sinus also drained into the ethmoidal sinus. The dorsal and lateral walls of the sphenoidal sinus were very thin and directly adjacent to cranial nerves II, III, IV, V and VI and major blood vessels., Conclusions: The equine sphenoidal and palatine sinuses are very variable in their anatomy, but are always in close proximity to multiple cranial nerves and major blood vessels., Potential Relevance: Many cranial nerves and blood vessels could be damaged with disorders involving the sphenopalatine sinus, potentially causing major and variable neurological syndromes, haemorrhage and extension of sepsis.

This study set out to determine the pattern of development and distribution of the interstitial cells of Cajal (ICC) in the intestinal tract of the equine fetus and neonate. Intestinal tissue samples from 12 naturally aborted equine fetuses and three euthanized neonates were collected and fixed in formalin prior to applying standard immunohistochemical labelling techniques targeting the c-Kit protein of the ICC. At 6 months of gestation, a network of ICC was present in the myenteric plexus region of both the small and the large intestine. ICC were also present within the circular muscle layer. In the large intestine, a proximal to distal gradient of distribution was evident, with few ICC observed in the more distal parts of the large intestine in the younger fetuses compared with the near-term animals. A transmural gradient of distribution was also evident within the large intestine, with the most luminal part of the muscularis externa being the last area to be colonized by ICC. This region did not appear fully developed until the early neonatal period. An increased density of ICC was noted throughout the large intestine in the regions of the taenial bands in all animals. This study is the first to describe ICC development and distribution in the equine fetus and neonate.

Fifteen English cocker spaniels with confirmed vitamin E deficiency were examined physically, ophthalmologically and neurologically. Eleven of them had clinical signs of neurological dysfunction which included ataxia, proprioceptive deficits, abnormal spinal reflexes and muscle weakness. In the two dogs examined histopathologically there was central neuronal fibre degeneration with prominent neuroaxonal dystrophy, particularly within the sensory relay nuclei of the brainstem, and one of the dogs had severe intestinal lipofuscinosis.

Reasons for Performing Study: The aetiopathogenesis of equine grass sickness (EGS) is unknown. The role of free radical-mediated neuronal damage has not previously been investigated in this condition., Objectives: To investigate the potential contribution of oxidative damage and antioxidant status to neurodegeneration in EGS., Methods: Systemic levels of surrogate biomarkers were determined in 10 horses with acute EGS and in 2 control populations; 10 healthy horses co-grazing with the 10 EGS horses at the onset of clinical disease, and 10 healthy mares grazing where EGS has not been reported., Results: EGS horses had alterations in levels of several antioxidants, consistent with oxidative stress, the acute phase response and/or the secondary metabolic complications of EGS. EGS horses had elevated plasma dihydroxyphenylalanine (DOPA) levels., Conclusions: The elevated DOPA levels probably reflected a generalised disturbance of catecholamine metabolism rather than increased DOPA production via free radical-mediated oxidation of tyrosine. However, there was no evidence of systemic macromolecular oxidative damage., Potential Clinical Relevance: Further work is required to determine whether macromolecular oxidative damage occurring at the neuronal level contributes to EGS.